curs cardiologie intervent 3 martie 2011-final

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INTERVENTIONAL INTERVENTIONAL CARDIOLOGY CARDIOLOGY Prof Univ Prof Univ Dr Ion C. Tintoiu Dr Ion C. Tintoiu 1

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Page 1: Curs Cardiologie Intervent 3 Martie 2011-Final

INTERVENTIONAL INTERVENTIONAL CARDIOLOGYCARDIOLOGY

Prof Univ Dr Ion C. Prof Univ Dr Ion C. Tintoiu Tintoiu

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IIII

INTERVENTIONAL CARDIOLOGYINTERVENTIONAL CARDIOLOGY

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Subclinical

TARGET ORGANS DAMAGESPresence ofMultiple

Coronary Plaques

VascularInflammation

Clinical

ATHEROTIC LESIONS “Iceberg”

ACS = acute coronary syndromes; UA = unstable angina; NSTEMI = nonST-segment elevation myocardial infarction; STEMI = ST-segment elevation myocardial infarction.

Adapted from Bhatt DL. J Invasive Cardiol. 2003;15(suppl B):3B-9B.

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5 Dr.Sarma@works

WHERE IS INTERVENTIONAL CARDIOLOGY?

HEARHEAR

SURGEONSURGEONCARDIOLOGISTCARDIOLOGIST

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CONTEINS Procedures for Interv.

Cardiol. (Coronarography,IVUS ,OCT)

Coronary heart disease Carotid artery Renal artery Congenital heart disease Valvular pathology Peripherical artery disease Aorta pathology Cardiac pacing

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CONTEINS

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Coronarography IVUS,OCT What’s behind ???

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What is Interventional What is Interventional CardiologyCardiology

Interventional Interventional cardiology cardiology is the non-surgical is the non-surgical treatment using radiologic imaging, with treatment using radiologic imaging, with contrast, to guide instruments (catheters, contrast, to guide instruments (catheters, balloons, etc) through the body’s blood balloons, etc) through the body’s blood vessels and other organs. This type of vessels and other organs. This type of procedure is done for both diagnostic and procedure is done for both diagnostic and therapeutic procedures and is usually done therapeutic procedures and is usually done on an outpatient basis.on an outpatient basis.

Some common types of procedures done in Some common types of procedures done in interventional interventional cardiology cardiology include: include:

1.1. AngiographyAngiography2.2. AngioplastyAngioplasty3.3. AtherectomyAtherectomy4.4. Stent insertionStent insertion5.5. Hemodinamic evaluation(catetherism)Hemodinamic evaluation(catetherism)6.6. BiopsiesBiopsies7.7. Occlusionand and opening proceduresOcclusionand and opening procedures8.8. treatmenttreatment

INTERVENTIONALCARDIOLOGYINTERVENTIONALCARDIOLOGY

Ion
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Objectives and GoalsObjectives and Goals

Basic understanding of Basic understanding of interventional interventional cardiologycardiology

Gain knowledge of key terms and Gain knowledge of key terms and phrasesphrases

Practice – participate in case Practice – participate in case examples and exercisesexamples and exercises

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INTERVENTIONAL CARDIOLOGY

CORONARY

REGIONAL

CAROTID,RENAL

VALVULAR,Pace makerCONGENITAL HEART DISEASE

A0RTAPUL. ART

INCENTIVES & REWARDSCLINICIANSINDICATION

DIAGNOSTIC

TREATMENT

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The Cardiovascular System: The Cardiovascular System: The HeartThe Heart

Heart pumps Heart pumps over 1 million over 1 million gallons per gallons per yearyear

Over 60,000 Over 60,000 miles of blood miles of blood vesselsvessels

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jugular veins

superior vena cava

pulmonary veins

hepatic portal vein

renal vein

inferior vena cava

iliac veins

femoral vein

carotid arteries

ascending aorta

pulmonary arteries

coronary arteries

renal artery

brachial artery

abdominal aorta

iliac arteries

femoral artery

Major VesselsMajor Vessels

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The result is a heart that functions more like a The result is a heart that functions more like a reptilian heart, in which approximately half of the reptilian heart, in which approximately half of the myocardial blood supply comes from sinusoidal myocardial blood supply comes from sinusoidal perfusion by the left ventricular cavity.perfusion by the left ventricular cavity.

CORONARY HEART DISEASECORONARY HEART DISEASE

ANATOMY AND PATHOGENESIS ANATOMY AND PATHOGENESIS

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Time for CoronarographyTime for Coronarography

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Coronary CirculationCoronary Circulation

Coronary circulation is blood supply to Coronary circulation is blood supply to the heartthe heart

Heart as a very active muscle needs lots Heart as a very active muscle needs lots of Oof O22

When the heart relaxes high pressure of When the heart relaxes high pressure of blood in aorta pushes blood into coronary blood in aorta pushes blood into coronary vessels vessels

Many anastomosesMany anastomoses connections between arteries supplying blood connections between arteries supplying blood

to the same region, provide alternate routes to the same region, provide alternate routes if one artery becomes occludedif one artery becomes occluded

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INTERVENTIONAL CARDIOLOGY IN

ISCHEMIC HEART DISEASE

CORONAROGRAPHY INTRAVASCULAR ULTRASOUND

(IVUS) OPTICAL COHERENCE

TOMOGTRAPHY (OCT) CORONARY ANGIOSCOPY

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CORONAROGRAPHY

PROCEDURES LESION DIAGNOSTIC TREATMENT (Percutaneous

coronary intervention-PCI) COMPLICATION –In Stent

Restenosis

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Coronary ArteriesCoronary Arteries

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Posterior View

Posterior ViewPosterior View

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Semilunar Valves and Semilunar Valves and Coronary Coronary

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Coronary artery Coronary artery circulationcirculation

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Coronary VeinsCoronary Veins

Collects wastes from cardiac muscleCollects wastes from cardiac muscle Drains into a large sinus on posterior surface Drains into a large sinus on posterior surface

of heart called the coronary sinusof heart called the coronary sinus Coronary sinus empties into right atriumCoronary sinus empties into right atrium

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Coronary Artery DiseaseCoronary Artery Disease Pathological Pathological

anatomyanatomy

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CORONAROGRAPHY

TECHNICAL PROCEDURE

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CORONAROGRAPHY Unic lesion Secvential lesion COMPLEX LESIONS bi-coronarian tri-coronarian ostial lesion bifurcation lesions trifurcation lesions total oclusion left main (protected or

unprotected)

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SELDINGERS SELDINGERS TEKNIKKTEKNIKK

SVEN-IVAR SELDINGERSVEN-IVAR SELDINGER (1921-1999), radiologist, (1921-1999), radiologist, was was born in Moraborn in Mora, , Sweden.Sweden. Graduating in medicine from the Graduating in medicine from the Karolinska Institute in 1948, he began his training in radiology Karolinska Institute in 1948, he began his training in radiology in 1950. in 1950. In 1953, Dr. Seldinger published the description of a In 1953, Dr. Seldinger published the description of a percutaneous entry technique in the journal, percutaneous entry technique in the journal, Acta Radiologica.Acta Radiologica. The equipment required to perform the basic technique The equipment required to perform the basic technique includes only includes only (1) a thinwall introducer needle, (2) a wire guide (1) a thinwall introducer needle, (2) a wire guide and (3) a plastic preformed catheter. Through a simple and (3) a plastic preformed catheter. Through a simple puncture, access is gained to any part of the body via the puncture, access is gained to any part of the body via the cardiovascular system, using a series of x-ray films as a guide. cardiovascular system, using a series of x-ray films as a guide.

Dr. Seldinger pioneered in applying his technique to the Dr. Seldinger pioneered in applying his technique to the localization of tumors by arteriography, selective renal localization of tumors by arteriography, selective renal angiography, percutaneous transhepatic cholangiography, and angiography, percutaneous transhepatic cholangiography, and portal venography. portal venography.

The simplicity of the Seldinger technique which The simplicity of the Seldinger technique which continues to revolutionize cardiology and radiology has continues to revolutionize cardiology and radiology has provided the catalyst for innovative application in the areas of provided the catalyst for innovative application in the areas of interventional radiology, urology, anesthesiology and critical interventional radiology, urology, anesthesiology and critical care medicine.care medicine.

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Seldingers teknikkSeldingers teknikk

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Copyright © 2008 by the American Roentgen Ray Society

Sun, J. et al. Am. J. Roentgenol. 2008;190:748-754

--

Left coronary arteryLeft coronary artery

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RCA RCARCARCA--

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QUANTITATIVE CORONAROGRAPHYQUANTITATIVE CORONAROGRAPHY

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RCA UNICORONARIAN LESIONRCA UNICORONARIAN LESION--

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OstiumOstium

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CORONAROGRAPHY

CONCLUSION: -comon used in coronary heart

disease -parameters: -type of lesions -quantitative evaluation of

stenosis -treatment solutions -PCI procedures

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Time for IVUSTime for IVUS

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INTRAVASCULAR ULTRASOUND (IVUS)

-TECHNIC PROCEDURE -INDICATIONS-ADVANTACE -CLINICAL

IMPLICATION-TREATMENT

CORONARY LESIONS

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Principle of IVUS transducer pullback.

Schoenhagen P , Nissen S Heart 2002;88:91-96

©2002 by BMJ Publishing Group Ltd and British Cardiovascular Society

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Vulnerable Plaque Vulnerable Plaque and IVUS and IVUS

Greyscale ImagingGreyscale Imaging

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STEMI– THE VOLCANO

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70% of ACS 70% of ACS culprit culprit lesionslesions

30% of ACS 30% of ACS culprit lesionsculprit lesions

((Naghavi et al. Circulation 2003;108:1664-72)Naghavi et al. Circulation 2003;108:1664-72)

““Vulnerable Plaque” = thrombosis-Vulnerable Plaque” = thrombosis-proneprone plaque and plaque with a high plaque and plaque with a high

probability of undergoing rapidprobability of undergoing rapid

progressionprogression

≈ ≈ 5%5%

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Davies MJ. Circulation. 1996;94:2013-2020.

Fissures inthe fibrous cap

The Matrix Skeleton of Unstable

Coronary Artery Plaque

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Continuing Medical Implementation …...bridging

the care gap

ST Elevation MI ST Elevation MI (STEMI)(STEMI)

90% of acute MIs are caused by thrombus formation from rupture of unstable plaques

Ruptured Plaque

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Pathogenesis Plaque rupture or erosion Thrombosis with/without occlusion Necrosis contingent on

Severity of plaque rupture Duration of ischaemia Lability of occlusive thrombus Adequacy of collaterals Vasoconstriction Downstream platelet/fibrin emboli

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1mm1mm 4mm4mm00

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00 1.51.5 6.0mm6.0mm

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In panel A, the left anterior descending (LAD) artery appears normal on the angiogram, yet on IVUS there is a clear crescent of soft atheromatous plaque.

Schoenhagen P , Nissen S Heart 2002;88:91-96

©2002 by BMJ Publishing Group Ltd and British Cardiovascular Society

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3.1 mm3.1 mm

3.1 mm3.1 mm

Angiography Fails to Depict Coronary Arterial Remodeling

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IVUS versus AngiographyIVUS versus Angiography

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IVUS

CONCLUSIONS -local lesions -aterosclerotic plaque structure

and composition-virtual hystology -thrombus formation -precise evaluation in lesion -stent malposition,fracture -revascularisation (PCI)

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Time for OCTTime for OCT

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Commercially available intracoronary Fourier domain OCT system (Lightlab Imaging Inc, Westford, MA) A) OCT system consisting in a) console containing the light source, a computer and imaging display screen and b) the automated pullback device allowing for pullback speeds up to 20mm/sec B) OCT imaging catheter ( Dragonfly™, Lightlab Imaging Inc, Westford, MA, USA) C) magnification of the distal OCT catheter tip. The OCT imaging catheter is introduced into the coronary artery using a conventional guide wire in short monorail technique. The short monorail catheter segment is indicated by a) the radiopaque distal catheter tip marker and b) a more proximal radiopaque marker. C) The imaging core is located approx 15mm proximal to the distal tip marker and moderately radiopaque. During pullback, the imaging core is withdrawn within the transparent catheter sheath, while the OCT imaging catheter itself is stationary within the artery.

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Example of stable severe lesion located in the right coronary artery.

Prati F et al. Eur Heart J 2009;eurheartj.ehp433

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: [email protected]

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A) coronary angiogram of the right coronary artery and B-E) OCT image display (commercially available intracoronary Fourier domain OCT system; Lightlab Imaging Inc, Westford, MA, USA). B) online, 3Dimensional lumen reconstruction of the imaged artery segment, side branches as well as the guiding catheter can be easily recognized and used as landmarks C) automated display of the minimal lumen area and proximal and distal reference segments D) conventional, 2D longitudinal view E) conventional, cross sectional view of the minimal lumen area.

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Longitudinal OCT study in a patient treated with a self-expanding, non drug eluting stents in the right coronary artery at A) baseline. B) 3 days follow-up and at C) 6 months follow up. The columns represent corresconding cross sections at each time point. OCT is able to visualize the changes is the stent area and tissue coverage over time. Early, very thin tissue coverage of the stent struts can be recognized at 3 days, while at 6 monthsd there is moderate neointima hyperplasia showing marked optical inhomogeneity with black, signal-poor regions around the stent struts, SB side branch (OCT Lightlab Imaging Inc, Westford, MA, USA)

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A) Coronary angiogram showing focal in-stent restenosis in a veneous bypass graft. B) Online QCA reveals a diameter stenosis of 69% with a reference diameter of 2,97mm.C) OCT - longitudinal view of the imaged vessel segment D) Graphic representation of the lumen area as measure by OCT confirms focal lumen narrowing. The blue lines indicate the distal (left side) and the proximal(right side) end of stent. The dotted lines represent the location of the corresponding OCT cross sections a-d. OCT reveals two layers of stents in (a), (c) and (d) and various degrees of restenotic tissue formation. Interestingly, there is clearly atherosclerosis within the neointimal tissue visible (b, see FIGURE 9). The minimal lumen area (d) is 1.3mm2 , consists of two layers of stents and shows homogenous, high backscattering tissue with smooth lumen borders

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Optical coherence tomography shows the three layer appearance of normal vessel wall, with the muscular media being revealed as a low signal layer comprised between internal and

external lamina.

Prati F et al. Eur Heart J 2009;eurheartj.ehp433

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: [email protected]

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Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply.

Schinkel, A. F.L. et al. J Am Coll Cardiol Intv 2008;1:449-451

Intracoronary Imaging After Thrombus Aspiration

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Culprit lesion in the left circumflex in a patient with unstable angina.

Prati F et al. Eur Heart J 2009;eurheartj.ehp433

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: [email protected]

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Example of white and red thrombus.

Prati F et al. Eur Heart J 2009;eurheartj.ehp433

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: [email protected]

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IVUS

IVUS

IVUSIVUS

OCTOCTOCTOCTOCTOCT

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Time for Coronary AngioscopyTime for Coronary Angioscopy

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Schematic figure of a vulnerable plaque (B) in longitudinal and cross-sectional views and in comparison with a normal arterial segment (A).Plaque vulnerability features that have been

included in the criteria of the vulnerable plaque definition are indicated.

Alsheikh-Ali A A et al. Ann Intern Med doi:10.1059/0003-4819-153-6-201009210-00272

©2010 by American College of Physicians

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Copyright ©2009 American College of Cardiology Foundation. Restrictions may apply.

Awata, M. et al. J Am Coll Cardiol Intv 2009;2:453-458

Coronary Angiograms and Angioscopic Images 8 Months After the Tandem Implantation of SES and PES

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Thrombus in a restenotic lesion after PES implantation.

Takano M et al. Circ Cardiovasc Interv 2008;1:20-27

Copyright © American Heart Association

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Angioscopic images viewed from inside the stent (top) and from outside the stent (bottom) demonstrate partial occlusion at the distal end of the stent (arrow).

Orbach D B et al. Radiology 2006;238:309-320

©2005 by Radiological Society of North America

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Copyright © 2009 by the American Roentgen Ray Society

Nakanishi, T. et al. Am. J. Roentgenol. 2000;174:1345-1347

--64-year-old man with ischemic heart disease

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. Angioscopic images of NSC grade and thrombus.

Takano M et al. Circ Cardiovasc Interv 2008;1:20-27

Copyright © American Heart Association

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. Angiographic and angioscopic findings of 6-month follow-up in PES and SES.

Takano M et al. Circ Cardiovasc Interv 2008;1:20-27

Copyright © American Heart Association

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CORONAROGRAPHY

CORONAROGRAPHY

CORONAROGR

CORONAROGR

OCTOCT

CORONAROGRAPHYCORONAROGRAPHY

IVUSIVUS

ANGIOSCOPYANGIOSCOPY

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Time for Interventional TreatmentTime for Interventional Treatment

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CORONARY HEART DISEASE

INTERVENTIONAL TREATMENT: PTCA PCI (PTCA-STENT) ROTABLATION ATHERECTOMY BRACHYTERAPY LASER

REVASCULARISATION

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INTERVENTIONAL REVASCULARISATION PCIINTERVENTIONAL REVASCULARISATION PCI

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CORONARY LESIONCORONARY LESIONHardening of the arteries (atherosclerosis) is a disorder in which the arteries become narrowed because fat in the form of cholesterol is deposited in the wall after poisons damage the lining of the arteries, for example cigarette smoke .The fatty tissue then becomes calcified and hard and forms an elevation known as a plaque (atherosclerosis). As this plaque grows, it narrows the inside of the artery reducing blood flow .The result is that various parts of the body such as the heart, eyes, kidney, legs, gut, or the brain get less food and oxygen. The plaque may eventually and often suddenly completely block the artery, causing death of the tissue supplied by that artery, causing for example ,a heart attack, stroke or gangrene.

Hardening of the arteries (atherosclerosis) is a disorder in which the arteries become narrowed because fat in the form of cholesterol is deposited in the wall after poisons damage the lining of the arteries, for example cigarette smoke .The fatty tissue then becomes calcified and hard and forms an elevation known as a plaque (atherosclerosis). As this plaque grows, it narrows the inside of the artery reducing blood flow .The result is that various parts of the body such as the heart, eyes, kidney, legs, gut, or the brain get less food and oxygen. The plaque may eventually and often suddenly completely block the artery, causing death of the tissue supplied by that artery, causing for example ,a heart attack, stroke or gangrene.

(Hardening of the arteries)

Sometimes the wall of the arteryweakens instead of narrowing and enlarges under the blood pressure causing what is known as an aneurysm

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Balloon angioplasty

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Percutaneous Percutaneous Transluminal Coronary Transluminal Coronary

AngioplastyAngioplasty

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What is an intravascular stent?

A small tubular mesh usually made of either stainless steel or Nitinol. (Shape memory alloy)

Inserted into stenotic (blocked) arteries to keep the lumen patent. Normally during angioplasty.

Used at various sites including the coronary, renal, carotid and femoral arteries.

Non-arterial uses e.g. in bronchus, trachea, ureter, bile duct.

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Stent in Coronary Stent in Coronary ArteryArtery

Maintains patency of blood vesselMaintains patency of blood vessel

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Varied stent geometries

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PCI-RCAPCI-RCA

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Miscellaneous /Miscellaneous /AtherectomyAtherectomy

Atherocathcourtesy Guidant

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RotablatorRotablator

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LaserLaser

Some catheters have also been fitted with special lasers which can photo-dissolve the tissue obstructing the arteries.

Laser cathetercourtesy Spectranetics

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ACUTE ACUTE CORONARY CORONARY

SYNDROMES:SYNDROMES:

STEMI STEMI PROGRAMPROGRAM

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Coronary Heart Disease

(CHD) - STEMI

Coronary Heart Disease

(CHD) - STEMI

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STEMI –PCI :DES (PACLITAXEL)

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STEMI-CABG

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History of Device Development: Past, Present and Future

1

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

20022003

2004

20052006

16

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History of History of Interventional CardiologyInterventional Cardiology

1977

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Coronary Angioplasty (PTCA) Coronary Angioplasty (PTCA) Andreas GruntzigAndreas Gruntzig

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History of History of Interventional CardiologyInterventional Cardiology

1977

1984

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Directional Coronary Atherectomy Directional Coronary Atherectomy (DCA)(DCA)

John SimpsonJohn Simpson

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

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Rotational Atherectomy Rotational Atherectomy (PTCRA)(PTCRA)

David AuthDavid Auth

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

1989

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Directional Coronary Atherectomy Directional Coronary Atherectomy (DCA)(DCA)

John SimpsonJohn Simpson

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

1989

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Coronary StentingCoronary StentingJulio PalmazJulio Palmaz

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

1989

1997

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Drug Eluting Drug Eluting StentsStents

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

1999

2000

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Percutaneous Treatment of Percutaneous Treatment of Carotid Artery StenosisCarotid Artery Stenosis

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

1999

2000

2002

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Percutaneous Aortic Valve Percutaneous Aortic Valve TherapyTherapy

Alain CribierAlain Cribier

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Self-expandingNitinol

multi-level frame

Porcine pericardium Tissue Valve

Disposable Loading System

Delivery Catheter 18 French 12 Fr body

The CoreValve Revalving™ SystemThe CoreValve Revalving™ SystemSelf-Expanding Support FrameSelf-Expanding Support Frame

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THE END???

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Bye!!!!!dont forget interventio

nal cardiology

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THE END

Thank you Thank you

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Normal

FattyStreak

Fibrous

Plaque

Occlusive Atherosclerot

icPlaque

PlaqueRupture/Fissure &

Thrombosis

MI

Stroke

Critical Leg Ischemia

Clinically Silent

Coronary

Death

Increasing Age

Effort AnginaClaudication

Unstable

Angina

Courtesy of P Ganz.

Atherosclerosis A Progressive Process

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Dear GOD, let a miracle happen !

Please, save my Dad/Mom

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RESTENOZA INTRASTENT

Centrul Clinic de Urgenta de Boli Centrul Clinic de Urgenta de Boli Cardiovasculare al ArmateiCardiovasculare al Armatei

Clinica de Cardiologie InterventionalaClinica de Cardiologie InterventionalaClinica de Chirurgie CardiacaClinica de Chirurgie Cardiaca

I. Tintoiu, M. Iacob, Florina Pinte, V Goleanu, D.Nita ,S.Dumitrescu,Cr.Gabriel,V.Roates,V.Greere,Ioana Raduta,Kela Cjicoli,L.Gheorghe

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150

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RESTENOZA DEFINITIE

Proces complex inflamator de

reendotelizare, degenerativ care

conduce la diferite grade de ocluzie in

stent, graft venos sau arterial

PCI

RESTENOZA

CABG

Restenoza - fenomen comun pentru PCI si CABG – rezolvare reciproca dupa principiul “TOTUL SAU NIMIC” sau

supravietuire miocardica

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In-Stent Restenosis = Intimal In-Stent Restenosis = Intimal HyperplasiaHyperplasia

The Limitation of Stents

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b

Aspectul morfopatologic şi imaginea endoscopicǎ (b) a stentului restenozat(a)

a

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In-stent restenosis (ISR) = within the margins of the stent

Peri-stent restenosis (PSR) = 5 mm proximal or distal to the margins of the stent

In-segment restenosis = either within the margins of the stent OR 5mm proximal or distal to the stent

5 mm5 mm 5 mm5 mm

in-stentin-stentproximalproximal distaldistal

in-segmentin-segment

5 mm5 mm

SIRIUS –SIRIUS – Restenosis Definitions Restenosis Definitions

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Reprezentarea schematică şi integrată a cascadei restenozei

A=vasul aterosclerotic înainte de intervenţieB=imediat post PCI-denudarea endoteliului şi depozitarea de trombocite şi fibrinogenC şi D = infiltrarea de leucocite şi proliferare de CMN urmate de migrarea celulară în zilele următoareE=îngroşarea intimei şi proliferarea CMN în acumularea de monociteF=modificări în compoziţia celulară (după 4 săptămâni-luni prin diminuare celulară şi bogăţia de matrice extracelulară (MEC)

(după Costa M.A.- Circulation 2005,111,2256)

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To DES or not to DES?

