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Chronic Aortic Regurgitation

CHRONIC AR most commonly results from rheumaticdisease in the developing countries like ours with clinicalpresentation in second to third decade while calcificdegeneration is the commonest cause in the west,presenting in the fourth to sixth decade of life.Other causes include congenital abnormalities (mostcommonly, bicuspid valves), myxomatous degeneration,idiopathic dilatation of aorta, systemic hypertension andMarfan syndrome. Rarely, AR may be associated withrheumatoid arthritis, ankylosing spondylitis, syphiliticaortitis, Reiter’s syndrome or in association with severalcongenital abnormalities.

Pathophysiology and Natural History

The above mentioned causes result in slow insidiousvolume overload of the left ventricle (LV) and aprolonged asymptomatic course. The LV responds tochronic volume overload by increasing the LV enddiastolic volume, a combination of eccentric andconcentric hypertrophy, thus maintaining the fillingpressures and ejection fraction within normal range.However, the increased LV size results in increased LVafter load. These compensatory mechanisms maycontinue for decades before impaired myocardialcontractility results in fall in ejection fraction and thusproduction of dyspnea. However, this LV dysfunctionmay, in some cases, insidiously progress to severe LVdysfunction before onset of symptoms. Some patients

AORTIC REGURGITATION: CURRENT PERSPECTIVE

Rahul Mehrotra*, Sanjay Mittal**and R.R. Kasliwal***Consultant, *Senior Consultant, Department of Cardiology, Indraprastha Apollo Hospitals,

Sarita Vihar, New Delhi 110 076,India.Correspondence to: Dr. R.R Kasliwal, Senior Consultant (Cardiology), Indraprastha Apollo Hospitals,

Sarita Vihar, New Delhi 110 076, India.

Aortic Regurgitation (AR) is fairly common with the overall prevalence being 4.9% in the Framingham HeartStudy1 and 10 percent in the Strong Heart Study2 carried out in American Indians. The prevalence of ARincreases with age and severe AR is more commonly observed in men than in women. AR is usually chronic butrarely, it may be acute and life threatening.We discuss in this article, the evidence based approach to evaluation and management of pure AR.

Key words: Tran thoracic Echocardiography, Tran esophageal echocardiography, AVR, IABP.

may also develop exertional angina due to diminishedcoronary flow reserve in response to hypertrophiedmyocardium.

Large number of studies have examined the naturalhistory of asymptomatic chronic severe AR andconcluded that the rate of progression to systolicdysfunction and/or LV symptoms averaged 4.3% peryear, sudden death occurred at a rate of less than 0.2%per year and once symptoms developed, mortality rateexceeded more than 10% per year [3-9].

A very important fact to be remembered in thesepatients is that more than a quarter of them die ordevelop LV dysfunction before development ofsymptoms, thus mandating regular follow up evaluationto ensure appropriate timing of intervention (surgery).

AR is associated with considerable morbidity andmortality. The variables identified as high risk markersbased on clinical studies are age, LV end systolicdimension (or volume) and LVEF during exercise.

Evaluation and Management

AR is usually detected by clinical examination orincidentally during echocardiography.

Clinical diagnosis of chronic severe AR is based ondetection of displaced apical impulse, wide pulsepressure (with its characteristic peripheral findingsand eponymous signs), and a high pitched blowing

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decrescendo diastolic murmur in the left third and fourthintercostal spaces. If this murmur is louder on the rightside, aortic root dilatation is the likely cause. A left sidedthird heart sound is often heard and is not necessarilydue to LV dysfunction. The Mid diastolic Austin-Flintrumble is considered a specific sign of severe AR.ECGand chest X-ray help in the evaluation of overall heartsize, rhythm, conduction disorders and evidence of LVhypertrophy.

Tran thoracic Echocardiography is anindispensable tool in the work-up and is indicated toconfirm the diagnosis, to assess the cause of AR andvalve morphology, to measure aortic root, to provide asemi quantitative estimate of severity of AR [10] (Table1) and to assess LV dimensions, systolic function andmass. Echocardiography is essential for selection ofpatients for surgery and subsequent follow up.

