Mechanisms of the valve defect
The development of aortic regurgitation follows two pathogenetic pathways. The defect can be associated with either damage to the valve apparatus itself or pathology of the aorta.
- Primary lesion of the valve cusps. Sclerosis, shrinking, or direct destruction of the tissue occurs. The most frequent cause is rheumatic fever (often combined with aortic stenosis). Infective endocarditis, congenital malformations, and trauma accompanied by cusp rupture also lead to the defect.
- Aortic root lesion. In this case, the cusps themselves remain intact (healthy), but dilation of the fibrous ring occurs, developing relative insufficiency. Syphilis, aortic dissection, cystic medial necrosis in Marfan syndrome, prolonged arterial hypertension, and inflammatory processes (aortitis, ankylosing spondylitis) lead to this scenario.
Intracardiac hemodynamics and remodeling
The foundation of hemodynamic disorders in this defect is volume overload. Due to incomplete cusp closure, regurgitation occurs: part of the blood flows backward from the aorta. Consequently, in diastole, the left ventricle (LV) fills from two sources: normal inflow from the left atrium and pathological return from the aorta.
- End-diastolic volume (EDV) increases, and the chamber walls are overstretched.
- To expel this mass of blood, the heart increases its contractions. A "pendulum-like" movement of blood is formed, when a significant part of the powerful stroke volume flows back into the ventricle.
Adaptation proceeds in two stages. In the early stage, marked cavity dilation occurs and eccentric hypertrophy develops (wall thickening with chamber enlargement), which maintains adequate output for a long time. In the decompensation stage, contractility drops, and end-diastolic pressure rises. "Mitralization" of the defect occurs: due to the massive enlargement of the LV, the fibrous ring of the mitral valve stretches, causing its relative insufficiency. Subsequently, retrograde pressure overloads the left atrium and pulmonary circulation, culminating in right ventricular failure.
Systemic circulation and the ischemia paradox
Hemodynamic shifts at the systemic level are vividly reflected in blood pressure (BP). Systolic BP rises due to the enormous stroke volume, and diastolic BP drops sharply due to blood flowing back into the heart. As a result, pulse pressure increases significantly.
A specific problem of this defect is myocardial ischemia. It arises due to a mismatch between oxygen demand and supply:
- Demand increases sharply due to the giant mass of the hypertrophied myocardium.
- Supply drops because coronary arteries fill during diastole, and diastolic pressure in the aortic root is critically reduced due to regurgitation. Ischemia, in turn, weakens the myocardium and exacerbates the severity of the defect.
Clinical presentation and physical examination data
The disease is characterized by a long asymptomatic period thanks to the powerful reserves of the left ventricle. The first subjective symptoms are usually a sensation of pounding heartbeat, followed by signs of left ventricular failure: exertional dyspnea, orthopnea, and attacks of cardiac asthma. About 20% of patients complain of angina.
Objective examination reveals a vivid picture of a hyperkinetic circulation type:
- Skin is pale.
- Pulsation of peripheral vessels is pronounced, especially the carotid arteries ("Corrigan's pulse" or carotid dance).
- de Musset sign: rhythmic nodding movements of the head synchronous with systole.
- Bounding and rapid pulse (pulsus celer et altus).
- A double murmur can be auscultated over the femoral artery (Duroziez's sign).
Palpation and percussion of the heart reveal a sharp displacement of the borders to the left. The apex beat is displaced to the 6th intercostal space, becoming diffuse and dome-shaped. In some cases, diastolic thrill ("cat's purr") can be felt over the cardiac base and in the suprasternal notch.
Briefly: answers to topical questions
Where and what main murmur is auscultated over the heart in a patient with aortic valve regurgitation?
The main auscultatory sign of aortic valve regurgitation is a diastolic murmur.
- Localization — over the aorta (in the 2nd intercostal space to the right of the sternum) and at Botkin-Erb's point (3rd–4th intercostal space at the left sternal border).
- Characteristics — a soft, high-pitched, holodiastolic decrescendo murmur.
- Radiation — transmitted to the cardiac apex.
This phenomenon is best auscultated with the patient sitting, leaning forward, and holding breath in deep expiration.
What is Quincke's capillary pulse and how to elicit it?
Capillary pulse (Quincke's sign) is the alternating flushing and blanching of the tissues synchronous with the phases of the cardiac cycle. This sign can be elicited by the following methods:
- Examination of the nail bed — rhythmic color change is revealed by applying light pressure to the tip of the nail.
- Examination of the lips — pulsation is detected by pressing a glass slide against the lips.
Flushing of the nail bed or lips occurs during systole, and blanching during diastole.
What is the Austin Flint murmur and what is the mechanism of its occurrence?
The Austin Flint murmur is a functional diastolic (mesodiastolic or presystolic) murmur heard at the cardiac apex in severe aortic regurgitation. The mechanism of its occurrence is associated with the development of relative stenosis of the left atrioventricular orifice. The regurgitant blood jet from the aorta strikes the anterior leaflet of the mitral valve. As a result, the anterior leaflet is displaced toward the posterior leaflet, narrowing the orifice, although organic changes in the mitral valve itself are absent. In character, this sound is low-pitched and rumbling.
What changes in heart configuration (what shape) are determined by percussion and radiography in aortic regurgitation?
Percussion and radiography reveal a typical aortic heart configuration. It is characterized by the following changes:
- Percussion findings — expansion of cardiac dullness borders to the left and downward due to left ventricular hypertrophy and dilation.
- Radiological findings — a deep notch ("accentuated waist") is visualized on the left contour between the 1st arch (aorta) and 4th arch (left ventricle).
Visually, in the early stages, the shape of the cardiac shadow resembles a boot or a duck.
The rule of the "dancing" defect: in aortic regurgitation, everything pulsates (carotid dance, de Musset sign, pulsus celer et altus, diffuse dome-shaped apex beat) due to the enormous pulse pressure.
Class and exam questions
Why can the "infinite tone" phenomenon be heard during vascular auscultation in such patients?
During blood pressure measurement by Korotkoff's method, sounds may be auscultated all the way down to the zero mark on the manometer. This is due to the rapid runoff of blood back into the ventricle and a critical drop in diastolic pressure in the arteries.
What does a decrease in pulse pressure indicate in the late stages of the disease?
A decrease in pulse pressure (as well as an increase in diastolic BP) is an alarming prognostic marker. It indicates exhaustion of compensatory mechanisms, a drop in myocardial contractility, and rising pressure in the failing left ventricle.
What is "mitralization" of an aortic valve defect?
This is a process in which, due to severe dilation of the left ventricular cavity, the mitral valve ring stretches. Relative insufficiency occurs, although the mitral valve cusps themselves are undamaged.
What else to study on this topic
- Detailed mechanism of Duroziez's sign in vessel auscultation.
- Pathogenesis features in syphilitic aortic root disease.
- Differential diagnosis of organic versus relative valve involvement.
- Pathophysiology of right ventricular failure development in aortic defects.
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