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TROMBOZA IN STENT (TS) IN ERA “DES”

Metaanaliza

Nr. pacienti

TS

8 trialuri 3817 p (DES)1995

(BMS)

15 p (0,4%)14 p (0,7%)

10 trialuri 5030 p(SES+PES

)

30 p (0,6%)

1trial 3974 p(SES+PES

)

38 p (1,27%)

36 p (92%) PCI 2 p (8%)

CABG

Solutii terapeutice• Stent bioabsorbabil• Clopidogrel 23 luni• PCI• CABG (dupa Kuchulakanti P.K. Circulation 2006, 113, 8, 1108-1114)

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“drug”eluting “just” bare metal

The DES euphoriaThe DES euphoria

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The Big 5 Myths of DES

1.1. Restenosis rates are always very low Restenosis rates are always very low

2.2. DES improves long term TLR and MACE DES improves long term TLR and MACE

3.3. No complicationsNo complications4.4. It is cost effectiveIt is cost effective5.5. If you will not use DES you will be suedIf you will not use DES you will be sued

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Early and Late Stent Early and Late Stent ThrombosisThrombosis

Stent Stent

Stent Stent

Problems in PCIProblems in PCI

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Total OcclusionTotal OcclusionTotal OcclusionTotal Occlusion

Exposed StrutsExposed StrutsExposed StrutsExposed Struts

44-year-old man was admitted with (AMI),31 months after a initial SES placement

Late Stent Thrombosis from LIA

Eur Heart J. 21 Oct 2005.

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Waiting…….

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Intravascular stents

A biased and limited account

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If a physician will not use DES, he might be suedIf a physician will not use DES, he might be sued

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Outline Background

Occlusive vascular disease and its treatment by PCI and stenting

Assessment of a novel compliance matching stent and comparison with a commercially available device In vivo radiographic measurement in pig

carotid and iliac arteries Development of a micro CT method for stented

vessel morphometry on excised arteries

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Cardiovascular Disease statistics

Heart and circulatory disease are the UK's biggest killers. 

In 2006, cardiovascular disease caused 40% of deaths in the UK, and killed over 245,000 people.

Coronary arterial disease causes over 120,000 deaths a year in the UK: approximately one in four deaths in men and one in six deaths in women.

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Revascularisation techniques

Coronary Artery Bypass Graft (CABG)

Percutaneous Coronary Intervention (PCI) Angioplasty Plus stenting (94%)

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Right VentricleRight Ventricle

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Left AtriumLeft Atrium

Forms most of the base of the heartForms most of the base of the heart Receives blood from lungs - 4 pulmonary veins (2 Receives blood from lungs - 4 pulmonary veins (2

right + 2 left)right + 2 left) Bicuspid valve: blood passes through into left Bicuspid valve: blood passes through into left

ventricleventricle has two cuspshas two cusps to remember names of this valve, try the pneumonic to remember names of this valve, try the pneumonic

LAMBLAMB Left Atrioventricular, Mitral, or Bicuspid valveLeft Atrioventricular, Mitral, or Bicuspid valve

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Left VentricleLeft Ventricle

Forms the apex of heart Forms the apex of heart Chordae tendineae anchor bicuspid valve to Chordae tendineae anchor bicuspid valve to

papillary muscles papillary muscles (also has trabeculae carneae like (also has trabeculae carneae like right ventricle)right ventricle)

Aortic semilunar valve: Aortic semilunar valve: blood passes through valve into the ascending aortablood passes through valve into the ascending aorta just above valve are the openings to the coronary just above valve are the openings to the coronary

arteriesarteries

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Myocardial Thickness and Myocardial Thickness and FunctionFunction

Thickness of myocardium varies according to the Thickness of myocardium varies according to the function of the chamberfunction of the chamber

Atria are thin walled, deliver blood to adjacent ventriclesAtria are thin walled, deliver blood to adjacent ventricles

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Thickness of Cardiac Thickness of Cardiac WallsWalls

Myocardium of left ventricle is much thicker than the right.

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A-V valves open and allow blood to flow A-V valves open and allow blood to flow from atria into ventricles when ventricular from atria into ventricles when ventricular pressure is lower than atrial pressurepressure is lower than atrial pressure occurs when ventricles are relaxed, chordae occurs when ventricles are relaxed, chordae

tendineae are slack and papillary muscles are tendineae are slack and papillary muscles are relaxedrelaxed

Atrioventricular Valves Atrioventricular Valves OpenOpen

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Atrioventricular Valves Atrioventricular Valves CloseClose

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Which side is anterior surface?

What are the ventricles doing?

Valve Function ReviewValve Function Review

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Blood CirculationBlood Circulation

Blood flowBlood flow

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Conduction System of Conduction System of HeartHeart

Coordinates contraction of heart muscle.

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Autorhythmic CellsAutorhythmic Cells Cells fire spontaneously, act as pacemaker Cells fire spontaneously, act as pacemaker

and form conduction system for the heartand form conduction system for the heart SA nodecluster of cells in wall of Rt. AtriaSA nodecluster of cells in wall of Rt. Atria

begins heart activity that spreads to both begins heart activity that spreads to both atriaatria

excitation spreads to AV nodeexcitation spreads to AV node AV nodeAV node

in atrial septum, transmits signal to bundle in atrial septum, transmits signal to bundle of Hisof His

AV bundle of His AV bundle of His the connection between atria and ventriclesthe connection between atria and ventricles divides into bundle branches & purkinje divides into bundle branches & purkinje

fibers, large diameter fibers that conduct fibers, large diameter fibers that conduct signals quicklysignals quickly

Conduction System of Conduction System of HeartHeart

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Developmental Anatomy of Developmental Anatomy of the Heartthe Heart

The heart develops The heart develops from mesoderm from mesoderm before the end of before the end of the third week of the third week of gestation.gestation.

The tubes develop The tubes develop into the four-into the four-chambered heart chambered heart and great vessels and great vessels of the heart.of the heart.

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Clinical ProblemsClinical Problems MI = myocardial infarctionMI = myocardial infarction

death of area of heart muscle from lack of Odeath of area of heart muscle from lack of O22

replaced with scar tissuereplaced with scar tissue results depend on size & location of damageresults depend on size & location of damage

Blood clotBlood clot use clot dissolving drugs streptokinase or t-use clot dissolving drugs streptokinase or t-

PA & heparinPA & heparin balloon angioplastyballoon angioplasty

Angina pectoris----heart pain from Angina pectoris----heart pain from ischemia of cardiac muscleischemia of cardiac muscle

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By-pass GraftBy-pass Graft

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AtherectomyAtherectomy http://www.nms.ac.jp/jnms/2000/067

05335e.pdf

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Interventional Cardiology Interventional Cardiology TermsTerms AngiographyAngiography – Pictures taken of a blood – Pictures taken of a blood

vesselvessel AntegradeAntegrade – with the flow – with the flow BifurcationBifurcation – a “splitting” or “forking” of – a “splitting” or “forking” of

vessels into two separate vesselsvessels into two separate vessels Aortic ArchAortic Arch – anomaly in the vessels coming – anomaly in the vessels coming

off the aortic arch where the left common off the aortic arch where the left common carotid actually comes off the right carotid actually comes off the right innominate artery instead of off the aortainnominate artery instead of off the aorta

CatheterCatheter – instrument used in most – instrument used in most percutaneous interventional radiology percutaneous interventional radiology proceduresprocedures

Contralateral Contralateral – opposite side– opposite side First orderFirst order – primary vascular branch – primary vascular branch

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Case Example RulesCase Example Rules

Unless otherwise specified, all Unless otherwise specified, all access is through the femoral access is through the femoral arteryartery

All findings are assumed reported All findings are assumed reported unless otherwise statedunless otherwise stated

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190190

Case Examples Case Examples (Abdominal Aorta & (Abdominal Aorta &

Visceral)Visceral)1.1. Catheter placement Catheter placement

in aorta for in aorta for abdominal abdominal aortogramaortogram

2.2. Catheter placement Catheter placement in aorta for bilateral in aorta for bilateral renal artery and renal artery and abdominal abdominal aortogramaortogram

3.3. Catheter placed in Catheter placed in aorta and bilateral aorta and bilateral renal arteries for renal arteries for angiogramsangiograms

4.4. Catheter placed in Catheter placed in aorta for abdominal aorta for abdominal aortogram. Catheter aortogram. Catheter then placed in the then placed in the celiac trunk, inferior celiac trunk, inferior mesenteric artery, mesenteric artery, and superior and superior mesenteric artery; mesenteric artery; contrast injected and contrast injected and images taken.images taken.

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Peripheral Arterial Disease - PAD

When hardening of the arteries with narrowing affects your legs it is called peripheral arterial disease or PAD. The symptoms it causes are often mistaken for something else and is often undiagnosed. If the underlying causes are not attended to (smoking, high blood pressure, high cholesterol and lack of exercise) it can progress and end with loss of the leg in 5-7% of cases. Symptoms are:• Pain on walking which goes away on resting and restarts when you walk again• The pain is worse if you walk faster or go up hills and comes on quicker• The distance you can walk gets shorter and shorter• Eventually you get pain in your foot even when you are resting and the foot looks red when it is hanging down• Pain in the foot when you are sleeping• Finally the toes go black and gangrene has occurred.

When hardening of the arteries with narrowing affects your legs it is called peripheral arterial disease or PAD. The symptoms it causes are often mistaken for something else and is often undiagnosed. If the underlying causes are not attended to (smoking, high blood pressure, high cholesterol and lack of exercise) it can progress and end with loss of the leg in 5-7% of cases. Symptoms are:• Pain on walking which goes away on resting and restarts when you walk again• The pain is worse if you walk faster or go up hills and comes on quicker• The distance you can walk gets shorter and shorter• Eventually you get pain in your foot even when you are resting and the foot looks red when it is hanging down• Pain in the foot when you are sleeping• Finally the toes go black and gangrene has occurred.

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Continuing Medical Implementation …...bridging

the care gap

What Is the Culprit Lesion?

What Is the Culprit Lesion?

• 58-year-old male with chronic stable angina

• Positive stress test with small reversible ischemic defect on nuclear scintigraphy

Medication prescribed, but six weeks later…3-day history of unstable angina, including30 minutes of rest pain

• Medically “cooled off” followed by angiography

Case provided by the McLaren Heart and Vascular Center, Flint, Michigan; used with permission.

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Continuing Medical Implementation …...bridging

the care gap

Atherosclerosis is a DiffuseAtherosclerosis is a Diffuse Process Process

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Continuing Medical Implementation …...bridging

the care gap

Unstable Angina: Platelet Unstable Angina: Platelet Plugging of the CapillariesPlugging of the Capillaries

From: Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death Davies MJ, Circulation 1986

“The results support the view that platelet aggregates in the myocardium represent an embolic phenomenon and are a potential cause of unstable angina. The association of myocardial necrosis with such emboli could precipitate sudden death from ventricular fibrillation.”

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Continuing Medical Implementation …...bridging

the care gap

Plaque Transition toPlaque Transition toAcute Coronary SyndromeAcute Coronary Syndrome

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Continuing Medical Implementation …...bridging

the care gap Extensive subendocardial myocardial infarction (yellow arrows)

Sub-endocardial MISub-endocardial MI

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Lower ExtremityLower Extremity5.5. Left femoral artery Left femoral artery

accessed, contrast accessed, contrast injected for lower injected for lower extremity extremity angiographyangiography

6.6. Left femoral artery Left femoral artery accessed, catheter accessed, catheter threaded up, over threaded up, over the abdominal aorta the abdominal aorta into the common into the common iliac artery, contrast iliac artery, contrast injected for injected for angiography of the angiography of the right lower right lower extremity.extremity.

7.7. Left femoral artery Left femoral artery accessed; catheter accessed; catheter threaded up into the threaded up into the aorta and placed at aorta and placed at the bifurcation the bifurcation contrast injected for contrast injected for bilateral lower bilateral lower extremity extremity angiographyangiography

8.8. Femoral artery Femoral artery accessed. Catheter accessed. Catheter placed in placed in contralateral contralateral common femoral common femoral artery for lower artery for lower extremity angio. extremity angio. Catheter then pulled Catheter then pulled back to ipsilateral back to ipsilateral common iliac and common iliac and contrast injected for contrast injected for lower extremity lower extremity angioangio

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Case Examples (Upper Case Examples (Upper Extremity)Extremity)

9.9. Catheter threaded Catheter threaded into the right into the right subclavian for subclavian for upper extremity upper extremity angiographyangiography

10.10. Catheter placed in Catheter placed in the right the right brachiocephalic brachiocephalic artery and the left artery and the left subclavian artery. subclavian artery. Upper extremity Upper extremity angiography angiography performedperformed

11.11. Access in the right Access in the right retrograde brachial retrograde brachial artery. Upper artery. Upper extremity angio extremity angio performed.performed.

12.12. Access in the right Access in the right brachial artery for brachial artery for upper extremity upper extremity angiography. angiography. Catheter then Catheter then threaded up, into, threaded up, into, and over the aortic and over the aortic arch and into the arch and into the left subclavian for left subclavian for upper extremity upper extremity angiography.angiography.

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Case Examples (Head & Case Examples (Head & Neck)Neck)13.13. Catheter placed in Catheter placed in

the aortic arch and the aortic arch and aortogram aortogram performed showing performed showing patent origins of the patent origins of the right right brachiocephalic, brachiocephalic, left common, and left common, and left subclavian left subclavian vessels. Slight vessels. Slight tortuosity seen in tortuosity seen in the arch itselfthe arch itself..

14.14. Catheter placed in Catheter placed in the aortic arch. the aortic arch. Contrast is injected Contrast is injected and angiography is and angiography is taken of the taken of the bilateral common bilateral common carotids and carotids and bilateral internal bilateral internal carotids.carotids.

15.15. Same as number 14 Same as number 14 with the addition of with the addition of the external carotid the external carotid arteriesarteries

CAROTID ARTERYCAROTID ARTERY

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Any Questions?Any Questions?

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Post CABG Post CABG coronary coronary

insufficiency: insufficiency: from from

prevention to prevention to interventionintervention

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Operative mortality 2-4% Operative mortality 2-4% Peri-operative myocardial infarction 2-4%Peri-operative myocardial infarction 2-4% Low cardiac output Low cardiac output Tachy-arrhythmias (AF in 40%}Tachy-arrhythmias (AF in 40%} Brady-arrhythmias Brady-arrhythmias ( in1-4% a permanent pacing is required)( in1-4% a permanent pacing is required) Bleeding(4-6% re-operation)Bleeding(4-6% re-operation) Neurological complications (2-4%)Neurological complications (2-4%) Infection (mediastinitis 1% with 14% mortality) (14% in Infection (mediastinitis 1% with 14% mortality) (14% in

DM with bil. IMAs)DM with bil. IMAs) Acute renal failure (30% defined as a 50% + in S. Acute renal failure (30% defined as a 50% + in S.

cereat.)cereat.) Pleural effusion (90%)Pleural effusion (90%) Phrenic nerve damage (1%) Phrenic nerve damage (1%) Intercostal nerve damageIntercostal nerve damage Aortic dissection Aortic dissection Thrombocytopenia (Limit post operative heparin)Thrombocytopenia (Limit post operative heparin) Early readmission Early readmission

COMPLICATIONS OF CORONARY COMPLICATIONS OF CORONARY ARTERY BYPASS GRAFT SURGERYARTERY BYPASS GRAFT SURGERY

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Post CABG coronary insufficiencyPost CABG coronary insufficiency Recurrent Ischemia (17% @ 1 year)Recurrent Ischemia (17% @ 1 year)

New disease in vessels not previously bypassed,Progressive disease in native vessels beyond the graft anastomosis,Disease in the bypass conduits themselves

• Vein graft failure: 8% at 1 year, 38% at 5 years and 75% at 10years. Campeau L, et al, 1984. Silent occlusion occurs in 28%, 32%, and 35% of SVG at 1-3, 4-6, and 7-11 years after CABG respectively

• Repeat Revascularsation: Repeat CABG or PTCA is required in 4% of patients at 5 years, 19% of patients 10 years,and31% of patients 12 years after initial CABG. Mark Freed, 1996

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Graft occlusionGraft occlusion

EarlyEarly

IntermediateIntermediate

LateLate

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Graft occlusion passes in one out Graft occlusion passes in one out of three phases:of three phases:

Early occlusionEarly occlusion:: Prior to discharge in 10%Prior to discharge in 10%

Small vessel (1.5 mm)Small vessel (1.5 mm)

Stenosis <70%Stenosis <70%

Technical factors, such as kinks from excessive Technical factors, such as kinks from excessive length of the graft or poor distal artery run offlength of the graft or poor distal artery run off

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Mechanisms of Post CABG Mechanisms of Post CABG ischemiaischemia

Thrombosis (Early)Thrombosis (Early)

Intimal hyperplasia (Intermediate)Intimal hyperplasia (Intermediate)

Atherosclerosis (Late)Atherosclerosis (Late)

Coronary steal after internal mammary graft Coronary steal after internal mammary graft insertion (IMA)insertion (IMA)

Subclavian stenosisSubclavian stenosis

Un-ligated IMA branchesUn-ligated IMA branches

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PREDISPOSING FACTORS FOR POST PREDISPOSING FACTORS FOR POST

CABG CORONARY INSUFFICIENCYCABG CORONARY INSUFFICIENCY

Native Vessel DiameterNative Vessel Diameter Grafted VesselGrafted Vessel Severity of Bypassed Proximal StenosisSeverity of Bypassed Proximal Stenosis Age of GraftAge of Graft Cigarette SmokingCigarette Smoking HyperlipidemiaHyperlipidemia HypertensionHypertension Diabetes MellitusDiabetes Mellitus Effect of GenderEffect of Gender

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MANAGEMENT OF POST CABG MANAGEMENT OF POST CABG

CORONARY INSUFFICIENCYCORONARY INSUFFICIENCY IMA anastomotic site: balloonIMA anastomotic site: balloon IMA elsewhere: stentIMA elsewhere: stent SVG: ????????SVG: ????????

PCI restenosis is 40-70%PCI restenosis is 40-70%

Redo CABG is riskyRedo CABG is risky

Try not to use themTry not to use them

---

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PCI in venous graftsPCI in venous grafts

Early is better than late Early is better than late (recent VG with focal lesion is (recent VG with focal lesion is favorable yet with high re-stenosis rate around 25% with stents)favorable yet with high re-stenosis rate around 25% with stents)

High thrombotic burdenHigh thrombotic burden Distal protection is an option Distal protection is an option (Percu-Surge Guard-(Percu-Surge Guard-

Wire)Wire)

Covered stentsCovered stents Atherectomy devicesAtherectomy devices Catheter thrombectomyCatheter thrombectomy Ultrasound thrombectomyUltrasound thrombectomy

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Trans-myocardial Trans-myocardial Revascularization (TMR)Revascularization (TMR)

Laser TMR attempts to treat coronary disease Laser TMR attempts to treat coronary disease through the heart's own microvasculature. through the heart's own microvasculature.

The concept emerged from what was determined The concept emerged from what was determined with time to be a nominal observation; human with time to be a nominal observation; human hearts were not nourished from sinusoidal hearts were not nourished from sinusoidal connections to the ventricular chamber as were connections to the ventricular chamber as were reptilian hearts. reptilian hearts. Wearns et al., 1933.Wearns et al., 1933.

The early clinical trials suggest that angina relief is The early clinical trials suggest that angina relief is

excellent, averaging two angina classes of excellent, averaging two angina classes of improvement. improvement. Horvath et al., 1997.Horvath et al., 1997.

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PAD – Your Risk Increases If You:

Are over the age of 50. Smoke or used to smoke.  Those who smoke or have a history of smoking have up to four times greater risk of P.A.D. Have diabetes.  One in every three people over the age of 50 with diabetes is likely to have P.A.D. Have high blood pressure.  Also called hypertension, high blood pressure raises the risk of developing plaque in the arteries. Have high blood cholesterol.  Excess cholesterol and fat in your blood contribute to the formation of plaque in the arteries, reducing or blocking blood flow to your heart, brain, or limbs. Have a personal history of vascular disease, heart attack, or stroke.  If you have heart disease, you have a one in three chance of also having P.A.D.

Are over the age of 50. Smoke or used to smoke.  Those who smoke or have a history of smoking have up to four times greater risk of P.A.D. Have diabetes.  One in every three people over the age of 50 with diabetes is likely to have P.A.D. Have high blood pressure.  Also called hypertension, high blood pressure raises the risk of developing plaque in the arteries. Have high blood cholesterol.  Excess cholesterol and fat in your blood contribute to the formation of plaque in the arteries, reducing or blocking blood flow to your heart, brain, or limbs. Have a personal history of vascular disease, heart attack, or stroke.  If you have heart disease, you have a one in three chance of also having P.A.D.

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Diagnosis of PAD

Your vascular surgeon will take a medical and family history, perform a physical exam, and conduct diagnostic tests.  

Medical and Family History

Your doctor will spend time reviewing you medical history, including the presence of diabetes, high blood pressure, high cholesterol , if you are a smoker or former smoker , have a personal and family history of cardiovascular disease, any symptoms that you may be experiencing in your legs while either sitting, standing, climbing, walking other physical activities, and your current medications and diet.

Physical ExamDuring the physical exam, your health care provider may check:Pulses in your legs and feet to determine if there is enough blood flowing to these areas, the color, temperature, and appearance of your legs and feet, and will check for signs of poor wound healing on the legs and feet.

Your vascular surgeon will take a medical and family history, perform a physical exam, and conduct diagnostic tests.  

Medical and Family History

Your doctor will spend time reviewing you medical history, including the presence of diabetes, high blood pressure, high cholesterol , if you are a smoker or former smoker , have a personal and family history of cardiovascular disease, any symptoms that you may be experiencing in your legs while either sitting, standing, climbing, walking other physical activities, and your current medications and diet.

Physical ExamDuring the physical exam, your health care provider may check:Pulses in your legs and feet to determine if there is enough blood flowing to these areas, the color, temperature, and appearance of your legs and feet, and will check for signs of poor wound healing on the legs and feet.

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Diagnostic Tests for PAD

A simple noninvasive test called an ankle-brachial index (ABI) test may per performed.   Painless and easy, the ABI compares the blood pressure readings in your ankles with the blood pressure readings in your arms.  An ABI can help determine whether you have PAD, but it cannot identify which arteries are narrowed or blocked.  Your health care provider may decide to do a Duplex scan to see whether a specific artery is open or blocked.  This test uses sound waves to measure the blood flow in the veins and arteries in your arms and legs.  Your health care provider may also perform blood tests to see if you have diabetes and check your cholesterol levels.  Other tests are also used to help diagnose P.A.D. 

A simple noninvasive test called an ankle-brachial index (ABI) test may per performed.   Painless and easy, the ABI compares the blood pressure readings in your ankles with the blood pressure readings in your arms.  An ABI can help determine whether you have PAD, but it cannot identify which arteries are narrowed or blocked.  Your health care provider may decide to do a Duplex scan to see whether a specific artery is open or blocked.  This test uses sound waves to measure the blood flow in the veins and arteries in your arms and legs.  Your health care provider may also perform blood tests to see if you have diabetes and check your cholesterol levels.  Other tests are also used to help diagnose P.A.D. 

A duplex scan of the leg arteries

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How is PAD Treated

The overall goals for treating PAD are to reduce any symptoms, improve quality of life and mobility, and prevent heart attack, stroke, and amputation.

There are three main approaches to treating PAD: making lifestyle changes; taking medication; and in some cases, having a special procedure or surgery.  

Your vascular surgeon will determine the best treatment options for you, based on your medical history and the severity of your condition.

The overall goals for treating PAD are to reduce any symptoms, improve quality of life and mobility, and prevent heart attack, stroke, and amputation.

There are three main approaches to treating PAD: making lifestyle changes; taking medication; and in some cases, having a special procedure or surgery.  

Your vascular surgeon will determine the best treatment options for you, based on your medical history and the severity of your condition.

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Medication for PAD

• Drugs to control cholesterol

• Drugs to control your blood pressure

• An anti platelet drug such as aspirin

• Very few if any drugs can actually improve the blood supply to your legs and are generally not worth taking

• Good control of your diabetes if you are a diabetic

• Drugs to control cholesterol

• Drugs to control your blood pressure

• An anti platelet drug such as aspirin

• Very few if any drugs can actually improve the blood supply to your legs and are generally not worth taking

• Good control of your diabetes if you are a diabetic

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Surgical treatment of PAD

Generally speaking if you cant walk too well because of pain your condition can be improved by the life style changes already mentioned or an sustained increase in your daily exercise .If this fails or your condition deteriorates to the point where you have pain at rest or at night in bed then you need treatment. Your vascular surgeon will advise you about the treatments available and which one suits you best. Some problems can be easily dealt with by stretching the narrowed artery with a balloon and inserting a stent but others will need something called a bypass operation where the blocked artery is bypassed with a piece of vein or plastic to reestablish blood flow. These techniques work well but there are risk and your vascular surgeon will discuss these with you.

