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When calcium binds to the troponin C, it causes conformational changes which lead to dislocation of troponin I. Afterwards, tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle. The letter I is given due to its inhibitory character. It is a useful marker in the laboratory diagnosis of heart attack. [2]
It can be difficult to distinguish unstable angina from non-ST elevation (non-Q wave) myocardial infarction. [4] [5] They differ primarily in whether the ischemia is severe enough to cause sufficient damage to the heart's muscular cells to release detectable quantities of a marker of injury, typically troponin T or troponin I.
A person who recently had a myocardial infarction has areas of damaged heart muscle and elevated cardiac troponin levels in the blood. [15] This can also occur in people with coronary vasospasm, a type of myocardial infarction involving severe constriction of the cardiac blood vessels. After a myocardial infarction troponins may remain high for ...
Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis. Troponins can also calculate infarct size but the peak must be measured in the 3rd day. After myocyte injury, troponin is released in 2–4 hours and persists for up to 7 days.
Cardiac muscle troponin T (cTnT) is a protein that in humans is encoded by the TNNT2 gene. [5] [6] Cardiac TnT is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration.
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The TIMI risk score can identify high risk patients in ST-elevation and non-ST segment elevation MI ACS [30] [31] and has been independently validated. [32] [33] Based on a global registry of 102,341 patients, the GRACE risk scoreestimates in-hospital, 6 months, 1 year, and 3-year mortality risk after a heart attack. [34]
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