acute and chronic aortic insufficiency-dr magdi sasi 2016

ACUTE AORTIC REGURGITATION DR MAGI AWAD SASI 2016

ACUTE and CHRONIC AORTIC INSUFFICIENCY

Essential for diagnosis of Chronic AR:

Heart murmur

Haemodynamically stable

Progressive cardiac enlargement

Classic and dramatic findings

Absence of terminally decompensated CCF

Essential for diagnosis of Acute AR

Destruction of normal AR

CCF refractory to treatment

Require urgent replacement

Quite ill with CCF to the point of cardiogenic shock

Normal left ventricle

2ry physical signs are absent

Definition OF ACUTE AR:

Haemodynamically significant AII of sudden onset ,occurring across a previously

competent AV into LV not previously subjected to volume overload.

AETIOLOGY OF AR: Acute causes of AR:

1. Acute rheumatic fever 2. Infective endocarditis 3. Dissection of aorta 4. Ruptured sinus of valsalva aneurysm 5. Failure of prosthetic valve

Chronic causes of AR: 1. Congenital ---bicuspid AV ,VSD 2. RHD 3. IE 4. HTN 5. Connective tissue disease:

Inherited ---- Marfan syndrome Ehler-Donals syndrome Osteogenesis imperfect Acquired---- SLE /RA Ankylosing spondylitis Primary antiphospholipid syndrome Reiters syndrome

6. Aortitis---Takayasu srteritis 7. Syphyilis 8. Associated with AS

Ca be primary of the valve or 2ry to aortic root dilatation


Aetiology :

1. Infective endocarditis:

A. Staphylococcus Aureus----acute AR

It causes necrosis ,perforation ,and detachment of valve leaflets.

Infection of aortic annulus with necrosis and abscess formation may cause

weakness and progressive dilatation.

An annular abscess may distort aortic valve.

One or two large valvular vegetation occurs.

B. Fungal endocarditis:

Bulky vegetation

Asperigillus

Candida albicans

Histoplasma

C. Acute endocarditis in drug addicts ,in S/C drug users –skin popping

D. Patient with congenitally bicuspid AV at increased risk for bacterial endocarditis

even in absence of AS/AR because:

i. Bicuspid valve is the commonest congenital valvular malformation

associated with turbulent flow

ii. The valve lesion is commonly asymptomatic and escape detection

iii. Antibiotic has not be prescribed prophylatically.

COMPLICATIONS:

A. Annular abscesses ,nearly always associated with severe AR

Gradual or sudden

Necrosis ,inflammation encroach AV node and proximal his prukinje region

First /second degree heart block

LBBB

CHB

B. Abscess may erode into pericardium

Purulent pericarditis

Hemopericardium

Cardiac temponade

C. Annular abscess extending into the membranous interventricular septum

Septal rupture with left to right shunt.

D. Extension of the infection to the muscular part

This leads to ventricular irritability and infranodal block

E. Infection may extend into the contagious right ventricle or right atrium

This leads to development of an aorto ventricular /right atrial fistula

C/F:

Machinery murmur related to left to right shunt & worsening CCF

F. Superior extension of infection may cause a mycotic aneurysm

This involves sinus valsalva and proximal ascending aorta.


THE TREATMENT FOR ALL IS AORTIC VALVE REPLACEMENT.

Diagnosis of infective endocarditis is suggested by:

1) One /more large or small vessel embolic events

2) Systemic signs of toxicity

2. Dissecting of ascending aorta:

Ascending aorta dissection with consequent hematoma may extend to involve the

aortic valve.

Displace the cusps downward &medially

One/more prolapsed or Evert into the outflow tract of the LV during diastole

AR

AR occurs in 65% of patients with dissection of ascending aorta.

Another complication ----acute myocardial infarction that usually involves the inferior wall

due to compromise of right coronary ostium by hematoma ---dissecting medial.

Sudden death may occur due to cardiac temponade if the process is protracted by

extension through aortic adventia.

C/F:

Severe chest pain

Evidence of vascular compromise to:

1. Head 3. Upper extremities

2. Lower extremities 4. Gut 5. Kidney

Treatment:

a. Urgent CT scan chest , aorto-graphy

b. Operative intervention

3. Connective tissue disease:

SLE---sterile perforation of one/more aortic valve cups by fibrinoid necrosis

involving valve parenchyma.