Generally speaking if you cant walk too well because of pain your condition can be improved by the life style changes already mentioned or an sustained increase in your daily exercise .If this fails or your condition deteriorates to the point where you have pain at rest or at night in bed then you need treatment. Your vascular surgeon will advise you about the treatments available and which one suits you best. Some problems can be easily dealt with by stretching the narrowed artery with a balloon and inserting a stent but others will need something called a bypass operation where the blocked artery is bypassed with a piece of vein or plastic to reestablish blood flow. These techniques work well but there are risk and your vascular surgeon will discuss these with you.

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AneurysmsAneurysmsThis is a swelling of the artery caused by a weakening of the wall and most commonly affects the main artery in the body – the Aorta.This artery is “the motorway” of the arterial system and carries blood to all parts of the body. It most commonly becomes an aneurysm in the abdomen (stomach).The aneurysm gradually increases in size and if left untreated will suddenly burst and lead to internal bleeding ending in death. The aim of treatment is to prevent rupture and death.

This is a swelling of the artery caused by a weakening of the wall and most commonly affects the main artery in the body – the Aorta.This artery is “the motorway” of the arterial system and carries blood to all parts of the body. It most commonly becomes an aneurysm in the abdomen (stomach).The aneurysm gradually increases in size and if left untreated will suddenly burst and lead to internal bleeding ending in death. The aim of treatment is to prevent rupture and death.

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Abdominal Aortic Aneurysm (AAAAbdominal Aortic Aneurysm (AAA))

Pulsating sensation in the abdomen Pain in the abdomen or back -- severe, sudden and often constant. The pain may radiate to the groin, buttocks, or legs. Tenseness of the abdominal muscles Anxiety Nausea and vomiting Clammy skin Rapid heart rate Collapse Abdominal swelling

Pulsating sensation in the abdomen Pain in the abdomen or back -- severe, sudden and often constant. The pain may radiate to the groin, buttocks, or legs. Tenseness of the abdominal muscles Anxiety Nausea and vomiting Clammy skin Rapid heart rate Collapse Abdominal swelling

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Abdominal Aortic Aneurysm (AAA)

Diagnosis

First your vascular surgeon will examine your abdomen and the pulses in your legs .

Your vascular surgeon may order the following tests:

Abdominal ultrasound CT Scan of Abdomen Angiography of aorta

First your vascular surgeon will examine your abdomen and the pulses in your legs .

Your vascular surgeon may order the following tests:

Abdominal ultrasound CT Scan of Abdomen Angiography of aorta

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Treatment Options Abdominal Aortic Aneurysm (AAA)

If the aneurysm is small and there are no symptoms your vascular surgeon may recommend periodic evaluations This can include a yearly ultrasound, to see if the aneurysm is getting bigger.

Aneurysms that cause symptoms require surgery to prevent complications. Patients with aneurysms bigger than 5.5 cm in diameter and aneurysms that rapidly increase in size require surgery. Surgery can prevent further complications such as a ruptured and death from occuring.

Routine screening for people over 65 is now becoming available and will allow this otherwise often silent but potentially lethal condition to be diagnosed and treated

If the aneurysm is small and there are no symptoms your vascular surgeon may recommend periodic evaluations This can include a yearly ultrasound, to see if the aneurysm is getting bigger.

Aneurysms that cause symptoms require surgery to prevent complications. Patients with aneurysms bigger than 5.5 cm in diameter and aneurysms that rapidly increase in size require surgery. Surgery can prevent further complications such as a ruptured and death from occuring.

Routine screening for people over 65 is now becoming available and will allow this otherwise often silent but potentially lethal condition to be diagnosed and treated

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Abdominal Aortic Aneurysm (AAA)InterventionalTreatment

There are two surgical approaches to treatment. In a traditional (open) repair, a cut is made in the abdomen to access the aneurysm. The abnormal vessel is replaced with a graft made of synthetic material, such as Dacron.The other approach is called endovascular grafting (keyhole surgery). With this approach the graft is inserted into the aneurysm through a plastic tube called a catheter .The catheter is inserted via the groin using small incisions and the stent graft released to bridge the aneurysm. Not all patients with abdominal aortic aneurysms are suitable for this type of keyhole surgery.

There are two surgical approaches to treatment. In a traditional (open) repair, a cut is made in the abdomen to access the aneurysm. The abnormal vessel is replaced with a graft made of synthetic material, such as Dacron.The other approach is called endovascular grafting (keyhole surgery). With this approach the graft is inserted into the aneurysm through a plastic tube called a catheter .The catheter is inserted via the groin using small incisions and the stent graft released to bridge the aneurysm. Not all patients with abdominal aortic aneurysms are suitable for this type of keyhole surgery.

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In the hands of a trained vascular surgeon more than 95% of patients will survive open surgery and have an excellent outcome if the operation is done before the aneurysm ruptures. Once it does, only 60 % will survive hence the importance of early diagnosis and treatment in appropriate cases. Endovascular surgery (keyhole) is a relatively recent treatment and although it has a slightly lower mortality its long term outlook is as yet uncertain. Your vascular surgeon will be able to tell you the pros and cons of both treatments and advise which one is best for your particular case. Suffice to say tht both are very effective in saving your life.

In the hands of a trained vascular surgeon more than 95% of patients will survive open surgery and have an excellent outcome if the operation is done before the aneurysm ruptures. Once it does, only 60 % will survive hence the importance of early diagnosis and treatment in appropriate cases. Endovascular surgery (keyhole) is a relatively recent treatment and although it has a slightly lower mortality its long term outlook is as yet uncertain. Your vascular surgeon will be able to tell you the pros and cons of both treatments and advise which one is best for your particular case. Suffice to say tht both are very effective in saving your life.

Abdominal Aortic Aneurysm (AAA)outcome

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Abdominal Aortic Aneurysm (AAA)How can you avoid one

• Do not smoke as smoking is a potent cause of aneurysms• Watch your diet and remember that vegetables are good for you• Have your cholesterol checked and if it is high have it treated• Have your blood pressure measured and if it is high get treatment• Look into your family history and find out if any of your relatives died of this condition. If they did see a vascular surgeon and get a check up• If you are 65 and particularly if you are male,get a scan of your abdomen to check for an aneurysm.

• Do not smoke as smoking is a potent cause of aneurysms• Watch your diet and remember that vegetables are good for you• Have your cholesterol checked and if it is high have it treated• Have your blood pressure measured and if it is high get treatment• Look into your family history and find out if any of your relatives died of this condition. If they did see a vascular surgeon and get a check up• If you are 65 and particularly if you are male,get a scan of your abdomen to check for an aneurysm.

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StrokesStrokesThere are several causes of stroke but a common one is narrowing of the carotid artery caused by atherosclerosis. The carotid arteries come off the aorta in the chest and one runs up each side of the neck dividing into two branches just below the angle of the jaw. One branch supplies the face and the other passes directly to the brain (internal carotid artery) .The diseased area occurs in the internal carotid artery just after the branching. Blood clot forms on this narrow area (stenosis) and bits can come off and travel upstream to block off the small arteries which supply the brain or eye.

There are several causes of stroke but a common one is narrowing of the carotid artery caused by atherosclerosis. The carotid arteries come off the aorta in the chest and one runs up each side of the neck dividing into two branches just below the angle of the jaw. One branch supplies the face and the other passes directly to the brain (internal carotid artery) .The diseased area occurs in the internal carotid artery just after the branching. Blood clot forms on this narrow area (stenosis) and bits can come off and travel upstream to block off the small arteries which supply the brain or eye.

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Do not panic Seek advice from your physician immediately Stop smoking

Do not panic Seek advice from your physician immediately Stop smoking

What You Should Do If You Experience These Symptoms

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You should then be referred to a vascular surgeon by your Physician and be investigated

• Physical examination• Blood tests (cholesterol)• A Duplex scan ( to see your carotid arteries)• You will probably be put on a small dose of aspirin

The scan is non invasive and does not hurt. It is essential thatIt is done by a properly trained practitioner and will show the doctorIf you have a significant narrowing of your carotid artery which needs treatment

Duplex scan

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Strokes and Carotid ArteryStrokes and Carotid ArteryWhen these bits of clot pass into the brain, they are usually very small and cause a temporary stroke a so called mini stroke which recovers after a few minutes or hours. This is called a transient ischaemic attack.During these attacks the patient can lose the use of the arm or leg or both on the opposite side. If the left carotid artery is affected in a right handed person there may be a temporary loss of speech. If the clot goes into the eye it can cause a temporary loss of vision which is often likened to a blind being drawn down over the eye and then lifted again as the sight recovers.These attacks are called amaurosis fugax .Attacks of TIA or amaurosis fugax are a warning sign and you MUST contact your physician. If the narrowed artery blocks completely then a permanent stroke will usually occur.

When these bits of clot pass into the brain, they are usually very small and cause a temporary stroke a so called mini stroke which recovers after a few minutes or hours. This is called a transient ischaemic attack.During these attacks the patient can lose the use of the arm or leg or both on the opposite side. If the left carotid artery is affected in a right handed person there may be a temporary loss of speech. If the clot goes into the eye it can cause a temporary loss of vision which is often likened to a blind being drawn down over the eye and then lifted again as the sight recovers.These attacks are called amaurosis fugax .Attacks of TIA or amaurosis fugax are a warning sign and you MUST contact your physician. If the narrowed artery blocks completely then a permanent stroke will usually occur.

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Interventional Treatment for carotid stenosis

• lowering the cholesterol , controlling the blood pressure , giving antiplatelet drugs such as aspirin and stopping smoking are essential in all cases• A mild degree of stenosis (narrowing) needs nothing else• Severe stenosis needs an operation and this can be either carotid endarterectomy (open surgery) or the insertion of a stent

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Carotid Angioplasty & Stenting This is a new technique where the narrowed carotid artery is widened without direct surgery. A wire is passed by the vascular surgeon from the groin and into the narrowed artery in the neck using local anesthesia. A small balloon is then passed over this guide wire and the narrow area stretched. A metal stent is then passsed into the stretched area and expanded to keep it wide .There are dangers to this technique because the wire and balloon can dislodge bits of clot and they can go into the brain and cause a stroke. Trials have shown that the open operation (carotid endarterectomy) is safer than angioplasty which is reserved for patient who are not fit for surgery or in whom surgery is risky, for example in patients who have had neck irradiation. Your vascular surgeon will be able to advise which is the best option for you.

This is a new technique where the narrowed carotid artery is widened without direct surgery. A wire is passed by the vascular surgeon from the groin and into the narrowed artery in the neck using local anesthesia. A small balloon is then passed over this guide wire and the narrow area stretched. A metal stent is then passsed into the stretched area and expanded to keep it wide .There are dangers to this technique because the wire and balloon can dislodge bits of clot and they can go into the brain and cause a stroke. Trials have shown that the open operation (carotid endarterectomy) is safer than angioplasty which is reserved for patient who are not fit for surgery or in whom surgery is risky, for example in patients who have had neck irradiation. Your vascular surgeon will be able to advise which is the best option for you.

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CEA is a surgical procedure in which a vascular surgeon makes an incision in the neck using local or general anesthesia. The Carotid artery is opened and the narrowed part removed in an operation called an endarterectomy. This is a bit like peeling an orange, you keep the skin and throw the orange away.This restores the artery to its normal thin consistency and some surgeons widen it further by sewing on a patch .No procedure is completely safe and stroke or death can occur in about 5% of cases. Trials have shown that the vast majority of patients having this operation do very well and future strokes are avoided.It is vital after surgery that you do NOT start to smoke again and take appropriate drugs to control your cholesterol and blood pressure.

CEA is a surgical procedure in which a vascular surgeon makes an incision in the neck using local or general anesthesia. The Carotid artery is opened and the narrowed part removed in an operation called an endarterectomy. This is a bit like peeling an orange, you keep the skin and throw the orange away.This restores the artery to its normal thin consistency and some surgeons widen it further by sewing on a patch .No procedure is completely safe and stroke or death can occur in about 5% of cases. Trials have shown that the vast majority of patients having this operation do very well and future strokes are avoided.It is vital after surgery that you do NOT start to smoke again and take appropriate drugs to control your cholesterol and blood pressure.

Carotid Endarterectomy (CEA)

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Endovascular SurgeryEndovascular SurgeryDiagnostic Angios, Angioplasty & Stenting, Diagnostic Angios, Angioplasty & Stenting,

Endovascular AAA repairEndovascular AAA repair

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1.1. Diagnostic AngiogramDiagnostic Angiogram Diagnosis Diagnosis Surgical PlanningSurgical Planning

2.2. Angioplasty & StentAngioplasty & Stent Treatment of Symptomatic Treatment of Symptomatic

LesionsLesions

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Stenosis vs. OcclusionStenosis vs. Occlusion

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Puncture Site & Puncture Site & CompressionCompression

Retrograde vs. AntegradeRetrograde vs. Antegrade

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Carotid EndarterectomyCarotid Endarterectomy

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CEACEA

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Abdominal Abdominal Aortic Aortic AneurysAneurysmm

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Open AAA RepairOpen AAA Repair

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Endovascular AAA RepairEndovascular AAA Repairaka Endograftaka Endograft

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Prep has some Prep has some challengeschallenges

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Leg RevascularizationLeg Revascularizationaka Fem-Popaka Fem-Pop

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Fem-pop, Fem-Tib, ISSVG, Synthetic Fem-pop, Fem-Tib, ISSVG, Synthetic GraftsGrafts

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Reversed Saphenous Vein Reversed Saphenous Vein GraftGraft

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LE AngioLE Angio

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Vascular SurgeryVascular SurgeryOcclusiveOcclusivePeripheral Peripheral

Vascular DiseaseVascular Disease

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Occlusive Peripheral Occlusive Peripheral Vascular DiseaseVascular Disease

Peripheral vascular diseasePeripheral vascular disease Includes any disease affecting the Includes any disease affecting the

peripheral vascular systemperipheral vascular system Occlusive – essentially blocked Occlusive – essentially blocked

arteriesarteries

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OutlineOutline

Review of the circulationReview of the circulation Pathogenesis of blocked arteriesPathogenesis of blocked arteries Manifestations of blocked arteriesManifestations of blocked arteries Monitoring the circulationMonitoring the circulation Occlusive peripheral vascular Occlusive peripheral vascular

diseasedisease Acute IschemiaAcute Ischemia Chronic IschemiaChronic Ischemia

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Review Of CirculationReview Of Circulation

Cells need supply of nutrients and Cells need supply of nutrients and removal of by productsremoval of by products

In a unicellular organism this may In a unicellular organism this may occur via the cell membrane into say occur via the cell membrane into say a pond or seaa pond or sea

Multicellular organisms need a Multicellular organisms need a circulatory systemcirculatory system

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Vascular SurgeryVascular SurgeryOcclusiveOcclusivePeripheral Peripheral

Vascular DiseaseVascular Disease

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Occlusive Peripheral Occlusive Peripheral Vascular DiseaseVascular Disease

Peripheral vascular diseasePeripheral vascular disease Includes any disease affecting the Includes any disease affecting the

peripheral vascular systemperipheral vascular system Occlusive – essentially blocked Occlusive – essentially blocked

arteriesarteries

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OutlineOutline

Review of the circulationReview of the circulation Pathogenesis of blocked arteriesPathogenesis of blocked arteries Manifestations of blocked arteriesManifestations of blocked arteries Monitoring the circulationMonitoring the circulation Occlusive peripheral vascular Occlusive peripheral vascular

diseasedisease Acute IschemiaAcute Ischemia Chronic IschemiaChronic Ischemia

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OPVD Anatomic OPVD Anatomic ClassificationClassification

Aorto-iliacAorto-iliac Le-RicheLe-Riche

Femero-Femero-poplitealpopliteal

Tibio-peronealTibio-peroneal

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William Harvey (1578-1657)

On the Motion of the Heart and Blood in Animals (1628)

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Problem With Blocked Problem With Blocked CirculationCirculation

Tissues lack adequate supply of nutrientsTissues lack adequate supply of nutrients Tissues suffer build of toxic by productsTissues suffer build of toxic by products

May cause symptoms and signs May cause symptoms and signs particularly when more blood flow is particularly when more blood flow is required;required; To muscles during exerciseTo muscles during exercise To tissues that are injured (more blood To tissues that are injured (more blood

needed)needed)

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Pathogenesis Of Blocked Pathogenesis Of Blocked ArteriesArteries

AtherosclerosisAtherosclerosis Genes, hyperlipidemiasGenes, hyperlipidemias LifestyleLifestyle

SmokingSmoking High fat dietHigh fat diet Lack of exerciseLack of exercise

Co-morbiditiesCo-morbidities Diabetes, hypertension, hypothyroidism, Diabetes, hypertension, hypothyroidism,

homocysteinehomocysteine

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Manifestations Of Blocked Manifestations Of Blocked ArteriesArteries

Depends on circulation affectedDepends on circulation affected HeartHeart

Stable angina, unstable angina, myocardial Stable angina, unstable angina, myocardial infarctioninfarction

BrainBrain Transient ischemic attact, strokeTransient ischemic attact, stroke

KidneyKidney Hypertension, renal failureHypertension, renal failure

LegsLegs Claudication, rest pain, necrosisClaudication, rest pain, necrosis

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Manifestations Of Blocked Manifestations Of Blocked ArteriesArteries

Depends on speed of development of Depends on speed of development of blockageblockage Slow blockageSlow blockage

Permits development of collateral blood Permits development of collateral blood supply so that occlusion may be supply so that occlusion may be asymptomaticasymptomatic

Rapid blockageRapid blockage No time for development of collateralsNo time for development of collaterals

Symptoms/ signs depend on adequacy of Symptoms/ signs depend on adequacy of preexisting collateralspreexisting collaterals

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Monitoring CirculationMonitoring Circulation

Mottling, colour, temperature, Mottling, colour, temperature, movements, sensationmovements, sensation

Palpable pulses, doppler signalsPalpable pulses, doppler signals

Non invasive pressure studies Non invasive pressure studies (Doppler)(Doppler)

Duplex imagingDuplex imaging Angiography (IAA, DSA, MRA)Angiography (IAA, DSA, MRA)

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Duplex of carotid Duplex of carotid stenosisstenosis

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AngiograpAngiographyhy

(DSA)(DSA)

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MRMRAA

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Occlusive Peripheral Vascular Occlusive Peripheral Vascular DiseaseDisease

Classification based upon clinical Classification based upon clinical presentationpresentation Acute ischemiaAcute ischemia Chronic ischemiaChronic ischemia

Anatomic classifcation based upon Anatomic classifcation based upon site(s) of diseasesite(s) of disease

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Acute IschemiaAcute Ischemia

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Effects Effects OOf f Acute Acute IIschemiaschemia

Reduced blood flowReduced blood flow Pulseless, pallor, perishing coldPulseless, pallor, perishing cold

Nerve ischemiaNerve ischemia Pain, paralysis, ParesthesiaPain, paralysis, Paresthesia

Muscle ischemiaMuscle ischemia RhabdomyolysisRhabdomyolysis

Compartment syndromeCompartment syndrome Ischemia reperfusion syndromeIschemia reperfusion syndrome

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Compartment SyndromeCompartment Syndrome

PathophysiologyPathophysiology DiagnosisDiagnosis ManagementManagement

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Compartment Compartment SyndromeSyndrome

PathophysiologyPathophysiology Strong fascia encases the limb to aid Strong fascia encases the limb to aid muscle function and return of venous muscle function and return of venous bloodblood

Injury results in swellingInjury results in swelling Swelling raises pressureSwelling raises pressure Pressure occludes lymphatic return, then Pressure occludes lymphatic return, then

venous return, then arterial inflowvenous return, then arterial inflow Result is dead or severly damaged tissues due Result is dead or severly damaged tissues due

to pressure and ischemiato pressure and ischemia

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Compartment SyndromeCompartment Syndrome DiDiagnosisagnosis

Strong index of suspicionStrong index of suspicion Nature of injury and duration of Nature of injury and duration of

ischemiaischemia Clinical manifestationsClinical manifestations

Nerve and muscle dysfunctionNerve and muscle dysfunction Decreased perfusionDecreased perfusion Tense compartmentTense compartment

May measure compartment pressure May measure compartment pressure as adjunct to treatment > 40 mm hgas adjunct to treatment > 40 mm hg

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Compartment SyndromeCompartment SyndromeManagementManagement

FasciotomyFasciotomy

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Acute IschemiaAcute Ischemia

CausesCauses ThrombosisThrombosis EmbolismEmbolism

The P’sThe P’s Thrombosis or embolism?Thrombosis or embolism? Clinical assessment of severityClinical assessment of severity Clinical algorithmClinical algorithm

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Causes of Acute IschemiaCauses of Acute Ischemia

TraumaTrauma ThrombosisThrombosis EmbolismEmbolism

Small printSmall print AneurysmAneurysm ThrombophiliaThrombophilia Paradoxial embolismParadoxial embolism Anatomic variationAnatomic variation Csytic adventitial diseaseCsytic adventitial disease

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ThrombosisThrombosisOcclusive Occlusive atherosclerosis atherosclerosis

AneurysmAneurysmMalignancyMalignancyThrombophiliaThrombophilia

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EmbolismEmbolism Macro-embolismMacro-embolism

arterial sidearterial side venous side (patent foramen ovale)venous side (patent foramen ovale)

Micro-embolismMicro-embolism ulcerated atherosclerotic plaquesulcerated atherosclerotic plaques aneurysmaneurysm

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The The PP ’s ’s No flow in arteryNo flow in artery

PPallorallor PPulse absentulse absent PPerishing colderishing cold

Nerve becomes ischemicNerve becomes ischemic PPainain PParesthesia / anesthesiaaresthesia / anesthesia PParalysisaralysis

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Thrombosis or Thrombosis or Embolism?Embolism?

Thrombosis EmbolismSex Male FemaleEmbolic source No YesOnset Progressive AcuteIschemia Milder SeverePHx Claudication NoneOther leg Abnormal Normal

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Clinical Assessment of Clinical Assessment of SeveritySeverity

ViableViable no immediate no immediate threatthreat

ThreatenedThreatened MarginallyMarginally ok if treated ok if treated

promptlypromptly

ImmediatelyImmediately ok if treated ok if treated immediatelyimmediately

IrreversibleIrreversible dead legdead leg

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Irreversible Irreversible IIschemiaschemia

Sensory lossSensory loss Profound,Profound, anaestheticanaesthetic

Muscle weaknessMuscle weakness ProfoundProfound, , paralysisparalysis

Arterial dopplerArterial doppler InaudibleInaudible Venous dopplerVenous doppler InaudibleInaudible

Amputation

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Viable no immediate Viable no immediate threatthreat

Sensory lossSensory loss NoneNone Muscle weaknessMuscle weakness NoneNone Arterial dopplerArterial doppler AudibleAudible Venous dopplerVenous doppler AudibleAudible

Restore perfusion

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Clinical Assessment of Clinical Assessment of SeveritySeverity

ViableViable No immediate threatNo immediate threat ThreatenedThreatened

marginallymarginally Ok if treated Ok if treated promptlypromptly

immediatelyimmediately Ok if treated Ok if treated immediatelyimmediately

IrreversibleIrreversible Dead legDead leg

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Threatened Threatened MarginallyMarginally

Sensory lossSensory loss Minimal (toes) Minimal (toes) to noneto none

Muscle weaknessMuscle weakness NoneNone Arterial dopplerArterial doppler InaudibleInaudible Venous dopplerVenous doppler AudibleAudible

Restore perfusion

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Threatened Threatened ImmediatelyImmediately

Sensory lossSensory loss More than More than toes, toes, PainPain

Muscle weaknessMuscle weakness Mild to Mild to moderatemoderate

Arterial dopplerArterial doppler InaudibleInaudible Venous dopplerVenous doppler AudibleAudible

Restore perfusion

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acute non traumatic ischemia

Irreversible Threatened Viable

Amputation

Clear embolus ?Thrombosis

Duplex

Embolectomy

Adequate Inadequate

Angiogram

Treat

Thrombolyse+/- PTA

Reconstruct

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PrognosisPrognosis EmbolismEmbolism

Overall 60% dead within three yearsOverall 60% dead within three years One episode 15-20% mortality (in One episode 15-20% mortality (in

hospital)hospital) Two episodes 40% mortality (in Two episodes 40% mortality (in

hospital)hospital) ThrombosisThrombosis

Overall 40% dead within three yearsOverall 40% dead within three years

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Chronic IschemiaChronic Ischemia

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LaFontaine ClassificationLaFontaine Classification

Stage 1Stage 1 claudicationclaudication

Stage 2Stage 2 rest painrest pain

Stage 3Stage 3 necrosis/ulcerationnecrosis/ulceration

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Prognosis in ClaudicantsPrognosis in Claudicants

About 15% will progress to requiring About 15% will progress to requiring revasculartion or amputationrevasculartion or amputation

Much higher risk of death from IHD Much higher risk of death from IHD and strokeand stroke

Rule out diabetes, hypertension and Rule out diabetes, hypertension and hypercholesterolemiahypercholesterolemia

Exercise, Smoking cessation, Aspirin Exercise, Smoking cessation, Aspirin and a Statin + control of risksand a Statin + control of risks

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Re-Vascularisation ?Re-Vascularisation ?

