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The role of the physical examination in the evaluation of patients with valvular heart disease is also considered in Chaps. 38 and 234; of electrocardiography (ECG) in Chap. 235; of echocardiography and other noninvasive imaging techniques in Chap. 236; and of cardiac catheterization and angiography in Chap. 237.


Mitral regurgitation (MR) may result from an abnormality or disease process that affects any one or more of the five functional components of the mitral valve apparatus (leaflets, annulus, chordae tendineae, papillary muscles, and subjacent myocardium) (Table 259-1). Acute MR can occur in the setting of acute myocardial infarction (MI) with papillary muscle rupture (Chap. 269), following blunt chest wall trauma, or during the course of infective endocarditis (IE) owing to leaflet perforation or destruction. With acute MI, the posteromedial papillary muscle is involved much more frequently than the anterolateral papillary muscle because of its singular blood supply. Transient, acute MR can occur during periods of active ischemia and bouts of angina pectoris. Rupture of chordae tendineae can result in “acute-on-chronic MR” in patients with myxomatous degeneration of the valve apparatus.

TABLE 259-1Major Causes of Mitral Regurgitation

Chronic MR can result from several disease processes (Table 259-1). Distinction should be drawn between primary MR, in which the leaflets and/or chordae tendineae are primarily responsible for abnormal valve function, and secondary (functional) MR, in which the leaflets and chordae tendineae are usually normal but the regurgitation is caused by left ventricular (LV) remodeling with annular enlargement, papillary muscle displacement, leaflet tethering, or their combination. Patient assessment, treatment approach, and long-term prognosis differ significantly between primary and secondary MR. Mitral valve prolapse (MVP) is discussed more extensively in Chap. 260. The rheumatic process produces rigidity, deformity, and retraction of the valve cusps and commissural fusion, as well as shortening, contraction, and fusion of the chordae tendineae. MR can persist after resolution of the acute phase of infection and inflammation. MR may occur as a congenital anomaly (Chap. 264), ...

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