Rapid enzyme release from acutely infarcted myocardium after early thrombolytic therapy: washout or reperfusion damage?

• Published in: The American heart journal Vol. 115; no. 4; pp. 711 - 716
• Main Authors: VAN DER LAARSE, A, VAN DER WALL, E. E, VAN DEN POL, R. C, VERMEER, F, VERHEUGT, F. W. A, KRAUSS, X. H, BAR, F. W. H. M, HERMENS, W. T, WILLEMS, G. M, SIMOONS, M. L
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier 01.04.1988
• Subjects: Biological and medical sciences; Blood. Blood coagulation. Reticuloendothelial system; Coronary Circulation; Humans; Hydroxybutyrate Dehydrogenase - blood; Medical sciences; Myocardial Infarction - drug therapy; Myocardial Infarction - enzymology; Pharmacology. Drug treatments; Random Allocation; Streptokinase - therapeutic use; Time Factors; Human; Infarct; Enzyme; Acute; Coronary artery; Cardiovascular disease; Coronary heart disease; Local administration; Chemotherapy; Reperfusion; Streptokinase; Myocardium; Serum; Intraarterial administration; Fibrinolytic
• ISSN: 0002-8703; 1097-6744
• DOI: 10.1016/0002-8703(88)90869-1

In a randomized study on early intracoronary thrombolytic therapy in patients with acute myocardial infarction (AMI), serial plasma enzyme activities were measured to analyze the rate of enzyme appearance in plasma with reference to treatment allocation, area at risk, and infarct size. Cumulative activities of alpha-hydroxybutyrate dehydrogenase (HBDH) appearing in plasma in the first 24 hours (Q24), 48 hours (Q48), and 72 hours (Q72) were calculated to obtain infarct size (= Q72) and rate of HBDH appearance in plasma (= Q24/Q72). Analyzed on the basis of "intention to treat" in 448 patients with AMI, the mean Q24/Q72 value (+/- SEM) was 0.653 +/- 0.011 in 230 patients receiving thrombolytic therapy; this value was significantly (p less than 0.001) higher than that observed in 218 patients receiving conventional therapy (0.504 +/- 0.012). In the thrombolysis group Q24/Q72 was independent of infarct size, whereas in the control group Q24/Q72 was negatively correlated with infarct size (r = -0.26; p less than 0.001). Plotted against the sum of ST segment elevations at admission (sigma ST) mean Q24 values were similar in both treatment groups, but mean Q48 and especially Q72 values were larger in the control group than in the thrombolysis group. We conclude that: (1) in reperfused infarctions the time course for development of infarct is accelerated in comparison to unreperfused infarcts; (2) this accelerated process of necrosis lasts about 40 to 50 hours, a duration that is hardly influenced by infarct size; and (3) the reperfusion-induced acceleration of enzyme release resembles the reoxygenation-induced enzyme release from anoxic hearts.