Risk factor control, aspirin, statinRisk factor control, aspirin, statin Pain controlPain control DressingDressing Sympathectomy (chemical, surgical)Sympathectomy (chemical, surgical) IloprostIloprost Angioplasty +/- Stent (? Drug elute)Angioplasty +/- Stent (? Drug elute) Surgical Surgical

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Surgical Re-Surgical Re-VascularisationVascularisation

Embolectomy and ThrombolysisEmbolectomy and Thrombolysis Patchplasty (synthetic/ autogenous)Patchplasty (synthetic/ autogenous) Endarterectomy Endarterectomy

(open/closed/eversion)(open/closed/eversion) Bypass with synthetic materialBypass with synthetic material Bypass with autogenous materialBypass with autogenous material

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Definition Of Critical Definition Of Critical IschemiaIschemia

Presence of tissue lossPresence of tissue lossOROR

Rest pain with ankle pressure less Rest pain with ankle pressure less than 50 mm Hgthan 50 mm Hg

FORFOR More than 2 weeksMore than 2 weeks

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Acute on ChronicAcute on Chronic

BypassBypass

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Digital Subtraction Digital Subtraction AngiogramAngiogram

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ChronicChronic

EndarterectomyEndarterectomy

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ChronicChronic

In situ distal bypassIn situ distal bypass

Fem to distal 1/3 posterior Fem to distal 1/3 posterior tibial with insitu long tibial with insitu long

saphenous veinsaphenous vein

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Carotid Vascular Carotid Vascular Disease:Disease:

Treatment Treatment options using options using surgery and surgery and

Interventional Interventional CardiologyCardiology

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Carotid Vascular DiseaseCarotid Vascular Disease

Stroke is 3Stroke is 3rdrd leading cause of death in leading cause of death in US (behind heart disease and cancer)US (behind heart disease and cancer)

Mortality from acute event is 20%Mortality from acute event is 20% 50% of patients are alive after 5 years50% of patients are alive after 5 years 4% of survivors require long-term 4% of survivors require long-term

skilled nursing careskilled nursing care 25% of survivors will have a second 25% of survivors will have a second

neurologic eventneurologic event

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Signs/symptoms of Signs/symptoms of carotid vascular diseasecarotid vascular disease

TIA (Transient Ischemic Attacks): focal TIA (Transient Ischemic Attacks): focal neurologic defects with resolution of neurologic defects with resolution of symptoms within 24 hourssymptoms within 24 hours

RIND (Reversible Ischemic Neurologic RIND (Reversible Ischemic Neurologic Deficit): transient neurologic defects lasting Deficit): transient neurologic defects lasting 24-72 hrs24-72 hrs

Amaurosis fugax: temporary blindness in Amaurosis fugax: temporary blindness in one eye, frequently described as “curtain one eye, frequently described as “curtain coming down” due to microemboli in retinacoming down” due to microemboli in retina

CVA (Cerebrovascular accident): neurologic CVA (Cerebrovascular accident): neurologic deficit with permanent brain damagedeficit with permanent brain damage

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Evaluating carotid Evaluating carotid diseasedisease

Duplex Doppler ultrasonographyDuplex Doppler ultrasonography Carotid Doppler ultrasonographyCarotid Doppler ultrasonography Magnetic resonance angiography Magnetic resonance angiography

(MRA)(MRA) Carotid angiography (gold standard)Carotid angiography (gold standard)

Sensitivity/specificity of noninvasive Sensitivity/specificity of noninvasive tests to predict stenoses >70% is 83-tests to predict stenoses >70% is 83-86%/89-94%86%/89-94%

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Duplex Doppler Duplex Doppler ultrasonographyultrasonography

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MRA of carotid stenosisMRA of carotid stenosis

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Carotid angiographyCarotid angiography

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Treatment optionsTreatment options Medical treatment (not as effective for Medical treatment (not as effective for

more advanced disease)more advanced disease) Carotid endarterectomy (CEA)Carotid endarterectomy (CEA) Nonsurgical carotid revascularization Nonsurgical carotid revascularization

using angioplasty and stentingusing angioplasty and stenting

Treatment recommended for:Treatment recommended for: Asymptomatic pts with >60% stenosisAsymptomatic pts with >60% stenosis Symptomatic pts with >50% stenosisSymptomatic pts with >50% stenosis

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Carotid endarterectomyCarotid endarterectomy

Performed through neck incision, usually Performed through neck incision, usually along sternocleidomastoid musclealong sternocleidomastoid muscle

Proximal and distal control of artery is Proximal and distal control of artery is obtainedobtained

While patient is heparinized, internal and While patient is heparinized, internal and external carotid arteries are clampedexternal carotid arteries are clamped

Longitudinal arteriotomy is performed, Longitudinal arteriotomy is performed, carotid plaque is removed, and vessel is carotid plaque is removed, and vessel is closed over a patchclosed over a patch

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Complications of carotid Complications of carotid endarterectomyendarterectomy

(perioperative mortality <0.5-3.0%, related (perioperative mortality <0.5-3.0%, related level of expertise of surgeons)level of expertise of surgeons)

Cardiac eventsCardiac events Postoperative Postoperative

strokestroke Hyperperfusion Hyperperfusion

syndromesyndrome Nerve injuryNerve injury

BleedingBleeding InfectionInfection ParotitisParotitis Re-stenosisRe-stenosis

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Postoperative cardiac Postoperative cardiac eventsevents

Appropriate cardiac work-up is Appropriate cardiac work-up is essentialessential

Because these patients have Because these patients have atherosclerotic disease in the carotids, atherosclerotic disease in the carotids, it must be assumed that they have it must be assumed that they have atherosclerotic disease elsewhereatherosclerotic disease elsewhere

Exercise stress testing, dobutamine Exercise stress testing, dobutamine echocardiography, dipyridamole echocardiography, dipyridamole imaging, or coronary catherization imaging, or coronary catherization should be usedshould be used

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Postoperative strokePostoperative stroke

Factors that contribute to Factors that contribute to postoperative stroke:postoperative stroke: Plaque emboliPlaque emboli Platelet aggregatesPlatelet aggregates Improper flushingImproper flushing Poor cerebral protectionPoor cerebral protection Relative hypotension Relative hypotension

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Hyperperfusion Hyperperfusion syndromesyndrome

Cerebral hyperperfusion is the Cerebral hyperperfusion is the leading cause of intracerebral leading cause of intracerebral hemorrhage and seizures during the hemorrhage and seizures during the first two weeks following CEAfirst two weeks following CEA

Causes changes in low-flow carotid Causes changes in low-flow carotid vascular bed vascular bed

Small vessels compensate by Small vessels compensate by dilating, then cannot re-constrict dilating, then cannot re-constrict properly and therefore cannot properly and therefore cannot protect vascular bedprotect vascular bed

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Nerve injuryNerve injury

Nerves at risk for injury during CEA Nerves at risk for injury during CEA include:include: Vagus nerveVagus nerve Recurrent laryngeal nerveRecurrent laryngeal nerve Facial nerveFacial nerve Glossopharyngeal nerveGlossopharyngeal nerve Hypoglossal nerveHypoglossal nerve Branches of trigeminal nerveBranches of trigeminal nerve

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Re-stenosisRe-stenosis

Re-stenosis following CEA occurs in 20% Re-stenosis following CEA occurs in 20% of patients overall, and 2.6-10% at 5 yearsof patients overall, and 2.6-10% at 5 years

Re-stenosis within 6 months is more Re-stenosis within 6 months is more common when smooth muscle cells are common when smooth muscle cells are abundant in lesion and is less common abundant in lesion and is less common when lesions are rich in lymphocytes and when lesions are rich in lymphocytes and macrophagesmacrophages

Late re-stenosis results from progression Late re-stenosis results from progression of atherosclerotic diseaseof atherosclerotic disease

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Carotid endarterectomyCarotid endarterectomy

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Predictors of mortality Predictors of mortality following CEAfollowing CEA

Increased ageIncreased age Male sex (relative risk 1.58)Male sex (relative risk 1.58) Diabetes (RR 1.48)Diabetes (RR 1.48) Systemic hypertension (RR 1.31)Systemic hypertension (RR 1.31) Smoking (RR 1.13)Smoking (RR 1.13)

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Predictors of recurrence Predictors of recurrence following CEAfollowing CEA

Elevated cholesterolElevated cholesterol Systemic hypertension (RR 1.42)Systemic hypertension (RR 1.42) Smoking (RR 1.47)Smoking (RR 1.47)

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Nonsurgical carotid Nonsurgical carotid revascularizationrevascularization

Percutaneous catheterization Percutaneous catheterization techniques have led to carotid techniques have led to carotid angioplasty and stent placementangioplasty and stent placement

Less invasive (performed with local Less invasive (performed with local anesthesia and sedation)anesthesia and sedation)

Less likely to precipitate cardiac Less likely to precipitate cardiac eventsevents

Technique can also be used to repair Technique can also be used to repair stenosis that is more cephaladstenosis that is more cephalad

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Technique used in Technique used in nonsurgical carotid nonsurgical carotid

repairrepair Catheter with umbrella tip is Catheter with umbrella tip is

inserted in stenotic carotid via inserted in stenotic carotid via femoral arteryfemoral artery

Balloon is inflated to dilate arteryBalloon is inflated to dilate artery Stent is placed in artery to maintain Stent is placed in artery to maintain

patencypatency Filters are used to capture embolic Filters are used to capture embolic

particlesparticles

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Examples of stents used Examples of stents used in carotid in carotid

revascularizationrevascularization

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Filters used in carotid Filters used in carotid repairrepair

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Pre- and post-stenting Pre- and post-stenting angiographyangiography

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Risks of nonsurgical Risks of nonsurgical vascular repairvascular repair

Plaques may be dislodged during Plaques may be dislodged during procedure leading to neurologic eventsprocedure leading to neurologic events

Re-stenosis is common in long term Re-stenosis is common in long term follow-up (15%) and may be difficult to follow-up (15%) and may be difficult to treat surgicallytreat surgically

Dissection has been shown to occur in 5% Dissection has been shown to occur in 5% of patients following stentingof patients following stenting

More studies comparing CEA to More studies comparing CEA to nonsurgical repair must be completednonsurgical repair must be completed

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Coarctation of AortaCoarctation of Aorta

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Coarctation of AortaCoarctation of Aorta

1. Definition1. Definition A congenital narrowing of upper descending thoracic aorta A congenital narrowing of upper descending thoracic aorta adjacent to the site of attachment of ductus arteriosusadjacent to the site of attachment of ductus arteriosus

2. History2. History Morgagni Morgagni : 1st description in 1760 : 1st description in 1760 BonnettBonnett : postductal & preductal type in 1903 : postductal & preductal type in 1903 CrafoordCrafoord : 1st coarctation repair in 1944 : 1st coarctation repair in 1944 Vorsschulte : prosthetic onlay graft or vertical incision Vorsschulte : prosthetic onlay graft or vertical incision and transverse closure in 1957and transverse closure in 1957 Waldhausen : subclavian patch aortoplasty in 1966Waldhausen : subclavian patch aortoplasty in 1966

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Coarctation of AortaCoarctation of Aorta

Developmental factorDevelopmental factor 1. Underdevelopment or hypoplasia of aortic1. Underdevelopment or hypoplasia of aortic arch or isthmusarch or isthmus

Definition of hypoplasiaDefinition of hypoplasia * Proximal arch : 60% of ascending aorta* Proximal arch : 60% of ascending aorta * Distal arch : 50% of ascending aorta * Distal arch : 50% of ascending aorta * Isthmus : 40% of ascending aorta * Isthmus : 40% of ascending aorta

2. Presence of ectopic ductal tissue in the aorta2. Presence of ectopic ductal tissue in the aorta

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Aortic Arch HypoplasiaAortic Arch Hypoplasia

DefinitionDefinition Hypoplastic arch has higher ratio of elastin lamellae to Hypoplastic arch has higher ratio of elastin lamellae to

vessel diameter & increase in collagen and decrease in vessel diameter & increase in collagen and decrease in

alpha-actin-positive cell that may hinder the ability of alpha-actin-positive cell that may hinder the ability of

arch to distendarch to distend..

1. 50% reduction of terminal end of ascending aorta, sometimes,1. 50% reduction of terminal end of ascending aorta, sometimes, because of small ascending aorta in coarctation, descending because of small ascending aorta in coarctation, descending thoracic aorta is compared.thoracic aorta is compared. 2. Transverse arch diameter less than body weight in Kg plus 12. Transverse arch diameter less than body weight in Kg plus 1 3. Z-value less than –2 or more3. Z-value less than –2 or more

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Coarctation of AortaCoarctation of Aorta MorphologyMorphology1. Localized stenosis1. Localized stenosis * More than 50% reduction in cross sectional area* More than 50% reduction in cross sectional area * Shelf, projection, infolding of aortic media into the* Shelf, projection, infolding of aortic media into the lumen opposite the ductus arteriosuslumen opposite the ductus arteriosus * Usually intimal hypertrophy ( intimal veil ) extends* Usually intimal hypertrophy ( intimal veil ) extends the shelf circumferentially and further narrows thethe shelf circumferentially and further narrows the lumen (Rodbard)lumen (Rodbard)

2. Tubular hypoplasia2. Tubular hypoplasia * Severe with lesser narrowing * Severe with lesser narrowing * Proximal aortic & arterial wall* Proximal aortic & arterial wall * Distal aortic arch narrowing* Distal aortic arch narrowing * Fetal flow pattern (Rudolph)* Fetal flow pattern (Rudolph)

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Coarctation of AortaCoarctation of Aorta

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Collaterals Collaterals in CoAin CoA

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Coarctation of AortaCoarctation of Aorta

PathophysiologyPathophysiology Narrowed aorta produces increased left Narrowed aorta produces increased left

ventricular afterload and wall stress, left ventricular afterload and wall stress, left ventricular hypertrophy, and congestive ventricular hypertrophy, and congestive heart failure.heart failure.

Systemic perfusion is dependent on the Systemic perfusion is dependent on the ductal flow and collateralization in severe ductal flow and collateralization in severe coarctation coarctation

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Coarctation of AortaCoarctation of Aorta Associated pathologyAssociated pathology 1. Collateral circulation1. Collateral circulation * Inflow : primary from branches of both subclavian arteries* Inflow : primary from branches of both subclavian arteries . internal mammary artery . vertebral artery. internal mammary artery . vertebral artery . costocervical trunk . thyrocervical trunk. costocervical trunk . thyrocervical trunk * Outflow : into descending aorta, two pairs of intercostal arteries* Outflow : into descending aorta, two pairs of intercostal arteries

2. Aneurysm formation of intercostal arteries2. Aneurysm formation of intercostal arteries * 3rd, & 4th rib notching * rare before 10 years of age* 3rd, & 4th rib notching * rare before 10 years of age

3. Coronary artery dilatation and tortuosity3. Coronary artery dilatation and tortuosity * due to LVH* due to LVH

4. Aortic valve4. Aortic valve * bicuspid (27-45%) * stenosis ( 6 - 7%)* bicuspid (27-45%) * stenosis ( 6 - 7%)

5. Intracranial aneurysm5. Intracranial aneurysm * berry type intracranial aneurysm in some patients* berry type intracranial aneurysm in some patients

6. Associated cardiac anomaly6. Associated cardiac anomaly * 85% of neonates presenting COA* 85% of neonates presenting COA

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CoA CoA LocalizedLocalized

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CoA CoA Tubular HypoplasiaTubular Hypoplasia

PDA

Distal arch

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Coarctation of AortaCoarctation of Aorta Natural historyNatural history 1. Incidence1. Incidence * 5-8% of CHD (5 per 10000 live births)* 5-8% of CHD (5 per 10000 live births) * Isolated CoA (82% of total CoA) ; male:female = 2:1* Isolated CoA (82% of total CoA) ; male:female = 2:1 CoA + VSD 11%, COA + other cardiac anomalies 7%CoA + VSD 11%, COA + other cardiac anomalies 7% * Complex CoA ; no sex difference* Complex CoA ; no sex difference 2. Survival of pure CoA2. Survival of pure CoA * 15% : CHF in neonate or infancy* 15% : CHF in neonate or infancy * 85% : survive late childhood without operation* 85% : survive late childhood without operation * 65% : survive 3rd decade of life (2% at 60 years) * 65% : survive 3rd decade of life (2% at 60 years) 3. Bacterial endocarditis 3. Bacterial endocarditis : common in 1: common in 1stst 5 decades 5 decades 4. Aortic rupture4. Aortic rupture : 2~3rd decade: 2~3rd decade 5. Intracranial lesion5. Intracranial lesion : subarachnoid hemorrhage(cong. Berry : subarachnoid hemorrhage(cong. Berry aneurysm)aneurysm)

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Coarctation of AortaCoarctation of Aorta Clinical features & diagnosisClinical features & diagnosis 1. Infancy1. Infancy 1) Closure of ductus (7-10 days) produces severe obstruction1) Closure of ductus (7-10 days) produces severe obstruction 2) Ductus arteriosus remains patent - differential cyanosis2) Ductus arteriosus remains patent - differential cyanosis 3) Associated intracardiac defect - more severe, early onset3) Associated intracardiac defect - more severe, early onset 4) Degree of collateral circulation 4) Degree of collateral circulation 2. Childhood2. Childhood * Asymptomatic without significant associated lesion* Asymptomatic without significant associated lesion * Hypertension (90%) * Cardiomegaly (33%)* Hypertension (90%) * Cardiomegaly (33%) * Rib notching (15%) * Rib notching (15%) 3. Adolescence and adult 3. Adolescence and adult * Hypertension ; very common * Valvar heart disease* Hypertension ; very common * Valvar heart disease * Heart failure at 30 years of age* Heart failure at 30 years of age 4. Associated syndrome4. Associated syndrome * Turner syndrome (XO) : 2% * Von Recklinghausen’s D * Turner syndrome (XO) : 2% * Von Recklinghausen’s D * Noonan’s syndrome or congenital rubella* Noonan’s syndrome or congenital rubella

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Coarctation of AortaCoarctation of Aorta

Indications for operationIndications for operation 1. Reduction of luminal diameter greater1. Reduction of luminal diameter greater than 50% at any agethan 50% at any age 2. Upper body hypertension over 150mmHg2. Upper body hypertension over 150mmHg in young infant ( not in heart failure )in young infant ( not in heart failure ) 3. CoA with congestive heart failure 3. CoA with congestive heart failure at any ageat any age

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Coarctation of AortaCoarctation of Aorta

Techniques of operationTechniques of operation 1. Subclavian flap aortoplasty1. Subclavian flap aortoplasty Neonate, infant and child up to 10 yearsNeonate, infant and child up to 10 years

2. End-to-end anastomosis2. End-to-end anastomosis Preferred in any age groupPreferred in any age group * Extended end-to-end anastomosis * Extended end-to-end anastomosis * Radically extended end-to-end anastomosis* Radically extended end-to-end anastomosis

3. Patch angioplasty or graft replacement3. Patch angioplasty or graft replacement

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Prevention of RecoarctationPrevention of Recoarctation

Ideal operative procedureIdeal operative procedure Successfully address transverse arch hypoplasia (if Successfully address transverse arch hypoplasia (if

present),present), Resection of all ductal tissue, andResection of all ductal tissue, and Prevention of residual circumferential scarring at the Prevention of residual circumferential scarring at the

aortic anastomotic sit.aortic anastomotic sit.

FactorsFactors Younger age at operationYounger age at operation Presence of aortic arch hypoplasia remain risk factors Presence of aortic arch hypoplasia remain risk factors

for recoarctation for recoarctation

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CoACoAExposureExposure

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CoA CoA Patch AugmentationPatch Augmentation

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CoA CoA Subclavian Artery FlapSubclavian Artery Flap

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CoA CoA End-to-End AnastomosisEnd-to-End Anastomosis

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CoA CoA Extended end-to-end AnastomosisExtended end-to-end Anastomosis

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Coactation of AortaCoactation of Aorta Resection and AnastomosisResection and Anastomosis

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Coactation of Aorta Coactation of Aorta Resection & Extended end-to-end AnastomosisResection & Extended end-to-end Anastomosis

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Coarctation of AortaCoarctation of Aorta End-to-Side AnastomosisEnd-to-Side Anastomosis

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Coarctation of Aorta Coarctation of Aorta Enlargement of VSD, Resection of Conal SeptumEnlargement of VSD, Resection of Conal Septum

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CoA + VSD, One-stage RepairCoA + VSD, One-stage Repair

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CoA + VSD, One-stage RepairCoA + VSD, One-stage Repair

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Coarctation of AortaCoarctation of Aorta End-to-Side AnastomosisEnd-to-Side Anastomosis

Opening of Resected Segment

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Coactation of AortaCoactation of Aorta

Operative resultsOperative results Hospital mortalityHospital mortality Causes of early death areCauses of early death are acute and chronic cardiac failure or severe acute and chronic cardiac failure or severe pulmonary insufficiencypulmonary insufficiency Incremental risk factor for deathIncremental risk factor for death 1) Older age1) Older age 2) Hypoplastic left heart class2) Hypoplastic left heart class 3) Techniques of operation3) Techniques of operation

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Coactation of AortaCoactation of Aorta Operative resultsOperative results MobidityMobidity 1) Paraplegia (0.2 ~ 1.5%)1) Paraplegia (0.2 ~ 1.5%) 2) Hypertension and abdominal pain2) Hypertension and abdominal pain 3) Persistent or recurrent coarctation3) Persistent or recurrent coarctation - more than 20mmHg - more than 20mmHg - high incidence in young - high incidence in young 4) Upper body hypertension without resting gradient4) Upper body hypertension without resting gradient - increased vascular activity in the forearm- increased vascular activity in the forearm - age at operation is risk factor - age at operation is risk factor 5) Late aneurysm formation5) Late aneurysm formation - higher in onlay patch technique- higher in onlay patch technique 6) Valvular disease6) Valvular disease 7) Congestive heart failure with hypertension7) Congestive heart failure with hypertension 8) Bacterial endocarditis 8) Bacterial endocarditis

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Coactation of AortaCoactation of Aorta

Special features of postoperative careSpecial features of postoperative care 1. Systemic arterial hypertension1. Systemic arterial hypertension Usually, but infant or young child doesn’t Usually, but infant or young child doesn’t need to be treated.need to be treated.

