Alterations in left ventricular function during therapy of unstable angina pectoris: Relationship to clinical outcome

Abstract

We studied 30 consecutive patients with unstable angina during pain-free intervals with gated blood pool scintigraphy. The initial study was performed within 18 hours of admission to the coronary care unit. A second study was performed near the time of hospital discharge, after stabilization with medical therapy. Three months thereafter patients were categorized according to their worst anginal status following hospital discharge. Fifteen patients were New York Heart Association functional class I or II (group A); 15 patients were in functional class III or IV (group B). Left ventricular ejection fraction was similar at the time of initial study (55.9 ± 2.18% and 56.0 ± 3.55% for groups A and B respectively). At the time of hospital discharge the ejection fraction had risen to 60.3 ± 1.85% ( p < 0.01) in group A and in group B it had fallen to 48.1 ± 3.4% ( p < 0.005). End-systolic volume index in group B rose from 37 ml/m 2 ± 6.1 to 43 ± 6.2 ml/m 2 ( p < 0.005) at the time of the follow-up study. There were no significant intergroup differences in the amount of nitrates or beta blockers received by the patients during the two scintigraphic examinations. Eleven group B patients subsequently underwent coronary artery bypass surgery. A significant increase in ejection fraction and a significant decrease in end-systolic volume index were noted when these patients were restudied an average of 3.2 months after surgery. This study suggests that changes in left ventricular function during the course of unstable angina pectoris are common and may be detected by serial gated blood pool scintigraphy. The direction of the change in ejection fraction was associated with the severity of angina in the follow-up period. A fall in ejection fraction and a rise in end-systolic volume index from admission to the time of the follow-up study were associated with an unfavorable clinical outcome and may represent clinically silent ischemic depression of left ventricular function.