Troponin T (shortened TnT[1] or TropT) is a part of the troponin complex, which are proteins integral to the contraction of skeletal and heart muscles. They are expressed in skeletal and cardiac myocytes. Troponin T binds to tropomyosin and helps position it on actin,[2] and together with the rest of the troponin complex, modulates contraction of striated muscle.[3] The cardiac subtype of troponin T is especially useful in the laboratory diagnosis of heart attack because it is released into the blood-stream when damage to heart muscle occurs.[4] It was discovered by the German physician Hugo A. Katus at the University of Heidelberg, who also developed the troponin T assay.
Fast skeletal troponin T3, TNNT3 (11p15.5, 600692)
Reference values
The 99th percentile cutoff for cardiac troponin T (cTnT) is 0.01 ng/mL.[5] The reference range for the high sensitivity troponin T is a normal < 14 ng/L, borderline of 14-52 ng/L, and elevated of >52 ng/L.[6]
Background
The troponin complex is responsible for coupling the sarcomere contraction cycle to variations in intracellular calcium concentration. Increased troponin T levels after an episode of chest pain indicates myocardial infarction.[7] It was discovered by the German physician Hugo A. Katus at the University of Heidelberg. He also developed the troponin T assay.[8] In patients with non-severe asymptomatic aortic valve stenosis and no overt coronary artery disease, the increased troponin T (above 14 pg/mL) was found associated with an increased 5-year event rate of ischemic cardiac events (myocardial infarction, percutaneous coronary intervention, or coronary artery bypass surgery).[9] In patients with stable coronary artery disease, the troponin T concentration has long been found to be significantly associated with the incidence of cardiovascular death and heart failure, but it was 2014 before it began to be accepted as a predictor of who would later suffer acute myocardial infarction (heart attack).[10][11]