2. Abdominal pain2. Abdominal pain Usually mild abdominal discomfort for a few days,Usually mild abdominal discomfort for a few days, and prominent in 5 - 10%.and prominent in 5 - 10%. Control hypertension, nasogastric decompression, Control hypertension, nasogastric decompression, IV maintainIV maintain 3. Chylothorax 3. Chylothorax 5%5%

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Coactation of Aorta Coactation of Aorta RepairRepair

ParaplegiaParaplegia 1. Duration of spinal cord ischemia1. Duration of spinal cord ischemia 2. Duration of intercostal artery ischemia2. Duration of intercostal artery ischemia 3. Intraoperative proximal hypotension3. Intraoperative proximal hypotension 4. Postoperative hypotension4. Postoperative hypotension 5. Hyperthermia during operation5. Hyperthermia during operation 6. Anastomosis with tension6. Anastomosis with tension 7. Acidosis in the perioperative periods7. Acidosis in the perioperative periods

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The Multi-Modality Cath Lab The Multi-Modality Cath Lab ProblemProblem

Multiple re-entry of Patient IDMultiple re-entry of Patient ID Error proneError prone Results fragmented across systemsResults fragmented across systems Results inconsistently time-taggedResults inconsistently time-tagged Custom solutions needed for data Custom solutions needed for data

sharingsharing Difficult to manageDifficult to manage

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Implanted Device Implanted Device ObservationsObservations

Explosion in number of implantable Explosion in number of implantable cardioverter defibrillatorscardioverter defibrillators

Clinicians need to manage patients with aClinicians need to manage patients with awide variety of devices in many contextswide variety of devices in many contexts ICDs, CRTDs, pacemakers, etc. ICDs, CRTDs, pacemakers, etc. Implant, office follow up, home monitoringImplant, office follow up, home monitoring

Need standard set of observations, Need standard set of observations, communicated in standard messagescommunicated in standard messages Therapy settings, events, device self-Therapy settings, events, device self-

monitoringmonitoring Enables consistent presentation of data from Enables consistent presentation of data from

all devicesall devices

Trial Implementation

Trial Implementation

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History of Device Development: Past, Present and Future

1

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Anatomy of a Start-up…Anatomy of a Start-up…

IPO

FDA Approval; Product Launch

Distribution Agreement

Hired CEO; Key management in placeFDA submission

Animal studies completed; Start clinical trials

Prototype completed; Funds raised

Patents Disclosed

Time (years)

Val

uat

ion

($

)

10

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Golden RulesGolden Rules Device or procedure must be simple to Device or procedure must be simple to

apply an can be adopted by the average apply an can be adopted by the average practitionerpractitioner

Invention addresses an otherwise unmet Invention addresses an otherwise unmet clinical needclinical need

Device regulatory path is associated with Device regulatory path is associated with a “reasonable” chance for success in an a “reasonable” chance for success in an otherwise well defined study with a finite otherwise well defined study with a finite sample sizesample size

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History of Device Development: Past, Present and Future

1

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Anatomy of a Start-up…Anatomy of a Start-up…

IPO

FDA Approval; Product Launch

Distribution Agreement

Hired CEO; Key management in placeFDA submission

Animal studies completed; Start clinical trials

Prototype completed; Funds raised

Patents Disclosed

Time (years)

Val

uat

ion

($

)

10

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Timing is Timing is everythingeverything

It is often, but not It is often, but not always best to be always best to be firstfirst

Some markets Some markets change quickly; change quickly; others very slowlyothers very slowly

New market New market development is development is expensiveexpensive

Window of Window of OpportunitOpportunit

yy

11

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Rigor of randomized clinical trialsRigor of randomized clinical trials

Clinical adoptionClinical adoption

Ease of useEase of use

Learning curvesLearning curves

12

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Goals of StartupsGoals of Startups

Balancing

13

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Golden RulesGolden Rules Device or procedure must be simple to Device or procedure must be simple to

apply an can be adopted by the average apply an can be adopted by the average practitionerpractitioner

Invention addresses an otherwise unmet Invention addresses an otherwise unmet clinical needclinical need

Device regulatory path is associated with Device regulatory path is associated with a “reasonable” chance for success in an a “reasonable” chance for success in an otherwise well defined study with a finite otherwise well defined study with a finite sample sizesample size

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

20022003

2004

20052006

16

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History of History of Interventional CardiologyInterventional Cardiology

1977

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Coronary Angioplasty (PTCA) Coronary Angioplasty (PTCA) Andreas GruntzigAndreas Gruntzig

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In- Stent RestenosisIn- Stent Restenosis

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BrachytherapyBrachytherapy

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

2002

2003

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Percutaneous “Mitral” Percutaneous “Mitral” Valve RepairValve Repair

Coronary Sinus AnnuloplastyCoronary Sinus Annuloplasty

Edge-to-Edge RepairEdge-to-Edge Repair

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Coronary Sinus Coronary Sinus AnnuloplastyAnnuloplasty

Edwards LifeScienceEdwards LifeScience

HandleHandleSliding Knob

Sliding Knob

Location of Implant

(Internal)

Location of Implant

(Internal)

Distal AnchorDistal AnchorProximal AnchorProximal Anchor

BridgeBridge

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Mitral Valve Edge-to-Edge Repair

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

20022003

2004

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Atrial fibrillation is a major Atrial fibrillation is a major source of cardiogenic source of cardiogenic

embolism-related strokeembolism-related stroke

Source: Neurology, 1978; Stroke, 1985; European Heart Journal, 1987; Lancet, 1987

500,000 strokes per year500,000 strokes per year AHA estimates that 15 – 20% of AHA estimates that 15 – 20% of

strokes/year are related to AFstrokes/year are related to AF

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WATCHMANWATCHMAN®® Device Device

Frame:Frame: Nitinol (shape memory) Nitinol (shape memory) Contour shape accommodates most LAA anatomyContour shape accommodates most LAA anatomy Barbs engage the LAA tissueBarbs engage the LAA tissue

Fabric Cap:Fabric Cap: Polyethyl terephthalate (PET) Fabric Polyethyl terephthalate (PET) Fabric Prevents harmful emboli from exiting during the healing processPrevents harmful emboli from exiting during the healing process

Barbs

160 µ PET fabric Device available in various Device available in various sizes:sizes: 21, 24, 27, 30 and 33 mm 21, 24, 27, 30 and 33 mm

(diameter)(diameter)

Device diameter is measured Device diameter is measured

across face of deviceacross face of device

Device Length = Device DiameterDevice Length = Device Diameter

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Left Atrial Appendage Left Atrial Appendage ClosureClosure

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

20022003

2004

2005

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The Next Frontier in The Next Frontier in Coronary StentingCoronary Stenting

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Treating Bifurcation LesionsTreating Bifurcation LesionsLimitations of Current DESLimitations of Current DES

Stents are tubular structures Stents are tubular structures not intended for Y-shaped not intended for Y-shaped

anatomyanatomy Side branch jailingSide branch jailing Limited ostial coverage Limited ostial coverage

(“Gaps”)(“Gaps”) Technically demandingTechnically demanding Multiple layers of metalMultiple layers of metal Increasing risk of thrombosisIncreasing risk of thrombosis Myriad of Techniques Myriad of Techniques

Gap

MultipleLayers

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The TAXUS PetalThe TAXUS PetalTMTM

Boston Scientific CoroporationBoston Scientific Coroporation

Stent AdvantagesStent Advantages Special stent feature to cover Special stent feature to cover

ostium of side branch (~2mm)ostium of side branch (~2mm) Reduces / eliminates side branch Reduces / eliminates side branch

“gap”“gap” May reduce frequency of 2nd May reduce frequency of 2nd

stentstent Placing 2nd stent, when Placing 2nd stent, when

necessary, is technically more necessary, is technically more straight forwardstraight forward

Delivery System Delivery System AdvantagesAdvantages

Side Branch wire lumen Side Branch wire lumen aids in alignment at ostiumaids in alignment at ostium

Side branch Side branch ““pre-wiredpre-wired””, no , no need to re-access through need to re-access through stentstent

Final Petal size determined Final Petal size determined by post dilatation balloonby post dilatation balloon

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Chronic Total Occlusion Chronic Total Occlusion (CTO)(CTO)

.

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History of History of Interventional CardiologyInterventional Cardiology

19771984

1988

19891997

19992000

20022003

2004

2005

2006

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Why Degradable Stents?Why Degradable Stents?

No late adverse eventsNo late adverse events Late thrombosisLate thrombosis Hypersensitivity reactions Hypersensitivity reactions

(chronic inflammation)(chronic inflammation) Stent fracturesStent fractures

Does not restrict arterial Does not restrict arterial remodelingremodeling

Permits non-invasive Permits non-invasive imaging of arteryimaging of artery

Permits bypass surgery Permits bypass surgery in futurein future

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Bioabsorbable Stent DesignBioabsorbable Stent Design

.

Core: Polymer A

Undercoat: Polymer B

Topcoat: Polymer B

Drug Layer: Polymer B + Sirolimus Coating Layers

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Multi-Layer, Combination Multi-Layer, Combination Drug DeliveryDrug Delivery

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Biodegradable StentsBiodegradable Stents

Could also be the ideal vehicle for Could also be the ideal vehicle for several other applications: non-several other applications: non-obstructive vulnerable plaque, gene obstructive vulnerable plaque, gene transfer for infract repair and transfer for infract repair and angiogenesis…..angiogenesis…..

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““Biodegradable Stents: Biodegradable Stents:

They Do Their Job and They Do Their Job and Disappear”Disappear”

- Ron WaksmanRon Waksman

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Future Opportunities in Interventional Cardiology

Peripheral Vascularization

-Claudication

-Limb Salvage

-Angiogenesis

Structural Heart/ Stroke Prevention

-PFO/ASD Closure

-Left Atrial Appendage closure

- Atrial Fib. Ablation

Cerebral Revascularization

-Carotid Stenting

-Embolic Protection Devices

-Acute Stroke Intervention

Congestive Heart Failure

-Resynchronization Therapy

-Impulse Modulation

-Implantable Pressure Regulators

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Transmyocardial LaserTransmyocardial LaserRevascularizationRevascularization

1. What is transmyocardial laser 1. What is transmyocardial laser revascularization?revascularization?

2. In whom should this technique be employed?2. In whom should this technique be employed? 3. How does transmyocardial laser 3. How does transmyocardial laser

revascularization work/ Pathophysiology?revascularization work/ Pathophysiology? 4. What are the details of operative techniques?4. What are the details of operative techniques? 5. What is the potential morbidity of this 5. What is the potential morbidity of this

procedure?procedure? 6. What are the long term results?6. What are the long term results? 7. Can any laser system be used?7. Can any laser system be used?

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1.1. What is transmyocardial laser What is transmyocardial laser revascularization?revascularization?

TMR: TMR: Relatively new technique that attempts to Relatively new technique that attempts to improve the blood supply to ischemic improve the blood supply to ischemic myocardium by using a high-powered COmyocardium by using a high-powered CO22 laser laser

to create multiple transmyocardial channels. to create multiple transmyocardial channels.

These new channels bring blood from the These new channels bring blood from the ventricular cavity directly into the myocardium. ventricular cavity directly into the myocardium.

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LASER HISTORY (1917-1996)LASER HISTORY (1917-1996)

EinsteinEinstein can be considered as the can be considered as the father of the laser. father of the laser.

~ 80-90 years ago he postulated ~ 80-90 years ago he postulated photons and stimulated emission and photons and stimulated emission and won the Nobel prize for related won the Nobel prize for related research on the photoelectric effect. research on the photoelectric effect.

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""A splendid light has dawned on A splendid light has dawned on me..."me..."

- Albert Einstein- Albert Einstein

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Although Einstein did not invent laser, his Although Einstein did not invent laser, his work laid the foundation. It was Einstein who work laid the foundation. It was Einstein who pointed out that stimulated emission of pointed out that stimulated emission of radiation could occur. radiation could occur.

He used his photon mathematics to examine He used his photon mathematics to examine the case of a large collection of atoms full of the case of a large collection of atoms full of excess energy and ready to emit a photon at excess energy and ready to emit a photon at some random time in a random direction. If a some random time in a random direction. If a stray photon passes by, then the atoms are stray photon passes by, then the atoms are stimulated by its presence to emit their stimulated by its presence to emit their photons early.photons early.

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Remarkably, the emitted Remarkably, the emitted photons go in the same photons go in the same direction and have exactly direction and have exactly the same frequency as the the same frequency as the original photon ! Later, as original photon ! Later, as the small crowd of the small crowd of identical photons moves identical photons moves through the rest of the through the rest of the atoms, more and more atoms, more and more photons will leave their photons will leave their atoms early to join in the atoms early to join in the subatomic parade. subatomic parade.

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All it took to invent the laser was for All it took to invent the laser was for someone to find the right kind of someone to find the right kind of atoms and to add reflecting mirrors atoms and to add reflecting mirrors & lenses to help the stimulated & lenses to help the stimulated emission along. emission along.

LASER: LASER: LLight ight AAmplification by (using mplification by (using Einstein's ideas about) Einstein's ideas about) SStimulated timulated EEmission of mission of RRadiation.adiation.

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LASER historyLASER history

* 1917 :1917 : Einstein postulates photons and Einstein postulates photons and stimulated emission stimulated emission

* 1954 :1954 : First microwave laser First microwave laser * 1960 :1960 : First optical laser First optical laser * 1965 :1965 : Discovery of cosmic background Discovery of cosmic background

radiation using microwave laser radiation using microwave laser * 1970 :1970 : First postulate of laser action in First postulate of laser action in

starsstars* 1979 :1979 : Near Infrared laser star found in Near Infrared laser star found in

Orion nebulaOrion nebula

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LASER historyLASER history

* 1981 :1981 : Carbon dioxide laser discovered in Carbon dioxide laser discovered in atmosphere of mars and venus atmosphere of mars and venus

* 1984 :1984 : First x-ray laser First x-ray laser * 1994 :1994 : Artificial laser guide stars Artificial laser guide stars * 1995 :1995 : Far Far infrared infrared laser star discovered laser star discovered * 1996 :1996 : UltravioletUltraviolet laser star discovered laser star discovered * 2003 :2003 : Knowledge base of the world’s Knowledge base of the world’s

most powerful research and military lasersmost powerful research and military lasers

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The Procedure… History & The Procedure… History & TechniqueTechnique

TMR is a derivative of older procedures developed TMR is a derivative of older procedures developed before CABG surgery to augment coronary blood flowbefore CABG surgery to augment coronary blood flow..

Arthur Vineberg Arthur Vineberg 1903-1903-19881988

(Canadian Cardiac (Canadian Cardiac Surgeon)Surgeon)

in in 19461946 attempted to attempted to improve myocardial blood improve myocardial blood flow by tunneling the left flow by tunneling the left internal mammary artery internal mammary artery directly into the left directly into the left ventricular myocardium.ventricular myocardium.

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He found, using early angiographic techniques, He found, using early angiographic techniques, that with this procedure a communication was that with this procedure a communication was created between the left mammary artery and created between the left mammary artery and the coronary circulation that remained patent for the coronary circulation that remained patent for at least 4 months after the procedure was at least 4 months after the procedure was performed.performed.

How this communication forms and persists was How this communication forms and persists was unanswered. unanswered.

His procedure fell out of favor with the advent of His procedure fell out of favor with the advent of the more physiologic CABG surgery in the the more physiologic CABG surgery in the 1960s1960s..

Vineberg AM. CMAJ. 1946;55:117–119

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2. In whom should this technique be 2. In whom should this technique be employed? Indications..employed? Indications..

Previous CABG/PTCA (high risk candidates for re-Previous CABG/PTCA (high risk candidates for re-do). do).

Genetic metabolic disease which has produced Genetic metabolic disease which has produced extensive peripheral coronary disease. extensive peripheral coronary disease.

... Poor runoff and no place to perform a ... Poor runoff and no place to perform a conventional revascularization ...conventional revascularization ...

““End-stage coronary vascular disease (diffuse)"End-stage coronary vascular disease (diffuse)" and can not be reconstructed by the usual means. and can not be reconstructed by the usual means.

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Indications (continued)Indications (continued)

Evidence of reversible ischemia on a radioactive Evidence of reversible ischemia on a radioactive perfusion scan. perfusion scan.

Reasonable ventricular function Reasonable ventricular function (EF > 20%).(EF > 20%). Very severe disabling angina, Very severe disabling angina, class III or IVclass III or IV, on , on

maximal anti-anginal therapy. maximal anti-anginal therapy.

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3. How does TMR work?3. How does TMR work?

Mechanism of action/ PathophysiologyMechanism of action/ Pathophysiology Exact mechanism: considerable controversy.Exact mechanism: considerable controversy. Several mechanisms have been proposed:Several mechanisms have been proposed:

- - direct blood flow to the myocardium direct blood flow to the myocardium (Open Channel Hypothesis)(Open Channel Hypothesis) - Sympathetic denervation of the myocardium- Sympathetic denervation of the myocardium - Angiogenesis- Angiogenesis - Placebo ??- Placebo ??

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Open Channel HypothesisOpen Channel Hypothesis

Theoretically, the new channels should allow Theoretically, the new channels should allow blood supply from the LV cavity up the channels to blood supply from the LV cavity up the channels to form buds off of the main channels. form buds off of the main channels.

It has been difficult to demonstrate that It has been difficult to demonstrate that revascularization has occurred consistently in all revascularization has occurred consistently in all patients. patients.

Does not Does not blood flow acutely. blood flow acutely. blood flow after 2-6 months.blood flow after 2-6 months.

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Open Channel HypothesisOpen Channel Hypothesis

Is there objective evidence of Is there objective evidence of increased myocardial increased myocardial

perfusion?perfusion?

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Open Channel Hypothesis (Pros)Open Channel Hypothesis (Pros)

Some autopsy specimens have shown open Some autopsy specimens have shown open channels (investigators in Hilemberg, Germany, channels (investigators in Hilemberg, Germany, using special angulated color doppler echo on using special angulated color doppler echo on human beings, have seen patent channels 30 human beings, have seen patent channels 30 days after the creation of these channels). days after the creation of these channels).

Animal studies have also been conflicting, but, Animal studies have also been conflicting, but, angioneogensis has definitely been shown to be a angioneogensis has definitely been shown to be a factor in both experimental and clinical studies.factor in both experimental and clinical studies.

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Rationale for TMR

• Epicardial approach(surgery)

• Endocardial approach(percutaneous)

• Holmium:yttrium –argon – garnet(Ho:YAG) & CO2lasers approved by USFood and Drug Admin

• Ho:YAG beamtransmitted by opticalfiber

• CO2 laser beamtransmitted by mirrorsand lenses

• Different lasers havenot been compared inclinical trials

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4. Details of operative techniques?4. Details of operative techniques?

Left anterior thoracotomyLeft anterior thoracotomy usually through the usually through the fifth intercostal space. (Europe : thoracoscopic fifth intercostal space. (Europe : thoracoscopic approach has been used). approach has been used).

The pericardium is opened, a cradle is made, The pericardium is opened, a cradle is made, and the dissection of the pericardium is and the dissection of the pericardium is carefully carried off of the heart. carefully carried off of the heart.

(No heparin is administered, nor is the patient (No heparin is administered, nor is the patient cannulated for cardiopulmonary bypass). cannulated for cardiopulmonary bypass).

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Technique of TMR vs PMR

TMR• L anterior

thoracotomy ormedian sternotomy

• Cannulation andheparin needed ONLYif concurrent CABG

• 25-50 channels madewith 1 cm separationin L ventricle

PMR• 3 catheter based

Ho:YAG devices

• Lack FDA approval

• Introduced into LV viafemoral artery

• Laser againstendocardium

• Multiple pulses to createup to 20 channels

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A A transesophageal echo (TEE)transesophageal echo (TEE) is necessary is necessary to document the transmural nature of the laser to document the transmural nature of the laser pulse by preservation of laser "steam" in the pulse by preservation of laser "steam" in the left ventricle. left ventricle.

Once the heart is in its pericardial cradle, the Once the heart is in its pericardial cradle, the probes are placed directly on the myocardium. probes are placed directly on the myocardium. The laser beam is synchronized with the The laser beam is synchronized with the ECGECG and then a foot switch allows for production of and then a foot switch allows for production of the laser pulse and vaporization of the the laser pulse and vaporization of the transmural myocardial channels. transmural myocardial channels.

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The channels are made The channels are made one cm apartone cm apart in all of in all of the ischemic areas and the borders in and the ischemic areas and the borders in and around the ischemic areas noted from the around the ischemic areas noted from the thallium sestamibi scans. thallium sestamibi scans.

After After 25 to 40 channels25 to 40 channels are drilled, the are drilled, the pericardium is loosely re-approximated and the pericardium is loosely re-approximated and the patient is closed in the usual fashion for a small patient is closed in the usual fashion for a small thoracotomy and returned to the ICU. thoracotomy and returned to the ICU.

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5. What is the potential morbidity of 5. What is the potential morbidity of this procedure? this procedure?

Complications: Complications: - atrial arrhythmias (atrial fibrillation)- atrial arrhythmias (atrial fibrillation) - hypotension- hypotension - ventricular arrhythmias- ventricular arrhythmias - ventricular dysfunction- ventricular dysfunction - myocardial infarctions- myocardial infarctions - pleural effusion- pleural effusion

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Adverse outcomesAdverse outcomes

Perioperative mortality rates : 1% - 9% .Perioperative mortality rates : 1% - 9% . Complications: Complications: - atrial arrhythmias (atrial fibrillation)- atrial arrhythmias (atrial fibrillation) - hypotension- hypotension - ventricular arrhythmias- ventricular arrhythmias - ventricular dysfunction- ventricular dysfunction - myocardial infarctions- myocardial infarctions - pleural effusion- pleural effusion

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7. Can any laser system be used?7. Can any laser system be used?

Unknown ??. Unknown ??. The most commonly used lasers for this The most commonly used lasers for this

procedure have been the holmium:yttrium-procedure have been the holmium:yttrium-aluminum garner laser (Ho:YAG) and the carbon aluminum garner laser (Ho:YAG) and the carbon dioxide dioxide COCO22 laser (more commonly used… less laser (more commonly used… less

thermal injury to surrounding tissues, more thermal injury to surrounding tissues, more efficient tissue penetration).efficient tissue penetration).

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CIRCULATIONCIRCULATION

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Circulatory SystemsCirculatory Systems

Blood flows through blood vesselsBlood flows through blood vessels Heart generates force to keep Heart generates force to keep

blood movingblood moving Closed system Closed system

Blood is confined to vessels and heartBlood is confined to vessels and heart Open systemOpen system

Blood mingles with fluid in tissuesBlood mingles with fluid in tissues

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Flow AnalogyFlow Analogy

river in river out

lake

1 2 3 1 2 3

1 2 3

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The HeartThe Heart The The heartheart is a cone-shaped, muscular is a cone-shaped, muscular

organ located between the lungs organ located between the lungs behind the sternum.behind the sternum.

The heart muscle forms the The heart muscle forms the myocardiummyocardium, with tightly , with tightly interconnected cells of interconnected cells of cardiac musclecardiac muscle tissue. tissue.

The The pericardiumpericardium is the outer is the outer membranous sac with lubricating fluid.membranous sac with lubricating fluid.

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The heart has four chambers: two upper, The heart has four chambers: two upper, thin-walled thin-walled atriaatria, and two lower, thick-, and two lower, thick-walled walled ventriclesventricles..

The The septumseptum is a wall dividing the right and is a wall dividing the right and left sides. left sides.

Atrioventricular valvesAtrioventricular valves occur between the occur between the atria and ventricles – the atria and ventricles – the tricuspidtricuspid valvevalve on on the right and the the right and the bicuspid valvebicuspid valve on the left; on the left; both valves are reinforced by both valves are reinforced by chordae chordae tendinaetendinae attached to muscular projections attached to muscular projections within the ventricles.within the ventricles.

Semilunar valvesSemilunar valves occur between the occur between the ventricles and the attached arteriesventricles and the attached arteries

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External heart anatomyExternal heart anatomy

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Passage of Blood Through Passage of Blood Through the Heartthe Heart

Blood follows this sequence through the Blood follows this sequence through the heart: superior and inferior vena cava heart: superior and inferior vena cava → right atrium → tricuspid valve → right → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve ventricle → pulmonary semilunar valve → pulmonary trunk and arteries to the → pulmonary trunk and arteries to the lungs → pulmonary veins leaving the lungs → pulmonary veins leaving the lungs → left atrium → bicuspid valve → lungs → left atrium → bicuspid valve → left ventricle → aortic semilunar valve → left ventricle → aortic semilunar valve → aorta → to the body. aorta → to the body.

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Internal view of the heartInternal view of the heart

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Valvular Heart Disease

Kenneth S. Korr M.D.Associate Professor of Medicine,

Brown Medical SchoolDirector, Division of Cardiology

The Miriam Hospital

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Normal Valve Function

Maintain forward flow and prevent reversal of flow.

Valves open and close in response to pressure differences (gradients) between cardiac chambers.

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Abnormal Valve Function

Valve Stenosis Obstruction to valve flow during that phase of the cardiac

cycle when the valve is normally open. Hemodynamic hallmark -“pressure gradient” ~ flow// VA

Valve Regurgitation, Insufficiency, Incompetence Inadequate valve closure--- back leakage

A single valve can be both stenotic and regurgitant; but both lesions cannot be severe!!

Combinations of valve lesions can coexist Single disease process Different disease processes One valve lesion may cause another Certain combinations are particularly burdensome (AS &

MR)

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Mitral Valve Competence:

Integrated function of several anatomic elements Posterior LA wall Anterior & Posterior

valve leaflets Chordae tendineae Papillary muscles Left ventricular wall

where the papillary muscles attach

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Mitral Regurgitation-Pathophysiology

MR: Leakage of blood into LA during systole

10 Abnormality -Loss of forward SV into LA

Compensatory Mechanisms Increase in SV (& EF) Forward SV +

regurgitant volume LV (LA) dilatation Left Ventricular Volume

Overload (LVVO)

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Chronic Mitral Regurgitation - LVVO

LVVO LV dilatation Eccentric hypertrophy

Increased LA pressure

Pulmonary HTN Dyspnea Atrial arrhythmias Low output state

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Pathophysiology –Acute vs Chronic Mitral Regurgitation

Acute MR Normal (noncompliant)

LA Increase LA pressure large “V” waves Acute Pulmonary Edema

Chronic MR Dilated, compliant LA LA pressure normal or

slightly increased Fatigue, low output state Atrial arrhythmias- a. fib.