Other :

i. Aortitis

ii. Ankylosing spondylitis

iii. Whipples disease

iv. Giant cell aortitis

v. Takayusu s arteritis


4. Trauma :

Pathogenesis:

Closed chest or abdominal trauma ----falls ,crush injuries ,automobile accident

Water hammer effect

Sudden compression of the thoracoabdominal aorta diastole with the aortic valve

closed may acutely increase intravascular pressure and cause aortic cuspal tearing

,perforation or detachement.

Trauma cause damage to normal valve and myxematous degenerated valves are

more susceptible.

Traumatic AR may occur as a consequence of severe muscle strain or strenuous

physical activity.

TO DIAGNOSE:

Require careful and thorough careful CVS examination

1) Initially when the victims presents to the hospital

2) After resuscitation and interventions complete

3) After several weeks of recovery

5. Spontaneous AR:

AV may be normal or myxematous.

Sudden eversion of an aortic cusp may result in spontaneous acute AR .

Bicuspid valve have an asymmetric nature ,the larger valve leaflet must oppose an

abnormally large total force in diastole ;resulting in an asymmetric + deformed

raphe.

Larger valve leaflet may not be sufficiently buttressed by smaller leaflet along

the line of coaptation leading to AR.

6. Prosthetic aortic valve insufficiency:

Can be caused by:

i. Sudden dehiscence of the sewing ring of prosthetic valve from the aortic

annulus .

It is an occasional complication of emergency AVR for acute fulminant ABE

when the valve must be implanted into an infected annulus.

ii. Pannus ingrowth ,thrombus formation ,vegetation may impede proper

seating of the ball or poppet in diastole.

iii. Poppet wear /failure

iv. Homograft valves and porcine bio-prostheses previously prepared undergo

progressive degeneration

Pathophysiology :

Chronic AR

Volume overload regurgitating into the LV during diastole increased overtime

LV wall undergoing minimal thickening ((septal +posterior wall thickening)) Eccentric hypertrophy((LVEDP+LVEDV))


Allows LV to operated at a larger end diastolic volume

Increased LV size to maintain CO ((starling law)) ((LV dilatation ---apex beat deviated line))

As long as systolic function is preserved ,the ventricle is capable to ejecting this

abnormal large total volume + LV diastolic pressure dose not raise and symptoms

of decompensation does not ensure.

Ejection of this large stroke volume results in widened arterial pulse pressure.

This widened arterial pulse pressure of brisk upstroke and fall-off with its myriad of

associated peripheral signs is used to assess the severity of AR.

These signs also indicate reasonable preservation of ventricular systolic function in

chronic AR.

At later stages ,due to volume overload or other intercurrent myocardial insult

Congestive cardiomyopathy

Systolic function deteriorates +

Left ventricle diastolic pressure rises

This results in : 1. Decrease organ perfusion

2. Pulmonary congestion

CARDIAC DECOMPENSATION

LV overload LV size ((eccentric hypertrophy))

to maintain COP

Run off phenomena

Large amount of blood escape Large LV needs more O2

From cardiac cycle

Angina pectoris

Diastolic BP/ LVEDP

Takes decades to develop CCF if chronic

Coronary perfusion

CCF Decompensation occurs when:

1. LV systolic pressure begins to fail

2. Progressive LV dilatation occurs

3. Spherical geometry develops


C/F: chronic AR

Fatigue

Decreased exercise capacity

Dyspnea

As forward COP declines ,arterial resistance rises to preserve blood pressure.

The peripheral manifestation of chronic AR are no longer manifest ,although the

patient is now severely ill from cardiac decompensation.

The dramatic clinical ,radiographic ,echocardiographic of ventricular enlargement is helpful to testify the chronicity of volume overload state.

LV systolic function and ESD are the most predictors of post operative survival and

LV function.

Symptoms of LV dysfunction---Dyspnea ,PND ,orthopnea

Symptoms of coronary insufficiency—angina ,nocturnal > exertional

With extreme reduction of diastolic pressure <40mmHg ,angina may be seen.

Symptoms of high COP----------pounding of the heart

The peripheral signs of chronic AR "signs of high COP in CHRONIC AR":

Presence of large bounding collapsing pulse is the first clue to chronic AR.

1. De Mussets sign:

The head frequently bobs with each heart beat ,caused by large stroke volume.

2. Müller sign is systolic pulsations of the uvula

3. Corrigans sign:

the pulse is of the water hammer or collapsing with abrupt distention and

quick collapse" sharp & full upstroke of the carotid pulse and a precipitous

decrease in diastole" .

