The left ventricular papillary muscles appear to be the last portions of the heart to be perfused by coronary arterial blood. As a consequence they are sensitive anatomic markers of myocardial ischemia. Foci of necrosis or fibrosis therefore are commonly seen in these structures, particularly the posteromedial papillary muscle, which has a poorer blood supply than does the anterolateral muscle. Coronary arterial luminal narrowing is the most common cause of necrosis or fibrosis of the left ventricular papillary muscles. Other conditions, all associated with inadequate cardiac output, which may produce these lesions include left ventricular outflow tract obstruction, especially that resulting from congenitally malformed aortic valves, acute valvular regurgitation (infective endocarditis), various cardiomyopathies, and primary endocardial fibroelastosis with or without anomalous origin of one or both coronary arteries from the pulmonary trunk. Various infiltrative diseases, including inflammation (Aschoff bodies, sarcoid, abscesses), amyloid, iron, and neoplasms, also may involve the papillary muscles. Their most common congenital malformation is the parachute or single papillary muscle. Fibrosis or necrosis of adjacent left ventricle free wall without involvement of the papillary muscles themselves may simulate clinically “papillary muscle dysfunction.’ The anterior papillary muscle of the right ventricle is frequently affected by conditions which also affect the left ventricular papillary muscles. Whether or not necrosis or fibrosis of the right ventricular papillary muscle causes tricuspid regurgitation, however, is unknown at present.