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European Heart Journal Advance Access published online on March 4, 2009

European Heart Journal, doi:10.1093/eurheartj/ehp047
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org

Cardiac troponin-I and risk of heart failure: a community-based cohort study

Johan Sundström1,5,*, Erik Ingelsson2,3, Lars Berglund1,5, Björn Zethelius2, Lars Lind1, Per Venge1 and Johan Ärnlöv2,4

1 Department of Medical Sciences, Uppsala University Hospital, SE-751 85 Uppsala, Sweden
2 Department of Public Health and Caring Sciences, Uppsala University Hospital, Uppsala, Sweden
3 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
4 Department of Health and Social Sciences, Högskolan Dalarna, Falun, Sweden
5 Uppsala Clinical Research Center, Uppsala University Hospital, Uppsala, Sweden

Received 22 June 2008; revised 18 December 2008; accepted 16 January 2009 * Corresponding author. Tel: +46 18 6119889 or +46 70 4225220, Fax: +46 18 509297, Email: johan.sundstrom{at}medsci.uu.se

Aims: We examined if circulating levels of cardiac troponin-I (cTnI) predict subsequent heart failure in the community.

Methods and results: Using Cox proportional hazards models, we examined the risk of a first hospitalization for heart failure during a maximum of 11.4 years in a community-based sample of 1089 70-year-old men without heart failure, valvular disease, or electrocardiographic left ventricular hypertrophy. Adjusting for smoking, systolic blood pressure, antihypertensive medication use, diabetes, body mass index, serum cholesterol, and myocardial infarction before baseline or during follow-up, 0.01 µg/L higher cTnI conferred a hazard ratio (HR) of 1.26 (95% confidence interval 1.15–1.38) for subsequent heart failure. Persons with cTnI ≥0.03 µg/L had an HR of 5.25 (2.00–13.77) compared with persons with cTnI <0.01 µg/L. Adjusting additionally for serum NTproBNP attenuated the estimates somewhat [HR 1.22 (1.11–1.34) per 0.01 µg/L of cTnI]. Excluding persons with myocardial infarction before baseline and censoring at time of myocardial infarction during follow-up, 0.01 µg/L higher cTnI was associated with a multivariable-adjusted HR of 1.31 (1.16–1.47) for heart failure.

Conclusion: In a community-based sample, a direct measure of cardiomyocyte damage, cTnI, indicated a substantially increased risk of heart failure, accounting for other risk factors. Studies investigating the clinical utility of measuring cTnI in asymptomatic individuals are warranted.

Key Words: Heart failure • Risk factors • Epidemiology • Population


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