Circulation, Vol 52, 297-305, Copyright © 1975 by American Heart Association
DO Nutter, C Wickliffe, CA Gilbert, C Moody and SB King 3d
Left ventricular structure, function, and the coronary circulation were
studied in a subset of patients with mitral valve leaflet prolapse. This
group of 26 patients (21 females, five males, with mean age of 46 years),
had the syndrome identified as idiopathic mitral valve prolapse (IMVP),
which was characterized by a systolic click-murmur, clinical symptoms that
were highly variable in duration and intensity, angiographically-documented
mitral prolapse, and no obvious associated systemic or cardiovascular
disease. Mitral regurgitation was of moderate degree in four, mild in 14,
and absent in eight. The left ventricular (LV) end-diastolic volume index
was elevated in ten of 25 (40%), the LV mass index was elevated in six of
17 (35%), but the LV anterior wall thickness was increase in only one of
17. Three major patterns of ventricular contraction were identified: 1)
normal in seven; 2) abnormal, usually an inferior deformity and/or anterior
asynergy, in eight; and 3) hyperkinetic in 11. Normal resting left
ventricular function, assessed as an ejection fraction greater than 55%,
was present in 17 of 25 (68%). Selective coronary arteriography was
essentially normal in all 25 patients studied. An ischemic ECG response was
detected during only one of 12 maximal treadmill exercise tests and in none
of ten atrial pacing stress tests (AP). Myocardial lactate extraction did
not change significantly during AP in six patients. We conclude that
cardiomyopathy does not appear to be a primary cause or an important
associated component of the IMVP syndrome. Abnormalities of the coronary
circulation or of myocardial metabolism were not demonstrated by available
methods. A proposed pathophysiological mechanism to explain the clinical
and angiographic findings in IMVP is discussed.
ARTICLES
The pathophysiology of idiopathic mitral valve prolapse