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19th World Congress on Heart Disease



Saul Schaefer, M.D., University of California, Davis, CA, USA


Cardiac troponin I and T (cTnI and cTnT) are components of the cardiac myocyte myofibrillar apparatus that are released when these cells are injured. Current assays set “normal” at levels that incorporate 99% of the non-diseased population, with usual upper limits in the range of 0.05ug/ml. Troponin elevations are useful in diagnosing acute coronary syndrome (ACS) in conjunction with clinical, electrocardiographic, and imaging data. Numerous other systemic processes that directly injure myocytes, or alter the supply-demand balance, can cause elevation of cTn, including ESRD, heart failure, sepsis, myocarditis, tachycardia, and hypertension. Distinguishing ACS from other causes can be difficult. In our retrospective study of low-risk troponinemia, 140 patients without clinical ACS but with a cTnI between 0.06 and 2.0 ug/ml were referred for cardiac catheterization to define the cause of elevated cTnI. Only 16 patients (11%) had significant CAD, with no patients under the age of 49 having CAD. Predictors of CAD included diabetes or presentation with an arrhythmia or syncope. Patients without CAD most frequently had conditions associated with increased cardiac wall stress. High-sensitivity troponin (hs-cTn) can detect levels of troponin in the order of 10 ng/ml. This increased sensitivity may speed the diagnosis of true ACS with minimal elevations of troponin, but may also result in a greater number of non-ACS patients being identified and treated. For example, 100% of patients with ESRD have an elevated cTnT – although this signifies increased risk for future cardiovascular events, should all these patients be identified as potentially having ACS? The decreased specificity of hs-cTn has slowed the adoption of this assay in the United States, but it's eventual use will likely increase the prevalence of troponinemia with unknown consequences for risk assessment, diagnosis and treatment.



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