4. Dancing carotid

5. Bisferiens pulse may be present & recognized in the brachial and femoral

It is bounding ,visible and forceful peripheral pulses.

6. Signs in femoral artery:

a. Traubes sign or pistol shot sound:

Booming sharp systolic sound heard over femoral artery((like gunshot)).

b. Duroziezs sign:

Systolic murmur ((bruit))heard over the femoral artery when it is compressed

proximally and diastolic murmur when it is compressed distally.

7. Quinckes sign:

By pressing a glass slide on the patients lip or transmitting a light through the

patients finger tips. It is a systolic blushing and diastolic blanching of the nail

skin when pressure is applied gently to the tip of nail.

8. Hills sign:

Disproportionate increase of systolic BP> 2ommHg when measured in the leg

as compared with systolic BP in the arm.

Mild > 20 mmHg , Modearte>40mmHg , Sever >60 mmHg

Popliteal cuff systolic pressure >brachial cuff pressure by > 60mmHg

The presence of such sign suggests sever chronic AR.

9. Final Jeopardy:

Landolfi’s sign = alternating constriction/dilatation of pupils


10. Mayne’s sign - moderate or mild degrees of of AR may be detected by

demonstration of a diminution of >15 mmHg in the diastolic BP in the arm

when it is elevated over the head compared with values taken when the arm is

at heart level

11. Blood pressure:

Systolic blood pressure is elevated

Diastolic pressure is abnormally low.

Korotkoff sound often persistent to zero.

As heart failure develops ,peripheral vasoconstriction occurs ;arterial diastolic

pressure rise------------------ increase severity of AR

The consequences are:

1. Increased LVEP---increased left atrium P---increased PCP ---PULMONARY E.

2. Early in the diastole ;LVP rises rapidly causing mitral leaflets to drift

toward closed position -----------------AUSTIN FLINT MURMUR.

3. Premature closure of mitral valve before onset of systole

4. The mitral valve may open late because the ejections period of acutely

volume---overloaded ventricle is prolonged.

5. Compensatory tachycardia shortens diastole

All factors reduce the time during which MV is open in diastole.

Premature closure of mitral valve causes:

A. Limits the degree of transmission of high pressure from LVEDP to left atrium and

pulmonary capillary bed.

B. Absence of the first heart sound

C. Limitation of diastolic interval compromises LV inflow and effective COP

IN ACUTE AR:

Acute damage to AV : A. Lacking eccentric hypertrophy Ventricle compliance is not increased

B. LV remains normal and poorly tolerated

If AR is severe ,end diastolic LV pressure may approaches aortic diastolic P.

The normal ventricle (( neither hypertrophied nor dilated)) cant acutely increased LV

stroke volume sufficiently to maintain stoke volume.

In normal ventricle ,there is little increase in stroke volume when EDP exceeds 12—

15mmHg .The starling curve relating ventricle stroke volume to EDV is rather flat at

pressures>15mmHg.So; increased EDP doesn't improve COP.

Pericardium may be a rule as it is suddenly stretched to the limit of its distensibility.

This leads to forward COP to declines.

This results in reflex increased in peripheral vascular resistance.

Acute AR:

Pallor and coolness of the skin

Decreased cutaneous blood flow

Impaired regional arterial flow


Reduced COP

Oliguria due to decreased blood flow

Deranged temperature regulation

GIT dysfunction

Hepatic dysfunction

Decreased tissue perfusion : a. Cardiogenic shock b. Lactic acidosis

Clinical presentation:

Acute AR---

The symptoms are of rapid onset due to increased left atrial pressure—pulmonary

congestion and decreased forward cardiac output.

Symptoms include: ACUTE PULMONAR EDEMA2

1. Exertional dyspnea

2. Orthopnea +dry cough increased by recumbency

3. PND

4. Dyspnea at rest even while sitting upright

Symptoms reflecting decreased COP are more subtle and overshadowed by those of

capillary congestion.

1. Fatigue on exertion

2. Apathy

3. Agitation

4. Deterioration in intellectual function

This reflects impaired skeletal muscle and cerebral perfusion.

An etiological diagnosis; Sever chest/back pain of abrupt onset--------Dissection Fever, Chills ,Malaise ,evidence of peripheral arterial emboli---infective endocarditis H/O chest /abdominal trauma------trauma induced Absence of symptoms or H/O heart disease suggest sudden perforation of AV

Chronic AR

There is a long period during which LV under goes enlargement while the

patient remains asymptomatic.

