This study tests the hypothesis that careful control of the composition of the initial reperfusate and the conditions of the reperfusion during emergency CABG will restore immediate segmental contractility in the previously ischemia area despite ischemic intervals of>2 hours. Between January 1987, and October 1990, 41 consecutive patients with acute coronary occlusion (90% due to PTC A failures) were reperfused during emergency myocardial revascularization according to one of two different protocols: in 25 patients the reperfusate was normal blood given at systemic pressure (“uncontrolled reperfusion”); in 16 patients the ischemic segment was reperfused during the first 20 minutes with a regional blood cardioplegic solution (substrate‐enriched, hyperosmotic, hypocalcemic, alkalotic, diltiazem‐containing) at 37°C at a pressure of 50 mmHg. Thereafter, total bypass was prolonged for an additional 30 minutes before extracorporeal circulation was discontinued (“controlled reperfusion”). Assessment of regional contractility (echocardiography, radionuclide ventriculography), electrocar‐diographic evidence of myocardial infarction, release of CK and CK‐MB enzymes, and hospital mortality were performed. Quantification of regional contractility was done with a scoring system from 0 (normokinesis) to 4 (dyskinesis). Data are expressed as mean ± standard error of the mean. Both groups were well matched for age, sex, and the distribution of the occluded artery. In the controlled reperfusion group there was a higher incidence of previous infarctions (50% vs 30%), additional significant stenosis (1.1 ± 0.2 vs 0.8 ± 0.1), and cardiogenic shock (38% vs 20%) as compared to uncontrolled reperfusion. Furthermore, the interval between coronary occlusion and reperfusion was significantly longer in the controlled reperfusion group (3.9 ± 0.3 vs 2.2 ± 0.3 hr, P<0.05) with a range between 2 and 6 hours. Regional contractility (assessed on the 7thpostoperative day) returned to normal in all patients treated by controlled reperfusion (wall motion score = 0.6 ± 0.2, normokinesis = 0, slight hypokinesis = 1). In contrast, regional contractility remained severely depressed after uncontrolled reperfusion (score 2.5 ± 0.2, P<0.05) with only 4 out of 25 patients having a score<2(2 = severe hypokinesis). Postoperatively, enzymes and ECG changes showed fewer abnormalities in the controlled reperfusion group but these differences did not reach statistical significance. One patient died of mitral insufficiency in the controlled reperfusion group, despite complete recovery of wall motion in the PTCA related artery (1 out of 16). Conversely, the 4 out of 25 deaths after uncontrolled reperfusion occurred in patients that sustained infarct in the area of the coronary occlusion (mortality 6% vs 16%). In conclusion, these results indicate that wall‐motion abnormalities can be avoided after PTCA failure if the initial reperfusion is controlled during emergency CABG. Further clinical studies comparing controlled and uncontrolled reperfusion in patients after acute coronary occlusion caused by