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Troponin, a molecule that is bound to the thin filament (actin) of striated muscle fibers, acts with intracellular calcium to control the interaction of the thin filament with the thick filament (myosin), thus regulating muscle contraction. Troponin consists of three subunits: T, which connects the troponin complex and tropomyosin (another cardiac muscle regulatory protein); I, which prevents muscle contraction in the absence of calcium; and C, which binds calcium.
Cardiac troponin I (MW 22.5 kDa) and the two skeletal muscle isoforms of troponin I have considerable amino acid sequence homology, but cTnI contains an additional N-terminal sequence and is highly specific for myocardium. Clinical studies have demonstrated the release of cTnI into the blood stream within hours following acute myocardial infarctions (AMI) or ischemic damage. Elevated levels of cTnI are detectable in blood within 4 to 6 hours after the onset of chest pain, reach peak concentrations in approximately 8 to 28 hours, and remain elevated for 3 to 10 days following AMI. Due to the high myocardial specificity and the long duration of elevation, cTnI has become an important marker in the diagnosis and evaluation of patients suspected of having an AMI.
The current guidelines of The Joint European Society of Cardiology/American College of Cardiology Committee support the use of cTnI as a preferred marker of myocardial injury. Several major studies have shown that cTnI is also a predictor of cardiac risk in patients with unstable angina. The American College of Cardiology and the American Heart Association’s current guidelines recommend using troponin results when making treatment decisions regarding unstable angina and non-ST segment elevation MI (NSTEMI).
Cardiac troponin I (MW 22.5 kDa) and the two skeletal muscle isoforms of troponin I have considerable amino acid sequence homology, but cTnI contains an additional N-terminal sequence and is highly specific for myocardium. Clinical studies have demonstrated the release of cTnI into the blood stream within hours following acute myocardial infarctions (AMI) or ischemic damage. Elevated levels of cTnI are detectable in blood within 4 to 6 hours after the onset of chest pain, reach peak concentrations in approximately 8 to 28 hours, and remain elevated for 3 to 10 days following AMI. Due to the high myocardial specificity and the long duration of elevation, cTnI has become an important marker in the diagnosis and evaluation of patients suspected of having an AMI.
The current guidelines of The Joint European Society of Cardiology/American College of Cardiology Committee support the use of cTnI as a preferred marker of myocardial injury. Several major studies have shown that cTnI is also a predictor of cardiac risk in patients with unstable angina. The American College of Cardiology and the American Heart Association’s current guidelines recommend using troponin results when making treatment decisions regarding unstable angina and non-ST segment elevation MI (NSTEMI).
CatalogRCM-010C
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ProductTroponin I
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FormatCassette
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Specimen *S/P
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Kit Size20 est
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* whole blood test could be conducted with assistant of assay buffer; but it may not work for every patient due to blood coagulation
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