DISEASES OF AORTIC VALVE,ETIOPATHOGENESIS AND MANAGEMENT

STUDENT : DR.MAHABALESHWAR S MCHAIRPERSON:DR.BASAVARAJ BALIGAR

LEONARDO DA VINCI STUDY OF OX HEART(15 TH CENTURY)

NORMAL AORTIC VALVE

AORTIC VALVE ANATOMY

The aortic vestibule or outflow tract of left ventricle,is continuous superiorly with ascending

aorta. Opening from left ventricle in to the aorta is by

aortic valve. Aortic valve has 3 semilunar cusps with free edge

of each projecting in to aortic lumen. Right and left coronary arteries arise from right

and left aortic sinus-CORONARY CUSPS. As blood recoils after ventricular contraction and

fills aortic sinuses,its automatically forced in to coronary arteries.

AORTIC VALVE ANATOMY

IMPORTANCE OF TODAY’S TOPIC The diseases involving valve may be

congenital and acquired and result in either narrowing or dilatation of valve.

Approximately 2/3 rd of heart operations are for aortic vlave replacement(AVR) often for Aortic Stenosis.

Newer approaches in managament- TAVI ,device closure of paravalvular

regurgitation

AORTIC STENOSIS Obstruction to outflow of blood from left

ventricle to aorta. Etiology: Congenital or acquired CONGENITAL A)VALVULAR B)SUPRAVAVULAR C)SUBVALVULAR

A)SUPRAVALVULAR AS Supravalvular AS is least frequent of all types. Obstruction occurs above the valve in the

ascending aorta. It is classified as1. Focal hourglass contraction2. Fibromuscular narrowing3. Generalized hypoplasia of ascending aorta

SUPRAVALVULAR AS TYPES

SUPRAVALVULR AS ASSOCIATED ANOMALIES It may occur as part of a congenital syndrome

such as Williams syndrome caused by a mutation in

the elastin gene (i.e., associated hypercalcemia, elfin facies, developmental delay, small stature)

multiple stenoses in the aorta and peripheral arteries

It may also be caused by lipid deposits in severe forms of familial hypercholesterolemia

Rubella syndrome Mental retardation

COANDA EFFECT:

Hallmark of supravalvular aortic stenosis Systolic pressure in the right arm is usually

higher than that in the left arm. This pulse disparity may be related to the

tendency of a jet stream to adhere to a vessel wall (Coanda effect) and selective streaming of blood into the innominate artery.

COANDA EFFECT MECHANISM

B)SUBVALVULAR AS This is a congenital condition, although it may

not be apparent at birth. Typically, a circumferential fibromuscular

membrane involving the anterior mitral valve leaflet is present in the LVOT below the aortic valve.

Its classified in to three types1. Membranous diaphragm2. A fibromuscular narrowing or tunnel

deformity3. Muscular subaortic hypertrophy

SUBVALVULAR AS

The pathogenesis of this condition is not perfectly understood but is thought to represent a maladaptive response to abnormal flow dynamics in the LVOT.

It may exist with other left-sided obstructive lesions- coarctation as part of Shone’s syndrome.

The condition may recur even after successful membrane resection.

Differential diagnosis of HOCM to be considered in patients with LVH

C)VALVULAR AORTIC STENOSIS1. Congenital(bicuspid,unicuspid)2. Acquired

Degenerative calcific Rheumatic fever Radiation injury to aortic valve Homozygous typeII hyperlipoproteinemia Rheumatoid involvement Ochronosis and alkaptonuria

BICUSPID VALVE

BICUSPID VALVE Most common congenital malformation occurs

in 1% to 2% of the population Most common cause of isolated valvular aortic

stenosis Male :female ratio of 3:1 Autosomal dominant inheritance;mutation in

NOTCH1 gene.

BICUSPID VALVE IMAGE

SIR WILLIAM OSLER ABOUT BICUSPID VALVE

“This point [right-left coronary cusp fusion], previously overlooked, may prove of interest in the etiology, and should be carefully noted in future observations”-1800

PATHOPHYSIOLOGY

The most common anatomic abnormality seen in a bicuspid valve is the fusion of the right and left coronary cusps-70 to 80%

Another type with fusion of right and posterior cusp -20 to 30% cases

A prominent ridge of tissue-raphe mimics a trileaflet valve

in diastole Echo confirmation – systolic leaflet opening

with only two aortic commisures.

