Aspartate aminotransferase, cytoplasmic
L-aspartate:2-oxoglutarate aminotransferase activity
Effects of therapeutic coronary reperfusion on aspartate aminotransferase isoenzymes in sera of patients with acute myocardial infarction.
We examined the kinetics of the catalytic activities of aspartate aminotransferase (AST, EC 2.6.1.1) isoenzymes in serum of 28 patients with myocardial infarction who were to receive either intracoronary urokinase--reperfusion angiographically proved--or conventional therapy (control group). Cytosolic (soluble) AST (s-AST) activity in serum increased rapidly immediately after recanalization, reaching a maximum 12 h after the onset of infarction. In the control group, this peak was reached 28 h after the onset (P less than 0.001). Peak s-AST activity was similar in the two groups. Peak activity and peak time for mitochondrial AST (m-AST) were the same for the two groups of patients; intervention that affects myocardial perfusion caused only a slight additional increase in m-AST activity in the early post-infarct period. There may be advantages to measuring m-AST, which is briefly influenced by reperfusion, instead of the usual cytosolic enzymes for assessment of myocardial damage in patients with myocardial infarction treated with thrombolytic therapy.