Angiocardiography in the Apical Systolic Click Syndrome

Mitral insufficiency is characteristically associated with a high-pitched, apical pansystolic murmur which radiates toward the left axilla and subscapular areas. Murmurs heard in late systole and systolic clicks were considered benign and were thought to originate in extracardiac structures (9), possibly related to pleural and pericardial disease. Recently, however, it has been demonstrated that a number of patients with late apical systolic murmurs, whether initiated by a click or not, have varying degrees of mitral insufficiency. A late apical systolic murmur may be heard in rheumatic mitral insufficiency, subaortic stenosis, coarctation of the aorta, and postmyocardial infarction and with a calcified mitral annulus associated with mitral insufficiency. The cases being reported are all in young females without previous history of congenital or acquired cardiac disease. The term “click” is used to describe a very short, high-pitched systolic clicking sound. This term was introduced by Gallavardin (5) in 1913 and popularized by Leatham (6) in 1958. Early systolic clicks have been heard in conditions such as aortic valvular disease, aortic dilatation, pulmonary valvular stenosis, and dilatation of the main pulmonary artery. The current discussion is devoted to clicks occurring in mid or late systole which initiate a late systolic murmur at the apex. The evidence that has accumulated in the past few years from right and left heart catheterization and from intracardiac phonocardiography has localized the origin of these clicks and late systolic murmurs to the region of the mitral valve and its supporting structures (7, 8, 11–13). The available data do not permit conclusions as to which morphological components of the mitral valve give rise to the clicks. It has been suggested that the mid or late systolic clicks are produced by abnormal chordae tendineae as their tension abruptly alters during ventricular systole. Reid (11) coined the term “chordal snap” to describe the click. He theorized that a disturbance of contraction of the papillary muscle or elongation of the chordae may produce relaxation or slackening of the chordae in midsystole. A pressure difference between the left ventricle and the left atrium with the continuation of systole could then produce sudden tightening of a slack chorda, creating a click. Whether mitral insufficiency occurs or not will depend on improper or proper cusp apposition at that time (2, 3). Five patients were chosen for investigation on the basis of the auscultatory and phonocardiographic demonstration of a late systolic murmur associated with and preceded by a clicking sound (Fig. 1) and because of T-wave abnormalities in the electrocardiogram (Fig. 2). The T-wave was sharply inverted in leads 2, 3, aVF, and, usually, V5 or V6. Left ventricular hypertrophy by voltage criteria was present in 3 patients.