TY - JOUR
T1 - Resistin, Adiponectin, and Risk of Heart Failure. The Framingham Offspring Study
AU - Frankel, David S.
AU - Vasan, Ramachandran S.
AU - D'Agostino, Ralph B.
AU - Benjamin, Emelia J.
AU - Levy, Daniel
AU - Wang, Thomas J.
AU - Meigs, James B.
N1 - Funding Information:
Supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study (contract no. N01-HC-25195), 2K24HL404334 (Dr. Vasan), RO1 HL076784 (Dr. Benjamin), 1R01 AG028321 (Dr. Benjamin), and an American Diabetes Association Career Development Award (Dr. Meigs). Dr. D'Agostino has received honoraria from Sanofi-Aventis and serves on advisory boards for Pfizer and Bayer. Dr. Meigs currently has research grants from GlaxoSmithKline and serves on safety boards for GlaxoSmithKline and Lilly. The funding agencies had no influence over the content or conduct of the analysis or the decision to publish the findings. Dr. Frankel had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
PY - 2009/3/3
Y1 - 2009/3/3
N2 - Objectives: We tested the association of the adipokines resistin and adiponectin with incident heart failure. Background: Abnormal concentrations of adipokines may partially explain the association between obesity and heart failure. Methods: We related circulating adipokine concentrations to the incidence of heart failure in 2,739 participants in the Framingham Offspring Study. Results: During 6 years of follow-up, 58 participants developed new-onset heart failure. In proportional hazards models (adjusting for age, sex, blood pressure, antihypertensive treatment, diabetes, smoking, total/high-density lipoprotein cholesterol ratio, prevalent coronary heart disease, valvular heart disease, left ventricular hypertrophy, and estimated glomerular filtration rate) using the lowest third of the resistin distribution as the referent, the hazard ratios for heart failure in the middle and top thirds were 2.89 (95% confidence interval [CI]: 1.05 to 7.92) and 4.01 (95% CI: 1.52 to 10.57), respectively (p = 0.004 for trend). Additional adjustment for body mass index, insulin resistance (measured with the homeostasis model), C-reactive protein, and B-type natriuretic peptide did not substantively weaken this association (multivariable hazard ratios [HRs]: 2.62 and 3.74, p = 0.007). In the maximally adjusted model, each SD increment in resistin (7.45 ng/ml) was associated with a 26% increase in heart failure risk (95% CI: 1% to 60%). Concentrations of adiponectin were not associated with heart failure (multivariable HRs: 0.87 and 0.97, p = 0.9). Conclusions: Increased circulating concentrations of resistin were associated with incident heart failure, even after accounting for prevalent coronary heart disease, obesity, and measures of insulin resistance and inflammation. The findings suggest a role for resistin in human disease and a novel pathway to heart failure.
AB - Objectives: We tested the association of the adipokines resistin and adiponectin with incident heart failure. Background: Abnormal concentrations of adipokines may partially explain the association between obesity and heart failure. Methods: We related circulating adipokine concentrations to the incidence of heart failure in 2,739 participants in the Framingham Offspring Study. Results: During 6 years of follow-up, 58 participants developed new-onset heart failure. In proportional hazards models (adjusting for age, sex, blood pressure, antihypertensive treatment, diabetes, smoking, total/high-density lipoprotein cholesterol ratio, prevalent coronary heart disease, valvular heart disease, left ventricular hypertrophy, and estimated glomerular filtration rate) using the lowest third of the resistin distribution as the referent, the hazard ratios for heart failure in the middle and top thirds were 2.89 (95% confidence interval [CI]: 1.05 to 7.92) and 4.01 (95% CI: 1.52 to 10.57), respectively (p = 0.004 for trend). Additional adjustment for body mass index, insulin resistance (measured with the homeostasis model), C-reactive protein, and B-type natriuretic peptide did not substantively weaken this association (multivariable hazard ratios [HRs]: 2.62 and 3.74, p = 0.007). In the maximally adjusted model, each SD increment in resistin (7.45 ng/ml) was associated with a 26% increase in heart failure risk (95% CI: 1% to 60%). Concentrations of adiponectin were not associated with heart failure (multivariable HRs: 0.87 and 0.97, p = 0.9). Conclusions: Increased circulating concentrations of resistin were associated with incident heart failure, even after accounting for prevalent coronary heart disease, obesity, and measures of insulin resistance and inflammation. The findings suggest a role for resistin in human disease and a novel pathway to heart failure.
KW - adipokines
KW - adiponectin
KW - epidemiology
KW - heart failure
KW - resistin
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U2 - 10.1016/j.jacc.2008.07.073
DO - 10.1016/j.jacc.2008.07.073
M3 - Article
C2 - 19245965
AN - SCOPUS:60449091233
SN - 0735-1097
VL - 53
SP - 754
EP - 762
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 9
ER -