4th ;5th decade -----decreased cardiac preserve or myocardial ischemia develop

after cardiomegally and myocardial dysfunction have occurred.

Principal symptoms -----exertional dyspnea ,orthopnea and PND.

In comparison to AS, ((where syncope and angina pectoris are common));

nocturnal angina often accompanied by diaphoresis which occurs when heart

rate slows and diastolic pressure falls to low levels may be trouble.

These episodes may be accompanied by abdominal discomfort.

Patient with severe AR complain of :

Uncomfortable awareness of the heart beat---on laying down


Thoracic pain due to bounding of heart against chest wall

Tachycardia ,stress or exertion may produce palpitation and head

pounding.

VPC are distressing due to great heave of volume loaded LV.

NOTE:

These complaints may be present for many years before symptoms of LV

dysfunction develops.

Acute AR: Gravely ill patients Sever dyspnea weakness hypotension Sever peripheral vasoconstriction Tachycardia Cyanosis Angina is uncommon

Acute AR--Physically :

Acute AR----ill patient ,dyspnic

The finding are related to:

1. Severity of pulmonary congestion

2. Impairment of forward COP + tissue perfusion

Thorough examination is mandatory.

3 major category:

a. Pulmonary congestion

b. Decreased COP

c. No signs of LV volume overload +stroke volume decreased

Tachycardia is the rule.

LV stroke volume is reduced(systolic BP is normal/increased;diastolic BP slightly

increased)

Precordium is relatively quiet to inspection and palpation.

There is lacking lateral displacement and heaving.

Auscultation in acute AR :

S1—first heart sound is usually soft as regurgitant volume rapidly fills ventricle and drives

the mitral leaflets toward the closed position at time of systole.

Absent S1---LVDP exceeds left atrial pressure prior to ventricular activation ,MV closure

occurs late in diastole ,preceding ventricular and atrial systole.

Premature MV closure have a protective rule over pulmonary circulation +pul.HTN

S2--- soft + may be absent if AV leaflets destroyed as no diastolic coaptation.

The murmur ---an ejection of variable intensity is heard to the base.

The diastolic murmur of AR is low pitched +shorter because as LVEDP raises ,the pressure

gradient between aorta and left ventricle is rapidly decreased.


A flail cusp may evoke a musical ((narrow frequency band)) and very intense diastolic M.

The Austin flint murmur if present is brief.

S3 is often present ,reflecting rapid early diastolic ventricular filling from LT atrium& aorta.

S3 S4 may be heard.

Loud P2 indicate pulmonary HTN.

The cacophony of sounds and murmurs may mimic pericarditis.

SUMMARY POINTS:

A. Fever, petechia ,purpura, arterial emboli (small or large)---INFECTIVE ENDOCARDITIS

B. Sever chest or back discomfort or unequal pulse in upper limbs—DAA

C. H/O of trauma------------------------------------------------------------------TRAUMATIC AR

D. Tall ,thin ,long arm span ,hyper-extensile joints ,ectopia lentis ----MARFANS

E. No finding---------------------------------------------------------------------------SPONTANEOUS

COMPARISON OF CLINICAL FINDING

CLINCAL FAETURES ACUTE AR CHRONIC AR

CCF Early & sudden Late &insidious

Arterial pulse 1. Rate/min

Increased

N

2. Rate of rise Not increased INCRAESED

Blood pressure 1. Systolic BP

N/ low

INCREASED

2. Diastolic BP N/low DECREASED

3. Pulse pressure N INCREASED

Contour of peak single bisferians

Left ventricle impulse Near normal Laterally displaced

Pulsus alternus common uncommon

Ausculatation S1

Soft to absent

Normal

A2 Soft N/decraesed

P2 N/decraesed N

S3 COMMON Absent

S4 Consistently absent Usually absent

Aortic systolic murmur Grade 3/less Grade 3/ more

Aortic regurgitant murmur Short .medium pitched Long ,high pitched

Austin flint murmur Mid diastolic Presystolic ;mid diastolic

Peripheral signs Absent Present


From such comparisons ,vital signs are helpful to clarify the cause of aortic regurgitation

weather it is acute or chronic .

It is mandatory to check the pulse and blood pressure and CVS examination.

WHAT ARE THE DIGANOSTIC DIFFERENCES BETWEEN ACUTE AR& CHRONIC AR?

