Troponin Release Following Brief Myocardial Ischemia

R elease of the cardiac-specific isoform of troponin I (cTnI) into the systemic circulation is frequently taken as a biomarker of cardiomyocyte necrosis and used in the diagnosis of myocardial infarction. But, transient increases in blood cTnI concentrations are observed in seemingly healthy individuals following strenuous exercise, asymptomatic patients, and disease states other than acute coronary syndromes (1). The latter include short bouts of ischemia insufficient to cause infarction, heart failure, myocarditis, pulmonary embolism, arrhythmias, sepsis, and trauma. Although cardiomyocyte death is a component of some of these conditions, its involvement in others may be less prominent or questionable. Blood cTnI concentrations remain an important diagnostic test in the clinical context of acute coronary syndromes, but these observations highlight the need for caveats in their interpretation. Moreover, they raise questions regarding the cellular mechanisms that mediate cTnI release and, accordingly, the cellular processes for