Aortic Regurgitation Mechanisms

Introduction

Aortic regurgitation (AR), also called aortic insufficiency, is a valvular heart disease in which the aortic valve fails to close completely during diastole, allowing blood to leak backward from the aorta into the left ventricle (LV). This abnormality leads to volume overload of the LV, progressive dilation, and eventually systolic heart failure if untreated.

The pathophysiology and clinical spectrum of AR depend heavily on whether the disease develops acutely or chronically. Acute AR is a medical emergency, whereas chronic AR often progresses silently until the LV can no longer compensate.

1. Etiology: Causes of Aortic Regurgitation

The causes of AR can be classified into valve leaflet abnormalities and aortic root diseases.

A. Congenital Causes

Bicuspid aortic valve – most common congenital cause. A bicuspid valve is prone to degeneration, prolapse, and endocarditis.
Congenital fenestrations or cusp malformations – rare, may cause insufficiency at a younger age.

B. Rheumatic Heart Disease

Often follows acute rheumatic fever.
Causes leaflet thickening, retraction, and commissural fusion, preventing full closure.
Typically associated with mitral valve disease, especially mitral stenosis.

C. Infective Endocarditis

Causes valve cusp perforation, destruction, or vegetations.
Leads to acute severe AR.
Associated with systemic infection, fever, and embolic complications.

D. Connective Tissue and Aortic Root Disorders

Marfan syndrome – due to fibrillin-1 gene mutation → aortic root dilation.
Ehlers-Danlos syndrome – collagen abnormality, predisposes to root dilation.
Annuloaortic ectasia – dilation of the aortic root and annulus.
Syphilitic aortitis (rare today) – damages ascending aorta → AR.

E. Degenerative and Other Causes

Calcific degeneration – less common than stenosis but may cause cusp restriction.
Hypertension – chronic pressure may dilate ascending aorta.
Aortic dissection – acute tear of the aortic intima involving the valve annulus → sudden AR.

2. Pathophysiology: Acute vs Chronic Aortic Regurgitation

The clinical manifestations of AR differ dramatically between acute and chronic forms.

A. Acute Aortic Regurgitation

Mechanism:

Sudden large regurgitant volume enters a non-compliant LV.
LV cannot dilate acutely → marked rise in LV end-diastolic pressure (LVEDP).
Elevated LVEDP transmits backward to left atrium and pulmonary veins, causing acute pulmonary edema.

Hemodynamics:

Stroke volume decreases abruptly.
Severe hypotension and cardiogenic shock may develop.

Causes:

Infective endocarditis (valve destruction).
Aortic dissection.
Traumatic rupture of valve cusps.

Clinical Picture:

Sudden onset dyspnea, pulmonary edema, hypotension.
Often fatal without urgent surgery.

B. Chronic Aortic Regurgitation

Mechanism:

Regurgitation develops gradually.
LV adapts through eccentric hypertrophy and dilation.
Initially maintains forward cardiac output despite regurgitation.
Over years, progressive LV dilation leads to systolic dysfunction.

Hemodynamics:

Wide pulse pressure due to:
- High systolic pressure (large stroke volume).
- Low diastolic pressure (runoff back into LV).
Increased LV compliance delays symptom onset.

Clinical Course:

Long asymptomatic phase.
Symptoms (dyspnea, fatigue, palpitations) appear when LV decompensation begins.

3. Clinical Features

The physical examination in AR is one of the most striking in cardiology, with peripheral signs of wide pulse pressure in chronic AR.

A. Symptoms

Acute AR:

Sudden severe dyspnea.
Pulmonary edema.
Cardiogenic shock.

Chronic AR:

Often asymptomatic for years.
Exertional dyspnea, fatigue, palpitations.
Angina may occur due to increased LV oxygen demand.

B. Signs and Peripheral Manifestations

Pulse and Blood Pressure:

Bounding (“water-hammer”) pulse – rapid upstroke and collapse.
Wide pulse pressure – hallmark of chronic AR.
Corrigan’s pulse – visible carotid pulsations.
De Musset’s sign – head bobbing with each heartbeat.
Quincke’s sign – capillary pulsations in nail beds.
Traube’s sign – pistol-shot sounds over femoral arteries.
Duroziez’s sign – systolic/diastolic murmurs over femoral artery with pressure.

Cardiac Examination:

Apex beat displaced and hyperdynamic (due to LV dilation).
Diastolic decrescendo murmur – best at left sternal border, patient leaning forward in end-expiration.
Austin Flint murmur – low-pitched mid-diastolic murmur at apex (regurgitant jet striking mitral valve, mimicking mitral stenosis).

4. Auscultatory Findings

Early diastolic, high-pitched, decrescendo murmur – classic for AR.
Heard best with diaphragm of stethoscope, left parasternal, patient sitting forward.
Murmur intensity may not correlate with severity (depends on pressure gradient).
Systolic flow murmur may be heard due to increased stroke volume.
Third heart sound (S3) in chronic AR indicates LV dysfunction.

5. Imaging and Diagnostic Modalities

A. Echocardiography

First-line investigation.
Identifies cause: valve cusp disease vs aortic root dilation.
Assesses severity:
- Jet width, regurgitant volume, vena contracta.
- Pressure half-time (shorter = more severe AR).
Evaluates LV size and function (key for surgical timing).

B. Doppler Echocardiography

Quantifies regurgitation.
Measures diastolic flow reversal in descending aorta – specific for severe AR.

C. Cardiac MRI

Gold standard for quantifying regurgitant fraction and LV volumes.
Useful in borderline cases and follow-up.

D. Cardiac Catheterization

Historically gold standard, now rarely needed.
Used when non-invasive imaging is inconclusive or before surgery.

E. Chest X-ray

Chronic AR: cardiomegaly, aortic root dilation.
Acute AR: may be normal or show pulmonary congestion.

F. ECG

LV hypertrophy and repolarization abnormalities in chronic AR.
Nonspecific in acute AR.

6. Stages and Clinical Course

Compensated stage: LV dilation with preserved function, often asymptomatic.
Decompensated stage: LV systolic dysfunction develops, symptoms of heart failure appear.
End-stage: Severe LV dysfunction, poor prognosis without valve replacement.

7. Prognostic Implications

Chronic severe AR has a long asymptomatic course.
Once symptoms (dyspnea, angina, syncope) appear, survival drops significantly.
LV function (ejection fraction, end-systolic dimension) is the strongest predictor of outcome.