Acute AR Chronic AR

ECG NORMAL LVH

CXR LV NORMAL PROMINANT

Aortic root and arch NORMAL PROMINENT

Pulmonary venous pattern Redistributed to upper lobes NORMAL

Interstitial and alveolar fluid Present absent

Chronic AR:

Apical impulse -----diffuse, displaced laterally & inferiorly ,forceful &unsustained.

There may be systolic retraction over the parasternal region.

A rapid ventricular filling wave is palpable at the apex.

A systolic thrill at the base of the heart ,suprasternal notch ,carotid arteries is palpable.

Auscultation :

S1—soft and prolongation of PR

A2—soft /absent

P2—obscured by murmur

S2—variable –absent ,single ,narrow or paradoxical splitting

An ejection systolic murmur is audible.

S3 gallop correlated with increased LVED volume and has been suggested as sign useful to

consider surgery.

Murmur—early diastolic high pitched blowing ,decrescendo murmur that begins

immediately after A2 ,best heard in the 2nd &3rd intercostals space left parasternal border.

It is accentuated by sitting up ,leaning forward ,hold breathing in full expiration.

In sever AR correlates better with the duration >intensity of the murmur.

Mild AR----------limited to early phase of diastole +high pitches


Moderate/sever AR—it is holodiastolic +rough quality

When the murmur is musical ((cooing dove)) ,it signifies eversion or perforation of an

aortic cusp.

Sever AR +LVF----equilibration of LVP+aorta P.-----abolish this component of murmur.

Site –1ry valve disease ---left sternal border –3rd/4th

Dilatation of ascending aorta ------right sternal border

What is Austin Flint murmur?----it is a low pitched mid & late diastolic rumble((like MS)) ,

heard over apical area due to anterior displacement of MV by the aortic regurgitant

stream. It indicates moderate to severe AR.

Sever aortic reflux---increased LVEDP ---narrowing MV---rapid antegrad flow through MV.

As LVEDP increased, Austin flint murmur terminates earlier.

A short ejection systolic murmur ,1—4/6 ,may be audible at the base of the heart due to

increased stroke volume and transmitted to the carotid arteries with thrill +high pitched.

HOW TO INCREASED MURMUR QUALITY?

Any intervention that raises the arterial pressure increases murmur.

Vasopressor drug

Squatting

Exercise –isometric ---increase murmur of AR+Austin Flint murmur.

An intervention that decrease arterial pressure:

Valsalva maneuver

Amyl nitrate inhalation

Clinical feature Mitral stenosis Austin flint murmur

S1 Increased Normal

S3 No Yes

Opening snap Yes ,heard no

LV enlargement No yes

RV enlargement Yes No

Murmur decrease with amyl nitrate No Yes

Atrial fibrillation yes no

ECHO MS yes No

What are the major hemodynamic features of AR?

FEATURES ACUTE AR CHRONIC AR


Left ventricle compliance Not increased Increased

Regurgitant volume increased Increased

LVEDP Markedly incraesed May be normal

LV ejection velocity dp/dt Not significantly incraesed

Markedly increased

Aortic systolic pressure Not increased Increased

Aortic diastolic pressure Normal to decraesed Markedly decreased

Systemic arterial pulse pressure Slight increased Markedly increased

Ejection fraction Not incraesed Normal to increased

Effective stroke volume N

Effective cardiac output N

Heart rate N

Peripheral vascular resistance Not incraesed

LABORATORY:

ECG—it is not an accurate indicator of severity of AR . Sinus tachycardia is the rule and

only indicative of severity of cardiac decompensation.

LVH is absent unless pre existing cardiac pathology.

Acute AR may evoke compensatory ventricular dilatation and increased cardiac mass.

ECG criteria are manifest as early as 2 weeks after onset.

Non specific ST/T wave changes:

1) Ischemia

2) Hypoxia

3) Acidosis

ECG finding in chronic AR: Normal LVH+ prominent upright left precordial T waves Non specific ST-T wave changes AV block or bundle branch block may be a sign of paravalvular /myocardial adscess

CXR:

<36 hr-----clear lung fields

Bilateral patchy interstitial infiltrates -----alveolar infiltrates

Redistribution of pulmonary venous return to apical veins.

Absence of cardiomegally

Displacement of ca in the wall of aortic knob

Cardiac size is a function of :

1) Duration of AR

2) Severity of AR


3) State of LV function

Calcification of AV is uncommon in patients with AR.

