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Troponin Helps Diagnose MI and Identify Future Cardiac Risk |
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"Each of these clinical groups [ESC/ACC/AHA] along with the laboratory community has independently reached the conclusion that cardiac troponin is the best marker for diagnosis, risk stratification and guidance of therapy in ACS.'
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F.S. Apple and A.H.B. Wu. Clinical Chemistry. 2001.1
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The troponins are regulatory proteins of the contractile apparatus. Both Troponin I and Troponin T have cardiac specific isoforms. They are referred to as Cardiac Troponin I (cTnI) and Troponin T (TnT). As such, they are not elevated by acute or chronic skeletal muscle injury; therefore, allowing for increased sensitivity and specificity in diagnosing AMI. These markers appear relatively early (on average, 4 to 6 hours) after muscle damage and may be present for several days after AMI.2
The National Academy of Clinical Biochemistry3 and the Joint European Society of Cardiolog/American College of Cardiology Committee4 agree that the cardiac troponins are currently the preferred markers for definitive myocardial damage because they have nearly absolute myocardial tissue specificity, as well as high sensitivity, thereby reflecting even microscopic zones of myocardial necrosis.
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"Our observations underscore the prognostic value of measuring cardiac troponin values in patients who are critically ill, including those who present to the ED."
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R.S. Wright, et al. The American Journal of Cardiology. 2002.6
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Triaging to the Appropriate Level of Care
Luigi M. Biasucci, MD,FESC,FACC Director, Research Program on Acute Coronary Syndromes Assistant Professor of Cardiology
Gemelli Hospital
Catholic University of Rome
Rome, Italy |
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cTnI–An Important Prognostic Variable in Unstable Angina...
Clinical studies have also shown a relationship between cTnI levels and long-term outcome after an episode of unstable angina. cTnI can even be detected when CK-MB levels are not normally elevated. For each 1 ng/mL increase in cTnI, the risk ratio for mortality increases significantly (p=0.02).5
And in Noncardiac Critical Illnesses
The significance of an elevated cTnI has been demonstrated in patients in the ICU, postoperative patients and in those with sepsis.6 Despite the fact that the typical symptoms of cardiac ischemia may not be exhibited in these patients, the multiple stresses associated with critical illness and its treatment increase the risk of myocardial ischemia. Further, other mechanisms, such as substances released during sepsis-related cardiac dysfunction, may likely result in elevations of cTnI, indicating a myocardial injury. |
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A recent study6 has shown that critically ill patients who present to the ED with noncardiac illnesses and elevated levels of cTnI have substantially increased risk of short-term mortality compared with those who have a normal cTnI (a mortality rate of 18.9% versus 5.6% [p=0.009]). Upon initial presentation to the ED, nearly one in four critically ill patients with noncardiac illnesses have evidence of cardiac injury, as demonstrated by an elevated cTnI. This is comparable to the incidence observed in the ICU, where most of the cardiac injuries go unrecognized in noncardiac illnesses.
These observations identify a significant incidence of acute myocardial injury associated with noncardiac critical illnesses in the ED that had been previously unrecognized. Therefore, even if the primary critical illness reflects a noncardiac etiology, an elevated cTnI is indicative of a greater short-term risk of mortality and a more aggressive cardiac evaluation in these patients is warranted.
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