Colour flow jet area and jet width are the preferredmodes for assessment of severity but indirect modes likeslope of AR jet, flow reversal in descending aorta andmagnitude of LV outflow tract velocity are also helpful.Quantitative parameters like regurgitant volume,regurgitant fraction and regurgitant orifice area aretechnically demanding, not routinely recommended butare very useful tools in expert hands. Accuratelydetermined vena contracta is also considered to be highlysensitive and specific (Fig. 1).

Tran esophageal echocardiography is needed

when inadequate images are obtained on Tran thoracicechocardiography in symptomatic patients. Radio-nuclide angiography or cardiac MRI can be used toassess LV volumes and systolic function in the samescenario. Cardiac catheterization is hardly everrequired nowadays for assessment of AR. Pre-operativecoronary angiography should be performed based onage, symptoms and associated risk factors. Exercisetesting is also sometimes needed for evaluation offunctional capacity and in patients with equivocalsymptoms.

Management of the patient is based on severity ofAR, symptomatic status, LV systolic function and LVsize, aortic root size and associated co morbidities.Figure 2 depicts the management strategy endorsed andrecommended by the American Heart association andAmerican College of Cardiology in the guidelinespublished in 2006.

Medical therapy

Vasodilator therapy is used with an aim to reduceregurgitant volume, LV end diastolic volume and wallstress thereby resulting in reduced after load, preservedsystolic function and LV mass. There are three potentialuses of vasodilators in chronic severe AR. They can beused on a long tem basis in patients who otherwise arecandidates for surgery but in whom surgery is notpossible, in severely symptomatic patients forstabilization before surgery and lastly in patients who are

Table 1: Doppler based echocardiography criteria for determination of AR severity.

Aortic regurgitation

Mild Moderate Severe

Qualitative

Angiographic grade 1+ 24 3-4+

Color Doppler jet width Central jet, width <25% Greater than mild but no Central jet, width greaterof LVOT sign of severe AR than 65% LVOT

Doppler vena contracta Less tha 0.3 0.3-0.6 Greater than 0.6

Quantitative (cath or echo)

Regurgitation volume (mL per beat) Less than30 30-59 Greater than or equal to 60

Regurgitation fraction (%) Less than30 30-49 Greater than or equal to 50

Regurgitation volume (mL per beat) Less than 0.10 0.10-0.29 Greater than or equal to 0.30

Additional essential criteria

Left ventricular size Increased

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asymptomatic, have normal LV function but are volumeloaded. The goal of medical therapy is to reduce systolicblood pressure and drug dosage should be increased untilthere is measurable decrease in systolic BP or the patientdevelops side effects. Nifedipine and ACE inhibitorshave been evaluated and approved for this purpose.Vasodilator therapy is not indicated in mild or moderateAR. Beta blockers are contraindicated as they increasethe diastolic regurgitation by producing bradycardia.There are no data to support the long-term use ofdigoxin, diuretics, nitrates or positive inotropic agents inasymptomatic patients.

Surgical management

Majority of patients with severe AR requiringsurgery undergo valve replacement (AVR) but somecenters are increasingly performing aortic valve repair,which is technically more demanding and requiresconsiderable experience.Fig. 1. Parasternal long axis view showing vena contracta.

Fig. 2. Suggested strategy for evaluation and management of patients with pure severe AR. DD refers to end-diastolicdimension, SD to end-systolic dimension, EF to ejection fraction and eval to evaluation.

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Mild or moderate aortic regurgitation thus, onlyrequires follow up for assessment of progression unlessdilatation of the ascending aorta justifies surgery. Astrategy of conservative management of severe aorticregurgitation in asymptomatic patients is reasonable ifthe patients have neither marked left ventricularenlargement nor left ventricular dysfunction, sinceseveral studies have shown that asymptomatic youngpatients with normal left ventricular function have asurvival rate identical to that in the general population[11-13].

