Aortic regurgitation overview

Aortic Regurgitation Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Varun Kumar, M.B.B.S., Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Aortic Insufficiency refers to the retrograde or backwards flow of blood from the aorta into the left ventricle during diastole .

Causes of Aortic Insufficiency

There are two broad causes of aortic insufficiency: diseases of the aortic valve itself and diseases of the aorta.

Aortic valve disease

• Rheumatic fever causes retraction of the cusps with resultant mixed aortic stenosis and aortic insufficiency with involvement of mitral valve disease.
• Infective endocarditis
• Traumatic aortic rupture following blunt chest trauma or deceleration injury.
• Congenital bicuspid aortic valve associated with increased risk of aortic dissection which then leads to aortic insufficiency.
• Dopamine agonists

Aortic root disease

• Hypertension
• Aortic dissection
• Marfan syndrome
• HLA B-27 positive conditions : Psoriatic arthritis ; Ankylosing spondylitis ; Reiter's syndrome
• Giant cell arteritis
• Syphilitic aortitis

Pathophysiology

Acute Pathophysiology

In acute aortic insufficiency, there is sudden decrease in stroke volume and subsequent increase in left ventricular end diastolic volume thereby causing decrease cardiac output with resultant reflex tachycardia. The sharply rising high left ventricular end diastolic pressure and reflex tachycardia causes profound hypotension and cardiogenic shock. Initially, the rising left ventricle end diastolic pressure causes early closure of mitral valve during diastole thereby preventing backward blood flow. But in severe cases, the rapidly rising left ventricular end diastolic pressure equalizes with the aortic end-diastolic pressure leading to backward flow of blood progressing towards development of pulmonary edema.

Chronic Pathophysiology

In chronic aortic insufficiency, initially the left ventricle remains complaint, thereby compensates for increased left ventricular end diastolic volume by progressive left ventricular dilatation and left ventricular hypertrophy, which maintains normal ratio of wall thickness to the cavity radius, thereby maintaining normal wall stress. Overtime, when the left ventricular hypertrophy fails to keep up with chronic volume overload, end systolic wall stress rises and at this point the left ventricle fails and results in left ventricle decompensation causing reduction in the left ventricular wall compliance with resultant congestive heart failure.

Diagnosis

Electrocardiogram

There is often evidence of left ventricular hypertrophy and left axis deviation.

Chest X Ray

There may be evidence of cardiomegaly.

Echocardiography

Echocardiography provides two-dimensional views of the regurgitant jet and allows measurement of both the velocity and the volume of the jet. In severe aortic insufficiency, the regurgitant jet width is more than 65% of the width of the left ventricular outflow tract (LVOT) and / or there is flow reversal in the descending aorta.

Aortography

A root shot on the aortogram can be used to gauge the amount of aortic insufficiency.

Cardiac MRI

Cardiac MRI can be used to quantify aortic insufficiency.

Treatment

Aortic insufficiency can be treated either medically with vasodilators or surgically with aortic valve replacement, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.

In general, acute aortic insufficiency with left ventricular dysfunction, symptomatic severe aortic insufficiency, asymptomatic aortic insufficiency with left ventricular dilatation or ejection fraction < 50% should be treated surgically with aortic valve replacement if there are no contraindications.

Chronic aortic insufficiency is managed with vasodilators such as ACE inhibitors , hydralazine or nifidipine to reduce the afterload. Indications for surgery in chronic aortic insufficiency include heart failure with a reduced ejection fraction and increased left ventricular dimensions.