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VALVULAR DEGENERATION CAUSED BY CALCIFICATION

The heart valves are subjected to high repetitive mechanical stresses, particularly at the hinge points of the cusps and leaflets owing to (1) 40 million or more cardiac cycles per year, (2)

substantial tissue deformations at each cycle, and (3) transvalvular pressure gradients in the closed phase of approximately 120 mm for the mitral and 80 mm for the aortic valve. It is

therefore not surprising that these normally delicate structures suffer cumulative damage complicated by formation of calcific deposits (composed of calcium phosphate mineral), which

may lead to clinically important disease (see Chapter 1 ). The most frequent calcific valvular diseases, illustrated in Figure 12-22 , are calcific aortic stenosis, calcification of a congenitally

bicuspid aortic valve, and mitral annular calcification. Each comprises primarily dystrophic calcification without significant lipid deposition or cellular proliferation, a process distinct from

but with some features of atherosclerosis.

Figure 12-22Calcific valvular degeneration. A, Calcific aortic stenosis of a previously normal valve having three cusps (viewed from aortic aspect). Nodular masses of calcium are heapedup

within the sinuses of Valsalva (arrow). Note that the commissures are not fused, as in postrheumatic aortic valve stenosis (see Fig. 12-24E ). B, Calcific aortic stenosis occurring on a

congenitally bicuspid valve. One cusp has a partial fusion at its center, called a raphe (arrow). C and D, Mitral annular calcification, with calcific nodules at the base (attachment margin)

of the anterior mitral leaflet (arrows). C, Left atrial view. D, Cut section of myocardium.

Figure 12-23Myxomatous degeneration of the mitral valve. A, Long axis of left ventricle demonstrating hooding with prolapse of the posterior mitral leaflet into the left atrium (arrow).

The left ventricle is on right in this apical four-chamber view. (Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.) B, Opened valve, showing pronounced hooding of the

posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact (arrows). C, Opened valve with pronounced hooding from patient who died suddenly (double arrows).

Note also mitral annular calcification (arrowhead).

Figure 12-24Acute and chronic rheumatic heart disease. A, Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small vegetations (verrucae) are visible

along the line of closure of the mitral valve leaflet (arrows). Previous episodes of rheumatic valvulitis have caused fibrous thickening and fusion of the chordae tendineae. B, Microscopic

appearance of Aschoff body in a patient with acute rheumatic carditis. The myocardial interstitium has a circumscribed collection of mononuclear inflammatory cells, including some large

histiocytes with prominent nucleoli and a prominent binuclear histiocyte, and central necrosis. C and D, Mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets,



commissural fusion (arrows), and thickening and shortening of the chordae tendineae. Marked dilation of the left atrium is noted in the left atrial view (C). D, Opened valve. Note

neovascularization of anterior mitral leaflet (arrow). E, Surgically removed specimen of rheumatic aortic stenosis, demonstrating thickening and distortion of the cusps with commissural

fusion (E, reproduced from Schoen FJ, St. John-Sutton M: Contemporary issues in the pathology of valvular heart disease. Human Pathol 18:568, 1967.)

Figure 12-25The pathogenetic sequence and key morphologic features of acute rheumatic heart disease.

Figure 12-26Infective (bacterial) endocarditis. A, Endocarditis of mitral valve (subacute, caused by Strep. viridans). The large, friable vegetations are denoted by arrows. B, Acute

endocarditis of congenitally bicuspid aortic valve (caused by Staph. aureus) with extensive cuspal destruction and ring abscess (arrow). C, Histologic appearance of vegetation of

endocarditis with extensive acute inflammatory cells and fibrin. Bacterial organisms were demonstrated by tissue Gram stain. (C, reproduced from Schoen FJ: Surgical pathology of

removed natural and prosthetic heart valves. Human Pathol 18:558, 1987.) D, Healed endocarditis, demonstrating mitral valvular destruction but no active vegetations.

Figure 12-27Diagrammatic comparison of the lesions in the four major forms of vegetative endocarditis. The rheumatic fever phase of RHD (rheumatic heart disease) is marked by a row

of small, warty vegetations along the lines of closure of the valve leaflets. IE (infective endocarditis) is characterized by large, irregular masses on the valve cusps that can extend onto the

chordae (see Fig. 12-26 ). NBTE (nonbacterial thrombotic endocarditis) typically exhibits small, bland vegetations, usually attached at the line of closure. One or many may be present (see

Fig. 12-28 ). LSE (Libman-Sacks endocarditis) has small or medium-sized vegetations on either or both sides of the valve leaflets.

TABLE 12-8-- Diagnostic Criteria for Infective Endocarditis *


Date: 2016-04-22; view: 206


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