Nathan D Wong1, Yanglu Zhao2, Ruben G W Quek3, Roger S Blumenthal4, Matthew J Budoff5, Mary Cushman6, Parveen Garg7, Veit Sandfort8, Michael Tsai9, J Antonio G Lopez3. 1. Division of Cardiology, Department of Medicine, University of California at Irvine, Heart Disease Prevention Program, Irvine, CA, USA; Department of Epidemiology, University of California Los Angeles, Los Angeles, CA, USA. Electronic address: ndwong@uci.edu. 2. Division of Cardiology, Department of Medicine, University of California at Irvine, Heart Disease Prevention Program, Irvine, CA, USA; Department of Epidemiology, University of California Los Angeles, Los Angeles, CA, USA. 3. Global Health Economics and United States Medical Organization, Amgen, Inc, Thousand Oaks, CA, USA. 4. Department of Medicine, Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. 5. Division of Cardiology, Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, CA, USA. 6. Department of Pathology, University of Vermont, Burlington, VT, USA. 7. Division of Cardiology, Department of Medicine, University of Southern California, Los Angeles, CA, USA. 8. Department of Cardiovascular Imaging, Clinical Center, National Institutes of Health, Bethesda, MD, USA. 9. Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Abstract
BACKGROUND: Residual atherosclerotic cardiovascular disease (ASCVD) risk in statin-treated US adults without known ASCVD is not well described. OBJECTIVE: To quantitate residual ASCVD risk and its predictors in statin-treated adults. METHODS: We studied 1014 statin-treated adults (53.3% female, mean 66.0 years) free of clinical ASCVD in the Multi-Ethnic Study of Atherosclerosis. We examined ASCVD event rates by National Lipid Association risk groups over 11-year follow-up and the relation of standard risk factors, biomarkers, and subclinical atherosclerosis measures with residual ASCVD event risk. RESULTS: Overall, 5.3% of participants were at low, 12.2% at moderate, 60.3% at high, and 22.2% at very high baseline risk. Despite statin therapy, age- and race-standardized ASCVD rates per 1000 person-years for men and women were both 4.9 for low/moderate risk, 19.1 and 14.2 for high risk, and 35.6 and 26.7 for very high risk, respectively. Specific independent predictors of residual risk included current smoking, family history, diabetes, high-sensitivity C-reactive protein, low-density lipoprotein particle number, carotid intimal medial thickness, and especially coronary artery calcium score. Those on moderate- or high-intensity statins at baseline (compared with low intensity) had 39% lower risks and those who increased statin intensity 62% lower ASCVD event risks (P < .01). CONCLUSION: Residual risk of ASCVD remains high despite statin treatment and is predicted by specific risk factors and subclinical atherosclerosis. These findings may be helpful for identifying those at highest risk needing more aggressive treatment.
BACKGROUND: Residual atherosclerotic cardiovascular disease (ASCVD) risk in statin-treated US adults without known ASCVD is not well described. OBJECTIVE: To quantitate residual ASCVD risk and its predictors in statin-treated adults. METHODS: We studied 1014 statin-treated adults (53.3% female, mean 66.0 years) free of clinical ASCVD in the Multi-Ethnic Study of Atherosclerosis. We examined ASCVD event rates by National Lipid Association risk groups over 11-year follow-up and the relation of standard risk factors, biomarkers, and subclinical atherosclerosis measures with residual ASCVD event risk. RESULTS: Overall, 5.3% of participants were at low, 12.2% at moderate, 60.3% at high, and 22.2% at very high baseline risk. Despite statin therapy, age- and race-standardized ASCVD rates per 1000 person-years for men and women were both 4.9 for low/moderate risk, 19.1 and 14.2 for high risk, and 35.6 and 26.7 for very high risk, respectively. Specific independent predictors of residual risk included current smoking, family history, diabetes, high-sensitivity C-reactive protein, low-density lipoprotein particle number, carotid intimal medial thickness, and especially coronary artery calcium score. Those on moderate- or high-intensity statins at baseline (compared with low intensity) had 39% lower risks and those who increased statin intensity 62% lower ASCVD event risks (P < .01). CONCLUSION: Residual risk of ASCVD remains high despite statin treatment and is predicted by specific risk factors and subclinical atherosclerosis. These findings may be helpful for identifying those at highest risk needing more aggressive treatment.
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