Lactic Dehydrogenase and Fraction 1 in Acute Myocardial Infarction

Whiting, Richard B.
November 1981
Angiology;Nov1981, Vol. 32 Issue 11, p764
Academic Journal
In this study, 2 patient populations were selected among those admitted to the coronary care unit with possible acute myocardial infarction. One group of 38 patients was felt to have definite myocardial infarction, and the second group of 44 individuals was felt not to have had acute infarction. The distinction between these 2 patient categories may be, at times, quite difficult. Serum levels of CK, LDH, and their respective isozymes were measured and timed from the clinical onset of the possible acute injury. The levels of LDH or LDH-1 did not adequately separate these 2 patient groups. The level of MB-CK provided the best separation of these patients. LDH-1 which was more than 35% of the total LDH value or reversal of the ratio LDH-1:LDH-2 so that it was greater than 1.00 each favors a clinical diagnosis of myocardial injury in the setting described in this study. Because LDH and its fractions are not quite as specific as MB-CK in these patients, it appears that measuring LDH and/or fractionation could be abandoned in the interest of economy in the coronary care unit. The exception would be those cases where the patient is presented relatively late for a diagnosis at a time when the CK and/or its MB may have returned toward the normal value and are therefore of no longer diagnostic use. The reversal of LDH-1:LDH-2 may be present for 1-3 weeks after infarction, thus providing support to such a diagnosis. There was a high correlation between increasing levels of CK and those of LDH found in this study in the patients with myocardial infarction, but it was not found in those with some other acute illness. This is not totally unexpected; at least theoretically, both enzymes are derived from a similar damaged tissue, the myocardium. Superimposed overt congestive heart failure disturbed this good correlation presumably by adding another tissue source of enzymes. However, the LDH-1 predominantly from myocardium still maintained a linear relationship with the CK, even in the presence of congestive heart failure. It appears likely that a serial measurement of LDH or its fractions could be used to calculate infarct size in a method quite analogous to those employing either CK total or MB-CK.


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