ASSOCIATIONS: Concurrent coarctation in 50% cases aortic root dilation Risk of aortic dissection is 5-9 times higher William’s syndrome-BAV with supravalvular

aortic stenosis in 12% cases Patent ductus arteriosus VSD Turner syndrome in 30% cases

CLINICAL FEATURES Can be diagnosed at any age Aortic ejection sound or a systolic or diastolic

murmur in young adult is most common presenting sign or symptom

Accidentally by 2D echo Family history of BAV Symptoms depending on severity of AS or AR

Severe stenosis typically develops by the fifth or sixth decade

Unicuspid valves open only at one commissure, are uncommon, and are usually severely stenotic at an early age.

Patients with Anteroposterior(as opposed to right-left) and eccentric(vs symmetric) have a faster rate of progression with an aortic valve pressure gradient increase averaging 27mmHg per decade.

DISESASE COURSE:

Most patients function normally untill late in life

Risk factors for cardiac eventsAge older than 30 yrsModerate or severe ARModerate to severe AS

Approximately 20% patients develop AR requiring AVR at 10-40 yrs of age

Increased risk of endocarditis

MANAGEMENT No medical therapies to prevent progressive

valve deteroiration Appropriate follow up for valve dysfunction Evaluation of ascending aorta with CT and

CMR

CALCIFIC DEGENERATIVE AS

CALCIFIC AORTIC VALVE DISEASE Calcific AS in the older patient is the most

common valve lesion requiring valve replacement

< 70 yrs-50% cases were due to bicuspid valve

-18% were due to degenerative causes

>70yrs-50% cases due to degenerative causes

-25% were due to bicuspid valve Aortic sclerosis is the initial stage of calcific

valve disease has irregular thickening of aortic valve leaflets

Aortic sclerosis has 50% increased risk of cardiovascular death and myocardial infarction over approx. 5yrs follow up.

Initially thought because of mechanical stress on normal valve,now because of profilerative and inflammatory changes.

RHEUMATIC AS

RHEUMATIC AS Adhesions and fusions of the commisures and

cusps and vascularization of the leaflets of valve ring

Retraction and stiffening of free borders of cusps

Calcific nodules develop on both surfaces – small round orifice

Often coexists with aortic regurgitation (AR) and mitral valve lesions.

It is a rare cause of isolated severe AS in the industrialized world.

Fusion of the commissures occurs leaving a small central orifice

Its usually at least 10 yrs after the attack of rheumatic fever before stenosis becomes critical or significant

TIMING OF ONSET OF SYMPTOMS AND SIGNIFICANTLY CALCIFIED AND STENOTIC VALVES VERSUS MAJOR ETIOLOGIES IN AS

ETIOLOGY

A SCHEMA OF A POTENTIAL CASCADE OF EVENTS LEADING TO AORTIC VALVE CALCIFICATION

AORTIC VALVE GROSS CHANGES

STRENGHTH OF ASSOCIATIONS IN OBSERVATIONAL AND EPIDEMIOLOGICAL STUDIES OF CLINICAL RISK FACTORS AND CALCIFIC AORTIC VALVE DISEASE

PATHOPHYSIOLOGY Aortic valve should be reduced to 1/4thof its

natural size before significant changes occur in circulation.

The normal aortic valve is 3.0 to 4.0cm2.Aortic stenosis

Valve area (cm2)

Gradient (mmhg)

Doppler jet velocity(m/sec)

Mild >1.5 <25 <3Moderate 1-1.5 25-40 3-4Severe <1 >40 >4

Gender difference in LV response to AS has been maintained.

Women more frequently exhibit normal LV performance and smaller,thick walled concentric LVH and diastolic dysfunction with normal or even subnormal systolic wall stress.

Men more frequently exhibit eccentric LVH,excessive systolic wall stress,systolic dysfunction and chamber dilation.

