Towards appreciating appropriate clinical responses to highly sensitive cardiac troponin assays

Abstract

Cardiac troponins (cTn) are structural components of the contractile apparatus of the cardiomyocyte and the recommended biochemical markers for diagnosing myocardial infarction. Although the diagnostic performance of both cTnT and cTnI as biochemical markers are quite similar, it is the analytical sensitivities of these assays that have been found to create the difference. High-sensitivity cTn assays, which are capable of measuring cTn levels 10-folds lower than conventional fourth generation assays, are results of continuous effort to develop more sensitive and accurate tests to detect cardiac injury. While the improvement in the sensitivity of these assays promises improvement in many aspects of patient care, such as earlier myocardial infarction diagnosis and cardiac disease risk assessment, shortcoming of these assays must be considered. Very low measurable levels of cardiac damage biochemical markers can deliver occult yet possible decisive message. Better understanding of the pros and cons of these assays will pledge an appropriate clinical reaction to highly sensitive results.

A Multiple Biomarker Approach in Patients with Cardiac Sarcoidosis

“…Cardiac troponins are sensitive and specific markers of myocardial injury. 29,30) Elevated circulating cardiac troponins associate with left ventricular dysfunction and may predict an adverse outcome, although further study is needed to verify this. 18) In addition, cardiac troponins in CS are suitable indicators of a favorable response to steroid therapy and are associated with prognosis.…”

“…However, many primarily non-cardiac conditions may lead to increased circulating cardiac troponins. 29,34) In advanced CS, it may be impossible to tell whether ele-vated concentrations are because of CS activity or the effects of cardiac and/or renal failure. 30) Further biomarkers in the diagnosis and prognosis of sarcoidosis are needed, and several biomarkers such as serum amyloid, tumor necrosis factor, tenascin-C, transforming growth factor-β1, and genome-wide gene expression signature strategies are potential candidates.…”

Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model

“…TnI is linked to myocardial injury while nt-proBNP reflects stretching of cardiomyocytes with distinct mechanisms and causes. 3 , 28 The adaptive changes that occur in the remaining nephrons resulting in hyperfiltration can influence nt-proBNP levels. The hemodynamic changes after the 5/6 nephrectomy are liked to structural glomerular lesions, that can be followed by proteinuria.…”