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To elucidate the relationship between lactate metabolism following reperfusion and restoration of left ventricular (LV) function, we assessed serial changes in transcardiac lactate metabolism following reperfusion therapy in 67 patients admitted to hospital within 6 h of the onset of acute anteroseptal myocardial infarction. Left ventriculograms taken about 30 min after reperfusion therapy revealed marked dyskinesis in the anteroapical region in all subjects. According to the regional ejection fraction (rEF), determined 4 weeks later as an index of LV function, patients were divided into 3 group: 1) Restored LV group: 28 patients with reperfusion and restored LV function (rEF greater than 30%); 2) Poor LV group: 26 patients with reperfusion but poor LV function (rEF less than 30%); 3) Failure group: 13 patients with failed reperfusion and occluded left anterior descending coronary artery. Although there was no difference in elapsed time and time to peak creatine phosphokinase (CPK) between the former 2 groups, the Restored LV group demonstrated lower peak CPK values, suggesting that these patients had less myocardial injury. Immediately after reperfusion, both groups showed transcardiac lactate production. In the Restored LV group, aerobic lactate metabolism was restored early after reperfusion (at 6 h), while in the Poor LV group prolonged anaerobic lactate metabolism was observed. These results suggest that an early restoration of aerobic metabolism might be a sign of stunned and viable myocardium, and a sustained lactate production might relate to a sustained process of myocardial injury.

Serial transcardiac lactate netabolism in post-reperfused stunned myocardium in evolving myocardial infarction.