Evan D Muse1, David I Feldman2, Michael J Blaha2, Zeina A Dardari2, Roger S Blumenthal2, Matthew J Budoff3, Khurram Nasir4, Michael H Criqui5, Mary Cushman6, Robyn L McClelland7, Matthew A Allison5. 1. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Scripps Translational Science Institute, The Scripps Research Institute, La Jolla, CA, USA. Electronic address: emuse@scripps.edu. 2. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. 3. Division of Cardiology, Harbor-UCLA Medical Center, Los Angeles, CA, USA. 4. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Center for Prevention and Wellness Research, Baptist Health Medical Group, Miami, FL, USA. 5. Department of Family and Preventive Medicine, University of California San Diego, San Diego, CA, USA. 6. Department of Medicine, University of Vermont, Burlington, VT, USA. 7. Department of Biostatistics, University of Washington, Seattle, WA, USA.
Abstract
OBJECTIVE: To describe the relationship between circulating resistin levels and cardiovascular diseases (CVD) and all-cause death in a multi-ethnic cohort. METHODS AND RESULTS: We studied 1913 participants from the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels. Absolute proportions experiencing new-onset atrial fibrillation (AF), atherosclerotic CVD (myocardial infarction, angina, resuscitated cardiac arrest, stroke), heart failure (HF), and all-cause death were calculated for each quartile of resistin. We used adjusted Cox proportional regression modeling resistin as a continuous variable per standard deviation of log-transformed resistin and secondarily as a categorical variable using resistin quartiles. Results were stratified by sex and race/ethnicity. The mean age of the population was 64.5 ± 10 years with half being female and a median resistin concentration of 15.1 ng/mL (11.9-19.1). Mean follow-up time was 7.2 ± 1.8 years. There was a graded increase in the occurrence of all outcomes across increasing quartiles of resistin. Modeled as a continuous variable, after adjustment for anthropomorphic measures, traditional risk factors, markers of inflammation, and other adipokines, significant associations were noted for HF (HR 1.4, CI 1.0-2.0), hard and all CVD (HR 1.3, 1.1-1.7 and 1.3, 1.1-1.6, respectively), and CHD (HR 1.31, 1.0-1.6), but not for AF or death. Significant interaction terms were noted between resistin and race, with Hispanic race/ethnicity showing the strongest relationship between resistin and outcomes. CONCLUSIONS: In an ethnically diverse population without known CVD at baseline, there was a strong, independent association between higher resistin levels and incident CVD, CHD and HF.
OBJECTIVE: To describe the relationship between circulating resistin levels and cardiovascular diseases (CVD) and all-cause death in a multi-ethnic cohort. METHODS AND RESULTS: We studied 1913 participants from the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels. Absolute proportions experiencing new-onset atrial fibrillation (AF), atherosclerotic CVD (myocardial infarction, angina, resuscitated cardiac arrest, stroke), heart failure (HF), and all-cause death were calculated for each quartile of resistin. We used adjusted Cox proportional regression modeling resistin as a continuous variable per standard deviation of log-transformed resistin and secondarily as a categorical variable using resistin quartiles. Results were stratified by sex and race/ethnicity. The mean age of the population was 64.5 ± 10 years with half being female and a median resistin concentration of 15.1 ng/mL (11.9-19.1). Mean follow-up time was 7.2 ± 1.8 years. There was a graded increase in the occurrence of all outcomes across increasing quartiles of resistin. Modeled as a continuous variable, after adjustment for anthropomorphic measures, traditional risk factors, markers of inflammation, and other adipokines, significant associations were noted for HF (HR 1.4, CI 1.0-2.0), hard and all CVD (HR 1.3, 1.1-1.7 and 1.3, 1.1-1.6, respectively), and CHD (HR 1.31, 1.0-1.6), but not for AF or death. Significant interaction terms were noted between resistin and race, with Hispanic race/ethnicity showing the strongest relationship between resistin and outcomes. CONCLUSIONS: In an ethnically diverse population without known CVD at baseline, there was a strong, independent association between higher resistin levels and incident CVD, CHD and HF.
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