Most patients fall between these two extremes!!

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Mitral Valve Disease – Echo findings

Mitral Stenosis Thickened, deformed

MV leaflets 2D MVA Doppler Gradient Associated LAE, RVH,

PHTN, TR,MR, LV function

Mitral Regurgitation Determine etiology –

leaflets, chordae, MVP, MI

Doppler severity of MR jet

LV function

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Balloon Mitral Commissurotomy

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Path of blood through the Path of blood through the heartheart

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• Interventional treatment

Balloon valvulotomy - It most commonly is used in young pts without extensive valvular calcification, in pregnant

women, and in pts who are unfavorable operative candidates Mitral valve replacement - performed if leaflets are immobile or heavily

calcified. - It also is performed if there is severe subvalvular

scarring.- Bioprosthetic or artificial mechanical valves can

be used as replacements.

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The HeartbeatThe Heartbeat Each heartbeat is called a Each heartbeat is called a cardiac cyclecardiac cycle.. When the heart beats, the two atria When the heart beats, the two atria

contract together, then the two contract together, then the two ventricles contract; then the whole ventricles contract; then the whole heart relaxes.heart relaxes.

SystoleSystole is the contraction of heart is the contraction of heart chambers; chambers; diastolediastole is their relaxation. is their relaxation.

The The heart soundsheart sounds, lub-dup, are due to , lub-dup, are due to the closing of the atrioventricular the closing of the atrioventricular valves, followed by the closing of the valves, followed by the closing of the semilunar valves.semilunar valves.

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Conduction system of the Conduction system of the heartheart

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Conduction and Conduction and ContractionContraction

SA node in right SA node in right atrium is atrium is pacemakerpacemaker

Electrical signals Electrical signals cause contraction of cause contraction of atriaatria

Signal flows to AV Signal flows to AV node and down node and down septum to ventriclesseptum to ventricles

SA node

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Pulmonary CircuitPulmonary Circuit

This loop This loop

oxygenates oxygenates

bloodblood

right pulmonary artery left pulmonary artery

capillarybed ofrightlung

pulmonarytrunk

capillary bedof left lung

(to systemic circuit)

pulmonary veins

lungs

(fromsystemiccircuit)

heart

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Systemic Systemic CircuitCircuit

Longer loop Longer loop

carries blood carries blood

to and from to and from

body tissuesbody tissues

capillary beds of headand upper extremities

(to pulmonarycircuit)

aorta

(frompulmonarycircuit)

heart

capillary beds of otherorgans in thoracic cavity

capillary bed of liver

capillary beds of intestines

capillary beds of other abdominalorgans and lower extremities

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Cardiovascular system Cardiovascular system diagramdiagram

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The The cardiovascular systemcardiovascular system has three has three types of blood vessels:types of blood vessels:

ArteriesArteries (and (and arteriolesarterioles) – carry ) – carry blood away from the heartblood away from the heart

CapillariesCapillaries – where nutrient and gas – where nutrient and gas exchange occurexchange occur

VeinsVeins (and (and venulesvenules) – carry blood ) – carry blood toward the heart.toward the heart.

The Blood VesselsThe Blood Vessels

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Blood vesselsBlood vessels

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Anatomy of a capillary Anatomy of a capillary bedbed

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Bulk Flow in Capillary Bulk Flow in Capillary BedBed

blood tovenule

inward-directedosmotic movement

cells oftissue

outward-directedbulk flowblood

from arteriole

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HemophiliaHemophilia HemophiliaHemophilia is an inherited clotting is an inherited clotting

disorder due to a deficiency in a disorder due to a deficiency in a clotting factor.clotting factor.

Bumps and falls cause bleeding in the Bumps and falls cause bleeding in the joints; cartilage degeneration and joints; cartilage degeneration and resorption of bone can follow.resorption of bone can follow.

The most frequent cause of death is The most frequent cause of death is bleeding into the brain with bleeding into the brain with accompanying neurological damage.accompanying neurological damage.

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Cardiovascular DisordersCardiovascular Disorders

Cardiovascular diseaseCardiovascular disease ( (CVDCVD) is the ) is the leading cause of death in Western leading cause of death in Western countries.countries.

Modern research efforts have Modern research efforts have improved diagnosis, treatment, and improved diagnosis, treatment, and prevention.prevention.

Major cardiovascular disorders include Major cardiovascular disorders include atherosclerosis, stroke, heart attack, atherosclerosis, stroke, heart attack, aneurysm, and hypertension.aneurysm, and hypertension.

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AtherosclerosisAtherosclerosis

AtherosclerosisAtherosclerosis is due to a build-up is due to a build-up of fatty material (of fatty material (plaqueplaque), mainly ), mainly cholesterol, under the inner lining of cholesterol, under the inner lining of arteries. arteries.

The plaque can cause a The plaque can cause a thrombusthrombus (blood clot) to form.(blood clot) to form.

The thrombus can dislodge as an The thrombus can dislodge as an embolusembolus and lead to and lead to thromboembolismthromboembolism..

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Stroke, Heart Attack, and Stroke, Heart Attack, and AneurysmAneurysm

A A cerebrovascular accidentcerebrovascular accident, or , or strokestroke, , results when an embolus lodges in a results when an embolus lodges in a cerebral blood vessel or a cerebral cerebral blood vessel or a cerebral blood vessel bursts; a portion of the blood vessel bursts; a portion of the brain dies due to lack of oxygen. brain dies due to lack of oxygen.

A A myocardial infarctionmyocardial infarction, or , or heart heart attackattack, occurs when a portion of heart , occurs when a portion of heart muscle dies due to lack of oxygen.muscle dies due to lack of oxygen.

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Coronary bypass Coronary bypass operationoperation

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AngioplastyAngioplasty

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Intravascular Intravascular stentsstents

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OutlineOutline BackgroundBackground

Occlusive vascular disease and its treatment Occlusive vascular disease and its treatment by PCI and stentingby PCI and stenting

Assessment of a novel compliance Assessment of a novel compliance matching stent and comparison with a matching stent and comparison with a commercially available devicecommercially available device In vivo radiographic measurement in pig In vivo radiographic measurement in pig

carotid and iliac arteriescarotid and iliac arteries Development of a micro CT method for stented Development of a micro CT method for stented

vessel morphometry on excised arteriesvessel morphometry on excised arteries

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Revascularisation Revascularisation techniquestechniques

Coronary Artery Bypass Graft Coronary Artery Bypass Graft (CABG)(CABG)

Percutaneous Coronary Intervention Percutaneous Coronary Intervention (PCI)(PCI) AngioplastyAngioplasty Plus Plus stentingstenting (94%) (94%)

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Balloon angioplastyBalloon angioplasty

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What is an intravascular What is an intravascular stent?stent?

A small tubular mesh usually made of A small tubular mesh usually made of either stainless steel or Nitinol. either stainless steel or Nitinol. (Shape (Shape memory alloy)memory alloy)

Inserted into stenotic (blocked) arteries to Inserted into stenotic (blocked) arteries to keep the lumen patent. Normally during keep the lumen patent. Normally during angioplasty.angioplasty.

Used at various sites including the Used at various sites including the coronary, renal, carotid and femoral coronary, renal, carotid and femoral arteries.arteries.

Non-arterial uses e.g. in bronchus, Non-arterial uses e.g. in bronchus, trachea, ureter, bile ducttrachea, ureter, bile duct..

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HistoryHistory The concept of vascular stents is The concept of vascular stents is

accredited to Charles Dotter in 1969, who accredited to Charles Dotter in 1969, who implanted stainless steel coils in canine implanted stainless steel coils in canine peripheral arteries.peripheral arteries. Not followed up in humans because of Not followed up in humans because of

haemodynamically significant narrowing.haemodynamically significant narrowing. Not in clinical practice until 1980s.Not in clinical practice until 1980s. Market leader is the Palmaz stent designed Market leader is the Palmaz stent designed

by Julio Palmaz in 1985.by Julio Palmaz in 1985. Initially, 18 grafts placed in canine vessels, with Initially, 18 grafts placed in canine vessels, with

patency rates approaching 80% at 35 weeks. patency rates approaching 80% at 35 weeks.

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Varied stent geometriesVaried stent geometries

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The problem with The problem with stents.stents.

Restenosis. (7 – 20%)Restenosis. (7 – 20%)

Rate depends onRate depends on

lesion type, length and severitylesion type, length and severity

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Mechanical cause of Mechanical cause of restenosisrestenosis

• ↓ ↓ shear stressshear stress Intimal HyperplasiaIntimal Hyperplasia ↓ ↓ lumenlumen ↑ ↑ shear stressshear stress If baseline shear stress not restored – If baseline shear stress not restored –

continuing intimal hyperplasia and continuing intimal hyperplasia and RESTENOSISRESTENOSIS

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Factors Which Factors Which Contribute toContribute to

In-stent Restenosis (1)In-stent Restenosis (1) Thrombus/platelet/fibrin adherence Thrombus/platelet/fibrin adherence

to stent struts.to stent struts. Anticoagulants Anticoagulants

Heparin – systemically or coated on stent.Heparin – systemically or coated on stent. Inhibition of the GP IIb-IIIa receptor:Inhibition of the GP IIb-IIIa receptor:

Prevents platelet aggregation. Prevents platelet aggregation.

Associated with raised incidence of MI.Associated with raised incidence of MI. PTFE coated stents.PTFE coated stents.

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Factors Which Factors Which Contribute toContribute to

In-stent Restenosis (2)In-stent Restenosis (2) Metabolic Metabolic

disorder/smoking/atherogenic diet.disorder/smoking/atherogenic diet. Life style changesLife style changes Restenosis rate double in insulin Restenosis rate double in insulin

dependent diabetics.dependent diabetics.

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Factors Which Factors Which Contribute toContribute to

In-stent Restenosis (3)In-stent Restenosis (3) Intimal hyperplasia due to wall injury from the Intimal hyperplasia due to wall injury from the

stentstent Brachytherapy:Brachytherapy:

Delivery: Radioactive stents, catheter radiation.Delivery: Radioactive stents, catheter radiation. May cause necrosis.May cause necrosis.

Drug eluting stentsDrug eluting stents Anti-proliferative agents e.g. rapamycin (Sirolimus)Anti-proliferative agents e.g. rapamycin (Sirolimus) Improved short term survival and maintenance of vessel Improved short term survival and maintenance of vessel

patencypatency More work needed to clarify longer term outcome (Circulation More work needed to clarify longer term outcome (Circulation

2008, 118, 18172008, 118, 1817

No improvement in outcome in insulin dependent diabetics No improvement in outcome in insulin dependent diabetics when compared to bare metal stentswhen compared to bare metal stents

Impaired ‘healing’ Impaired ‘healing’ late thrombosis, some doubt about how late thrombosis, some doubt about how serious this is. More studies needed. (Circulation 2008, serious this is. More studies needed. (Circulation 2008, 118118, , 1783)1783)

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Factors Which Factors Which Contribute toContribute to

In-stent Restenosis (4)In-stent Restenosis (4) Mechanical factorsMechanical factors

Stress concentration/bending at end of stent.Stress concentration/bending at end of stent. Raised hoop and bending stress sensed by vascular Raised hoop and bending stress sensed by vascular

smooth muscle cells → fibrosis/ remodellingsmooth muscle cells → fibrosis/ remodelling Flow disturbance within stented region.Flow disturbance within stented region.

Time varying shear stress sensed by vascular Time varying shear stress sensed by vascular endothelium → release of vasoactive mediators in the endothelium → release of vasoactive mediators in the short term and remodelling/intimal hyperplasia in short term and remodelling/intimal hyperplasia in the longer termthe longer term

Compliant-ended stentCompliant-ended stent

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Compliant Ended StentCompliant Ended Stent

Rigid in the centre to Rigid in the centre to provide recoil resistanceprovide recoil resistance

Parabolic and Parabolic and cantilevered strutscantilevered struts gradual change in gradual change in

compliance and matching compliance and matching to native vesselto native vessel

reduces stress reduces stress concentration and bendingconcentration and bending

Less disturbed flowLess disturbed flow

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Stents used in the Stents used in the StudyStudy

SMART stent

(Commercially available)

Compliant Ended Stent

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Palmaz CES

6 week post 6 week post implantationimplantation

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Cardiovascular Cardiovascular DisordersDisorders

PathophysiologyPathophysiology

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Review of Anatomy & PhysiologyReview of Anatomy & Physiology

AnatomyAnatomy ChambersChambers A-V valvesA-V valves Semilunar valvesSemilunar valves Coronary arteriesCoronary arteries

LeftLeft Ant. Ant.

DescendingDescending CircumflexCircumflex

RightRight

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• Cardiac Cycle = one complete heartbeat– Systole = contraction of heart ; Diastole = relaxation of the heart

– In systole:• first the two atria contract (atrial systole)• then the two ventricles contract (ventricular systole)

• Atrial diastole begins when ventricles contracting

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– Stroke Volume = volume of blood ejected from one ventricle during a beat– Cardiac Output = amount of blood one ventricle can pump each minute

» normal = 5 liters per minute (at rest)» Note: CO = SV x Heart Rate

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– Acyanotic Congenital Heart Disease (cont)

• These are obstructive lesions

• If severe they produce acyanotic CHF

• Coarctation of the Aorta • In time get left ventricular failure

• Hypotension distal to coarctation

• Coarctation usually juxtaductal (ductus arteriosus)

• When ductus closes ; patient goes into CHF

• Aortic stenosis

• Pulmonary stenosis• Severe form = pulmonary atresia

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Cyanotic Congenital Heart Cyanotic Congenital Heart DiseaseDisease

Tetralogy of FallotTetralogy of Fallot most common cyanotic most common cyanotic

congenital heart defectcongenital heart defect includes: VSD, pulm includes: VSD, pulm

stenosis, dextroposition stenosis, dextroposition of aorta, RVHof aorta, RVH

Transposition of the Great Transposition of the Great ArteriesArteries

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Valvular DisordersValvular Disorders

– 2 main types• insufficiency = failure of valves to close• stenosis = hardening of cusps

– both types allow for blood regurgitation– All come from disorders of endocardium

– 2 etiologies– Congenital– Acquired

* from rheumatic fever* from infective endocarditis

– Congenital malformations most commonly affect;– aortic & pulmonary valve (see previous slides)

– mitral valve most commonly affected in rheumatic heart disease

» Mitral Stenosis --- most commonly from rheumatic fever» Mitral Insufficiency

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Renal Artery Renal Artery StentingStenting

pre post

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Global Renal Global Renal RevascularizationRevascularization

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Pathology of Atheroembolism

• Plaque / cholesterol • Endothelial cells• Platelet-Fibrin Thrombi• Calcified tissue

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FILTERDEVICES

OCCLUSIONDEVICES

Preserve flowLimit Ischemic Time

More complete capture

Small debrisVascular Injury

No antegrade flowProlonged Ischemic Time

Vascular InjuryShoulder Regions

+

-

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FILTER DEVICES

Cordis

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OCCLUSIONDEVICES

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Atheroembolization Atheroembolization ProtectionProtection

Percusurge Guardwire

A. Traverse

B. Inflate

C. Intervene

D. Embolectomize

Percusurge Guardwire

A. Traverse

B. Inflate

C. Intervene

D. Embolectomize

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DSA Abdominal DSA Abdominal AortogramAortogram

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Abdominal Aortogram: Abdominal Aortogram: Late PhaseLate Phase

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Early Phase Late Phase

Selective Left Renal Selective Left Renal AngiogramAngiogram

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Selective Right Renal Selective Right Renal AngiogramAngiogram

?

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Angioplasty and Angioplasty and StentingStenting

6 x 18mm Herculink Stent 6.5mm Post-dilatation

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Right Renal Angio: Right Renal Angio: FinalFinal

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Modern advances Modern advances in the management in the management

of strokeof stroke

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Carotid Artery StenosisCarotid Artery Stenosis

Common Carotid

External Carotid

Stenosis at bifurcation of Internal Carotid

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High Grade Carotid High Grade Carotid StenosisStenosis

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European carotid trialists collaborative groupEuropean carotid trialists collaborative group European Carotid Surgery Trial (ECST)European Carotid Surgery Trial (ECST) North American symptomatic carotid endarterectomy trial I North American symptomatic carotid endarterectomy trial I

& II(NASCET)& II(NASCET)

3 RCT’s (symptomatic) – 6143 pts3 RCT’s (symptomatic) – 6143 pts

Severe Stenosis RRR 48% NNT Severe Stenosis RRR 48% NNT 1515

Carotid EndarterectomyCarotid Endarterectomy

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Internal carotid artery (ICA) origin angioplasty

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Section 1 Slide 17

Causes of Ischaemic Stroke

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“drug”eluting “just” bare metal

The DES euphoriaThe DES euphoria

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Siegburg / Stanford

Bare Metal Stent

Drug Eluting Stent

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In-stent Restenosis = Intimal Hyperplasia

The Limitation of Bare MetalStents

1 mm

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Drug Eluting Stents vs. Bare Metal Stents

BENEFIT

ReducedRestenosis

RISK

StentThrombosis

Siegburg / Stanford

Death, AMI, TLR

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Igaki-Tami (Igaki Medica Planning Co Ltd)

Magnesium (Biotronik)

REVA (REVA Medical)

BTI (Bioabsorbable Therapeutics Inc)

BVS (Abbott Vascular)

Bioabsorbable Stents

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NOI DIRECTII DESRE-ENDOTELIZARE

Trial HEALING II – FIM STENT: GENOUSTM EPC CAPTURE STENT

63 p: MACERESTENOZALATE LOSS

REZULTATE: MACE-7,9%Late loss=0,55±0,28TVR=8,8%TLR=0,5%Tromboza=0%

Concluzii HEALING II: stenturi cu EPC reduc restenoza si previn tromboza

(dupa H.J. Euro Interv 2007,3,1,67-75)

–30 zile30 zile–6 luni6 luni–9 luni9 luni

IVUSIVUS

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EPC Capture Technology

Healing Process of Technology DESNew Generation

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To DES or not to DES?

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RESTENOZA IN STENTUL CAROTIDIAN

MECANISM – RELEVANŢĂ CLINICĂ

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The atherosclerotic plaque with the stent and Neointimal hyperplasia

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RESTENOZA IN STENTUL CAROTIDIAN

MECANISME

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DES trials are a “shell game” thatyou have to watch carefully inside

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Endothelial injurypost implantation

Stent implantation causes arterial injury, which can initiate restenosis. The restenosisStent implantation causes arterial injury, which can initiate restenosis. The restenosisprocess includes inflammation, migration of smooth muscle cells, smooth muscle cellprocess includes inflammation, migration of smooth muscle cells, smooth muscle cellproliferation and extracellular matrix formation. proliferation and extracellular matrix formation.

Implanted stent

Plaque

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Dissecting the plaque

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Early and Late Stent Thrombosis

Stent Stent

Stent Stent

Problems in PCIProblems in PCI

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Transthoracic Transthoracic Echocardiograph of PFOEchocardiograph of PFO

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530

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Carotid dissection

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Unenhanced computed tomography from 69-year-old woman presenting brain hemorrhages due Amyloid Angiopathy

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Pathogenesis of Ischaemic Pathogenesis of Ischaemic strokestroke

Penumbra

Infarction

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Risk of death dependency and good Risk of death dependency and good functional outcome in randomised functional outcome in randomised

trials of rt-PA given within 3 hours of trials of rt-PA given within 3 hours of acute strokeacute stroke

17,3 18,4

36,451,4

44,330,2

0%

20%

40%

60%

80%

100%

Thrombolysis Control

Alive and independant

alive but dependant

Dead

Cochrane September 1999

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Intra arterial Intra arterial ThrombolysisThrombolysis

PROACT IIPROACT II Intra arterial ProurokinaseIntra arterial Prourokinase 6 Hour time window6 Hour time window Relative risk reduction of 15% in Relative risk reduction of 15% in

functional outcomefunctional outcome No difference in mortalityNo difference in mortality Procedural complication 9%Procedural complication 9% Early Intra cerebral haemorrhage 10%Early Intra cerebral haemorrhage 10%

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Mechanical clot removal in Mechanical clot removal in acute strokeacute strokeMERCI trialMERCI trial Phase 1 Trial Phase 1 Trial

Cerebral embolectomy Cerebral embolectomy successful recanalisation successful recanalisation in 69 /141 (48%)in 69 /141 (48%)

In combination with rtPA In combination with rtPA in 17 casesin 17 cases

Procedural complications Procedural complications 7.1%7.1%

Could extend the time Could extend the time window to 8 hourswindow to 8 hours

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An Outline of An Outline of Congenital Heart Congenital Heart

DiseaseDisease

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ObjectivesObjectives To provide an outline of congenital To provide an outline of congenital

heart diseaseheart disease Differentiate acyanotic from Differentiate acyanotic from

cyanotic lesionscyanotic lesions Recognize critical left ventricular Recognize critical left ventricular

obstructionobstruction Understand the action and Understand the action and

indications for PGE1indications for PGE1

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An Outline of Congenital An Outline of Congenital Heart DiseaseHeart Disease

Pink (Acyanotic)Pink (Acyanotic)

Blue (Cyanotic)Blue (Cyanotic)

Critical Left Sided Critical Left Sided

Obstruction Obstruction

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Acyanotic Congenital Acyanotic Congenital Heart DiseaseHeart Disease

Normal pulmonary blood flowNormal pulmonary blood flow Valvar lesionsValvar lesions Coarctation Coarctation

Increased pulmonary blood flowIncreased pulmonary blood flow Shunt lesionsShunt lesions

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Acyanotic Congenital Acyanotic Congenital Heart DiseaseHeart Disease

Valvar lesionsValvar lesions StenosisStenosis

• AorticAortic• PulmonaryPulmonary• MitralMitral

RegurgitationRegurgitation• AorticAortic• MitralMitral• Pulmonary Pulmonary

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Acyanotic Congenital Acyanotic Congenital Heart DiseaseHeart Disease

Stenotic lesions – semilunar valvesStenotic lesions – semilunar valves Valvar dysplasiaValvar dysplasia

Regurgitant lesions – semilunar Regurgitant lesions – semilunar valvesvalves Valvar dysplasiaValvar dysplasia Secondary to intervention for stenotic Secondary to intervention for stenotic

lesionslesions Secondary to endocarditisSecondary to endocarditis

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Valve LesionsValve Lesions Mitral valve lesionsMitral valve lesions

AV canal defectsAV canal defects complete vs. partialcomplete vs. partial

Isolated MV lesionsIsolated MV lesions

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Valve LesionsValve Lesions

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Valve lesionsValve lesions

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AVSDAVSD

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CoarctationCoarctation

Obstruction of the Obstruction of the aortic archaortic arch

Classically Classically juxtaductal, although juxtaductal, although may occur anywhere may occur anywhere along the aortaalong the aorta

May develop over May develop over time time Femoral pulses Femoral pulses

should be checked should be checked routinely throughout routinely throughout childhoodchildhood

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Coarctation Coarctation Characterized by weak femoral pulses, Characterized by weak femoral pulses,

brachio-femoral delay in pulses and a systolic brachio-femoral delay in pulses and a systolic ejection type murmur heard loudest in the ejection type murmur heard loudest in the backback

Arm-leg blood pressure gradient (arm > leg)Arm-leg blood pressure gradient (arm > leg) Gradient greater than 30mmHg considered significantGradient greater than 30mmHg considered significant upper limb hypertensionupper limb hypertension

Treatment may be surgical or interventionalTreatment may be surgical or interventional Balloon dilationBalloon dilation Stent implantationStent implantation

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Shunt LesionsShunt Lesions Pink, oxygenated blood crosses from Pink, oxygenated blood crosses from

the left side of the heart to the right the left side of the heart to the right side of the heartside of the heart

Signs and symptoms dependent on the Signs and symptoms dependent on the size of the lesion and relative vascular size of the lesion and relative vascular resistance – systemic vs. pulmonaryresistance – systemic vs. pulmonary

Significant lesions marked by Significant lesions marked by increased pulmonary flowincreased pulmonary flow

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Acyanotic Congenital Acyanotic Congenital Heart DiseaseHeart Disease

