Wilson Nadruz1,2, Alexandra Gonçalves1,3, Brian Claggett1, Gabriela Querejeta Roca1, Amil M Shah1, Susan Cheng1, Gerardo Heiss4, Christie M Ballantyne5, Scott D Solomon1. 1. Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. 2. University of Campinas, Campinas, Brazil. 3. University of Porto Medical School, Porto, Portugal. 4. Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA. 5. Section of Cardiology, Baylor College of Medicine and Houston Methodist DeBakey Heart and Vascular Center, Houston, TX, USA.
Abstract
AIMS: Cigarette smoking has been associated with incident heart failure independent of coronary artery disease (CAD), but the mechanisms linking smoking to cardiac damage are not well understood. This study sought to evaluate the relationship between smoking and N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity Troponin T (hs-TnT), which are, respectively, biomarkers of myocardial wall stress and injury, in a large community-based cohort. METHODS AND RESULTS: We examined the association between smoking history and NT-proBNP and hs-TnT in 9649 participants free of overt CAD or heart failure from the Atherosclerosis Risk in Communities (ARIC) Study who attended Visit 4 (1996-1998), as well as the association with change in these biomarkers from Visit 4 to Visit 5 (2011-2013) in 3151 participants. At Visit 4, higher cumulative cigarette exposure, assessed by total pack-years, was associated with elevated levels of NT-proBNP (P < 0.001) and hs-TnT (P = 0.01) among ever smokers in multivariable analyses adjusted for potential confounders. After 15 years of follow-up, participants who were active smokers at Visit 4 had greater incidence of elevated NT-proBNP {adjusted proportion = 48% [95% confidence interval (CI) 41, 54] vs. 35 (95% CI 32, 39); P = 0.006} and hs-TnT [adjusted proportion = 32% (95% CI 26, 38) vs. 23 (95% CI 20, 26); P = 0.021] compared with never smokers, adjusting for baseline and follow-up covariates. CONCLUSIONS: In a large community-based cohort free of overt CAD and heart failure, cigarette smoking was associated with biomarkers of myocardial wall stress and injury at baseline as well as with a continued measurable increase in these biomarkers after 15 years of follow-up.
AIMS: Cigarette smoking has been associated with incident heart failure independent of coronary artery disease (CAD), but the mechanisms linking smoking to cardiac damage are not well understood. This study sought to evaluate the relationship between smoking and N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity Troponin T (hs-TnT), which are, respectively, biomarkers of myocardial wall stress and injury, in a large community-based cohort. METHODS AND RESULTS: We examined the association between smoking history and NT-proBNP and hs-TnT in 9649 participants free of overt CAD or heart failure from the Atherosclerosis Risk in Communities (ARIC) Study who attended Visit 4 (1996-1998), as well as the association with change in these biomarkers from Visit 4 to Visit 5 (2011-2013) in 3151 participants. At Visit 4, higher cumulative cigarette exposure, assessed by total pack-years, was associated with elevated levels of NT-proBNP (P < 0.001) and hs-TnT (P = 0.01) among ever smokers in multivariable analyses adjusted for potential confounders. After 15 years of follow-up, participants who were active smokers at Visit 4 had greater incidence of elevated NT-proBNP {adjusted proportion = 48% [95% confidence interval (CI) 41, 54] vs. 35 (95% CI 32, 39); P = 0.006} and hs-TnT [adjusted proportion = 32% (95% CI 26, 38) vs. 23 (95% CI 20, 26); P = 0.021] compared with never smokers, adjusting for baseline and follow-up covariates. CONCLUSIONS: In a large community-based cohort free of overt CAD and heart failure, cigarette smoking was associated with biomarkers of myocardial wall stress and injury at baseline as well as with a continued measurable increase in these biomarkers after 15 years of follow-up.
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