Release of cardiac troponin in acute coronary syndromes: ischemia or necrosis?

Abstract

Analysis of cardiac troponin T and I have been shown to be effective in detecting minor myocardial injury in cardiac patients who present with acute coronary syndromes (ACS). Determination of minor myocardial injury is significant, as these patients have a higher short-term morbidity and mortality than other unstable angina patients with normal concentrations for these markers. In this report, two theories are given as to why cardiac troponin is superior to other markers such as CK-MB for risk stratification. The 'low cut-off concentration model' is based on the fact that troponin is not increased in patients with skeletal muscle disease or injury, resulting in low baseline concentrations of the cardiac isoforms in the absence of active cardiac disease. This enables the use of low decision limits. Troponin also has a higher myocardial tissue content relative to CK-MB, thereby also increasing its clinical sensitivity to irreversible injury. In the 'reversible ischemia model', cytoplasmic free troponin T and I leak across the membrane of myocytes as the result of reduced coronary blood flow. Jeopardized myocardial tissue can recover with acute recanalization. Support for this model comes from clinical observations and animal studies.