Valvular defects

Acquired valvular defects include:


 * 1. stenosis (narrowing)
 * 2. insufficiency (non-clotting) – its consequence is backflow of blood (regurgitation)

They most often affect the left-sided valves (ie mitral and aortic valves). Both defects are often combined on one valve (combined defect - the valve is simultaneously stenotic and insufficient), other times it is a pure defect (most often pure insufficiency). The term isolated defect means that only one valve is affected while the other is normal.

Relative insufficiency occurs without organic damage to the valve during dilatation of the heart or aorta, when the edges of an otherwise unchanged valve do not touch each other (e.g., when dilating the right ventricle, relative insufficiency of the tricuspid valve occurs in this way, or relative aortic insufficiency occurs when dilatation of the aorta on the basis of syphilitic mesoartotitis).

Valvular defects can be compensated for by hypertrophy of the myocardium, which maintains normal cardiac output. In more severe or acutely occurring valvular defects, decompensation and heart failure occur (the morphological manifestation of decompensation is the dilation of the relevant sections of the heart).

Mitral stenosis
Mitral stenosis most often arises as a result of rheumatic endocarditis (adhesions of commissures and tendons), or in case of large vegetations, infectious endocarditis on the valves, tumors of the left atrium (mainly myxoma ), massive annular sclerosis of the mitral annulus. Blood stagnates in the LS, which expands and wall thrombi form (especially in its ear), which can embolize into the general circulation, the dilated LS then exerts pressure on the esophagus and the left recurrent laryngeal nerve. The congestion of the blood is transferred to the small circulation, causing congestion and later rusty induration of the lungs, pulmonary hypertension induces subsequent PK hypertrophy. This later dilates and causes relative insufficiency of the tricuspid valve with subsequent dilation of the PS and transfer of congestion to the general circulation - in the late stages there is generalized venostasis (increased filling of jugular veins, hepatomegaly ...). The consequence of hypertension in the small circulation is sclerosis of the pulmonary arteries.

Macroscopically, the heart with mitral stenosis has a dilated LS, a hypertrophic PK (however, this is not cor pulmonale ! – this term is reserved for hypertrophy of the PK in pulmonary hypertension having a cause primarily in the lungs) and a dilated PS, while the size of the LV does not change, clinically a diastolic murmur.

Mitral insufficiency
It is caused by a defect in the valve leaflets (rheumatic endocarditis, mitral prolapse - myxoid degeneration of the valve, infective endocarditis ) or the suspension apparatus (scarring or rupture of the papillary muscle or tendon). During systole, the blood penetrates back into the LS, which expands and hypertrophies, from there the stagnation is transferred, as in mitral stenosis, to the small circulation, where it has the same consequences with the formation of PK hypertrophy, but the LV behaves differently than in mitral stenosis - it hypertrophies and dilates. Macroscopically, the heart in mitral insufficiency has hypertrophied and dilated all compartments, clinically a systolic murmur.

Aortic stenosis
The causes of aortic stenosis can be threefold:


 * rheumatic endocarditis (10%) - commissural adhesions (younger adults)
 * bicuspid aortic valve (40%) – no commissural fusions, dystrophic valve calcification (5th–6th decade)
 * senile (sclerotic) type (50%) – no commissural adhesions, dystrophic valve calcification (8th–9th decade)

Narrowing of the outflow tract of the left ventricle leads to an increase in afterload, to which the heart responds by hypertrophy of the left ventricle. As the defect worsens, anginal problems and the risk of sudden death appear - aortic stenosis is the most often fatal valve defect!

Aortic insufficiency
The cause is, on the one hand, involvement of the valve itself (rheumatic or infectious endocarditis), and on the other hand, involvement of the aorta (Luetic aortitis, Marfan syndrome, aortic dissection, ankylosing spondylitis). During diastole, non-closing valve blood flows back into the LV (diastolic murmur), which thus fills more and therefore hypertrophies and then dilates. The disorder is also transmitted to other heart sections, so in the final stage we find hypertrophy and dilation of all heart sections (the most pronounced hypertrophy of the whole heart, its weight can exceed 1000 g – cor bovinum). In the wall endocardium of the LV septum below the mouth of the aorta there are regurgitation cilia - Zahn's valves.

Tricuspid stenosis
A rare defect, it arises in rheumatic endocarditis or in the framework of carcinoid syndrome.

Tricuspid insufficiency
It is mostly relative in PK dilatation, or arises in post-rheumatic leaflet shortening, in carcinoid syndrome, infective endocarditis and Ebstein's malformation.

Mitral prolapse (myxoid degeneration, Barlow syndrome )
Enlargement of the leaflets of the mitral valve (which during systole arch - prolapse - into the LS). Anulus fibrosus sinister is dilated, the tendons are thin and elongated.

Microscopically, there is an increased content of mucus-like substances (acidic mucopolysaccharides) in the valve..

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 * Review of valvular defects