Aortic regurgitation is a condition characterized by abnormal structural changes in the aortic valve leaflets, resulting in inadequate coaptation. Etiologies include rheumatic heart disease, age-related degenerative changes of the valve, infective endocarditis, Marfan syndrome, congenital malformations of the aortic valve, and aortic dissection.
Pathophysiology
The primary hemodynamic change in aortic regurgitation is diastolic reflux of blood from the aorta into the left ventricle. Due to the significant diastolic pressure gradient between the aorta and the left ventricle, even a regurgitant orifice of only 0.5 cm² can lead to a regurgitant flow of 2–5 liters per minute. During diastole, the left ventricle receives both blood from the left atrium and from the regurgitant aortic flow, causing overfilling and progressive left ventricular enlargement and remodeling. In the compensated phase, the left ventricle can maintain an increased stroke volume, with cardiac output exceeding normal levels. However, during decompensation, cardiac output decreases, left atrial and pulmonary artery pressures rise, and left heart failure may occur. Additionally, reduced diastolic pressure impairs coronary perfusion, while significant left ventricular hypertrophy increases oxygen demand, resulting in myocardial ischemia.
Clinical Manifestations
Patients with mild regurgitation and good cardiac compensatory function may remain asymptomatic. Early symptoms include palpitations, discomfort in the precordial region, and a sensation of strong pulsations in the head. Severe cases often present with angina pectoris, dyspnea, and episodes of paroxysmal dyspnea, orthopnea, or acute pulmonary edema.
Physical Examination
Findings include an enlarged cardiac silhouette with displacement of the apical impulse downward and to the left, along with lifting apical beats. A sighing diastolic murmur—occurring in early, mid, or throughout diastole—can be heard along the left sternal border at the third or fourth intercostal space as well as the aortic valve area, often radiating to the apex. Signs of severe regurgitation include water hammer pulses, Traube's sign (pistol-shot sounds over arteries), and visible capillary pulsations.
Auxiliary Examinations
Electrocardiography (ECG)
ECG findings include left axis deviation along with evidence of left ventricular hypertrophy and strain.
X-ray Examination
Chest X-rays may show enlargement of the ascending aorta and left ventricle with increased pulsation amplitude. Pulmonary venous congestion may be evident in cases of left ventricular failure.
Echocardiography
Echocardiography is the most effective method for assessing the severity of the lesion. The speed of aortic valve opening and closure is increased, and multiple lines may be visible during diastole. Regurgitant blood flow impacting the mitral valve during diastole may cause the anterior mitral leaflet to exhibit high-frequency flutter. Echocardiography can also identify left ventricular enlargement, incomplete closure of the aortic valve leaflets during diastole, leaflet structural abnormalities, and retrograde diastolic blood flow from the aorta into the left ventricle.
Treatment
Patients who have developed symptoms such as angina pectoris or signs of left ventricular failure often experience rapid disease progression, with a risk of sudden death over the next few years. Early surgical intervention involving either valve replacement with a prosthetic valve or valve repair remains the recommended approach.