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      Temporal Associations Between Smoking and Cardiovascular Disease, 1971 to 2006 (from the Framingham Heart Study)

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          Abstract

          Smoking has consistently been related to cardiovascular risk. Public health efforts have yielded reduced smoking prevalence and gains in cardiovascular disease (CVD) prevention. We hypothesized that the contribution of tobacco to CVD risk would be attenuated over prospective decades (1971 to 2006) in a community-based cohort. We evaluated 5,041 Framingham Heart Study Offspring Cohort participants (mean age 36.1 years, 52% women) without prevalent CVD. We collected prospective data on smoking status, relevant CVD risk factors, and incident CVD events across prospective decades. We used multivariable-adjusted, Cox proportional hazard models to measure the effect of smoking on incident CVD over 3 prospective 12-year follow-up periods. Our results demonstrated a consistent twofold increased risk of CVD in men who smoke compared with nonsmokers for each 12-year time period spanning from 1971 to 2006. Women who smoked had a 1.5-fold increased CVD risk. Smoking remains an important risk factor despite substantial improvements in the prevention and treatment of CVD. Significant, contemporary improvements in CVD prevention—such as gains in hypertension and cholesterol treatment—have not attenuated the strong and persistent associations between smoking and CVD observed here. In conclusion, our results highlight the importance of continued public health efforts to address smoking as a modifiable exposure that strongly contributes toward CVD risk.

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          Author and article information

          Journal
          0207277
          408
          Am J Cardiol
          Am. J. Cardiol.
          The American journal of cardiology
          0002-9149
          1879-1913
          22 May 2019
          08 August 2017
          15 November 2017
          30 May 2019
          : 120
          : 10
          : 1787-1791
          Affiliations
          [a ]Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts;
          [b ]Department of Medicine, Division of Cardiology, UPMC Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, Pennsylvania;
          [c ]Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts;
          [d ]National Heart, Lung, and Blood Institute’s and Boston University’s Framingham Heart Study, Framingham, Massachusetts
          Author notes
          [* ]Corresponding author: Tel: 412 648 6920; fax: 412 802 6395., magnanij@ 123456pitt.edu (J.W. Magnani).
          Article
          PMC6541867 PMC6541867 6541867 nihpa1030593
          10.1016/j.amjcard.2017.07.087
          6541867
          28865894
          cc18af73-5d23-4e32-84a6-b35040b3bbd5
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