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Shunt LesionsShunt Lesions Atrial Level ShuntAtrial Level Shunt

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Right AtriumRight Atrium

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ASD - typesASD - types Secundum ASDSecundum ASD

Most commonMost common Defects at the level of the fossa ovalis, presumably Defects at the level of the fossa ovalis, presumably

secondary to deficiency, perforation or absence of the secondary to deficiency, perforation or absence of the septum primumseptum primum

Sinus Venosus ASDSinus Venosus ASD Involving the portion of septum adjacent to the entry of Involving the portion of septum adjacent to the entry of

the systemic veins, outside the fossa ovalisthe systemic veins, outside the fossa ovalis Often associated with anomalous pulmonary veinsOften associated with anomalous pulmonary veins

Primum ASDPrimum ASD Endocardial cushion defect involving the inferior portion Endocardial cushion defect involving the inferior portion

of the atrial septum, adjacent to the AV valves of the atrial septum, adjacent to the AV valves usually involving malformations of the AV valvesusually involving malformations of the AV valves

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Congenital Heart DefectsCongenital Heart Defects

Most arise during the first 8 weeks of gestationMost arise during the first 8 weeks of gestation

– Congenital heart disease is divided into 2 categories: acyanotic & cyanotic

– Acyanotic Congenital Heart Disease• Diagnoses are suspected by the presence of murmurs

• 2 types: (1) increase pulmonary blood flow & (2) obstructive lesions

• These lesions usually increase pulmonary blood flow

• Ventricular Septal Defect (VSD)» most common (1/3 of all congenital heart problems)

» not too serious as in over 50% of the cases the defect spontaneously closes by age 18

» Most close within first year of life

• Atrial Septal Defect (ASD)• Persistence of fossa ovale

• Patent Ductus Arteriosus (PDA)• 80% close within 2 weeks of age

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ASDsASDs

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ASDASD Atrial level shunts result in right-Atrial level shunts result in right-

sided volume overloadsided volume overload Wide fixed split S2 characteristic Wide fixed split S2 characteristic

finding of atrial level shuntsfinding of atrial level shunts Murmur due to increased flow across Murmur due to increased flow across

the pulmonary and possibly tricuspid the pulmonary and possibly tricuspid valvesvalves

Significant symptoms uncommon Significant symptoms uncommon even with large defectseven with large defects

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ASDASD

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Shunt LesionsShunt Lesions•Ventricular level shunt

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VSDVSD Can occur anywhere along the ventricular Can occur anywhere along the ventricular

septumseptum Defects in the perimembranous region are Defects in the perimembranous region are

less likely to spontaneously close or even less likely to spontaneously close or even reduce in size and are more likely to reduce in size and are more likely to require interventionrequire intervention

Atrioventricular septal defects (AVSD/AV Atrioventricular septal defects (AVSD/AV canal/endocardial cushion defects)canal/endocardial cushion defects) Will generally behave like large VSDsWill generally behave like large VSDs

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VSDVSD

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VSDVSD Symptoms dependent on the size of the Symptoms dependent on the size of the

defect and the relative vascular defect and the relative vascular resistance between the systemic and resistance between the systemic and pulmonary systemspulmonary systems Congestive heart failure (CHF) signs and Congestive heart failure (CHF) signs and

symptomssymptoms Timing of CHF in infantsTiming of CHF in infants

Hemodynamically significant lesions Hemodynamically significant lesions result in LA and LV dilationresult in LA and LV dilation

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VSDVSD Cardiac findings dependent largely on the Cardiac findings dependent largely on the

size of the defectsize of the defect Typical VSD murmur harsh, pansystolic, Typical VSD murmur harsh, pansystolic,

flat-topped murmurflat-topped murmur Intensity of the murmur generally Intensity of the murmur generally

inversely proportional to the size of the inversely proportional to the size of the defectdefect

Very large lesions may result in outflow Very large lesions may result in outflow tract or systolic ejection-type murmurs tract or systolic ejection-type murmurs and possibly a diastolic rumbleand possibly a diastolic rumble

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VSDVSD Medical therapy utilized to improved Medical therapy utilized to improved

patient symptoms and optimize patient symptoms and optimize patient growthpatient growth Diuretics, digoxin, after-load reduction, Diuretics, digoxin, after-load reduction,

optimization of feedsoptimization of feeds

Surgical patch repair the mainstay Surgical patch repair the mainstay of treatment of hemodynamically of treatment of hemodynamically significant lesionssignificant lesions

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Shunt LesionsShunt Lesions Patent Ductus Patent Ductus

ArteriosusArteriosus Great Artery Great Artery

level shunt level shunt

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PDAPDA Continuous or ‘machinery-type’ murmurContinuous or ‘machinery-type’ murmur Hemodynamically significant shunts Hemodynamically significant shunts

result in left-sided volume overloadresult in left-sided volume overload

Larger lesions in infants surgically Larger lesions in infants surgically ligatedligated

Smaller PDAs in older children Smaller PDAs in older children generally closed via interventional generally closed via interventional catheter techniquescatheter techniques

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PDAPDA

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Cyanotic Congenital Heart Cyanotic Congenital Heart DiseaseDisease

Right to left shunting resulting in entry of Right to left shunting resulting in entry of desaturated blood into the systemic arterial desaturated blood into the systemic arterial systemsystem

Increased pulmonary blood flowIncreased pulmonary blood flow Truncus arteriosusTruncus arteriosus Transposition of the great arteriesTransposition of the great arteries Total anomolous pulmonary venous returnTotal anomolous pulmonary venous return

Decreased pulmonary blood flowDecreased pulmonary blood flow Tetralogy of Fallot/pulmonary atresiaTetralogy of Fallot/pulmonary atresia Tricuspid atresiaTricuspid atresia Critical pulmonary stenosisCritical pulmonary stenosis

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Cyanotic Congenital Cyanotic Congenital Heart Disease WithHeart Disease With

↑↑Pulmonary Blood FlowPulmonary Blood Flow

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d-Transposition d-Transposition

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Normal HeartNormal Heart

Body RA RV PA

LALVAO Lungs

Circulation is in “series”

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d-Transposition d-Transposition Circulation is in “parallel”Circulation is in “parallel”

BodyBody RARA RVRV AoAo

LungsLungs LALA LVLV PAPA

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TGATGA

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TGATGA Must bring oygenated blood into the systemic Must bring oygenated blood into the systemic

circulationcirculation Great artery level shunt - PDAGreat artery level shunt - PDA Atrial level shunt – PFOAtrial level shunt – PFO

Prostaglandin E1 (PGE)Prostaglandin E1 (PGE) Re-opens and maintains patency of the ductus Re-opens and maintains patency of the ductus

arteriosusarteriosus Balloon atrial septostomy (BAS)Balloon atrial septostomy (BAS)

Increase intracardiac shunting across the atrial Increase intracardiac shunting across the atrial septumseptum

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d-Transposition d-Transposition

BodyBody RARA RVRV AoAo

PFO PFO BASBAS PDA PDA PGEPGE

LungsLungs LALA LVLV PAPA

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BASBAS

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TGATGA

Arterial switch Arterial switch repairrepair Transection and Transection and

switching of great switching of great arteriesarteries

Movement of Movement of coronary arteries coronary arteries via tissue buttonsvia tissue buttons

Patching of neo-Patching of neo-pulmonary arterypulmonary artery

Closure of ASDClosure of ASD Ligation of PDALigation of PDA

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Total Anomalous Total Anomalous Pulmonary Venous Pulmonary Venous

ReturnReturn

Pulmonary veins fail to connect to left atrium

Pulmonary veins communicate with systemic vein

Combined systemic and pulmonary venous returns to the RA and circulates to the systemic and pulmonary systems via the ASD and TV

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TAPVDTAPVD Results in cyanosis and increased pulmonary Results in cyanosis and increased pulmonary

flow flow Dilated RA and RVDilated RA and RV Reasonably stable in the absence of obstruction Reasonably stable in the absence of obstruction

along the pulmonary venous pathwayalong the pulmonary venous pathway

Not a PGE dependent lesionNot a PGE dependent lesion

Surgical correctionSurgical correction Rerouting/baffling of pulmonary veins to the LARerouting/baffling of pulmonary veins to the LA

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Truncus arteriosusTruncus arteriosus 1. common, single 1. common, single

outflow tract with outflow tract with pulmonary arteries pulmonary arteries originating from the originating from the ascending aortaascending aorta

2. abnormal truncal 2. abnormal truncal valvevalve

3. large VSD3. large VSD

4. not a PGE 4. not a PGE dependent lesiondependent lesion

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Truncus arteriosusTruncus arteriosus

Closure of VSD to Closure of VSD to include truncus on include truncus on LV sideLV side

Placement of RV-Placement of RV-PA conduit with PA conduit with removal of PA’s removal of PA’s from the truncus from the truncus and reanatomosis and reanatomosis to the conduitto the conduit

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Cyanotic Congenital Cyanotic Congenital Heart DiseaseHeart Disease

Decreased Pulmonary Blood FlowDecreased Pulmonary Blood Flow

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Cyanotic Congenital Heart Cyanotic Congenital Heart Disease Disease

↓ ↓ Pulmonary FlowPulmonary Flow==

RVOT Obstruction + RVOT Obstruction + R->L Shunt R->L Shunt

Tetralogy of Fallot Tetralogy of Fallot 1. Pulmonary stenosis1. Pulmonary stenosis

2. Overriding aorta2. Overriding aorta

3. RVH3. RVH

4. VSD4. VSD

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Pulmonary atresia/VSDPulmonary atresia/VSD

Tetralogy of Fallot Tetralogy of Fallot with atretic with atretic pulmonary valvepulmonary valve

Variable Variable pulmonary artery pulmonary artery anatomyanatomy

Generally a PGE Generally a PGE dependent lesiondependent lesion

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Critical pulmonary Critical pulmonary stenosisstenosis

Severe pulmonary Severe pulmonary stenosis with stenosis with inadequate inadequate pulmonary flowpulmonary flow Pulmonary Pulmonary

atresia/intact atresia/intact ventricular septumventricular septum

PGE dependent PGE dependent lesionlesion

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Tricuspid atresiaTricuspid atresia 1. tricuspid atresia 1. tricuspid atresia 2. severely 2. severely

hypoplastic RVhypoplastic RV 3. VSD3. VSD 4. ASD – large4. ASD – large 5. pulmonary 5. pulmonary

stenosisstenosis VariableVariable

Generally a PGE Generally a PGE dependent lesiondependent lesion

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Cyanotic Heart DiseaseCyanotic Heart Disease Decreased blood flow due to RVOT Decreased blood flow due to RVOT

obstruction may require obstruction may require augmentation of pulmonary blood augmentation of pulmonary blood flow via creation of a surgical flow via creation of a surgical systemic to pulmonary shuntsystemic to pulmonary shunt

Blalock-Taussig Shunt (BTS)Blalock-Taussig Shunt (BTS)

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Blalock-Taussig ShuntBlalock-Taussig Shunt Developed in 1944 by Helen Developed in 1944 by Helen

Taussig, a Pediatric Cardiologist and Taussig, a Pediatric Cardiologist and Alfred Blalock the Chief Surgeon at Alfred Blalock the Chief Surgeon at John Hopkins Hospital in John Hopkins Hospital in conjunction with his research conjunction with his research assistant Vivien Thomas to prolong assistant Vivien Thomas to prolong the lives of children with Tetralogy the lives of children with Tetralogy of Fallot and became known as the of Fallot and became known as the ‘blue baby operation’.‘blue baby operation’.

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Case 1 (continued)Case 1 (continued) BTSBTS

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A DVD, A DVD, Partners of the HeartPartners of the Heart, is available , is available from the University of Ottawa, recounting from the University of Ottawa, recounting the development of the ‘blue baby the development of the ‘blue baby operation’operation’

Visit the website: Visit the website: www.pbs.org/wgbh/amex/partners/breakthroughs/b_surgeon.html, to review the hemodynamic effects of , to review the hemodynamic effects of Tetralogy of Fallot and the development of Tetralogy of Fallot and the development of the BTS operation, and perform virtual the BTS operation, and perform virtual surgery accompanied by Vivien Thomas’ surgery accompanied by Vivien Thomas’ voiced explanations of the procedure.voiced explanations of the procedure.

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BT ShuntBT Shunt

The original operation consisted of The original operation consisted of anastomosing the right subclavian artery to anastomosing the right subclavian artery to the right pulmonary artery, thus reliably the right pulmonary artery, thus reliably increasing the amount of blood flow to the increasing the amount of blood flow to the lungs which would also grow over with the lungs which would also grow over with the patientpatient

Currently, a modified BT shunt is generally Currently, a modified BT shunt is generally performed, using a Gortex tube graft to performed, using a Gortex tube graft to anastomose the subclavian artery to the anastomose the subclavian artery to the pulmonary artery and is still often used for pulmonary artery and is still often used for children with Tetralogy of Fallot as well as children with Tetralogy of Fallot as well as other cyanotic heart lesions where pulmonary other cyanotic heart lesions where pulmonary blood flow is limited.blood flow is limited.

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Critical Left-Sided ObstructionCritical Left-Sided Obstruction

Neonatal presentationNeonatal presentation

Critical aortic stenosisCritical aortic stenosis

CoarctationCoarctation

Hypoplastic left heart syndromeHypoplastic left heart syndrome

Cardiogenic shockCardiogenic shock

PGE dependent lesionsPGE dependent lesions

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Left-sided ObstructionLeft-sided Obstruction

Coarctation of Coarctation of the aortathe aorta Critical Critical

narrowing of narrowing of the the “juxtaductal” “juxtaductal” aortaaorta

Blood cannot Blood cannot get past the get past the obstruction obstruction

SHOCK

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CoarctationCoarctation Characterized by weak or absent Characterized by weak or absent

pulses particularly in the lower pulses particularly in the lower limbslimbs

Initiation of PGE lifesavingInitiation of PGE lifesaving ‘‘splitting’ of saturations seen in critical splitting’ of saturations seen in critical

narrowings with patency of ductus narrowings with patency of ductus arteriosus ie: normal saturation in right arteriosus ie: normal saturation in right arm and lower saturation in the lower arm and lower saturation in the lower limbs due to right to left shunting across limbs due to right to left shunting across the PDAthe PDA

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Coarctation - treatmentCoarctation - treatment Surgical correction following Surgical correction following

initiation of PGE and stabilizationinitiation of PGE and stabilization

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Left-Sided ObstructionLeft-Sided Obstruction Critical Aortic Critical Aortic

StenosisStenosis CRITICALCRITICAL

InadequateInadequate

forward flow to forward flow to

maintain cardiac maintain cardiac

outputoutput

SHOCK

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Critical ASCritical AS Weak pulses throughoutWeak pulses throughout Low blood pressureLow blood pressure Variable murmurVariable murmur AcyanoticAcyanotic

PGEPGE

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Critical AS - TreatmentCritical AS - Treatment Balloon valvuloplasty or surgical Balloon valvuloplasty or surgical

valvuloplastyvalvuloplasty

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Left Ventricular Outflow Left Ventricular Outflow Tract ObstructionTract Obstruction

Hypoplastic Left Hypoplastic Left Heart Syndrome Heart Syndrome (HLHS)(HLHS)

1. Mitral atresia1. Mitral atresia

2. Aortic atresia2. Aortic atresia

3. Hypoplastic left 3. Hypoplastic left ventricleventricle

4. Hypoplastic 4. Hypoplastic ascending aortaascending aorta

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HLHSHLHS Initially cyanoticInitially cyanotic With closure of the PDA With closure of the PDA

SHOCK SHOCK Tachycardia, tachypnea, low blood Tachycardia, tachypnea, low blood

pressure, weak pulses, poor perfusion, pressure, weak pulses, poor perfusion, cyanotic/grey colourcyanotic/grey colour

PGEPGE

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HLHSHLHS

Norwood Norwood procedureprocedure Stage I single Stage I single

ventricle palliationventricle palliation

Heart TransplantHeart Transplant

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. Angiographic image of the 3 Amplatzer atrial septal occluder devices after release, indicated by the black arrows.

Copyright © American Heart Association

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(a) Graft angiogram obtained in the frontal projection shows abrupt cutoff (arrow) of the native brachial artery, which represents an acute embolus following use of the ATD.

Sofocleous C T et al. Radiology 1999;213:561-567

©1999 by Radiological Society of North America

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(a) Graft angiogram obtained in the frontal projection shows abrupt cutoff (arrow) of the native brachial artery, which represents an acute embolus following use of the ATD.

Sofocleous C T et al. Radiology 1999;213:561-567

©1999 by Radiological Society of North America

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. Transesophageal echocardiogram midesophageal aortic valve long axis at a multiplane angle of 128 degrees with the Amplatzer device in the left ventricular outflow tract.

MacKnight B M et al. Anesth Analg 2007;105:1229-1230

©2007 by Lippincott Williams & Wilkins

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Cine recording showing correct position of the fenestrated Amplatzer device.

Althoff T F et al. Chest 2008;133:283-285

©2008 by American College of Chest Physicians

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Copyright © 2008 by the American Roentgen Ray Society

Lee, T. et al. Am. J. Roentgenol. 2007;188:W431-W439

--43-year-old man with marked device protrusion after insertion of Amplatzer septal occluder (AGA Medical Corporation)

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Transhepatic technique (continued)

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Transhepatic technique (continued)

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Transhepatic technique (continued)

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Transhepatic technique (continued)

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Transhepatic interventions

Others

atrial septal defect device occlusion (2) Fontan fenestration device occlusion (2) coil embolization of pulmonary artery

pseudoaneurysm(2) device retrieval (1) endomyocardial biopsy (1)

Sheath sizes: 4-14 French

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Pulmonary valvuloplasty

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Pulmonary valvuloplasty(continued)

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Pulmonary valvuloplasty(continued)

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Pulmonary valvuloplasty(continued)

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Pulmonary valvuloplasty(continued)

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Fontan stent placement

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Fontan stent placement (continued)

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Fontan stent placement (continued)

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Fontan stent placement (continued)

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Fontan stent placement (continued)

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Conclusions

The transhepatic approach is effective as a route for right sided cardiac catheterization and can be performed with relative safety

The transhepatic approach will allow therapeutic procedures to be performed in a subset of children where this has been previously not possible

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Angiographic image of the 3 Amplatzer atrial septal occluder devices after release, indicated by the black arrows.

Arcidiacono C et al. Circ Cardiovasc Imaging 2008;1:e15-e16

Copyright © American Heart Association

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Live transthoracic 3D image of the right surface of the atrial septum with the 3 devices indicated by white and black arrows.

Arcidiacono C et al. Circ Cardiovasc Imaging 2008;1:e15-e16

Copyright © American Heart Association

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663

Autorhythmic CellsAutorhythmic Cells Cells fire spontaneously, act as pacemaker and Cells fire spontaneously, act as pacemaker and

form conduction system for the heartform conduction system for the heart SA nodeSA node

cluster of cells in wall of Rt. Atriacluster of cells in wall of Rt. Atria begins heart activity that spreads to both atriabegins heart activity that spreads to both atria excitation spreads to AV nodeexcitation spreads to AV node

AV nodeAV node in atrial septum, transmits signal to bundle of in atrial septum, transmits signal to bundle of

HisHis AV bundle of His AV bundle of His

the connection between atria and ventriclesthe connection between atria and ventricles divides into bundle branches & purkinje fibers, divides into bundle branches & purkinje fibers,

large diameter fibers that conduct signals large diameter fibers that conduct signals quicklyquickly

Conduction System of Conduction System of HeartHeart

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Rhythm of Conduction Rhythm of Conduction SystemSystem

SA node fires spontaneously 90-100 times per SA node fires spontaneously 90-100 times per minuteminute

AV node fires at 40-50 times per minuteAV node fires at 40-50 times per minute If both nodes are suppressed fibers in If both nodes are suppressed fibers in

ventricles by themselves fire only 20-40 times ventricles by themselves fire only 20-40 times per minuteper minute

Artificial pacemaker needed if pace is too slowArtificial pacemaker needed if pace is too slow Extra beats forming at other sites are called Extra beats forming at other sites are called

ectopic pacemakersectopic pacemakers caffeine & nicotine increase activitycaffeine & nicotine increase activity

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Ventricular PressuresVentricular Pressures

Blood pressure in aorta is 120mm HgBlood pressure in aorta is 120mm Hg Blood pressure in pulmonary trunk is 30mm Blood pressure in pulmonary trunk is 30mm

HgHg Differences in ventricle wall thickness Differences in ventricle wall thickness

allows heart to push the same amount of allows heart to push the same amount of blood with more force from the left ventricleblood with more force from the left ventricle

The volume of blood ejected from each The volume of blood ejected from each ventricle is 70ml (stroke volume) ventricle is 70ml (stroke volume)

Why do both stroke volumes need to be Why do both stroke volumes need to be same?same?

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Heart SoundsHeart Sounds

Where to listen on chest wall for heart sounds.

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Cardiac OutputCardiac Output

Amount of blood pushed into aorta or Amount of blood pushed into aorta or pulmonary trunk by ventriclepulmonary trunk by ventricle

Determined by stroke volume and heart rateDetermined by stroke volume and heart rate CO = SV x HRCO = SV x HR

at 70ml stroke volume & 75 beat/min----5 and at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min1/4 liters/min

entire blood supply passes through circulatory entire blood supply passes through circulatory system every minutesystem every minute

Cardiac reserve is maximum output/output Cardiac reserve is maximum output/output at restat rest average is 4-5 while athlete is 7-8average is 4-5 while athlete is 7-8

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Influences on Stroke Influences on Stroke VolumeVolume

Preload (affect of stretching)Preload (affect of stretching) Frank-Starling Law of HeartFrank-Starling Law of Heart more muscle is stretched, greater force of more muscle is stretched, greater force of

contractioncontraction more blood more force of contraction resultsmore blood more force of contraction results

ContractilityContractility autonomic nerves, hormones, Ca+2 or K+ levelsautonomic nerves, hormones, Ca+2 or K+ levels

AfterloadAfterload amount of pressure created by the blood in the amount of pressure created by the blood in the

wayway high blood pressure creates high afterloadhigh blood pressure creates high afterload

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Stroke Volume and Stroke Volume and Heart RateHeart Rate

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Congestive Heart Failure Congestive Heart Failure

Causes of CHFCauses of CHF coronary artery disease, hypertension, MI, valve coronary artery disease, hypertension, MI, valve

disorders, congenital defectsdisorders, congenital defects Left side heart failureLeft side heart failure

less effective pump so more blood remains in less effective pump so more blood remains in ventricleventricle

heart is overstretched & even more blood heart is overstretched & even more blood remainsremains

blood backs up into lungs as pulmonary edemablood backs up into lungs as pulmonary edema suffocation & lack of oxygen to the tissuessuffocation & lack of oxygen to the tissues

Right side failure Right side failure fluid builds up in tissues as peripheral edemafluid builds up in tissues as peripheral edema

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Physiology of Physiology of ContractionContraction

Depolarization, plateau, repolarizationDepolarization, plateau, repolarization

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Depolarization & Depolarization & RepolarizationRepolarization

DepolarizationDepolarization Cardiac cell resting membrane potential is -90mvCardiac cell resting membrane potential is -90mv excitation spreads through gap junctionsexcitation spreads through gap junctions fast Na+ channels open for rapid depolarizationfast Na+ channels open for rapid depolarization

Plateau phase Plateau phase 250 msec (only 1msec in neuron) 250 msec (only 1msec in neuron) slow Caslow Ca+2+2 channels open, let Ca channels open, let Ca +2+2 enter from enter from

outside cell and from storage in sarcoplasmic outside cell and from storage in sarcoplasmic reticulum, while Kreticulum, while K++ channels close channels close

Ca Ca +2+2 binds to troponin to allow for actin-myosin binds to troponin to allow for actin-myosin cross-bridge formation & tension developmentcross-bridge formation & tension development

Repolarization Repolarization CaCa+2+2 channels close and K channels close and K++ channels open & -90mv channels open & -90mv

is restored as potassium leaves the cellis restored as potassium leaves the cell Refractory period Refractory period

very long so heart can fillvery long so heart can fill

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673

Changes in cell membrane permeability.

