Miguel Cainzos-Achirica1, Michael D Miedema2, John W McEvoy3, Mary Cushman4, Zeina Dardari5, Philip Greenland6, Khurram Nasir7, Matthew J Budoff8, Mouaz H Al-Mallah9, Joseph Yeboah10, Roger S Blumenthal5, Josep Comin-Colet11, Michael J Blaha12. 1. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Bellvitge University Hospital, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain; Universitat de Barcelona, Barcelona, Spain; RTI Health Solutions, Pharmacoepidemiology and Risk Management, Barcelona, Spain. 2. Minneapolis Heart Institute, Minneapolis Heart Institute Foundation, Minneapolis, MN, USA. 3. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Johns Hopkins Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. 4. Departments of Medicine and Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, VT, USA. 5. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. 6. Departments of Medicine and Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. 7. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Center for Healthcare Advancement and Outcomes, Miami Cardiac and Vascular Institute, Baptist Heath South Florida, Miami, FL, USA. 8. Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA. 9. King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Cardiac Center, Ministry of National Guard, Health Affairs, Saudi Arabia. 10. Wake Forest University, Winston-Salem, NC, USA. 11. Bellvitge University Hospital, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain; Department of Clinical Sciences, University of Barcelona, Barcelona, Spain. 12. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: mblaha1@jhmi.edu.
Abstract
BACKGROUND: The prognostic value of hsCRP in contemporary multi-ethnic populations is unclear, particularly in statin users. The aim of this study was to characterize the prognostic utility of hsCRP for atherosclerotic CVD (ASCVD) risk prediction in a multi-ethnic population including non-users and users of statins followed for >13 years. Associations with heart failure (HF), atrial fibrillation (AF), venous thromboembolism (VTE), cancer, and all-cause death were also examined. METHODS AND RESULTS: We evaluated 6757 participants from the Multi-Ethnic Study of Atherosclerosis (MESA; 1002 using statins at baseline), median follow-up 13.2 years. Higher levels of hsCRP were associated with a higher risk of all study endpoints in the unadjusted Cox Proportional Hazards regression analyses, except AF. Among non-users of statins, hsCRP only remained associated with VTE after adjusting for ASCVD risk factors, and did not improve risk prediction. Among users of statins, hsCRP did not improve ASCVD risk prediction either, although it was strongly associated with incident HF (HR for hsCRP ≥ 2 vs <2 mg/L 3.99; 95% CI 2.02, 7.90) and all-cause death (HR 1.52; 95% CI 1.11, 2.08) in multivariable analyses, and hsCRP significantly improved prediction of HF (area under the curve [AUC] basic model 0.741, AUC basic + hsCRP 0.788). CONCLUSIONS: The utility of hsCRP for ASCVD prediction was modest. On the other hand, hsCRP was associated with incident VTE in statin non-users, and all-cause mortality and HF in statin users. In the latter, hsCRP improved the prediction of incident HF events. This finding should be replicated in larger cohorts.
BACKGROUND: The prognostic value of hsCRP in contemporary multi-ethnic populations is unclear, particularly in statin users. The aim of this study was to characterize the prognostic utility of hsCRP for atherosclerotic CVD (ASCVD) risk prediction in a multi-ethnic population including non-users and users of statins followed for >13 years. Associations with heart failure (HF), atrial fibrillation (AF), venous thromboembolism (VTE), cancer, and all-cause death were also examined. METHODS AND RESULTS: We evaluated 6757 participants from the Multi-Ethnic Study of Atherosclerosis (MESA; 1002 using statins at baseline), median follow-up 13.2 years. Higher levels of hsCRP were associated with a higher risk of all study endpoints in the unadjusted Cox Proportional Hazards regression analyses, except AF. Among non-users of statins, hsCRP only remained associated with VTE after adjusting for ASCVD risk factors, and did not improve risk prediction. Among users of statins, hsCRP did not improve ASCVD risk prediction either, although it was strongly associated with incident HF (HR for hsCRP ≥ 2 vs <2 mg/L 3.99; 95% CI 2.02, 7.90) and all-cause death (HR 1.52; 95% CI 1.11, 2.08) in multivariable analyses, and hsCRP significantly improved prediction of HF (area under the curve [AUC] basic model 0.741, AUC basic + hsCRP 0.788). CONCLUSIONS: The utility of hsCRP for ASCVD prediction was modest. On the other hand, hsCRP was associated with incident VTE in statin non-users, and all-cause mortality and HF in statin users. In the latter, hsCRP improved the prediction of incident HF events. This finding should be replicated in larger cohorts.
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