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Pathology · Cardiovascular Pathology

Aortic valve defects

*Vitium valvae aortae*

Aortic valve defects are a group of acquired structural anomalies of the semilunar aortic cusps that disrupt intracardiac hemodynamics. In the structure of valvular pathology, they rank second in frequency after mitral apparatus lesions and lead to extreme left ventricular hypertrophy.

EpidemiologyRank 2nd in frequency after mitral valve disease.
Heart massCan reach 700–1000 g in hypertrophy, forming a "bovine heart".
Common etiologyMost commonly develops as a result of rheumatic fever.
HemodynamicsPure stenosis is rare; it is usually combined with insufficiency.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiology and general morphological changes

The development of an aortic valve defect can be triggered by a number of various pathological processes. Traditionally, the most frequent cause of the defect is rheumatic fever. Conditions such as atherosclerosis, syphilis, brucellosis, and infective endocarditis lead to the deformation and destruction of the valvular apparatus significantly less frequently.

The general morphological picture of aortic valve defect development is largely similar to the destructive and sclerotic processes observed in mitral valve disease. Pathological changes develop sequentially and steadily:

  • The semilunar cusps gradually thicken, losing their natural elasticity and mobility.
  • Pronounced sclerosis of the valvular tissue develops.
  • The cusps fuse together, deforming the lumen of the aortic orifice.
  • In later stages, the tissue undergoes petrification (massive calcium salt deposition), making the valve completely rigid.

Specific changes depending on etiology

Depending on the underlying disease that caused the defect, characteristic, etiologically specific changes form on the valves:

  • Atherosclerosis: The pathological process has a clear localization. It develops predominantly on the side of the semilunar cusps facing directly toward the sinus of Valsalva. Pronounced lipoidosis and subsequent liposclerosis are observed in this zone.
  • Infective endocarditis and brucellosis: These severe infectious processes are characterized by profound destructive changes in the valvular apparatus. The cusp tissue undergoes ulceration and erosion. Transmural perforations and specific aneurysms of the semilunar cusps frequently occur, leading to acute insufficiency.
  • Syphilis: Deformation of the valvular apparatus in this specific infection is always accompanied by damage to the aortic wall itself, resulting in syphilitic mesaortitis. Aortic valve insufficiency in this case is secondary: it arises due to the formation of an aortic aneurysm, which mechanically stretches the valve ring, preventing the cusps from closing.
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Pathological anatomy and hemodynamic disturbances

From a hemodynamic perspective, aortic stenosis in its pure, isolated form is extremely rare. As a rule, the pathology is combined, with narrowing of the orifice (stenosis) accompanying valve insufficiency.

Myocardial changes The defect creates a colossal increased workload on the heart due to the necessity of overcoming resistance or compensating for the regurgitant blood flow. In response, marked working hypertrophy of the left ventricle develops. The mass of the heart can reach 700–1000 grams. In classical pathological anatomy, such a giant heart is figuratively called a "bovine heart" (cor bovinum).

Endocardial changes Due to severe intracardiac hemodynamic disturbances and constant turbulent blood flow, pronounced endocardial fibrosis of the left ventricle develops. An interesting morphological feature is that specific fibrous thickenings, visually resembling additional semilunar cusps, may appear on the ventricular endocardium below the main valve orifice.

Clinical manifestations in severe regurgitation

When an aortic defect is accompanied by severe regurgitation (backflow of blood from the aorta into the left ventricular cavity during diastole), a very characteristic clinical picture arises, driven by sharp pressure drops.

First, auscultation reveals specific murmurs reflecting pathological blood flow turbulence. Second, blood pressure parameters change drastically: there is a sharp, pathological drop between systolic and diastolic pressure. This naturally leads to a significant increase in pulse pressure, which is one of the most important clinical and diagnostic markers of this pathology.

Briefly: answers to topical questions

Specifically, which murmurs (and in what phase of the cardiac cycle) are auscultated in aortic stenosis and insufficiency?

Aortic valve defects are characterized by specific murmurs auscultated during systole and diastole.

DefectCycle phase and murmur characteristics
Aortic StenosisRough crescendo-decrescendo (diamond-shaped) systolic murmur over the aorta
Aortic insufficiencyProtodiastolic or holodiastolic murmur (occupying the entire diastole), as well as the Austin Flint presystolic murmur at the apex

What type of left ventricular hypertrophy (concentric or eccentric) develops in aortic stenosis?

In aortic stenosis, the type of left ventricular hypertrophy depends on the stage of the disease. In the compensation stage, concentric myocardial hypertrophy develops as an adaptive response to high intraventricular pressure, while the cavity volume does not increase. In the decompensation stage, when reserves are depleted, concentric hypertrophy is replaced by eccentric hypertrophy with cavity dilatation.

What systemic complications in other organs are caused by a decompensated aortic valve defect?

Decompensation of an acquired heart defect leads to blood stagnation in the pulmonary and systemic circulation, cavity effusions, and anasarca. Chronic general venous congestion causes progressive parenchymal atrophy, stromal sclerosis with organ induration (fibrosis), and secondary lymphatic drainage overload.

How to memorize

For quick memorization of specifics: Atherosclerosis — Atheromatosis (lipoidosis at the sinus of Valsalva), Sepsis — Spoils/destroys the valve (destruction, perforation), Syphilis — Sortic wall (mesaortitis and aneurysm).

Class and exam questions

What is the most common etiology of aortic valve disease?

Rheumatic fever is the most common cause. Atherosclerosis, syphilis, brucellosis, and infective endocarditis are significantly less common.

What is a "bovine heart"?

This is a macroscopic term (cor bovinum) designating a sharply enlarged heart weighing 700–1000 grams. It occurs due to pronounced left ventricular hypertrophy in response to increased hemodynamic load caused by the defect.

How does syphilis lead to aortic valve insufficiency?

Syphilis causes mesaortitis, which leads to the formation of an aortic aneurysm. Dilation of the aortic root stretches the valve ring, causing secondary insufficiency.

Does isolated aortic valve stenosis occur?

It is extremely rare in its pure form. As a rule, stenosis is combined with valve insufficiency.

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What else to study on this topic

  • Morphogenesis of rheumatic heart valve disease
  • Pathological anatomy of infective endocarditis
  • Syphilitic mesaortitis: macro- and microscopic presentation
  • Compensation mechanisms in left ventricular hypertrophy

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