Atrial fibrillation-induced cardiac troponin I release.

Link to article at PubMed

Atrial fibrillation-induced cardiac troponin I release.

Int J Cardiol. 2013 Apr 23;

Authors: Parwani AS, Boldt LH, Huemer M, Wutzler A, Blaschke D, Rolf S, Möckel M, Haverkamp W

Abstract
BACKGROUND: Cardiac troponin I (cTnI) is highly specific for myocardial damage and for the diagnosis of acute coronary syndrome. We investigated cTnI utility and predictive value in patients with atrial fibrillation (AF) in the acute setting. METHOD: We studied 354 consecutive patients with the primary diagnosis of AF and clinical symptoms suggestive of myocardial ischemia presenting to our emergency department. cTnI was obtained on presentation. Patients with ST-segment elevation myocardial infarction were excluded. Coronary angiography was performed in 100 patients. RESULTS: cTnI was elevated (>0.09μg/L) in 51 of 354 (15%) patients. The mean cTnI in these patients was 0.37μg/L (0.09-3.14). In 23 of 100 patients undergoing coronary angiography, cTnI was elevated. Only 6 of these 23 patients (26%) had significant stenosis. In 77 of 100 patients undergoing coronary angiography, cTnI was normal, revealing significant stenosis in 25 patients (33%). The positive predictive value of elevated cTnI for a coronary intervention was 26% and the negative predictive value was 68%. Using multivariate logistic regression, we found that heart rate on presentation, the presence of angina pectoris, left ventricular ejection fraction, serum creatinine, and hemoglobin independently predicted elevated cTnI level. CONCLUSION: These data are the first to show that AF in the acute setting is frequently associated with cTnI elevations. AF patients with high heart rate and/or angina pectoris often show false elevated cTnI levels. These findings are relevant for clinicians evaluating patients with acute AF and myocardial ischemia symptoms. Appropriate clinical guidelines must be established that also consider AF-related elevations in cTnI.

PMID: 23623668 [PubMed - as supplied by publisher]

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