CLINICAL FEATURES History: Most patients with valvular AS are

asymptomatic. History of Rheumatic fever in past Classical triad of symptoms being1. Angina pectoris-5yrs 2. Syncope-3 yrs3. Heart failure(dyspnea on

exertion,orthopnea,PND,pulmonary edema)-2yrs

Typical angina pectoris occurs concurrently with coronary artery disease or without it.

NATURAL HISTORY OF AS

Syncope 1. occuring on effort is caused by systemic

vasodilatation in the presence of fixed or inadequate cardiac output or arrhythmia or both

2. Occuring at rest because of arrhythmia mainly

Dyspnea on exertion,orthopnea,PND may occur secondary to pulmonary venous hypertension.

Systemic venous congestion develops late Heyde syndrome: Gastrointestinal

malformation causing increased suspectibility to GI hemorrhage and anemia.

Bleeding can be caused by acquired defect in VWF.

Calcific systemic embolism may occur in some cases.

COMPLICATIONS Infective endocarditis Cerebral vascular hemorrhage in patients with CoA Gastrointestinal bleeding-Heyde syndrome Aortic regurgitation – occurs in almost all types of

AS,more common with subvalvular Atrial fibrillation-brief filling of left ventricle Mitral annular calcification and calcification of AV

node in patients with Monckeberg’s aortic stenosis causing MR

Aortic dissection Hemolytic anemia-trauma to RBCs passing through

the stenotic orifice

CLINICAL FEATURES Arterial examination: Slow rising and late peaking arterial pulse

(parvus et ardus) Mechanism:

Stroke volume declines Systolic pressure falls and pulse pressure

narrows A systolic thrill in carotid arteries Feature of severe AS

SEVERE AS WITH ABSENT PULSUS PARVUS ET ARDUS??

Elderly (arteriosclerosis) Supravalvular AS Asociated AR,HTN Children with hyperdynamic circulation Can severe AS and hypertension coexist??

Palpation: With LVH and normal LV cavity dimensions,

the apical impulse is usually nondisplaced, diffuse, and sustained.

However, the apical impulse may later be displaced when there is LV systolic dysfunction.

A double apical impulse represents a palpable a wave or S4, caused by a noncompliant left ventricle.

A systolic thrill may be palpable in the second right intercostal space

AUSCULTATION

GALLAVERDIAN PHENOMENON:

Aortic thrill is usuall heard at the base of heart In patients with calcified aortic valves,the

systolic murmur is loudest at the base of the heart,but high frequency components may radiate to the apex.

Differentiating from valvular MR The intensity of systolic murmur varies from beat

to beat Radiation to carotids Amyl nitrate increases the murmur Associated features-type of apex beat,pulse

carecter soft S1,S3 in MR

SEVERE AS Symptoms-syncope Pulse type S2 split paradoxically Presence of S4 Late peaking,longer duration of murmur SBP >200mmHg rules out severe AS Apico carotid delay suggests area<1cm2

CHARECTERISTICS OF SUPRAVALVULAR AORTIC STENOSIS

A2 is accentuated Ejection click is absent Systolic thrill and murmur are more

conspicious and are transmitted to neck Systolic BP in right arm is more than

left(coanda effect) Post stenotic aortic dilatation is absent Coronary arterial circulation is abnormal

CHARECTRISTICS OF SUBVALVULAR AORTIC STENOSIS: Ejection click is absent Diastolic murmur of AR is prominent Post stenotic aortic root dilatation is absent Aortic valve is normal Doppler picks up gradient below the aortic

cusps

DISTINGUISHING VARIOUS FORMS OF LVOT

INVESTIGATIONS Electrocardiography: Left ventricular hypertrophy with or without

secondary ST-T wave changes (Pressure over-load pattern-ST depression and T wave inversion in lateral leads) 85%

Left atrial enlargement/hypertrophy(80%) Sometimes shows conduction delay, left

bundle branch block Heart blocks (calcifications) can occur rarely Atrial fibrillation indicates associated mitral

disease or heart failure

Electrocardiogram of an 18-year-old boy with severe aortic stenosis and moderate aortic regurgitation. There is left ventricular hypertrophy by voltage criteria. Small q waves in V5 and V6 denotes some volume overload due to aortic regurgitation

