post infarct vsd, nicvd

7/27/2019 Post Infarct VSD, NICVD

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POST INFARCT VSR AND ITSRECENT UPDATES

PRESENTER-DR A.Y.M. SHAHIDULLAH

MS STUDENT

MODERATOR-

DR. RAMPADA SARKER

ASST. PROFESSOR

DEPT. OF CARDIAC SERGURYNICVD


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DEFINITION

Post infarct ventricular septal rupture (VSR) is a defect in theventricular septum that results from rupture of acutely infarctedmyocardium.


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History

In 1845, Latham described a postinfarction ventricular septal rupture at

autopsy.

In 1923, Brunn first made the diagnosis antemortem.

In 1934, Sager added the 18th case to the world literature andestablished specific clinical criteria for diagnosis.

In 1956, Cooley and associates performed the first successful surgical

repair in a patient 9 weeks after the diagnosis of septal rupture.


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Incidence

Approximately 1% to 2% of cases of acute myocardial infarctions (AMI)results in VSR and account for about 5% of early deaths.

The average time from infarction to rupture is between 2 and 4 days, but it

may be as short as a few hours or as long as 2 weeks.

Post infarction VSR occur in men more often than women (3 to 2).


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Pathogenesis

Slippage of myocytes during infarct expansion allow blood to dissect throughthe necrotic myocardium and enter either the right ventricle or pericardialspace.

Hyaline degeneration of cardiomyocytes with subsequent fragmentation andenzymatic digestion allow fissures to form, predisposing to rupture.

Post infarction ventricular rupture usually associated with complete

occlusion rather than severe stenosis of a coronary artery.


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Types of VSR

Simple:

It consists of a direct through-and-through defect, located anteriorly, in

approximately 60% of cases, following occlusion of the left anterior

descending artery.

Complex:

It consists of a serpiginous dissection tract remote from the primary septal

defect, located inferiorly, about 20% to 40% of patients.


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PathophysiologyAcute Ventricular Infarction Acute Myocardial Infarction

Ventricular Septal Rupture Ventricular Dysfunction

Acute Left To Right Shunt Heart Failure ( Rt or Lt or Both)

Cardiogenic Shock

Multi Organ Failure


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Natural History

Mortality of postinfarction septal rupture without surgical intervention -

About 25% within the first 24 hours,About 50% within 1 week,

About 65% within 2 weeks,

About 80% within 4 weeks and

Only 7% lived longer than one year.


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Diagnosis

The typical presentation of a ventricular septal rupture -

- A new loud , harsh, pansystolic murmur ( 90% of cases)

best heard at the left lower sternal border, associated with apalpable thrill

- Recurrent chest pain,

- An abrupt deterioration in hemodynamics.


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cont. Diagnosis

ECG findings- changes associated with antecedent anterior, inferior,posterior or septal infarction, A-V conduction block.

Echocardiography findings-The defect,Site and size,

Right and left ventricular function,Pulmonary artery and right ventricular pressures, andExclude coexisting mitral regurgitation or free wall rupture.

Left heart catheterization-coronary artery disease,left ventricular wall motion, and

specifics of valvular dysfunction.


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Preoperative Management

The goals-

- To reduce the systemic vascular resistance, thus the left-to-right

shunt;- To maintain cardiac output and arterial pressure to ensure peripheralorgan perfusion;

- To maintain or improve coronary artery blood flow.

These are best accomplished by the intra-aortic balloon pump (IABP).

Counterpulsation reduces left ventricular afterload, thereby increasingcardiac output and decreasing the left-to-right shunt. Thus-

- decreased myocardial oxygen consumption,

- improved myocardial and peripheral organ perfusion.

Pharmacologic therapy-- Inotropic agents

- Diuretics

- Vasodilators.


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Principles of repair of postinfarction ventricular

septal defects-

Cardiopulmonary bypass with moderate hypothermia and meticulous

myocardial protection.

Transinfarct approach to ventricular septal defect with the site of

ventriculotomy determined by the location of the transmural infarction.

Trimming of the left ventricular margins of the infarct back to viable

muscle to prevent delayed rupture of the closure site.

