PROLONGED WAIL MOTION ABNORMALITIES AFTER CHEST PAIN AT REST IN PATIENTS WITH UNSTABLE ANGINA - A POSSIBLE MANIFESTATION OF MYOCARDIAL STUNNING

Although myocardial ''stunning'' would be expected to occur in unstable angina, there is no published report in which the recovery of regional left ventricular function was serially monitored in this syndrome. To determine whether the time course of the regional waif motion abnormalities associated with unstable angina is consistent with myocardial stunning, 20 consecutive patients with unstable angina were studied prospectively. Regional left ventricular wall motion was assessed by two-dimensional echocardiography during or immediately after angina at rest and at serial times thereafter. Six of the 20 patients fulfilled the inclusion criteria. The recovery of segmental wall motion after chest pain was consistently found to be delayed in all six patients, but a considerable variability was observed. in at least two subjects, the improvement was rapid and the wall motion abnormalities disappeared almost completely within 2 hours after the chest pain. Both of these patients had the shortest duration of angina (approximately 10 minutes). In contrast, in three other patients with longer duration of chest pain, the improvement was slower and significant wall motion abnormalities were still present at 24 hours after the chest pain. In five control patients who had angiographically-documented coronary artery disease but no recent episode of angina, there was no significant change in segmental wall motion during a period of observation equivalent to that used in the unstable angina group. This study evaluated for the first time the time course of wall motion abnormalities in patients with unstable angina. The results demonstrate that angina at rest is followed by a prolonged depression of contractile function, which may persist for up to 24 hours or even longer. Because none of the patients had evidence of acute myocardial infarction or recurrent ischemia, our observations suggest myocardial stunning as the pathophysiologic substrate for the slow recovery of wall motion. The present results are consistent with the concept that myocardial stunning does occur in unstable angina and indeed may be a component of the natural history of this disorder; however, further investigations using simultaneous measurements of function and flow will be necessary to unequivocally distinguish myocardial stunning from hibernation and silent ischemia.