Left atrial enlargement suggest MV disease.

CXR finding in Chronic AR :

LV enlargement

Dilated ascending aorta

Aortic wall calcification---Syphilis

Aortic valve calcification----AS+AR

ECHO:

Premature closure of mitral valve ---sever degree of AR ,LVD HTN

An ECHO ,irregular ,shaggy ,large structure related to the valve leaflet.

1. Calcification and fibrosis of normal valve

2. Chronic thickening of one of AV leaflets

3. Degeneration of bicuspid valve

4. Sterile vegetation

5. Infective endocarditis

Doppler ECHO is the principal non invasive means of identifying AR.

ECHO finding in chronic AR: Dilated LV Dilated aortic root Diastolic fluttering of mitral leaflets Doppler regurgitation jet


ECHO ACUTE CHRONIC

MITRAL VALVE 1. Closure 2. Opening 3. Anterior leaflet E/F slop 4. Diastolic fluttering 5. Aortic valve presystolic opening

Early Late

Reduced Yes Yes

N N N

YES NO

Septal wall motion Normal Hyperkinetic

Posterior wall motion Normal Hyperkinetic

End diastolic dimension Normal Increased

End systolic dimension Normal Normal

Shortening function Normal Increased

The echocardiographic findings of obvious premature mitral valve closure associated with

absent A wave (during sinus rhythm) and absent diastolic oscillations can be useful in

diiferentiating acute from chronic aortic regurgitation


Cardiac catheterization------------Acute AR

1. Arterial pulse pressure normal

2. Equilibration of LV + Aorta pressure late in diastole

3. Increased LVEDP > left atrial pressure in late diastole indicative of CCF

4. Increased pulmonary artery wedge presser > 25—30mmHg

5. Mild to modest increase in mean pulmonary artery pressure

Pressure gradient across lung 10—12mmHg

Pulmonary hypertension is acute.

6. Mild elevation in mean atrial pressure 8—10mmHg with pulmonary artery + right

ventricular systolic pressure >35—45mmHg.

Ventriculography

1) Normal LV segmental wall motion

2) Normal systolic function EF> 0.50

3) Slight increase in LVED + LVES volume

4) Thickening of AV leaflets or filling defects

5) Thickening of anterior MV leaflet

6) Fluttering /high frequency vibration of anterior MV leaflets as it is pushed toward

closed position in late diastole.

7) Abnormal filling defects projecting into LV outflow tract at level of aortic annulus

,membranous ,muscular ventricular septum suggesting abscess.

Risk :

1. Arrhythmia , Cardiac depression

2. Osmotic load ,Hypotension

3. Embolization

RULE OF ECHO IN MANAGEMENT OF CHRONIC AR:AHA/ACC 2006

SYMPTOMS

NO EQUIVOVAL Yes AVR

Exercise test symptoms

NO SYMPTOMS

NORMAL EF LV FUNCTION? Subnormal

EF border line/uncertain EF50%

RVG

LV DIMENSIONS LVSD>55 OR DD>75


By ECHO, sever AR:

1. Regurgitant fraction ≥ 50%

2. Regurgitant volume ≥ 60ml/beat

3. Effective regurgitant orifice ≥ 30mm2

LV DIMENSIONS

SD 45—50mm SD<45-50mm SD 50-55mm

DD 60-70mm DD<60-70mm DD70-75mm

Initial exam Stable clinical evaluation

Every 6M/ ECHO 6M

YES YES NO

NO

HEMODYNAMIC RESPONSE TO EXERCISE

Clinical evaluation 6-12m Revaluate 3m

ECHO every 12 months

AVR--------Abnormal Normal

TREATMENT of chronic AR:

The role of medical therapy in patients with AR is limited; there are currently no

randomized, placebo-controlled data showing that vasodilator therapy delays the

development of symptoms or LV dysfunction warranting surgery.

• Medical – Afterload reduction: ACEI, nifedipine, hydralazine – Use BB cautiously, if at all, given prolonged diastole and therefore

regurg volume


• Surgical – AVR – 4% mortality alone, 6.8% with CABG

– LV dysfunction often irreversible, despite AVR

• `

A. Vasodilator therapy (i.e., Nifedipine, ACE inhibitor, Hydralazine) is indicated to

reduce systolic blood pressure in hypertensive patients with AR.

Expected—decrease afterload; stroke volume ; decrease regurgitant volume.

