Subvalvular mitral insufficiency: roentgen aspects.

Abstract

The characteristic roentgen appearance of rheumatic mitral insufficiency is dominated by the large left ventricle and the large left atrium (14). This appearance is generated by the slow development of mitral incompetence over a period of years. As the rheumatic process heals, the leaflets scar and the chordae tendineae shorten, allowing regurgitation into the left atrium and elevation of left atrial pressure with subsequent left atrial dilatation (6, 10, 15). In addition to the valvular insufficiency of rheumatic heart disease, however, mitral incompetence may result from disruption of the subvalvular apparatus. Each leaflet of the valve is anchored by a number of chordae tendineae. In turn each of the chordae inserts into one or the other of the papillary muscles. Rupture of the chordae tendineae or of the papillary muscle causes prolapse of the unsupported leaflet into the left atrium with consequent acute mitral insufficiency. This may occur in an otherwise competent valve or may aggravate pre-existing mitral incompetence from another cause (15). The purpose of this report is to present the roentgen findings in eight patients with subvalvular mitral incompetence studied at the University of Kentucky Medical Center, Lexington. The clinical and hemodynamic findings will be analyzed elsewhere. Table I summarizes the clinical course of our patients and Table II the radiographic evaluation. The roentgen appearance is illustrated in Figures 1 to 3. A number of roentgen findings were present in almost all of our patients. These include absence of mitral valve calcification, cardiac enlargement, evidence of pulmonary venous and capillary hypertension, systolic pulsation of the left atrium by fluoroscopy, and moderate-to-massive mitral regurgitation on the left ventriculogram. Left atrial size is variable, and on that basis the findings in these patients form a spectrum. It is our feeling that the size of the left atrium and the appearance of the roentgenogram are dependent upon the following factors: (a) the etiology of the subvalvular incompetence; (b) the duration of mitral incompetence; (c) the number of chordae involved; (d) the age of the patient; (e) associated heart disease. Etiology Rupture of the chordae tendineae has been attributed to trauma (3) and rheumatic heart diseases (2). Several papers have implicated bacterial endocarditis as the leading cause of ruptured chordae, even where there is little if any other evidence of endocarditis (8, 11, 13, 16). Some cases have no obvious cause and are listed as spontaneous (7, 9, 17–19). Myocardial infarction is the cause of rupture or dysfunction of a papillary muscle in almost all instances (1,4). In patients in whom the acute subval-vular incompetence is not preceded by previous valvular heart disease, the left atrium is not enlarged radiographically but exhibits vigorous systolic pulsations by fluoroscopy (15,16).