Conservative trimming of the right ventricular muscle as required for

complete visualization of the margins of the defect.


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Cont

Inspection of the left ventricular papillary muscles and

concomitant replacement of the mitral valve only if there is frankpapillary muscular rupture.

Closure of the septal defect without tension, with the use of prostheticmaterial.

Closure of the infarctectomy without tension with the use of prostheticmaterial and epicardial placement of the patch to the free wall to avoidstrain on the friable endocardial tissue.

Buttressing of the suture lines with pledgets or strips of Teflon felt orsimilar material to prevent sutures from cutting through friablemuscle.


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Repair of anterior post infarction VSD

Continuous instead of

interrupted sutures

Pledgeted sutures are taken from VSD margin to patch margin

Ventriculotomy closure with suture over felt continuous suture for reinforcement


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INFARCT EXCLUSION TECHNIQUE

Oval bovine pericardial patch sutured toendocardium over noninfarcted ventricular septum

Left ventricular cavity excluded from

infarcted myocardium


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REPAIR OF POSTINFARCTION VSD IN APICAL PORTION

Infarcted portion of both ventriclesare excised with VSD Closure for a ex usin PTFE felt


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REPAIR OF POSTERIOR POST INFARCTION VSD

Heart is lifted out of pericardial cavity

Infarcted tissue of LV, RV &

se tum are excised

Septal patch is placed on LV side

Second patch is used to close RV wall

External patch is placed over

infarcted area


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INFARCT EXCLUSION TECHNIQUE

Left ventriculotomy is done

Bovine patch is sutured on healthy portion of LVstartin on fibrous mitral anulus

Lateral edge of patch

is sutured to LV wall

near post papillary

muscle

Exclude all infarcted muscle of LV cavit


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. Surgery for post-infarction ventricular septal defect (VSD): doublepatch and glue technique for early repairClaude Deville*, Louis Labrousse,Emmanuel Choukroun and Francesco Madonna

Department of Cardio-Vascular Surgery, Hpital Haut-Lvque, avenue de Magellan, 33604

Bordeaux-Pessac, France

Site of ventriculotomies close to the

septal margin.

Double ventriculotomy in one

case of anterior VSD.


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Right side of ventricular septum with

ventricular septal defect, tricuspid papillary

muscle tip on moderator band.

Patch on the right side of the ventricular

septum preserving important anatomical

structures.


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Septal surface of the left ventricle

presenting only fine trabeculations.Patch on the left side of the

ventricular septum.


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Patches crossing the ventriculotomies Dacron patch on each side of the

septum and glue injection.


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Strip of felt on the right and left

ventricular sides of the incisions.Simultaneous closure of the two

ventriculotomies with heavy

mattressed and transseptal suture


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The interrupted stitches suture closing

the two ventriculotomies.


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Results-

No recurrences of VSD was observed in 37 patients operated on with this

technique since 1986, compared to six recurrences in the 56 patients

operated with the classic repair, P=0.09. This confirms our previous results

published in 2002 .

Hospital mortality with the double patch and glue techniqueconcerns 10 out

of 37 patients (27%) compared to 28 among 56patients (50%) with the

classic repair, P=0.006


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Double-Patch Repair of Postinfarction Ventricular Septal

DefectMehmet Balkanay, MD, Ercan Eren, MD, Cuneyt Keles, MD, Mehmet Erdem

Toker, MD, and Mustafa Guler, MDDepartment of Cardiovascular Surgery, Kosuyolu Heart and Research Hospital, Istanbul,

Turkey

The ventricular septal perforation was closed directly by stitching, with

the same sutures, 2 autologous pericardial patches onto both sides of the

affected septum, through only a left ventriculotomy.

Complete closure of the defect was accomplished, and no residual

shunt was observed in any patient.

A) A longitudinal transinfarction


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A) A longitudinal transinfarction

incision is made in the left

ventricular myocardium

parallel to and 10 mm away

from the posterior descending

artery.