CHEST X RAY:

Normal sized heart Dilated proximal ascending aorta (post-

stenotic dilation) Calcification of aortic valve (better seen on

fluoroscopy) Calcification does not mean severe aortic

stenosis Late stages: Enlarged heart with pulmonary

venous hypertension

ECHOCARDIOGRAPHIC FINDINGS IN AORTIC STENOSIS

Valve thickening and doming on 2D and gradient across valve on continuous wave Doppler

All severe aortic stenosis (AS) in adults will be calcified

Allows definition of valve anatomy, cause of AS, calcification and assessment of severity of AS

Left ventricular hypertrophy, systolic functions (ejection fraction) can be evaluated

Assessment of aortic root dilatation and associated mitral valve disease

TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE). Planimetry of the aortic valve orifice is often

possible with TEE and relates well to that measured by cardiac catheterization.

TEE is often necessary to confirm the diagnosis of subaortic membrane and to differentiate it from hypertrophic cardiomyopathy or valvular AS.

2-DECHOCARDIOGRAM (LONG-AXIS VIEW) IN A PATIENT WITH CALCIFICAORTIC STENOSIS. THE CALCIUM IN THE VALVE GENERATESABNORMALLY INTENSE ECHOES. THERE IS SOME EVIDENCE OF THEASSOCIATED LEFT VENTRICULAR HYPERTROPHY.

Doppler echocardiography allows measurement of transaortic jet velocity,which is useful for measuring disease severity and predicting clinical outcome.

Stenotic orifice area is calculated by continuity equation

Mean transaortic gradient using modified Bernoulli equation.

DOPPLER AORTIC JET VELOCITY

Continuous-wave (CW) Doppler signals obtained fromthe right upper parasternal edge, where the high-velocityjet from the stenotic valve is coming towards thetransducer. AV, aortic valve; LA, left atrium; MV, mitral valve;LV, left ventricle; IVS, interventricular septum; PVW,posterior ventricular wall.

DOBUTAMINE ECHOCARDIOGRAPHY AND STRESS ECHOCARDIOGRAPHY Exercise testing in patients with asymptomatic

AS may provide useful information such as exercise-induced symptoms or abnormal blood pressure response (ACC/AHA class IIb indication).

Exercise testing is contraindicated (ACC/AHA class III indication) in symptomatic patients with AS.

Dobutamine echocardiography may be useful in evaluating low-flow/low-gradient AS in patients with LV dysfunction

CARDIAC CATHETERISATION AND ANGIOGRAPHY Its indicated only when non invasive tests are

inconclusive,when clinical and echo findings are discrepant

Also for coronary angiogram before surgical intervention.

Cardiac magnetic resonance (CMR): Assesing LV volume,function and mass in which echo

cannot give information

Positron Emission Tomography(PET): Visualize the location and severity of inflammation and

calcification in experimental models and in humans with calcific valve disease.

NATURAL HISTORY A prolonged latent period is characteristic of

the natural history of AS in an adult. Once moderate stenosis is present (jet

velocity >3 m/s), the average rate of progression is an increase in jet velocity of 0.3 m/s per year, an increase in mean pressure gradient of 7 mmHg per decade, and a decrease in valve area of 0.1 cm2 per year.

Once the symptoms of angina, syncope or HF develop, the average survival is 5, 3 and 2 years, respectively. There is also a high risk of sudden death

MEDICAL MANAGEMENT Antibiotic prophylaxis: infective

endocarditis,artificial prosthesis in situ Medical therapy in asymptomatic

patients: During the asymptomatic phase, therapy is directed at primary prevention of CAD, maintenance of sinus rhythm, and blood pressure control.

Medical therapy in symptomatic patients: diuretics in pulmonary congestion,Digoxin in atrial fibrillation.

Vasodilator therapy: used in patients with LV dysfunction

Treatment of hyperlipidemia: The association between AS and risk factors

for atherosclerosis has prompted trials with statins to retard the progression of AS

There is currently no indication for statin use specific to AS, although in hyperlipidemic patients with AS, aggressive lowering of LDL level with statins appears warranted.

