Effect of coronary reocclusion after initial reperfusion on ventricular function and infarct size

Abstract

Reocclusion of a coronary artery after thrombolytic therapy occurs in approximately 12% to 33% of patients; however, there are few experimental data concerning reocclusion. Accordingly, to compare the effects of reocclusion versus sustained occlusion on the myocardium, a canine model (n = 12) of 2 h of left circumflex artery occlusion, 1 h of reperfusion and 1 h of reocclusion was studied. In a control group (n = 11), 3 h of circumflex artery occlusion was followed by 1 h of reperfusion. As a result, both groups had the same total duration of ischemia (3 h) and reperfusion (1 h). Hemodynamic measurements, radioactive microsphere injections and two-dimensional echocardiography were performed at baseline, occlusion and reperfusion for both groups and at the end of reocclusion for the experimental group. In vivo risk area was determined with Evans blue dye and infarct size with triphenyltetrazolium staining methods.Similar decreases in myocardial blood flow after coronary occlusion and similar reperfusion blood flows occurred in both groups. Despite intervening reperfusion in the reocclusion group, no significant difference was found in the infarct size/risk area ratio between the reocclusion and control groups (54.5 ± 6.9% vs. 48.4 ± 5.1%, respectively, p = NS). Two-dimensional echocardiography demonstrated a similar degree and extent (159 ± 9 ° vs. 153 ± 12 °, p = NS) of left ventricular dysfunction with both the occlusion and reocclusion. In addition, there were no significant differences in global or regional left ventricular function between the two groups. However, reocclusion after reperfusion did produce a further deterioration in ischemic zone wall thickening (9.5 ± 2.0% to 0.7 ± 1.8%, p < 0.001).It is concluded that coronary reocdusion after initial reperfusion contributes to additional ischemic damage, so that the beneficial salvaging effects of reperfusion are negated. Furthermore, coronary reocdusion results in further ischemic dysfunction in the reperfused but hypokinetic myocardium.