Action Potential in Cardiac Action Potential in Cardiac MuscleMuscle

Page 672: Curs Cardiologie Intervent 3 Martie 2011-Final

674

Electrocardiogram---ECG or Electrocardiogram---ECG or EKGEKG

EKGEKG Action potentials of all Action potentials of all

active cells can be active cells can be detected and recorded detected and recorded

P waveP wave atrial depolarization atrial depolarization

P to Q intervalP to Q interval conduction time from conduction time from

atrial to ventricular atrial to ventricular excitation excitation

QRS complex QRS complex ventricular depolarizationventricular depolarization

T waveT wave ventricular repolarizationventricular repolarization

Page 673: Curs Cardiologie Intervent 3 Martie 2011-Final

675

One Cardiac CycleOne Cardiac Cycle At 75 beats/min, one cycle requires 0.8 sec.At 75 beats/min, one cycle requires 0.8 sec.

systole (contraction) and diastole (relaxation) of systole (contraction) and diastole (relaxation) of both atria, plus the systole and diastole of both both atria, plus the systole and diastole of both ventriclesventricles

End diastolic volume (EDV)End diastolic volume (EDV) volume in ventricle at end of diastole, about volume in ventricle at end of diastole, about

130ml130ml End systolic volume (ESV)End systolic volume (ESV)

volume in ventricle at end of systole, about 60mlvolume in ventricle at end of systole, about 60ml Stroke volume (SV)Stroke volume (SV)

the volume ejected per beat from each ventricle, the volume ejected per beat from each ventricle, about 70mlabout 70ml

SV = EDV - ESVSV = EDV - ESV

Page 674: Curs Cardiologie Intervent 3 Martie 2011-Final

676

Phases ofPhases of Cardiac CycleCardiac Cycle Isovolumetric relaxationIsovolumetric relaxation

brief period when volume in ventricles does not brief period when volume in ventricles does not change--as ventricles relax, pressure drops and change--as ventricles relax, pressure drops and AV valves openAV valves open

Ventricular fillingVentricular filling rapid ventricular filling:as blood flows from full rapid ventricular filling:as blood flows from full

atriaatria diastasis: as blood flows from atria in smaller diastasis: as blood flows from atria in smaller

volumevolume atrial systole pushes final 20-25 ml blood into atrial systole pushes final 20-25 ml blood into

ventricleventricle Ventricular systoleVentricular systole

ventricular systoleventricular systole isovolumetric contractionisovolumetric contraction

brief period, AV valves close before SL valves open brief period, AV valves close before SL valves open ventricular ejection: as SL valves open and blood ventricular ejection: as SL valves open and blood

is ejectedis ejected

Page 675: Curs Cardiologie Intervent 3 Martie 2011-Final

677

Cardiac CycleCardiac Cycle

Page 676: Curs Cardiologie Intervent 3 Martie 2011-Final

678

Ventricular PressuresVentricular Pressures

Blood pressure in aorta is 120mm HgBlood pressure in aorta is 120mm Hg Blood pressure in pulmonary trunk is 30mm Blood pressure in pulmonary trunk is 30mm

HgHg Differences in ventricle wall thickness Differences in ventricle wall thickness

allows heart to push the same amount of allows heart to push the same amount of blood with more force from the left ventricleblood with more force from the left ventricle

The volume of blood ejected from each The volume of blood ejected from each ventricle is 70ml (stroke volume) ventricle is 70ml (stroke volume)

Why do both stroke volumes need to be Why do both stroke volumes need to be same?same?

Page 677: Curs Cardiologie Intervent 3 Martie 2011-Final

679

AuscultationAuscultation

StethoscopeStethoscope Sounds of heartbeat are from Sounds of heartbeat are from

turbulence in blood flow caused by turbulence in blood flow caused by valve closurevalve closure first heart sound (lubb) is created with the first heart sound (lubb) is created with the

closing of the atrioventricular valvesclosing of the atrioventricular valves second heart sound (dupp) is created with second heart sound (dupp) is created with

the closing of semilunar valvesthe closing of semilunar valves

Page 678: Curs Cardiologie Intervent 3 Martie 2011-Final

680

Heart SoundsHeart Sounds

Where to listen on chest wall for heart sounds.

Page 679: Curs Cardiologie Intervent 3 Martie 2011-Final

681

Cardiac OutputCardiac Output

Amount of blood pushed into aorta or Amount of blood pushed into aorta or pulmonary trunk by ventriclepulmonary trunk by ventricle

Determined by stroke volume and heart rateDetermined by stroke volume and heart rate CO = SV x HRCO = SV x HR

at 70ml stroke volume & 75 beat/min----5 and at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min1/4 liters/min

entire blood supply passes through circulatory entire blood supply passes through circulatory system every minutesystem every minute

Cardiac reserve is maximum output/output Cardiac reserve is maximum output/output at restat rest average is 4-5 while athlete is 7-8average is 4-5 while athlete is 7-8

Page 680: Curs Cardiologie Intervent 3 Martie 2011-Final

682

Influences on Stroke Influences on Stroke VolumeVolume

Preload (affect of stretching)Preload (affect of stretching) Frank-Starling Law of HeartFrank-Starling Law of Heart more muscle is stretched, greater force of more muscle is stretched, greater force of

contractioncontraction more blood more force of contraction resultsmore blood more force of contraction results

ContractilityContractility autonomic nerves, hormones, Ca+2 or K+ levelsautonomic nerves, hormones, Ca+2 or K+ levels

AfterloadAfterload amount of pressure created by the blood in the amount of pressure created by the blood in the

wayway high blood pressure creates high afterloadhigh blood pressure creates high afterload

Page 681: Curs Cardiologie Intervent 3 Martie 2011-Final

683

Stroke Volume and Stroke Volume and Heart RateHeart Rate

Page 682: Curs Cardiologie Intervent 3 Martie 2011-Final

684

Congestive Heart Failure Congestive Heart Failure

Causes of CHFCauses of CHF coronary artery disease, hypertension, MI, valve coronary artery disease, hypertension, MI, valve

disorders, congenital defectsdisorders, congenital defects Left side heart failureLeft side heart failure

less effective pump so more blood remains in less effective pump so more blood remains in ventricleventricle

heart is overstretched & even more blood heart is overstretched & even more blood remainsremains

blood backs up into lungs as pulmonary edemablood backs up into lungs as pulmonary edema suffocation & lack of oxygen to the tissuessuffocation & lack of oxygen to the tissues

Right side failure Right side failure fluid builds up in tissues as peripheral edemafluid builds up in tissues as peripheral edema

Page 683: Curs Cardiologie Intervent 3 Martie 2011-Final

685

Desirable Levels of Desirable Levels of Blood Cholesterol for Blood Cholesterol for

AdultsAdults TC (total cholesterol) under 200 mg/dlTC (total cholesterol) under 200 mg/dl LDL under 130 mg/dlLDL under 130 mg/dl HDL over 40 mg/dlHDL over 40 mg/dl Normally, triglycerides are in the range of Normally, triglycerides are in the range of

10-190 mg/dl.10-190 mg/dl. Among the therapies used to reduce Among the therapies used to reduce

blood cholesterol level are exercise, diet, blood cholesterol level are exercise, diet, and drugs.and drugs.

Page 684: Curs Cardiologie Intervent 3 Martie 2011-Final

686

Exercise and the HeartExercise and the Heart

Sustained exercise increases oxygen Sustained exercise increases oxygen demand in muscles.demand in muscles.

Benefits of aerobic exercise (any activity Benefits of aerobic exercise (any activity that works large body muscles for at least that works large body muscles for at least 20 minutes, preferably 3-5 times per 20 minutes, preferably 3-5 times per week) are;week) are; increased cardiac outputincreased cardiac output increased HDL and decreased triglyceridesincreased HDL and decreased triglycerides improved lung functionimproved lung function decreased blood pressuredecreased blood pressure weight control.weight control.

Page 685: Curs Cardiologie Intervent 3 Martie 2011-Final

687

Developmental Anatomy of Developmental Anatomy of the Heartthe Heart

The heart develops The heart develops from mesoderm from mesoderm before the end of before the end of the third week of the third week of gestation.gestation.

The tubes develop The tubes develop into the four-into the four-chambered heart chambered heart and great vessels and great vessels of the heart.of the heart.

Page 686: Curs Cardiologie Intervent 3 Martie 2011-Final

688

Autorhythmic CellsAutorhythmic Cells Cells fire spontaneously, act as pacemaker and Cells fire spontaneously, act as pacemaker and

form conduction system for the heartform conduction system for the heart SA nodeSA node

cluster of cells in wall of Rt. Atriacluster of cells in wall of Rt. Atria begins heart activity that spreads to both atriabegins heart activity that spreads to both atria excitation spreads to AV nodeexcitation spreads to AV node

AV nodeAV node in atrial septum, transmits signal to bundle of in atrial septum, transmits signal to bundle of

HisHis AV bundle of His AV bundle of His

the connection between atria and ventriclesthe connection between atria and ventricles divides into bundle branches & purkinje fibers, divides into bundle branches & purkinje fibers,

large diameter fibers that conduct signals large diameter fibers that conduct signals quicklyquickly

Conduction System of Conduction System of HeartHeart

Page 687: Curs Cardiologie Intervent 3 Martie 2011-Final

689

Rhythm of Conduction Rhythm of Conduction SystemSystem

SA node fires spontaneously 90-100 times per SA node fires spontaneously 90-100 times per minuteminute

AV node fires at 40-50 times per minuteAV node fires at 40-50 times per minute If both nodes are suppressed fibers in If both nodes are suppressed fibers in

ventricles by themselves fire only 20-40 times ventricles by themselves fire only 20-40 times per minuteper minute

Artificial pacemaker needed if pace is too slowArtificial pacemaker needed if pace is too slow Extra beats forming at other sites are called Extra beats forming at other sites are called

ectopic pacemakersectopic pacemakers caffeine & nicotine increase activitycaffeine & nicotine increase activity

Page 688: Curs Cardiologie Intervent 3 Martie 2011-Final

690

Timing of Atrial & Timing of Atrial & Ventricular ExcitationVentricular Excitation

SA node setting pace since is the fastestSA node setting pace since is the fastest In 50 msec excitation spreads through In 50 msec excitation spreads through

both atria and down to AV nodeboth atria and down to AV node 100 msec delay at AV node due to 100 msec delay at AV node due to

smaller diameter fibers- allows atria to smaller diameter fibers- allows atria to fully contract filling ventricles before fully contract filling ventricles before ventricles contractventricles contract

In 50 msec excitation spreads through In 50 msec excitation spreads through both ventricles simultaneouslyboth ventricles simultaneously

Page 689: Curs Cardiologie Intervent 3 Martie 2011-Final

691

Autorhythmic CellsAutorhythmic Cells Cells fire spontaneously, act as pacemaker and Cells fire spontaneously, act as pacemaker and

form conduction system for the heartform conduction system for the heart SA nodeSA node

cluster of cells in wall of Rt. Atriacluster of cells in wall of Rt. Atria begins heart activity that spreads to both atriabegins heart activity that spreads to both atria excitation spreads to AV nodeexcitation spreads to AV node

AV nodeAV node in atrial septum, transmits signal to bundle of in atrial septum, transmits signal to bundle of

HisHis AV bundle of His AV bundle of His

the connection between atria and ventriclesthe connection between atria and ventricles divides into bundle branches & purkinje fibers, divides into bundle branches & purkinje fibers,

large diameter fibers that conduct signals large diameter fibers that conduct signals quicklyquickly

Conduction System of Conduction System of HeartHeart

Page 690: Curs Cardiologie Intervent 3 Martie 2011-Final

692

Rhythm of Conduction Rhythm of Conduction SystemSystem

SA node fires spontaneously 90-100 times per SA node fires spontaneously 90-100 times per minuteminute

AV node fires at 40-50 times per minuteAV node fires at 40-50 times per minute If both nodes are suppressed fibers in If both nodes are suppressed fibers in

ventricles by themselves fire only 20-40 times ventricles by themselves fire only 20-40 times per minuteper minute

Artificial pacemaker needed if pace is too slowArtificial pacemaker needed if pace is too slow Extra beats forming at other sites are called Extra beats forming at other sites are called

ectopic pacemakersectopic pacemakers caffeine & nicotine increase activitycaffeine & nicotine increase activity

Page 691: Curs Cardiologie Intervent 3 Martie 2011-Final

693

Timing of Atrial & Timing of Atrial & Ventricular ExcitationVentricular Excitation

SA node setting pace since is the fastestSA node setting pace since is the fastest In 50 msec excitation spreads through In 50 msec excitation spreads through

both atria and down to AV nodeboth atria and down to AV node 100 msec delay at AV node due to 100 msec delay at AV node due to

smaller diameter fibers- allows atria to smaller diameter fibers- allows atria to fully contract filling ventricles before fully contract filling ventricles before ventricles contractventricles contract

In 50 msec excitation spreads through In 50 msec excitation spreads through both ventricles simultaneouslyboth ventricles simultaneously

Page 692: Curs Cardiologie Intervent 3 Martie 2011-Final

694

Developmental Anatomy of Developmental Anatomy of the Heartthe Heart

The heart develops The heart develops from mesoderm from mesoderm before the end of before the end of the third week of the third week of gestation.gestation.

The tubes develop The tubes develop into the four-into the four-chambered heart chambered heart and great vessels and great vessels of the heart.of the heart.

Page 693: Curs Cardiologie Intervent 3 Martie 2011-Final

695

Physiology of Physiology of ContractionContraction

Depolarization, plateau, repolarizationDepolarization, plateau, repolarization

Page 694: Curs Cardiologie Intervent 3 Martie 2011-Final

696

Depolarization & Depolarization & RepolarizationRepolarization

DepolarizationDepolarization Cardiac cell resting membrane potential is -90mvCardiac cell resting membrane potential is -90mv excitation spreads through gap junctionsexcitation spreads through gap junctions fast Na+ channels open for rapid depolarizationfast Na+ channels open for rapid depolarization

Plateau phase Plateau phase 250 msec (only 1msec in neuron) 250 msec (only 1msec in neuron) slow Caslow Ca+2+2 channels open, let Ca channels open, let Ca +2+2 enter from enter from

outside cell and from storage in sarcoplasmic outside cell and from storage in sarcoplasmic reticulum, while Kreticulum, while K++ channels close channels close

Ca Ca +2+2 binds to troponin to allow for actin-myosin binds to troponin to allow for actin-myosin cross-bridge formation & tension developmentcross-bridge formation & tension development

Repolarization Repolarization CaCa+2+2 channels close and K channels close and K++ channels open & -90mv channels open & -90mv

is restored as potassium leaves the cellis restored as potassium leaves the cell Refractory period Refractory period

very long so heart can fillvery long so heart can fill

Page 695: Curs Cardiologie Intervent 3 Martie 2011-Final

697

Changes in cell membrane permeability.

Action Potential in Cardiac Action Potential in Cardiac MuscleMuscle

Page 696: Curs Cardiologie Intervent 3 Martie 2011-Final

698

Electrocardiogram---ECG or Electrocardiogram---ECG or EKGEKG

EKGEKG Action potentials of all Action potentials of all

active cells can be active cells can be detected and recorded detected and recorded

P waveP wave atrial depolarization atrial depolarization

P to Q intervalP to Q interval conduction time from conduction time from

atrial to ventricular atrial to ventricular excitation excitation

QRS complex QRS complex ventricular depolarizationventricular depolarization

T waveT wave ventricular repolarizationventricular repolarization

Page 697: Curs Cardiologie Intervent 3 Martie 2011-Final

699

One Cardiac CycleOne Cardiac Cycle At 75 beats/min, one cycle requires 0.8 sec.At 75 beats/min, one cycle requires 0.8 sec.

systole (contraction) and diastole (relaxation) of systole (contraction) and diastole (relaxation) of both atria, plus the systole and diastole of both both atria, plus the systole and diastole of both ventriclesventricles

End diastolic volume (EDV)End diastolic volume (EDV) volume in ventricle at end of diastole, about volume in ventricle at end of diastole, about

130ml130ml End systolic volume (ESV)End systolic volume (ESV)

volume in ventricle at end of systole, about 60mlvolume in ventricle at end of systole, about 60ml Stroke volume (SV)Stroke volume (SV)

the volume ejected per beat from each ventricle, the volume ejected per beat from each ventricle, about 70mlabout 70ml

SV = EDV - ESVSV = EDV - ESV

Page 698: Curs Cardiologie Intervent 3 Martie 2011-Final

700

Phases ofPhases of Cardiac CycleCardiac Cycle Isovolumetric relaxationIsovolumetric relaxation

brief period when volume in ventricles does not brief period when volume in ventricles does not change--as ventricles relax, pressure drops and change--as ventricles relax, pressure drops and AV valves openAV valves open

Ventricular fillingVentricular filling rapid ventricular filling:as blood flows from full rapid ventricular filling:as blood flows from full

atriaatria diastasis: as blood flows from atria in smaller diastasis: as blood flows from atria in smaller

volumevolume atrial systole pushes final 20-25 ml blood into atrial systole pushes final 20-25 ml blood into

ventricleventricle Ventricular systoleVentricular systole

ventricular systoleventricular systole isovolumetric contractionisovolumetric contraction

brief period, AV valves close before SL valves open brief period, AV valves close before SL valves open ventricular ejection: as SL valves open and blood ventricular ejection: as SL valves open and blood

is ejectedis ejected

Page 699: Curs Cardiologie Intervent 3 Martie 2011-Final

701

Cardiac CycleCardiac Cycle

Page 700: Curs Cardiologie Intervent 3 Martie 2011-Final

702

Ventricular PressuresVentricular Pressures

Blood pressure in aorta is 120mm HgBlood pressure in aorta is 120mm Hg Blood pressure in pulmonary trunk is 30mm Blood pressure in pulmonary trunk is 30mm

HgHg Differences in ventricle wall thickness Differences in ventricle wall thickness

allows heart to push the same amount of allows heart to push the same amount of blood with more force from the left ventricleblood with more force from the left ventricle

The volume of blood ejected from each The volume of blood ejected from each ventricle is 70ml (stroke volume) ventricle is 70ml (stroke volume)

Why do both stroke volumes need to be Why do both stroke volumes need to be same?same?

Page 701: Curs Cardiologie Intervent 3 Martie 2011-Final

703

AuscultationAuscultation

StethoscopeStethoscope Sounds of heartbeat are from Sounds of heartbeat are from

turbulence in blood flow caused by turbulence in blood flow caused by valve closurevalve closure first heart sound (lubb) is created with the first heart sound (lubb) is created with the

closing of the atrioventricular valvesclosing of the atrioventricular valves second heart sound (dupp) is created with second heart sound (dupp) is created with

the closing of semilunar valvesthe closing of semilunar valves

Page 702: Curs Cardiologie Intervent 3 Martie 2011-Final

704

Heart SoundsHeart Sounds

Where to listen on chest wall for heart sounds.

Page 703: Curs Cardiologie Intervent 3 Martie 2011-Final

705

Cardiac OutputCardiac Output

Amount of blood pushed into aorta or Amount of blood pushed into aorta or pulmonary trunk by ventriclepulmonary trunk by ventricle

Determined by stroke volume and heart rateDetermined by stroke volume and heart rate CO = SV x HRCO = SV x HR

at 70ml stroke volume & 75 beat/min----5 and at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min1/4 liters/min

entire blood supply passes through circulatory entire blood supply passes through circulatory system every minutesystem every minute

Cardiac reserve is maximum output/output Cardiac reserve is maximum output/output at restat rest average is 4-5 while athlete is 7-8average is 4-5 while athlete is 7-8

Page 704: Curs Cardiologie Intervent 3 Martie 2011-Final

706

Influences on Stroke Influences on Stroke VolumeVolume

Preload (affect of stretching)Preload (affect of stretching) Frank-Starling Law of HeartFrank-Starling Law of Heart more muscle is stretched, greater force of more muscle is stretched, greater force of

contractioncontraction more blood more force of contraction resultsmore blood more force of contraction results

ContractilityContractility autonomic nerves, hormones, Ca+2 or K+ levelsautonomic nerves, hormones, Ca+2 or K+ levels

AfterloadAfterload amount of pressure created by the blood in the amount of pressure created by the blood in the

wayway high blood pressure creates high afterloadhigh blood pressure creates high afterload

Page 705: Curs Cardiologie Intervent 3 Martie 2011-Final

707

Stroke Volume and Stroke Volume and Heart RateHeart Rate

Page 706: Curs Cardiologie Intervent 3 Martie 2011-Final

708

Congestive Heart Failure Congestive Heart Failure

Causes of CHFCauses of CHF coronary artery disease, hypertension, MI, valve coronary artery disease, hypertension, MI, valve

disorders, congenital defectsdisorders, congenital defects Left side heart failureLeft side heart failure

less effective pump so more blood remains in less effective pump so more blood remains in ventricleventricle

heart is overstretched & even more blood heart is overstretched & even more blood remainsremains

blood backs up into lungs as pulmonary edemablood backs up into lungs as pulmonary edema suffocation & lack of oxygen to the tissuessuffocation & lack of oxygen to the tissues

Right side failure Right side failure fluid builds up in tissues as peripheral edemafluid builds up in tissues as peripheral edema

Page 707: Curs Cardiologie Intervent 3 Martie 2011-Final

Renovascular Diseaserecognition and

management

Craig A. Thompson, M.D., MMSc.Cardiac and Vascular Interventional

ServicesDartmouth Hitchcock Medical

CenterLebanon, NH

Page 708: Curs Cardiologie Intervent 3 Martie 2011-Final

Etiology of Renal Artery Stenosis

Fibromuscular dysplasia

Atherosclerosis

Polyarteritis Nodosa

Radiation-induced

Takayasu’s arteritis

Page 709: Curs Cardiologie Intervent 3 Martie 2011-Final

Mark A. Pohl

Page 710: Curs Cardiologie Intervent 3 Martie 2011-Final

MRA & Contrast Angiography

Page 711: Curs Cardiologie Intervent 3 Martie 2011-Final

Screening Aortography

RN

LN

Page 712: Curs Cardiologie Intervent 3 Martie 2011-Final

Renal Artery Stenting

pre post

Page 713: Curs Cardiologie Intervent 3 Martie 2011-Final

Global Renal Revascularization

Page 714: Curs Cardiologie Intervent 3 Martie 2011-Final

OCCLUSIONDEVICES

Page 715: Curs Cardiologie Intervent 3 Martie 2011-Final

Gadolinium Renal AngiogramGadolinium Renal Angiogram

No trans-lesional gradient with 5F catheter

RR

Page 716: Curs Cardiologie Intervent 3 Martie 2011-Final

Gadolinium Renal AngiogramGadolinium Renal Angiogram

60mmHg gradient with 4F catheter

IVUS with87% stenosisc/t reference

vesselLL

Page 717: Curs Cardiologie Intervent 3 Martie 2011-Final

Abdominal Aortogram: Late Phase

Page 718: Curs Cardiologie Intervent 3 Martie 2011-Final

Early PhaseLate Phase

Selective Left Renal Angiogram

Page 719: Curs Cardiologie Intervent 3 Martie 2011-Final

Selective Right Renal Angiogram

?

Page 720: Curs Cardiologie Intervent 3 Martie 2011-Final

Selective Lumbar Angiogram: Wire

Position

0.018” Glidewire

5F Cobra

5F Cobra / 7F IM Guide

Page 721: Curs Cardiologie Intervent 3 Martie 2011-Final

CAMELOTCAMELOTCComparison of omparison of AmAmlodipine vs lodipine vs EEnalapril to nalapril to LLimit imit

OOccurrences of ccurrences of TThrombosishrombosis

NORMALISE NORMALISE NoNorvasc for rvasc for RRegression of egression of MManifest anifest AAtherosclerotic therosclerotic LLesions by esions by IIntravascular ntravascular SSonographic onographic EEvaluationvaluation

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724

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725

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726

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727

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728

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729

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730

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731

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732

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733

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734

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735

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736

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737

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738

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739

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740

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741

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742

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743

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744

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745

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746

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747

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748

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749

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751

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752

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753

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754

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755

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756

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Clinical application of IVUS.

Schoenhagen P , Nissen S Heart 2002;88:91-96

©2002 by BMJ Publishing Group Ltd and British Cardiovascular Society

Page 756: Curs Cardiologie Intervent 3 Martie 2011-Final

Clinical application of IVUS.

Schoenhagen P , Nissen S Heart 2002;88:91-96

©2002 by BMJ Publishing Group Ltd and British Cardiovascular Society

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759

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760

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761

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766

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767

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768

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769

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770

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771

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772

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788

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789

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790

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791

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792

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793

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794

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795

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796

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797

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798

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799

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802

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803

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804

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805

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806

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807

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808

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809

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810

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811

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812

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Pathogenesis of ACS

Non-Vulnerable

Atherosclerotic Plaque

Non-Vulnerable

Atherosclerotic Plaque

Vulnerable Atherosclerotic

Plaque

Vulnerable Atherosclerotic

Plaque