SURGICAL TREATMENT Children: Balloon aortic valvotomy is advisable

in the adolescent or young adults with 1. Severe congenital AS, 2. In all symptomatic patients and in

asymptomatic patients with a transvalvular gradient >60 mmHg or

3. In those with ECG showing ST changes at rest or with exercise.

The same indications are appropriate for surgical intervention, although balloon valvotomy is probably preferable at experienced centres with suitable valve anatomy.

STEPS FOR PERCUTANEOUS BALLOON VALVOTOMY. A, Dilation of the native stenoticvalve. B, A crimped stented valve has been inserted over a guidewire into the aortic annulus. C, Inflation of the balloon deploysthe valve. D, The balloon is deflated andremoved with the aortic valve replaced.

Adults: Aortic valve replacement (AVR) is the

treatment of choice for patients with severe AS.

ACC CLASSIFICATION Class I: Conditions for which there is evidence

and/or general agreement that this procedure is useful and effective.

Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure.

Class IIa: Weight of evidence/opinion is in favor of usefulness/ efficacy.

Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

Class III: Conditions for which there is evidence and/or general agreement that the procedure is not useful/effective and in some cases may be harmful.

RECOMMENDATIONS FOR AORTIC VALVEREPLACEMENT IN PATIENTS WITH AORTIC STENOSIS

Class I 1  AVR is indicated for symptomatic patients with

severe AS 2  AVR is indicated for patients with severe AS

undergoing CABG or surgery on the aorta or other heart valves

3  AVR is recommended for patients with severe AS and LV systolic dysfunction (ejection fraction < 0.50)

Aortic valve replacement video

AORTIC VALVE REPLACEMENT SURGICAL PROCEDURES Aortic valve replacement with

Homograft(Allograft) Tissue implanted is entirely biologic Today all are inserted as miniroot

replacement,implanting homograft and proximal aortic root as a unit

Patient’s coronary arteries are reimpalntedin to sinus of valsalva of homograft aortic root

Aortic valve replacement with pulmonary autograft(Ross procedure) Pulmonary homograft is impalnted as a miniroot to

replace the pulmonic valve and main pulmonary artery.

Significant CAD in 25-30% patients with aortic valve surgery,so CABG is combined with AVR

RESULTS

Mortality Survival rate of 5yrs – 80 to 85% 10yrs – 70% Overall mortality of 3.2% in patients undergoing isolated

AVR and 5.6% in patients with AVR and CABG In patients without frank LV failure operative risk is from 2-

5% Valve related complications:

Structural deteroiration of valve Hemodynamic prosthetic dysfunction Prosthetic valve thrombosis Anticoagulant related bleeding Infection,infective endocarditis Hemolysis,heart block

CHOICE OF VALVE There is no perfect aortic valve substitute

Consider patient age anatomy ventricular function lifestyle,fear of reoperation possible CI to anticoagulation

Bovine pericardial Bioprosthesis: No anticoagulation More durable than porcine prosthesis in elderly Eventually deteriorate

Mechanical valve: Double leaflet tilting disc valves – St.Jude and

carbomedics Single leaflet tilting disc valve- Medtronic hall Extremely durable Valve thrombosis,thromboembolism and need for

AC

Porcine bioprosthesis: More rapid structural dysfunction- 8 to 10yrs

Stentless porcine prosthesis: Relatively new Improved hemodynamic function Low incidence of thromboembolism

Cryopreserved Homograft valves: Thromboembolism and endocarditis are

uncommon Structural deterioration

Pulmonary autograft: Ross procedure – excellent hemodynamics,low

incidence of thromboembolism and endocarditis

Aortic regurgitation and pulmonic stenosis

TRANSAORTIC VALVE REPLACEMENT VIDEO

TAVI offers an alternative approach to treatment of severe AS,particularly in patients with prohibitive surgical risk

PARTNER trial randomized study in US concluded TAVI resulted in substantial reduction in rates of death and hospitalization compared to BV and medical therapy

AORTIC REGURGITATION Aortic regurgitation (AR) can result from

disease of the AV (aortic cusp) and due to dilatation of aortic root.

