Analysis of regional left ventricular wall motion during diastole in mitral stenosis.

Left ventricular angiograms of 16 patients with mitral stenosis and 18 normal subjects were digitised frame by frame to study regional diastolic wall motion. Left ventricular cavity volume and its rate of change were derived, and plots constructed to show regional wall motion throughout the cardiac cycle. Patients with mitral stenosis had a significantly reduced peak filling rate of 380±170 ml/s, in comparison with normal (690±260 ml/s). A slow rate of filling, however, was not associated with slow and uniform outward movement of the endocardium of the left ventricle. In patients with mitral stenosis, peak outward velocities were normal at the apex and along the inferior wall, and only slightly reduced anteriorly (9±3 cm/s, normal 11±4 cm/s). Instead, striking nonuniformity of wall motion was present, so that the interval over which peak wall motion occurred in the three regions of the cavity was extended to 93± 53 ms (normal 43±25 ms). The same applied to the termination of rapid outward movement, which occurred over an interval of 110±44 ms (normal 43 ±21). A second manifestation of regional asynchrony was abnormal outward wall movement during isovolunmic relaxation, and in nine patients it had reached its peak velocity in at least one region before the mitral valve opened. Finally, the ventricular cavity was seen to oscillate as it filled in six patients, with the endocardium moving inwards in one region after mitral valve opening associated with accentuated outward movement elsewhere. The reduced left ventricular filling rate in mitral stenosis thus manifests itself in small part only as slow outward wall motion. The main disturbance to regional left ventricular function was a reproducible series of disturbances causing striking asynchrony. This dissociation of regional wall motion from filling and the constant finding of motion of the anterior free wall of the ventricle preceding that elsewhere are similar to the disturbances seen in patients with coronary artery disease. Both may represent disorganisation in disease of the highly specialised restoring forces whose action is the basis of coordinate filling in the normal heart.