Troponins are bound to the actin filament within muscles and are involved in excitation-contraction coupling. Both cardiac troponin T and troponin I are coded by specific genes and are immunologically distinct from those in skeletal muscle. Neither is detectable in normal healthy individuals but both are released into the bloodstream from cardiomyocytes damaged by necrosis, toxins and inflammation. They become detectable by 4-6h after myocardial injury, peak at 14-18h, and persist for up to 12 days. Current assays are highly specific as they use recombinant human cardiac tropinin T as a standard.

Due to their high sensitivity, plasma levels rise with other cardiac insults, e.g. tachycardia (SVT/VT), pericarditis, myocarditis, sepsis, heart failure, severe exertion and pulmonary embolism. The degree of rise post-MI or during critical illness correlates with a worse outcome.

A positive test is when the cardiac troponin T or I value exceeds the 99th percentile of values for a control group on >1 occasion during the first 24h after the index clinical event. For cardiac troponin T this is quoted as 0.05-0.1ng/ml though many labs now consider values >0.03ng/ml as positive. Values for cardiac troponin I depend on the particular assay used (usually >0.5-1.5ng/ml). The negative predictive value after an acute MI is probably strongest after 6h. Sensitivity peaks at 12h but at the expense of a lower specificity. With renal dysfunction, higher levels are needed to diagnose myocardial damage due to impaired excretion.

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