Why We Do What We Do: Troponins

Many times we just accept what our superiors tell us and don’t understand the context. Below is an article that examines the effectiveness of troponin as a predictor of mortality. A thorough summary helps interpret the data…enjoy!

Cardiac-Specific Troponin I Levels to Predict the Risk of Mortality in Patients with Acute Coronary Syndromes – NEJM 1996

Cardiac Specific Troponin I Levels to Predict The Risk of Mortality in Patients with Acute Coronary Syndromes.
Antman ET et al. NEJM 1996.

√ Extent of myocardial necrosis is an important determinant of the risk of death
√ Ck and its isoenzyme (CK-MB) lack sufficient sensitivity and specificity, there is need for more sensitive and cardiac specific markers of myocardial necrosis
√ Cardiac troponin I is highly specific for myocardial tissue, is not detectable in the blood of healthy persons
√ Purpose: evaluate the potential prognostic value of this marker in patients with unstable angina or non-Q wave myocardial infarction

√ Used TIMI IIIB trial – compared tPA with placebo and to compare early invasive management strategy with an early, conservative strategy
√ 21-76 y.o. with episodes of CP for at least 5 minutes but less than 6hours within the preceding 24 hours and had a documented evidence of coronary artery disease
√ Samples were frozen after CK-MB tested at 4oC when transported then at -70oC
o Serum specimens with cardiac troponin I levels between 4.2 and 20 ng per mL, measures of troponin remain stable
√ Cutoff value is 0.4ng per mL

√ Patients with >0.4ng/mL Less likely to have a history of angina, hypertension, or MI; to have a primary angiogram sowing at least one epicardial vessel with 70% or more stenosis, or receive nitrates, beta blockers, ccb, or aspirin before the qualifying episode of ischemic discomfort
√ More likely to have ST-segment deviation
√ No significant differences between patients with cardiac troponin I levels of 0.4 nG per mL or higher than those with lower levels
√ CKMB compared to troponin showed a significant disparity
√ Mortality at 42 days – 29 patients (2.1 percent) died with Troponin I level elevation vs. 8 deaths with levels below 0.4ng per mL
√ Correlation between mortality at 42 days (without adjustment for base-line characteristics) and the cardiac troponin I level in the plasma specimen obtained at enrollment were statistically significant increases in mortality with increasing level of cardiac troponin
√ Risk ratio for mortality in the patients with trop I levels of 0.4ng per mL or more rose progressively with increasing troponin I levels
√ With every increase by 1ng/mL there is a resultant increase in risk ratio for Mortality at 42 days

√ Small sample size considering number deceased at 29
√ Sample storage does not consider those with low troponins

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