Currently troponin T and troponin I levels are the tests of choice for the detection of myocardial injury.

Cardiac troponins are regarded as the preferred biomarkers for the diagnosis of acute myocardial infarction.

Even minor elevations in plasma cardiac troponin levels reflect subtle myocardial damage, increasing the risk of progression to overt cardiovascular disease.
Assays have high clinical sensitivity and specificity for detection of myocardial injury.

Troponins have nearly absolute myocardial tissue specificity and high sensitivity indicating the presence of even small microscopic zones of myocardial necrosis.

The most common causes of troponin release is low level injury to the myocardium.

Despite is nearly absolute tissue specificity and superior sensitivity cardiac troponins are not specific for the etiology of myocardial necrosis: elevations may be seen in coronary ischemia, pulmonary embolism, heart failure, sepsis, and renal insufficiency (Jaffe AS et al).

Among patients with massive and sub massive pulmonary embolism troponin elevation occurs in one in three and one and seven patients, respectively.

Because of the above, clinical syndromes consistently ischemia and characteristic rise and fall in cardiac troponins during serial testing are essential for myocardial infarction diagnosis.

Most elevated troponin test results are in patients without chest pain or ischemic EKG changes and has no clinical utility and results in downstream testing (Shimoni Z).

Myocardial infarction is indicated by rising and falling pattern of troponin with at least one value above the 99 percentile of the upper reference level.

The 99th percentile value of upper reference limit maximizes the sensitivity and specificity for identifying patients at risk of possible acute coronary syndrome.

Cardiac troponins T and I are components of cardiomyocytes.

Biochemical markers of myocardial necrosis.

Detects myocardial injuries much smaller than those detected by CPK_MB.

A strong association between elevated troponin levels and recurrent coronary ischemic events.

Troponins T and I are occasionally detectable in the general population, and such findings strongly are associated with structural heart disease, increased risk of death and adverse cardiovascular events.

Troponins may be useful for detecting subclinical cardiovascular disease and assessing cardiovascular disease risk in the general population.

Chronic elevations of cardiac troponin occur in chronic kidney disease related to myocardial strain from altered hemodynamics, inflammation, endothelial dysfunction, subendocardial ischemia, and possibly reduced clearance.

Persistently elevated high-sensitivity troponin levels indicate ongoing chronic myocardial injury and strongly associated with the risk of death and cardiovascular events.

Cardiac troponin T levels begin to increase 3 to 5 hours after myocardial injury and remain elevated for 14 to 21 days.

Cardiac troponin I levels begin to increase 3 hours after myocardial ischemia, peaks at 14 to 18 hours and remain elevated for 5 to 7 days.

Sensitivity for cardiac troponin up to 100% for myocardial damage within 4 to 6 hours after acute myocardial infarction.

Cardiac troponin I and cardiac troponin T assays clinically perform comparably.

Cardiac troponin T is more commonly elevated in patients with chronic kidney disease, but with more sensitive cardiac troponin i assays the difference is narrowing.

Sensitivity of up to 100% for cardiac troponin I by 6 hours after acute myocardial infarction.

For clinical purposes, detectable elevations of troponin do not occur with ischemia alone unless there is a component of cardiac injury.

Elevated levels in patients with acute neurologic disease associated with adverse prognosis.

Elevations can be due to fibrin interference.

Elevations may be due to combination of cardiac troponin and immunoglobulins.

Small elevations in troponons are associated with increased risk of adverse outcome in patients with acute coronary syndromes ( James S et al).

Levels of cardiac troponin greater than 0.01 mcg per liter have been associated with increased mortality among patients clinically free of cardiovascular disease and in patients with acute coronary syndromes.

In patients with suspected acute coronary syndrome, utilization and sensitive troponin I assay increased the diagnosis of myocardial infarction and identify patients at high risk for recurrent MI and death: lowering the diagnostic threshold of plasma troponin is associated with major reductions in morbidity and mortality (Mills NI et al).

High-sensitivity troponin (hsTn) assays have limits of detection approximately tenfold lower than conventional essays, 99th percentiles in the low nanogram per liter range, and are analytically very precise.

High-sensitivity troponin (hsTn) assays promise to diagnose smaller myocardial infarctions otherwise undetected or identifying myocardial infarction earlier.

The proportion of patients with an acute myocardial infarction continuously increases with increasing levels of high sensitive-cardiac troponin T values.

High-sensitive troponin asays have expedited a more accurate and early diagnosis of acute MI and allows identification of increased number of patients with elevated troponin due to noncoronary and noncardiac reasons.

Cardiac troponin is currently live gold standard for the diagnosis of non-ST segment elevation myocardial infarction.

High-sensitivity cardiac troponin T levels should be interpreted as quantitative rather than qualitative.

Using high-sensitivity cardiac troponin T scores within one hour of patients with chest pain has a sensitivity for negative predictive value of 100% and a specificity of 97% and a positive predictive value of 84% , and shortens the time needed to rule out acute MI and may obviate prolonged monitored and serial blood sampling in three of four consecutive patients with acute chest pain ( Reichlin T et al).

High sensitivity cardiac troponin allows accurate rule out and rule in acute myocardial infarction within 1 hour in up to 75% of cases.

In the low-to-intermediate risk patients with suspected acute coronary syndrome, an undetectable hi sensitive troponin T value admission allows a safe discharge without occurrence of death myocardial infarction within 90 days (Vafaie M et al).

Among children and adolescents younger than 20 years of age presenting with chest pain, the most common causes of troponin elevation include myocarditis and vasospasm secondary to drug use

Most non-myocardial infarction causes of troponin elevation in young patients are associated with higher all cause mortality compared with acute myocardial infarction.

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