Etiology:1. Chronic AR: Leaflet abnormalities: Aortic root or ascending aorta abnormalities

CHRONIC AORTIC REGURGITATIONLEAFLET ABNORMALITIES AORTIC ROOT /ASCENDING AORTARheumatic fever(80% cases) Age related aortic dilatationInfective endocarditis Annuloaortic ectasiaTrauma Cystic medial necrosis(Marfan’s

syndrome)Myxomatous degeneration Systemic hypertensionCongenital AR Aortitis( syphilis)SLE Reiter’s syndromeRheumatoid Arthritis Ankylosing spondylytisTakayasu arteritis Behcet’s syndromeAnkylosing Spondylytis Psoriatic arthritiswhipple’s disease Osteogenesis imperfectaCrohn’s disease Relapsing polychondritisDrug induced valulopathy Ehler’s Danlos syndrome

ACUTE AORTIC REGURGITATIONLEAFLET ABNORNMALITIES AORTIC ROOT /ASCENDING

AORTATraumatic rupture Acute aortic dissectionInfective endocarditis(most common cause)

Perivalvular leak or dehiscence of prosthetic valves

Acute prosthetic valve dysfunctionPost aortic balloon valvuloplasty

VARIOUS CAUSES OF PURE AR

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY

Acute AR: Severe volume overload of LV with resultant

pulmonary congestion as LV chamber is small Usually present with signs of sudden

hemodynamic deterioration such as weakness, altered mental status, severe shortness of breath, or syncope.

If left untreated, these patients quickly progress to total cardiovascular collapse.

When severe chest pain is part of the initial clinical presentation, aortic dissection must be strongly suspected

HISTORY Patients with mild to moderate AR are usually

asymptomatic. even patients with AR in the chronic

compensated phase are often entirely asymptomatic.

As LV decompensation progresses, symptoms of dyspnoea, palpitations, orthopnoea, and in advanced cases, PND and peripheral oedema occur

Angina

Nocturnal angina occurs due to bradycardia and increased AR with reduced aortic diastolic pressure leading to diminished coronary perfusion

Attacks associated with profuse sweating Abdominal angina during sleep due to

splanchnic ischemia

PHYSICAL FINDINGS Look for peripheral manifestations of infective

endocarditis, signs of Marfan’s syndrome, evidence of chronic aortic dissection, and signs of collagen vascular disorders.

Peripheral pulse examination: The widened pulse pressure accounts for a

number of physical findings associated with chronic AR.

MECHANISM OF WIDE PULSE PRESSURE In AI,ventricular stroke volume is high

Rapid upstroke in pulse/ increased systolic BP

Collapsing character(fall in diastolic BP) is due to Diastolic leak back in to left ventricle from aorta Reflex vasodilataion mediated by carotid

baroreceptors secondary to large stroke volume The rapid run off to the periphery due to

decreased systemic vascular resistance

PHYSICAL SIGNS ASSOCIATED WITH CHRONIC AR 1.Light house sign (alternate flushing and blanching of forehead) 2.Landolfi’s sign (Change in pupillary size in accordance with

cardiac cycle and not related to light). 3. Retinal artery pulsations (Becker’s sign). 4. de Musset’s sign (head bobbing with each heart beat).It is due

to ballistic effect of severe AR. 5. Muller’s sign—Systolic pulsations of uvula. 6. Quincke’s sign (capillary pulsations) can be detected by

pressing a glass slide on patients lip or nailbed. 7. Dancing carotids (Corrigan’s sign). 8. Locomotor brachii. 9. Collapsing or water-hammer pulse (↑ systolic pressure and ↓

diastolic pressure); usually pulse pressure is more than the diastolic pressure.

10. Bisferiens pulse-a double impulse in systole

Bisiferiens pulse Conditions with large stroke volume:

Stroke volume is rapidly ejected from LV Since initial percussion wave is exaggerated due

to large stroke volume,the tidal wave also becomes prominent

Combintion of slow rising and collapsing pulse: AS and AR

DIFFERENT TYPES OF PULSE WAVEFORMS

SIGNS IN AR CONTINUED.. 11. Pistol shot femorals (Traube’s sign) arteries Pistol

shot sound over the femoral vein is heard in severe TR. 12. Duroziez’s sign—systolic murmur heard over

femoral artery when it is compressed proximally and a diastolic murmur when it is compressed distally using the ‘bell’ of the stethoscope.

