In reference to lactate dehydrogenase (LDH) testing1 as a useful component of assessing probability of myocardial injury, it seems long past due that routine measurement of LDH isoenzymes be discouraged if not altogether abandoned. After more than 10 years of attempting to make LDH isoenzymes a sensitive and specific test with varying assays, it continues to fall short of any appropriate standard.
Given the typical use of this enzyme (assessing for myocardial injury after creatine kinase measurements have returned to baseline values), it has been proposed that LDH isoenzyme analysis be replaced by determination of cardiac-specific troponin I levels. Troponin I levels rise in a time course similar to creatine kinase isoenzyme MB, but remain elevated for 5 to 10 days. Recent data have shown troponin I to be specific in the setting of trauma,2 rhabdomyolysis,3 recent surgery,4 and renal failure (Greg S. Martin, MD, B.N. Becker, MD, and G. Schulman, MD, unpublished data, 1996). In addition, analysis of troponin I levels may be useful prognostically in the evaluation of chest pain of unclear origin, as demonstrated in the setting of unstable angina.5 Other authors have already advocated the replacement of LDH isoenzyme assays with analysis of cardiac troponin I based on its superior release kinetics and sensitivity and specificity.6