B) Several 3-0 Prolene sutures

are passed through the 1st

pericardial patch; then the

needles are passed

transmurally by everting them

through the healthy portion of

the defect, from the right side

of the septum to the left.

C)1st patch is lowered to the right

side of the defect by tying the

sutures tightly; then the

needles of the same suturesare passed through the 2nd

pericardial patch.

D) All these sutures are then tied

securely on the left side of the

septum, thus closing the

defect completely on both

sides, with a double patch.


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Off-pump repair of a post-infarct ventricular septal defect: the 'Hamburger

procedure'Thomas A Barker, Alexander Ng, and Ian S Morgan

Department of Cardiothoracic Surgery, Heart and Lung Centre, Wolverhampton, UK

Department of Cardiothoracic Anaesthesia, Critical Care & Pain Management, Heart and Lung

Centre, Wolverhampton, UK

An off-pump closure technique called the 'Hamburger procedure' has been pioneered as

an alternative to open procedures that require CPB and ventriculotomy.

By bringing the left and right ventricles into close apposition with Teflon supported plication sutures, the defect

was closed with moderate reductions in cardiac chamber size.


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A dramatic reduction in pulmonary

arterial pressure and inotropic

doses occurred immediately after

surgery. As this technique was

performed off-pump, potential

sequelae of CPB (ie adverse

haemodynamic, neurological and

inflammatory effects) were obviated.

A short operative time of 40 minutes

compared with a longer, more

complex open patch repair requiringCPB and ventriculotomy.


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ASSOCIATED PROCEDURES

- Concomitant coronary artery bypass

- Mitral valve replacement- Left ventricular aneurysm

- Repair of free wall rupture


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Operative Mortality

Hospital mortality after repair is 30% to 50%.

Five year survival 44% - 57%.

Ten year survival 29% - 36%.

Modes of death-Early- Cardiac failure (up to 90%),

Bleeding,

Sepsis,

Stroke,

GIT bleeding

Recurrent VSD.

Late- Cardiac failure,

Sudden death,

Sepsis,

Stroke

MI


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INDICATION FOR OPERATION

Post infarction VSD is almost always an indication for operation.

Repair of post infarction VSD 2 to 3 weeks or more after septal rupture

is relatively safe.

Operation can be delayed if-

- adequate cardiac output with no evidence of shock

- easy controllable or absence of symptoms of pulmonary

venous hypertension

- easy controllable or absence of fluid retention

- good renal function


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PERCUTANEOUS CLOSURE

Successful transcatheter closure of postinfarction ventricular septal rupture

has been reported using several types of catheter-deployed devices-

- CardioSEAL device, double umbrella prosthesis.

- Amplatzer septal occluder and

- Rashkind double umbrella.

Results of early repair of post infarction VSR in literature


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Results of early repair of post infarction VSR in literature

source: MMCTS (April 25, 2005)

Year Author No. of

Pt

Mean

delay insurgery

(day)

Location

of VSDAnt

%

Location

of VSDPost

%

Hospital

mortality%

Recurrence

of VSD%

1996 Cox 109 5 - 6 50 50 27.5 22.9

1998 Chaux 31 - 42 58 32 6

1998 Dalrymplehay 150 2 59 41 32 -

1998 David 52 3 50 50 19 5.7

1999 Deja 110 - 69 31 37 43

1999 Prete 54 2 44.5 55.5 26 -

2000 Crenshaw 84 3.5 71.5 28.5 47 -

2003 Barker 65 11.5 46 54 23.1 -

2004 Daville

one patch

two patch

56

37

3.4

3.1

55.5

59.5

44.5

40.5

50

27

7

0

Surgical repair of post-infarction ventricular septal defect: 19


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Surgical repair of post-infarction ventricular septal defect: 19

years of experienceVittorio Mantovani, , Giovanni Mariscalco, Cristian Leva, Claudio Blanzola and Andrea Sala

Department of Cardiac Surgery, Ospedale di Circolo-Fondazione Macchi, Universit dell'Insubria-

Viale Borri 57, 21100 Varese, Italy

Received 10 November 2004;

Objectives

To review our experience of surgical repair of post-infarction ventricular septal defect (VSD).

