• Grant V Chow, Glenn A Hirsch, David D Spragg, Jennifer X Cai, Alan Cheng, Roy C Ziegelstein, and Joseph E Marine.
• Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224-2780, USA.
• Medicine (Baltimore). 2010 May 1; 89 (3): 141-8.

AbstractAlthough cardiac troponin I (cTnI) elevation in patients presenting to the hospital with supraventricular tachycardia (SVT) is well recognized, the prevalence, predictors, and prognostic significance of cTnI elevation associated with SVT presentation are not known. We screened records of all patients presenting to 2 hospitals over a 4-year period with the diagnosis of SVT confirmed by 12-lead electrocardiogram, and who had at least 1 measured cTnI level and at least 1 year of follow-up after discharge. The primary endpoint was the occurrence of 1 of the following outcomes: death, myocardial infarction, or cardiovascular rehospitalization. Seventy-eight patients met the study criteria (54% female; mean age, 62.2 +/- 15.8 yr), and 29 patients (37.2%) had an elevated cTnI level of > or =0.06 ng/mL (range, 0.06-7.78 ng/mL). Univariate predictors of elevated cTnI included left ventricular ejection fraction (LVEF) <50%, renal dysfunction, ST-segment depression or left bundle branch block on the electrocardiogram, and moderate or severe regurgitation of any cardiac valve. Predictors of elevated cTnI after multivariate analysis included peak heart rate during SVT (per 15 bpm) (odds ratio [OR], 1.58; 95% confidence interval [CI], 1.01-2.46; p = 0.04) and LVEF <50% (OR, 6.12; 95% CI, 1.40-26.7; p = 0.02). After multivariable adjustment, the presence of elevated cTnI with SVT was associated with increased risk of the primary endpoint of death, myocardial infarction, or cardiovascular rehospitalization (hazard ratio [HR], 3.67; 95% CI, 1.22-11.1; p = 0.02). Mild elevation of cTnI is common in patients presenting to the hospital with SVT, and is associated with increased risk of future cardiovascular events. Further study is needed to determine the mechanisms of SVT-related cTnI elevation and its association with elevated cardiovascular risk.

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