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Aortic Valve Disease

Q: What is "cor bovinum"?

It is a macroscopic term (cor bovinum) denoting a markedly enlarged heart weighing 700–1000 grams. It results from pronounced left ventricle hypertrophy compensating for increased hemodynamic load.

*Vitium valvae aortae*

For medical students2 min readUpdated 2026-10-10

Aortic valve disease encompasses a group of acquired structural anomalies of the aortic semilunar cusps that disrupt intracardiac hemodynamics. It is the second most common valvular pathology after mitral valve disease and leads to extreme left ventricular hypertrophy.

EpidemiologyRanks second in frequency after mitral valve disease.

Heart weightReaches 700–1000 g during hypertrophy, forming a "cor bovinum".

Common etiologyMost commonly develops as a consequence of rheumatic fever.

HemodynamicsPure stenosis is rare; it is usually combined with insufficiency.

Etiology and General Morphological Changes

Aortic valve disease can be triggered by a variety of pathological processes. The most common cause is traditionally rheumatic fever. Significantly rarer causes of deformation and destruction of the valvular apparatus include atherosclerosis, syphilis, brucellosis, and infective (subacute bacterial) endocarditis.

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

Semilunar cusps progressively thicken, losing their natural elasticity and mobility.
Pronounced sclerosis of the valvular tissue develops.
Cusps fuse together, deforming the aortic orifice lumen.
In late stages, the tissue undergoes calcification (massive deposition of calcium salts), rendering the valve completely rigid.

Specific Changes Depending on Etiology

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

Atherosclerosis: The pathological process has a distinct localization. It develops predominantly on the side of the semilunar cusps facing the aortic sinus (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 of the valvular apparatus. Cusp tissue undergoes ulceration and erosion. Perforations and specific aneurysms of the semilunar cusps frequently occur, leading to acute regurgitation.
Syphilis: Deformation of the valvular apparatus in this specific infection is always accompanied by lesions of the aortic wall itself, manifesting as syphilitic mesaortitis. Aortic regurgitation in this case is secondary: it arises from aortic aneurysm formation, which mechanically stretches the valve ring and prevents cusp coaptation.

Pathological Anatomy and Hemodynamic Alterations

Hemodynamically, aortic stenosis in a pure, isolated form is extremely rare. As a rule, the pathology is combined, where narrowing of the orifice (stenosis) is paired with valve insufficiency.

Myocardial Changes The defect creates a colossal workload on the heart due to the need to overcome resistance or compensate for the backflow of blood. In response, marked compensatory concentric hypertrophy of the left ventricle develops. The heart weight can reach 700–1000 grams. In classical pathology, such a giant heart is referred to as "cor bovinum" (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 resembling additional semilunar cusps may form on the ventricular endocardium just below the main valve orifice.

Clinical Manifestations of Severe Regurgitation

When aortic valve disease is accompanied by significant regurgitation (backflow of blood from the aorta into the left ventricular cavity during diastole), a characteristic clinical picture emerges, driven by sharp pressure differentials.

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

Mnemonic

For quick recall of specific etiologies: Atherosclerosis — Atheromatosis (lipoidosis facing the sinus of Valsalva), Sepsis — Spoils the valve (destruction, perforation), Syphilis — Strikes the aortic wall (mesaortitis and aneurysm).

Frequently asked questions

What specific murmurs (and in which phases of the cardiac cycle) are auscultated in aortic stenosis and insufficiency?

Aortic valve diseases produce specific murmurs during systole and diastole.

Disease	Cycle Phase and Murmur Characteristics
Aortic stenosis	Harsh crescendo-decrescendo systolic ejection murmur at the aortic area
Aortic regurgitation	Protodiastolic or holodiastolic murmur (occupying all of diastole), along with the Austin Flint pre-systolic murmur at the apex

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

In aortic stenosis, the type of left ventricular hypertrophy depends on the stage of the disease. During the compensation stage, concentric myocardial hypertrophy develops as an adaptive reaction to high intracavitary pressure, while cavity volume remains unchanged. In the decompensation stage, when reserves are depleted, concentric hypertrophy transitions into eccentric hypertrophy with chamber dilation.

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

Decompensated acquired heart disease leads to congestion in the pulmonary and systemic circulations, cavity effusions, and anasarca. Chronic systemic venous congestion drives parenchymal atrophy, stromal sclerosis with organ induration (fibrosis), and secondary lymphatic drainage overload.

What is the most frequent etiology of aortic valve disease?

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

What is "cor bovinum"?

It is a macroscopic term (cor bovinum) denoting a markedly enlarged heart weighing 700–1000 grams. It results from pronounced left ventricle hypertrophy compensating for increased hemodynamic load.

How does syphilis lead to aortic valve insufficiency?

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

Does isolated aortic valve stenosis occur?

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

Go deeper

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