1986Clinical CardiologyOpen access

“Flipped” lactic dehydrogenase pattern in acute coronary insufficiency

I Weinberger, Z Rotenberg, Alex Sagie, J Fuchs, Oded Sperling, Jacob Agmon

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Abstract

Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

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Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

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Available abstract

Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

Key concepts: Medicine, Lactic dehydrogenase, Lactate dehydrogenase, Creatine kinase, Myocardial infarction, Internal medicine, Cardiology, Unstable angina

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