Hemodynamic benefit shown with Hydralazine &Nifedipine ,less results with ACE I.

Dose titrated to achive decrease in systolic BP ,NOT NORMALIZATION.

B. Other than for treating HTN, vasodilator therapy has potential role in three situations:

1. Severe AR with symptoms or LV dysfunction but are not surgical candidates.

2.As a short-term therapy to improve hemodynamics in patients with severe HF

and severe LV dysfunction prior to surgery

3.May be considered for long-term therapy in asymptomatic patients with severe

AR who have some LV dilatation but normal LV systolic function.

C. Nitrates and diuretics may be used

D. B blocker--- Rerospective data suggest that b -blocker use may be associated with

a survival benefit in patients with severe AR, but prospective studies are needed.

It is used cautiously , gives prolonged diastole and therefore increases regurgitant

volume . It is mainly used in marfan syndrome.

E. Rheumatic fever prophylaxis

When endocarditis is suspected or confirmed, appropriate antibiotic coverage is

critical.

Vasodilator therapy indications: Class I

1) Severe AR with symptoms or severe LV dilatation with contraindication for surgery. 2) Severe AR without symptoms but LV dilatation and systolic HTN. 3) Any degree of AR with HTN. 4) Persistent LV systolic dysfunction short period before AVR. 5) Short term therapy prior to AVR.

Class III Mild to moderate AR without symptoms and signs with normal LV function.

Surgical Management :

In asymptomatic AR ,Decompensation occur when:

1. LV systolic function begins to fall

2. Progressive LV dilatation

3. Spherical geometry develops.

The most important predictors of postoperative &LV function are:


A. LV systolic function

B. End systolic diameter

ACC/AHA Guidelines—Class I indications for AVR for AR

1. Acute, severe AR is treated surgically. 2. Symptomatic NYHA functional status III/ IV 3. Asymptomatic with chronic severe AR and LV systolic dysfunction (mild to

moderate low EF <50%), LVSD>55mm ,LVDD >70mm ,Aorta D>55mm 4. Need for CABG, surgery on the aorta, or other valve surgery. 5. Class II angina

If the aortic root is dilated, it may be repaired or replaced at the time of AVR.

For patients with a bicuspid valve, Marfan’s syndrome (or related genetically

triggered aortopathy), surgery on the aorta should occur at the time of AVR if the

aortic root or ascending aorta is 4.5 cm.

Although worse NYHA functional Class, LV dysfunction, and the chronicity of these

abnormalities are predictors of higher operative and postoperative mortality, AVR is

usually a better alternative than medical therapy in improving overall mortality and

morbidity.

Class II FOR AVR in chronic AR: 1) Rapid increase in LV diameters 2) NYHA II with LVEF>50% with stable EF ,LV size and exercise tolerance 3) Asymptomatic patient with normal LVEF with sever LVD ((ESD >55 OR EDD>75mm)) 4) BAV or marfan syndrome with aortic diameter >50mm

Patients with EF<25% or LVESD>60mm ,LVEDD>70mm are at high operative risk.

AVR has clearly been shown to prolong survival and improve functional status in patients

with severe symptoms.

The prognosis is correlated with pump function.

Vasodilator therapy reduces LV dilatation in asymptomatic patients withAR who have

normal LV systolic function ,delaying the need for AVR.

Symptomatic patients have a poor prognosis under medical treatment.

European guidelines 2007:

Asymptomatic patient with sever AR –LVEF≤50% ,EDD>70mm ,ESD50mm((25mm/m2BSA))

NO YES

FOLLOW UP AVR


OUTCOME/PROGNOSIS

Asymptomatic patients with normal LV systolic function ---

a. Progression to symptoms and/or LV dysfunction ,6% per year.

b. Progression to asymptomatic LV dysfunction ,3.5% per year.

c. Sudden death ,0.2% per year.

Asymptomatic patients with LV dysfunction------

1) Progression to cardiac symptoms 25% per year.

2) Symptomatic patients

Mortality rate >10% per year.

Outcomes of AVR for AR:

3/5/10 year survival regardless of EF: 82%, 76%, 67%

Improved somewhat with nifedipine preop in low EF (<35%) pts

Again, many times, LV dysfunction is irreversible despite AVR, so still need

aggressive CHF regimen


Echocardiography in conjunction with a thorough history and physical examination, provides accurate, reproducible, and cost-effective methodology for the serial assessment of contractile dysfunction in patients with aortic regurgitation.

