Key result
cTnI matches CK-MB accuracy for predicting cardiac death or significant CAD in cocaine-associated chest pain.
Why the study?
Baseline ECG abnormalities and marker elevations not associated with myocardial necrosis complicate accurate MI diagnosis in patients with cocaine-associated chest pain, necessitating evaluation of troponin utility.
Does cardiac troponin I testing accurately diagnose myocardial infarction and predict significant coronary disease compared to CK-MB in patients with cocaine-associated chest pain?
Observational (n=246)
Does cardiac troponin I testing accurately diagnose myocardial infarction and predict significant coronary disease compared to CK-MB in patients with cocaine-associated chest pain?
Troponin I has equivalent diagnostic accuracy to CK-MB for diagnosing myocardial necrosis and underlying significant coronary disease in patients with cocaine-associated chest pain.
May support troponin I interchangeability with CK-MB in cocaine chest pain; leaves open prospective validation.
Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine‐associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. Objective: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. Methods: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule‐in protocol that included serial sampling of creatine kinase (CK), CK‐MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK‐MB MI (CK‐MB ≥ 8 ng/mL with a relative index [(CK‐MB × 100)/total CK] ≥ 4, cardiac death, and significant coronary disease (≥50%). Results: Of the 246 admitted patients, 34 (14%) met CK‐MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI‐positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK‐MB criteria for MI, and the other had a peak CK‐MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK‐MB MI and cTnI and were not significantly different. Conclusions: Most patients with cTnI elevations meet CK‐MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK‐MB for diagnosing necrosis in patients with cocaine‐associated chest pain and suspected MI.
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Kontos et al. (2002) conducted an observational in Cocaine-associated chest pain and suspected myocardial infarction (n=246). Cardiac troponin I (cTnI) vs. CK-MB was evaluated on Predicting cardiac death or significant coronary disease (≥50%). Cardiac troponin I demonstrated equivalent diagnostic accuracy to CK-MB for predicting cardiac death or significant coronary disease in patients with cocaine-associated chest pain.
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