Mechanisms of ischemic mitral insufficiency and their surgical correction
The function of the mitral valve is dependent on the precise interaction of cusps, chordae, ventricular base, and the posterior ventricular wall. For closure to take place with or without atrial contraction, a vortex forms behind the anterior cusp and mov
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The function of the mitral valve is dependent on the precise interaction of cusps, chordae, ventricular base, and the posterior ventricular wall. For closure to take place with or without atrial contraction, a vortex forms behind the anterior cusp and moves it posteriorly, and the ventricular muscle starts to develop tension . With this the ventricular pressure rises , reversing the diastolic forward flow of blood through the orifice . Closure occurs after systole has started, just before the aortic valve opens. The normal annulus narrows, bringing the posterior cusp nearer to the anterior cusp and the posterior left ventricular wall shortens allowing the cusps to rise to the plane of the atrioventricular ring . A small puff of regurgitation occurs as the cusps close. Most of this is blood displaced by the cusps as their contact progresses from a touching of the free edges to contact over a substantial area [2, 3]. The competent closed mitral valve has the following features: 1) The area of the cusps exceeds the systolic area of the mitral annulus. In general, the length of the anterior cusp through its center equals or exceeds the systolic diameter of the annulus from the base of the anterior cusp to the base of the central scallop of the posterior mitral cusp (at junction of ventricle, cusp , and atrium) . 2) The free edges of anterior and posterior cusps in systole are a) at the same level as each other and b) on the ventricular side of the plane of the atrioventricular orifice . 3) The combination of 1) and 2) results in the body of the cusps being parallel to the plane of the orifice while appositional areas (Y.3 of the anterior cusp and ~ of the posterior cusp) are in contact with each other in a plane more or less at right angles to the plane ofthe orifice (Fig. la, b) [1,2]. The effect of coronary artery disease on the mechanisms of normal mitral valve competence
Mitral insufficiency results from the failure of cusp coaption . Coronary artery disease may affect mitral valve coaption in three basic ways : 1) It may alter left ventricular systolic funciton of a) the mural annulus (Fig . 2a) ; b) the po sterior left ventricular wall between the annulus and the origin of one or both of the papillary muscles; (Fig . lc, d , Fig . 2c) , c) a segment of the posterior left ventricular muscle surrounding the origin of a papillary mu scle (Fig. 2a , Fig. 3a , b) ; d) combinations of a) b) and c) (Fig. 2b, d, Fig. 3c, d), and e) the whole left ventricle producing a dilated cardiomyopathy . 117 H. O. Vetter et al. (eds.), Ischemic Mitral Incompetence © Springer-Verlag Berlin Heidelberg 1991
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Fig. 1. In this and in all other long axis cross-sectional drawings of the left ventricle the lengths of anterior and posterior cusps and chordae are kept the same . The left ventricular dimensions change: if failure of coaption occurs it is entirely due to ventricular mechanisms. a) and b) Norm al ventricle; a) Diastole , and b) Systole . The vertical bars labelled A show the annular diameter change between diastol
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