Methods

In the period 19832002, 50 patients underwent repair of VSD. Mean age was 66 years, male sex 52%.

Infarct location was anterior in 60% and posterior in 40% of cases. Median interval between rupture

and surgery was 2 days. Preoperative intra-aortic balloon counterpulsation was employed in 56%; a

coronary angiogram was performed in 98% of cases. A patch repair technique was used in 90% of

cases. Coronary bypass grafting was associated in 50% of patients.

Results

Mean aortic clamp time was 101 31 min. Global operative mortality was 36%, respectively 26.7% in

anterior and 50% in posterior location (p = ns). Emergency operation and interval from rupture to

surgery less than 3 days were univariate predictor of early mortality. Five years survival excluding

operative deaths was 76%.

Conclusions

The surgical repair of post-infarction VSD entails a high operative mortality; different techniques were

employed with similar results. Emergency operation is associated with a worse short-term prognosis;long-term survival is acceptable.

Long Term Results After Surgical Repair of Postinfarction


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Long-Term Results After Surgical Repair of Postinfarction

Ventricular Septal Rupture by Infarct Exclusion TechniqueNestoras Papadopoulos MD, Anton Moritz MD, PhD, Omer Dzemali MD, Andreas Zierer MD, Amin Rouhollapour MD, Hanns

Ackermann PhD and Farhad Bakhtiary MD, PhD

Department of Thoracic and Cardiovascular Surgery, Johann-Wolfgang-Goethe University Hospital,

Frankfurt/Main, GermanyCenter of Health Science, Institute for Biostatistics and Mathematical Modelling, Johann Wolfgang-Goethe

University Hospital, Frankfurt/Main, germany

Background

Ventricular septal defect (VSD) is one of the most serious and life-threatening complications of acute myocardialinfarction. The aim of this study was to evaluate the early and long-term results of the patients after surgical repair ofpostinfarction VSD by infarct exclusion technique.

MethodsA total of 32 consecutive patients (mean age, 62.5 10.5 years) underwent postinfarction VSD repairusing astandardized technique in our department. A retrospective analysis of clinical and operative data, predictors of earlymortality, and long-term survival was performed. The localization of VSD was posterior in 50% and anterior in 50% ofthe patients.

Results

The hospital mortality was 31.2% (10 patients). The most common cause of hospital death was persistent low cardiacoutput. The mortality of the posterior VSD group was significantly lower than that of the anterior VSD group (18.7%

and 43.7%, respectively, p = 0.01). Intra-aortic balloon pump support and absence of cardiac shock were significantlyassociated with a lower risk of hospital mortality (p = 0.0001 and p = 0.0009, respectively). The actuarial survival ratesof in-hospital survivors at 5 and 10 years were 79% 2% and 51% 3%, respectively.

Conclusions

The repair of postinfarction VSD by the infarct exclusion is feasible and safe. This techniqueseems to offer sufficientfavorable early and long-term results compared with other techniques. Early indication, preoperative intra-aorticballoon pump support may improve the surgical results. Preoperative cardiogenic shock carries a poor prognosis forthis patient group.


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Postinfarction Ventricular Septal Defects: Towards a

New Treatment Algorithm?Simon Maltais MD, MS, Reda Ibrahim MD, Arsne-Joseph Basmadjian MD, Michel Carrier MD, Denis Bouchard MD, Raymond

Cartier MD, Philippe Demers MD, Martin Ladouceur MS, Michel Pellerin MDand Louis P. Perrault MD, PhD, ,

Cardiac Surgery, Montreal Heart Institute and Universit de Montral, Montreal,Cardiology Department, Montreal Heart Institute and Universit de Montral, Montreal,

Biostatistics Department, McGill University Health Centre, Montreal, Quebec, Canada

Accepted 20 November 2008.

Background

We reviewed our experience at the Montreal Heart Institute with early surgical and percutaneous closure

of postinfarction ventricular septal defects (VSD).

Methods

Between May 1995 and November 2007, 51 patients with postinfarction VSD were treated. Thirty-nine patients

underwent operations, and 12 were treated with percutaneous closure of the VSD.