Patients with severe AR with symptoms or with LVdysfunction (LVEF 50% or less) are candidates for AVR.AVR is also indicated in asymptomatic patients withchronic severe AR while undergoing coronary bypass,surgery on aorta or other valves. The above three areClass I recommendations as per ACC/AHA practiceguidelines for valvular heart disease-2006. AVR isconsidered reasonable (Class IIa) for asymptomaticpatients with normal LV systolic function but severe LVdilatation (end-diastolic dimension greater than 75mmor end-systolic dimension greater than 55 mm). AVR isnot indicated in mild, moderate or severe AR andnormal LV systolic function when LV dilatation is notmoderate or severe (end-diastolic dimension less than 70mm or end-systolic dimension less than 50 mm) (ClassIII ).Below is the suggested treatment algorithm forselecting patients for AVR.

AVR is the usual intervention for aortic regurgitationand in the United States, is associated with a mortality of4 percent when performed in isolation and 6.8 percentwhen performed with coronary bypass surgery [14]. Theoperative mortality is lower in high-volume centres [15]and among patients who have minimal or no symptoms(1 to 2% mortality [16] or better preoperative leftventricular function (8% mortality when the ejectionfraction is 35% or less vs 2% when the ejection fractionis 505 or more) [17].

Aortic Regurgitation with Aortic Root Disease

Diseases of the proximal aorta may also contribute tochronic AR. Dilatation of the ascending aorta is amongthe most common causes of isolated AR [18]. In suchpatients, the valvular regurgitation may be less importantin decision making than the primary disease of the aorta,such as Marfan syndrome, dissection, or chronicdilatation of the aortic root related to hypertension or abicuspid aortic valve. In such patients, if the AR is mildor the left ventricle is only mildly dilated, management is

focused on treating the underlying aortic root disease. Inmany patients, however, AR may be severe andassociated with severe LV dilatation or systolicdysfunction, in which case decisions regarding medicaltherapy and timing of the operation must consider bothconditions. In general, AVR and aortic root re-construction are indicated in patients with disease of theaortic root or proximal aorta and AR of any severitywhen the degree of dilatation of the aorta or aortic root isequal to or greater than 5.0 cm by echocardiography[19].

Acute Aortic Regurgitation

Acute aortic regurgitation when severe is a lifethreatening condition occurring as a consequence ofinfective endocarditis, dissection of aorta or followingballoon valvotomy and surgical commisurotomy forcongenital aortic stenosis (AS). The left ventricle,suddenly forced to accommodate the large regurgitantvolume, operates on the steep portion of the diastolicpressure volume curve, as a result of which the LV enddiastolic and LA pressures rise dramatically. Inability ofthe LV to dilate acutely results in fall in forward strokevolume. Pulmonary edema and Cardiogenic shockfrequently result. Elevated end diastolic pressurecoupled with increased myocardial oxygen demand dueto tachycardia and increased after load result insubendocardial ischemia and its attendant complica-tions, including, commonly, sudden death.

Diagnosis

There may not be any clinical sign other thantachycardia, a soft first heart sound and a short, soft,barely audible early diastolic murmur. A brief diastolicrumble may be heard at the apex due to diastolic MR.Chest X Ray and ECG frequently are normal. Transthoracic echocardiography is an indispensable tool indiagnosis, assessment of severity, determining the causeand assessment of hemodynamics. Tran esophagealechocardiography (TEE) is very useful in aortic rootdissection but CT scan or MRI may be used if they can beobtained earlier than TEE. Cardiac catheterization israrely required and Angiography is needed in patients ofknown Coronary artery disease.

Treatment

Urgent surgical intervention is needed in acute severeAR and medical therapy in the form of dopamine,dobutamine and nitroprusside only plays a temporizingrole by reducing LV end diastolic pressure andimproving cardiac output. Intra aortic balloon pump

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(IABP) is contraindicated and beta blockers should beused very cautiously as they blunt the compensatorytachycardia. Surgery should not be delayed as death dueto arrhythmia, acute pulmonary edema or circulatorycollapse is common.

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