Relation of isovolumic relaxation to left ventricular wall movement in man.

In order to determine the duration of isovolumic relaxation and its relation to left ventricular wall movement, 14 normal subjects, 44 patients with coronary artery disease, 16 with hypertension, and 10 with pure mitral stenosis were studied. Simultaneous echocardiograms, phonocardiograms, and apex cardiograms were performed, and the resulting traces digitised. In normal subjects, aortic valve closure (A2) occurred at a mean of 40 + 10 ms before the minimum left ventricular dimension, and the duration of isovolumic relaxation, taken as the period from A2 to the onset of mitral valve cusp separation was a mean of 65 + 15 ms. In patients with hypertension, the timing of aortic valve closure was normal, but isovolumic relaxation was prolonged to a mean of 105 + 25 ms, so that mitral valve opening was significantly delayed, occurring at a mean of 80 + 25 ms after the minimum left ventricular dimension. In patients with coronary artery disease, aortic valve closure was significantly delayed by a mean of 5 + 40 ms with respect to the minimum left ventricular dimension. The mean duration of isovolumic relaxation did not differ significantly from normal, though the scatter was wide, but mitral valve opening was also delayed by a mean of 80 + 35 ms. In these patients, there was a strong association between delay in aortic valve closure and abnormal wall movement during isovolumic contraction. In patients with mitral stenosis, aortic valve closure was significantly delayed (mean 30 35 ms), but isovolumic relaxation was short (mean 40 + 20 ms). Thus though delayed mitral valve opening occurs both in hypertension and coronary artery disease, its cause differs: in the former the cause is prolonged relaxa- tion, while in the latter it is primarily incoordinate systolic wall movement, resulting in prolongation of ejection and delayed aortic valve closure, with respect to normal regions.