Results

Half of the patients were in systemic shock, and 88% were supported with an intraaortic balloon pump before

the procedure. Before the procedure, 14% of patients underwent primary percutaneous transluminal coronary

angioplasty. The mean left ventricular ejection fraction was 0.44 0.11, and mean Qp/Qs was 2.3 1. Time

from acute myocardial infarction to VSD diagnosis was 5.4 5.1 days, and the mean delay from VSD diagnosisto treatment was 4.0 4.0 days. A moderate to large residual VSD was present in 10% of patients after

correction. Early overall mortality was 33%. Residual VSD, time from myocardial infarction toVSD diagnosis,

and time from VSD diagnosis to treatment were the strongest predictor of mortality. Twelve patients were

treated with a percutaneous occluder device, and the hospital or 30-day mortality in this group was 42%.

Conclusion

Small or medium VSDs can be treated definitively with a ventricular septal occluder or initially

to stabilize patients and allow myocardial fibrosis, thus facilitating delayed subsequent

surgical correction

Repair of post-infarct ventricular septal defect with or without coronary artery


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bypass grafting in the northwest of England: a 5-year multi-institutional

experienceBARKER T. A. ; RAMNARINE I. R. ; WOO E. B. ; GRAYSON A. D.; AU J. ; FABRI B. M. ; BRIDGEWATER B. ; GROTTE G. J. ;

(1) Department of Cardiothoracic Surgery, Manchester Royal Infirmary, Manchester, ROYAUME-UNI

(2) Department of Cardiothoracic Surgery, The Cardiothoracic Centre-Liverpool, Thomas Drive, Liverpool, L14 3PE, ROYAUME-UNI

(3) Department of Clinical Governance, The Cardiothoracic Centre-Liverpool, Thomas Drive, Liverpool, L14 3PE, ROYAUME-UNI

(4) Department of Cardiothoracic Surgery, Blackpool Victoria Hospital, Blackpool, ROYAUME-UNI(5) Department of Cardiothoracic Surgery, Wythenshawe Hospital, Manchester, ROYAUME-UNI

Objective: To present the 5-year experience of the northwest of England's surgical repair of post myocardialinfarction (MI) ventricular septal defects (VSD). Our primary aim was to evaluate the effect of concomitantcoronary artery bypass grafting (CABG) on mid-term survival and also to identify prognostic indicators.

Methods: A multi-centre regional observational study involving clinical data from 65 consecutive patientswho underwent post MI VSD repair in the northwest of England between April 1997 and March 2002. Bothprospective and retrospective collection of preoperative, operative and postoperative information wasperformed. Patient follow-up was performed by linking their records to the National Strategic Tracing Servicedatabase. Multivariate logistic regression and Cox proportional hazards analyses were used to identifyindependent risk factors for poor prognosis.

Results: Of the 65 patients included in the study, 42 (64.6%) underwent concomitant CABG with a median oftwo grafts. The majority of patients who had their coronary arteries grafted had multivessel disease (92.9%

Overall 30-day mortality was 23.1%. Predictors of poor prognosis included preoperative inotropes (P < 0.001)and total occlusion of infarct related artery (P = 0.03). The crude hazard ratio (HR) of mid-term mortality forconcomitant CABG patients was 0.82 [95% confidence interval (CI) 0.38-1.78; P = 0.62]. After adjustment fordifferences in patient and disease characteristics, the adjusted HR of mid-term mortality for concomitantCABG patients was 0.17 (95% CI 0.04-0.74; P = 0.019). The adjusted freedom from death in the concomitantCABG patients at 30 days, 1, 2, and 4 years was 96.2%, 91.6%, 88.8%, and 82.8%, respectively, comparedwith 79.1%, 58.8%, 49.1%, and 32.2% for the non-concomitant CABG patients.

Conclusion: These data provide evidence that concomitant CABG is significantly beneficial to mid-term

mortality rates. We recommend that patients who present with post MI VSD who have multivessel diseaseshould be routinely revascularised.


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post infarct vsd, nicvd

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