Becker A E, Anderson R H
Eur J Cardiol. 1975 Jan;2(3):351-9.
The pathological processes underlying the symptom of mitral insufficiency appearing during the course of acute myocardial infarction are reviewed. The mitral valve apparatus can be considered as being composed of fibrous elements (the annulus fibrosus, the valve leaflet and the chordae tendineae), the left atrial endocarduim and the muscular elements (the papillary muscles together with their supporting myocardium). Since the fibrous elements are avascular, it is concluded that they are unlikely to be directly affected by ischemia. For this and other reasons dilatation of the mitral annulus is not considered a cause of incompetence. It is suggested that muscular involvement is the most likely cause of mitral incompetence during acute myocardial infarction. The syndrome of 'papillary muscle dysfunction' is therefore reviewed under the headings of (1) conditions producing abnormal spatial orientation of the muscles, (2) conditions producing abnormal or absent contraction of the muscles and (3) conditions producing improper timing of muscular contraction. Cases are illustrated which demonstrated generalized dilatation of the left ventricle, localized dilatation and both complete and imcomplete papillary muscle rupture. Mitral insufficiency under these circumstances may ensue from either improper orientation or improper functioning of the muscular elements of the mitral valve apparatus, or from both. It is also emphasized that direct involvement of the papillary muscles by the ischemic process is not necessary for incompetence to occur, and that most cases of mitral incompetence complicating the acute stage of myocardial infarction are of transient nature, resolving during the recovery phase.