Duroziez’s murmur—diastolic murmur heard with the diaphragm of the stethoscope when distal pressure is applied.

13. Hill’s sign—popliteal cuff systolic pressure exceeds brachial cuff pressure by > 20 mm Hg.

a) Mild AR 20–40 mm Hgb) Moderate AR 40–60 mm Hgc) Severe AR > 60 mm Hg. 14. Rosenbach’s sign—pulsations of liver.

Hill sign(an exaggerated difference in blood pressure in upper and lower limb extremeties)is an artifact of sphygmomanometer measurements and no longer considered a sign of severe AR-BRAUNWALD

the wide pulse pressure,significant LV dilatation and Austin Flint Murmur are not features of acute AR

CAUSES OF NARROW PULSE PRESSURE IN AR??

Acute AR CHF Associated MS/AS Marked tachycardia

PALPATION:

With severe AR, the apical impulse is typically enlarged and displaced lateral to the midclavicular line in the fifth intercostal space because of LV enlargement.

The impulse may be sustained and hyperdynamic.

A diastolic thrill may be palpable in the second left intercostal space, as may a systolic thrill caused by increased aortic flow.

AUSCULTATION

AUSCULTATION

PICTORIAL REPRESENTATION OF MURMUR IN ACUTE AND CHRONIC AR

The severity of AR correlates better with duration than with the intensity of murmur.

When the murmur is musical (‘cooing dove’ murmur), it usually signifies eversion or perforation of an aortic cusp.

Acute AR: The early diastolic murmur of acute AR is

shorter and lower in pitch than the murmur of chronic AR

AUSTIN FLINT MURMUR

The Austin Flint murmur is a middle-to-late diastolic rumble that is believed to be caused by vibration of the anterior mitral leaflet as it is struck by the regurgitant jet or by turbulence in the mitral inflow from partial closure of the mitral valve by the regurgitant jet.

SEVERE AR The presence of the following indicate severe AR: a. Duration of murmur (> 2/3 of diastole) is

directly proportional to the severity. In moderate to severe AR, murmur becomes holodiastolic and may have a rough quality.

b. Bisferiens pulse c. Hill’s sign > 60 mm Hg?? d. Apical impulse (down and out) e. Austin-Flint murmur f. Marked peripheral signs. They are absent in depressed myocardial function.

ELECTRCARDIOGRAM Left axis deviation with left ventricular

hypertrophy of volume over-load, pattern (prominent Q waves in leads I, aVL, and V3 through V6)

Tall and upright T-waves. Later on inverted T-wave, with ST-segment depressions

Intraventricular conduction defects occur late in the course and are usually associated with left ventricle dysfunction

RADIOLOGICAL ABNORMALITIES

Marked enlargement of cardiac shadow Calcification of the aortic valve uncommon Dilation of the ascending aorta (more than in

AS) Severe aneurysmal dilation of the aorta

suggests aortic root disease (Marfan’s syndrome, cystic medial necrosis or annuloaortic ectasia)

Linear calcifications in the wall of the ascending aorta: syphilitic aortitis

Acute aortic regurgitation (AR): less cardiac dilatation and more pulmonary venous hypertension

Chest radiograph (posteroanterior view) of a 40-year-old male with severe aortic regurgitation. There is left ventricular type of cardiomegaly and mild pulmonary venous hypertension

ECHOCARDIOGRAPHY Transthoracic echocardiography: measurement of LV

end-diastolic and end-systolic dimensions and volumes, ejection fraction and mass Serial measurements for follow-up

High frequency fluttering of the anterior leaflet of the mitral valve during diastole

Echo may show bicuspid valve,thickened valve cusps,congenital abnormalities,vegetations.

