BACKGROUND: The role of alcohol in the development of subclinical cardiovascular disease is unclear. We examined the association between alcohol consumption and markers of subclinical cardiac damage and wall stress. METHODS: We studied the cross-sectional and prospective associations of alcohol consumption with highsensitivity cardiac troponin T (hs-cTnT) and N-terminal pro B-type natriuretic peptide (NT-proBNP) measured at 2 time points, 6 years apart (baseline, 1990-1992; follow-up, 1996-1998), in over 11000 participants of the Atherosclerosis Risk in Communities (ARIC) Study with no history of cardiovascular disease. Alcohol consumption was categorized as follows: never, former, current: 1, 2-7, 8-14, and 15 drinks/week. RESULTS: Compared to never drinkers, persons who consumed 2-7 drinks per week were less likely to have increased hs-cTnT (14 ng/L) at baseline (odds ratio 0.67, 95% CI, 0.46-0.96), and had a lower risk of incident increases in hs-cTnT at follow-up (relative risk0.70, 95% CI, 0.49-1.00). Conversely, there was a positive association between alcohol intake and NT-proBNP concentrations at baseline. Consumption of15 drinks/week was positively associated with incident increases in NT-proBNP (300 pg/mL) at the 6-year follow-up visit (relative risk 2.38, 95% CI, 1.43-3.96). CONCLUSIONS: In this community-based study of middle-aged adults without a history of cardiovascular disease, moderate drinking was associated with lower concentrations of hs-cTnT, a marker of chronic subclinical myocardial damage, and positively associated with NT-proBNP, a biomarker of cardiac wall stress. Our results suggest that the cardiac effects of alcohol are complex. Cardiac biomarkers may help improve our understanding of the full cardiovascular effects of alcohol consumption.
Bibliographical noteFunding Information:
Research Funding: Reagents for the NT-proBNP and hs-cTnT assays were donated by Roche Diagnostics. The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts, (HHSN 268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN2682011 00010C, HHSN268201100011C, and HHSN268201100012C). M. Lazo, support from the Johns Hopkins Institute for Clinical and Translational Research (ICTR) which is funded in part by Grant Number UL1 TR 001079 from the National Center for Advancing Translational Sciences (NCATS) a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research, and the Alcohol and Beverage Foundation (ABMRF); C.M. Ballantyne, personal fees and grant support from Roche Diagnostics; E. Selvin, NIH/NIDDK grants K24DK106414 and 2-R01 DK089174 and personal fees from Roche Diagnostics.
© 2016 American Association for Clinical Chemistry.
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