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- Dyspnea or orthopnea.
- Characteristic apical systolic murmur.
- Color-flow Doppler echocardiographic evidence of systolic regurgitation into the left atrium.
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The mitral apparatus consists of the left ventricular walls that support the papillary muscles, the chordae tendineae, mitral leaflets, annulus, and adjacent left atrial walls. Because defects in any of these components can lead to systolic regurgitation, the list of diseases that can cause mitral regurgitation includes many types of heart disease. Anything that causes left ventricular dilatation may disrupt the alignment of the papillary muscles, impairing their function and dilating the annulus, resulting in mitral regurgitation. Myocardial infarction involving the papillary muscles or the left ventricular walls that support them can impair the function of the mitral apparatus. Mitral chordae can rupture, especially in patients with hypertension or mitral valve prolapse. The most common diseases affecting the mitral leaflets are rheumatic heart disease and the myxomatous changes of mitral valve prolapse. In addition, infective endocarditis can destroy the mitral leaflets, and mitral annular calcification can impair the normal systolic contraction of the annulus, leading to mitral regurgitation. Finally, left atrial dilatation from any cause can disrupt annular function and cause mitral regurgitation. Some patients have combinations of these defects, making mitral regurgitation both more likely and more severe.
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For clinical purposes, mitral regurgitation can be divided into two broad categories: organic and functional. The former refers to diseases that involve the valve leaflets and their immediate supporting apparatus, ie, chordae and annulus. The latter refers to diseases that affect the left ventricle and atrium, leaving the valve apparatus intact (Table 20–1). Most clinical studies involve patients with organic mitral regurgitation, so, unless otherwise specified, the following discussion focuses on organic mitral regurgitation.
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Mitral valve prolapse is unique among the many causes of chronic organic mitral regurgitation in many ways. An increase in the middle connective tissue layer of the mitral valve causes an increase in leaflet size and elongated chordae. The resultant systolic prolapse of the valve into the left atrium may or may not be accompanied by regurgitation. In some patients, regurgitation depends on left ventricular volume. Large volumes tend to reduce prolapse and hence regurgitation; small volumes have the opposite effect.
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Consequently, the presence or absence of regurgitation and its severity and timing in systole (the ventricle becomes progressively smaller during systole) are determined by a complex interplay of left ventricular volume, pressure, and contractile state. Patients with mitral valve prolapse are also unique because the condition can be hereditary connective tissue disease (eg, Marfan syndrome) or acquired (inflammation of ...