Doppler echocardiography and colour flow Doppler imaging are the most sensitive and accurate non-invasive techniques in the diagnosis and evaluation of AR

AR can be quantified into mild, moderate and severe AR on above basis

ECHO-DOPPLER ASSESSMENT OF AR SEVERITY

Recent studies have shown that end systolic volume is astrong predictor of adverse clinical outcomes

Echocardiogram of a patient with aortic regurgitation caused by infectiveendocarditis. The left panel shows a linear vegetation (arrow) prolapsing into the leftventricular outflow tract from the aortic valve leaflet in diastole. The right panel is a colorflow Doppler image exhibiting turbulent blood flow filling the left ventricular tract duringdiastole. AO = aorta; LA = left atrium; LV = left ventricle; RV = right ventricle

AORTIC REGURGITATION (COLOUR DOPPLER).

CARDIAC CATHETERISATION AND ANGIOGRAPHY Cardiac catheterisation is undertaken when

the severity of AR is not clear on non-invasive evaluation.

The indications for selective coronary angiography are the same as for AS

CARDIAC MAGNETIC RESONANCE:

CMR provides accurate measurement of regurgitant volumes and orifice in AR.

Most accurate to assess end systolic volume,diastolic volume and mass.

Cardiac MRI showing a bicuspid aortic valve with AR and ascending aorta dilation. A, Fast single-shot steady-state free precession (SSFP) image in acoronal view. B, Retrospectively reconstructed magnitude image from a phase-contrast sequence showing a bicuspid aortic valve. C, Balanced SSFP image. Oblique axialleft ventricle inflow-outflow view, showing grade 2 aortic regurgitation.

NATURAL HISTORY The rate of progression to symptoms and/or

LV systolic dysfunction is about 4.3% per year in asymptomatic patients with severe AR.

Sudden death occurs at the rate of <0.2% per year in this subgroup of patients.

The average rate of symptom onset in patients with depressed LV function is >25% per year.

Mortality rates of >10% per year have been reported in patients with angina pectoris and >20% per year in those with HF.

MANAGEMENT Acute AR: Surgery is the treatment of choice within 24

hrs Iv diuretics and vasodilators(nitroprusside) are

of short time benefit Beta blockers are avoided so not to reduce

cardiac output and slow heart rate.

CHRONIC AR TREATMENT Early symptoms of dyspnea respond to

diuretics, vasodilators(ACE inhibitors,CCBs) Systolic BP goal of <140 mmHg Beta blockers and ARBs may be useful to

retard the aortic root dilatation as in Marfan’s syndrome.

Beta blockers may sometime provide incremental BP lowering in patients with chronic AR and hypertension.

Patients with severe AR without indication for operation should be followed up by clinical and ECHO examination every 6-12 months.

SURGICAL TREATMENT: Patients with severe AR usually do not

become symptomatic untill after the development of myocardial dysfunction

When delayed too long >1yr from onset of symptoms or LV dysfunction,surgical treatment often does not restore normal LV function.

INDICATIONS FOR AVR IN SEVERE ARINDICATION CLASSSymptomatic patients in severe AR irrespective of LV systolic function

I

Asymptomatic pts with chronic severe AR and Lv systolic dysfunction (EF<50% at rest)

I

Pts with chronic severe AR undergoing surgery on Aorta or CABG

I

Asymptomatic patients with severe AR and EF>50% but with Lvdilatation EDD>75mm and ESD >55mm

IIa

Patients with moderate AS while undergoing surgery on Aorta or CABG

IIb

Asymptomatic patients with severe AR when EF>50% but progressive LV dilatation with EDD>75mm and ESD >55mm and declining exercise tolerance

IIb

AVR not indicated for asymptomatic pts with mild,moderate,severe AR when normal LV systolic function at rest,degree ofdilatation is not severe (EDD<75mm and ESD <55mm )

III

REFERENCES Braunwald’s Heart disease- Textbook of

Cardiovascular Medicine – 10th edn Hurst’s the Heart-Manual of Cardiology-12th edn Manual of Cardiovascular Medicine by B.Griffin 4th

edn Harrison’s Principlesof Internal Medicine – 19th edn API Textbook of Medicine-10th edn A Textbook of Cardiovascualr disease by Kanu

chatterjee et al Clinical examination in Cardiology- B.N.V Rao Textbook of Cardiovascular Medicine by Eric Topol-

3rd edn

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