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"Flipped" lactic dehydrogenase pattern in acute coronary insufficiency
Insights
Serum lactic dehydrogenase (LDH) isoenzyme testing can detect myocardial damage in acute coronary insufficiency (ACI) patients, even when other cardiac enzymes are normal. A "flipped" LDH pattern indicates damage, aiding diagnosis and treatment decisions.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Acute coronary insufficiency (ACI) diagnosis can be challenging, especially when patients present late.
- Standard cardiac enzyme tests like creatine kinase-MB may return to normal within 24 hours.
Observation:
- Serum lactic dehydrogenase (LDH) isoenzymes were analyzed in 85 ACI patients and 10 stable angina controls.
- A "flipped" LDH pattern (LDH1 > LDH2) was observed in 15 ACI patients with normal total LDH and creatine kinase-MB levels.
Findings:
- The "flipped" LDH pattern, with LDH 1:2 ratios between 1.02-1.13, suggests myocardial damage in ACI patients.
- Control patients with stable angina showed normal LDH isoenzyme distribution.
- This pattern may be linked to myocytolysis and coagulation necrosis observed in postmortem studies.
Implications:
- LDH isoenzyme measurement is valuable for diagnosing myocardial damage in ACI, particularly in late presentations.
- A "flipped" LDH pattern may necessitate longer rest periods and earlier coronary angiography.
- This diagnostic tool aids in differentiating ACI from stable angina when other markers are normalized.
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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