• The use of guidelines and the development of algorithms for timing of surgery in patients with aortic regurgitation guide operative intervention to preserve contractile function, thereby improving long-term post operative outcome and minimizing unnecessary risk.

Asymptomatic Aortic Regurgitation:

Introduction:

• Despite Significant Volume and Pressure Overload on the Left Ventricle (LV),

patients with Aortic Regurgitation (AR) Typically Remain Asymptomatic For

Extended Periods of Time.

• Symptoms of Dyspnea, Orthopnea, Nocturnal angina and Syncope Develop

Relatively Late in the Course of the Disease.

• Aortic Valve Replacement (AVR) has Clearly been Shown to Prolong Survival and

Improve Functional Class in Patients with Severe Symptoms.

• The Optimal Timing for Valve Replacement in Asymptomatic Pts is Less Concrete.

• Should Prophylactic AVR be Performed to Preserve LV Contractile Function ?

• The Benefits of Preserving Contractile Function must be Weighted against the

Immediate Operative Risks Associated with Prosthetic Valves.

• Long asymptomatic phase, Followed by a symptomatic phase with a relatively

rapid progressive deterioration in clinical function.

• Asymptomatic Patients with normal LV pump function have an excellent long-term

prognosis : 90% of pts are Asymptomatic at 3 years, 81% at 5 years and 75% at 7 y.

The percentage of Pts requiring AVR was < 4% per year.

• Asymptomatic Patients with impaired LV ejection performance:

66 % require surgery within 3 years.


• Vasodilator Therapy (nifedipine, ACE Inh), reduces LV dilatation in Asymptomatic

Pts with AR who have normal LV systolic function, delaying the need for AVR

• Symptomatic Pts have a poor prognosis under medical TT (4% of survival after 10 y

FU, NYHA III-IV.

• Surgical Intervention appears to improve survival and functional class in patients

with AR.

• LV pump function improves after aortic valve replacement with correction of the

volume after load.

Indices of LV performance in Asymptomatic patients with AR:

• 1) Ejection Phase Indices: Asymptomatic Pts with normal LV function have an excellent long-term

survival rate, and < 4% of pts per year require AVR. Asymptomatic pts with impaired LV function, have a considerably more

aggressive clinical course and should be referred for elective AVR to avoid progression to irreversible contractile dysfunction.

• 2) End-Systolic Dimension: 80% of asymptomatic pts with an end-systolic dimension > 55 mm required

surgery within 34 months compared with 20% of pts with an end-systolic dimension < 55 mm.

No pt with an end-diastolic dimension <= 40 mm required aortic valve replacement at 4 years, whereas 65% of pts with an end-systolic dimension >= 50 mm required surgery within the follow up period

Time of surgery:

a) Sub clinical LV contractile dysfunction may develop when the LV ejection

fraction remains normal; LV function in AR generally improves after valve

replacement.

b) Asymptomatic Pts with a normal LV ejection fraction have an excellent

long-term prognosis with medical therapy.

c) Asymptomatic Pts with normal LV function should treated by vasodilators

(Nifedipine) for after load reduction to delay the progression of LV dilation

and the need for AVR

d) AVR in Symptomatic or Asymptomatic Pts with Mild or Moderate

depressed LV pump function improves survival over medically treated Pts

with AR

e) Severe, preoperative contractile dysfunction is associated with persistent

LV dilation and dysfunction, often resulting in postoperative congestive

heart failure and death.

Algorithm for the timing of surgery in asymptomatic AR:


POINTS CLINICAL LV EF% LV ESD(mm) Exercise capacity

0 none >60% <45 preserved

1 1 50-60% 45--55

2 2/more <50% >55 Decreased

Clinical age >65 ,cardiothoracic ratio ≥ 0.58 , LVH on ECG ,Cardiac index ≤2.5

l/m/m2 ,LVED Pressure >20mmHg

Exercise capacity 8 METS on graded exercise treadmill

0---1 Delay surgery ,clinical and ECHO follow up 12 months

2 Border line ,clinical and ECHO follow up 6 months

≥3 proceed with surgery

Additional predictors of adverse out come in AR:

A. Percentage fractional shortening <29%

B. End systolic volume index >60ml/m2

C. End systolic wall stress >235mmHg

D. End diastolic dimensions >80mm

E. EDD ((RADIUS))R

ED wall thickness ≥ 3.2

acute and chronic aortic insufficiency-dr magdi sasi 2016

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