Lactate metabolism in acute myocardial infarction and its relation to regional ventricular performance

Myocardial metabolism was assessed in 20 patients with acute anterior myocardial infarction using lactate uptake (defined as (aortic lactate — great cardiac venous lac-tate)/aortic lactate x 100) as an index. The regional ejection fraction of the anterior wall was obtained from left ventriculography. There was a linear relation between lactate uptake and regional ejection fraction (r = 0.79, p < 0.001). Four patients without total occlusion in the infarct vessel had a higher lactate uptake (19.6 ± 6.7 versus 4.2 ± 13.4%, p < 0.05) and regional ejection fraction (26.3 ± 7.9 versus 14.9 ± 7.0%, p < 0.05) than did 16 patients with total occlusion. The latter group of patients underwent intracoronary infusion of urokinase, which resulted in reperfusion in 13 patients. Lactate uptake before urokinase infusion (sample I), just after reperfusion (sample II), 30 minutes after reperfusion (sample III) and 4 weeks after reperfusion (sample IV) was 5.7 ± 13.2, −13.9 ± 14.7, 2.9 ± 15.2 and 20.2 ± 11.0%, respectively (sample I versus II and II versus III, p < 0.01; sample I versus IV and III versus IV, p < 0.05). The decrease in lactate uptake immediately after reperfusion, which was accompanied by an increase in creatine kinase-MB isoenzyme release into the blood, was considered to be the result of a “washout”effect. Lactate uptake was ameliorated 4 weeks later, accompanied by an improvement (from 15.1 ± 7.1 to 23.4 ± 7.2%, p < 0.01) in the regional ejection fraction. It is concluded that the degree of asynergy was closely related to the extent of metabolic deterioration in myocardial infarction.