Daniel R Drozd1, Mari M Kitahata, Keri N Althoff, Jinbing Zhang, Stephen J Gange, Sonia Napravnik, Greer A Burkholder, William C Mathews, Michael J Silverberg, Timothy R Sterling, Susan R Heckbert, Matthew J Budoff, Stephen Van Rompaey, Joseph A C Delaney, Cherise Wong, Weiqun Tong, Frank J Palella, Richard A Elion, Jeffrey N Martin, John T Brooks, Lisa P Jacobson, Joseph J Eron, Amy C Justice, Matthew S Freiberg, Daniel B Klein, Wendy S Post, Michael S Saag, Richard D Moore, Heidi M Crane. 1. *Department of Medicine, University of Washington School of Medicine, Seattle, WA; †Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; ‡Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC; §Department of Medicine, University of Alabama School of Medicine, Birmingham, AL; ‖Department of Medicine, University of California San Diego, San Diego, CA; ¶Kaiser Permanente Division of Research, Oakland, CA; #Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN; **Department of Epidemiology, University of Washington School of Public Health, Seattle, WA; ††Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA; ‡‡Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; §§Department of Medicine, George Washington University School of Medicine, Washington, DC; ‖‖Department of Clinical Investigations, Whitman Walker Health, Washington, DC; ¶¶Department of Epidemiology & Biostatistics, University of California San Francisco, San Francisco, CA; ##Division of HIV/AIDS Prevention, National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, GA; ***Department of Medicine, Yale School of Public Health, New Haven, CT; †††Department of Infectious Diseases, San Leandro Medical Center, San Leandro, CA; and ‡‡‡Department of Medicine, Johns Hopkins University, Baltimore, MD.
Abstract
BACKGROUND: Previous studies of cardiovascular disease (CVD) among HIV-infected individuals have been limited by the inability to validate and differentiate atherosclerotic type 1 myocardial infarctions (T1MIs) from other events. We sought to define the incidence of T1MIs and risk attributable to traditional and HIV-specific factors among participants in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) and compare adjusted incidence rates (IRs) to the general population Atherosclerosis Risk in Communities (ARIC) cohort. METHODS: We ascertained and adjudicated incident MIs among individuals enrolled in 7 NA-ACCORD cohorts between 1995 and 2014. We calculated IRs, adjusted incidence rate ratios (aIRRs), and 95% confidence intervals of risk factors for T1MI using Poisson regression. We compared aIRRs of T1MIs in NA-ACCORD with those from ARIC. RESULTS: Among 29,169 HIV-infected individuals, the IR for T1MIs was 2.57 (2.30 to 2.86) per 1000 person-years, and the aIRR was significantly higher compared with participants in ARIC [1.30 (1.09 to 1.56)]. In multivariable analysis restricted to HIV-infected individuals and including traditional CVD risk factors, the rate of T1MI increased with decreasing CD4 count [≥500 cells/μL: ref; 350-499 cells/μL: aIRR = 1.32 (0.98 to 1.77); 200-349 cells/μL: aIRR = 1.37 (1.01 to 1.86); 100-199 cells/μL: aIRR = 1.60 (1.09 to 2.34); <100 cells/μL: aIRR = 2.19 (1.44 to 3.33)]. Risk associated with detectable HIV RNA [<400 copies/mL: ref; ≥400 copies/mL: aIRR = 1.36 (1.06 to 1.75)] was significantly increased only when CD4 was excluded. CONCLUSIONS: The higher incidence of T1MI in HIV-infected individuals and increased risk associated with lower CD4 count and detectable HIV RNA suggest that early suppressive antiretroviral treatment and aggressive management of traditional CVD risk factors are necessary to maximally reduce MI risk.
BACKGROUND: Previous studies of cardiovascular disease (CVD) among HIV-infected individuals have been limited by the inability to validate and differentiate atherosclerotic type 1 myocardial infarctions (T1MIs) from other events. We sought to define the incidence of T1MIs and risk attributable to traditional and HIV-specific factors among participants in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) and compare adjusted incidence rates (IRs) to the general population Atherosclerosis Risk in Communities (ARIC) cohort. METHODS: We ascertained and adjudicated incident MIs among individuals enrolled in 7 NA-ACCORD cohorts between 1995 and 2014. We calculated IRs, adjusted incidence rate ratios (aIRRs), and 95% confidence intervals of risk factors for T1MI using Poisson regression. We compared aIRRs of T1MIs in NA-ACCORD with those from ARIC. RESULTS: Among 29,169 HIV-infected individuals, the IR for T1MIs was 2.57 (2.30 to 2.86) per 1000 person-years, and the aIRR was significantly higher compared with participants in ARIC [1.30 (1.09 to 1.56)]. In multivariable analysis restricted to HIV-infected individuals and including traditional CVD risk factors, the rate of T1MI increased with decreasing CD4 count [≥500 cells/μL: ref; 350-499 cells/μL: aIRR = 1.32 (0.98 to 1.77); 200-349 cells/μL: aIRR = 1.37 (1.01 to 1.86); 100-199 cells/μL: aIRR = 1.60 (1.09 to 2.34); <100 cells/μL: aIRR = 2.19 (1.44 to 3.33)]. Risk associated with detectable HIV RNA [<400 copies/mL: ref; ≥400 copies/mL: aIRR = 1.36 (1.06 to 1.75)] was significantly increased only when CD4 was excluded. CONCLUSIONS: The higher incidence of T1MI in HIV-infected individuals and increased risk associated with lower CD4 count and detectable HIV RNA suggest that early suppressive antiretroviral treatment and aggressive management of traditional CVD risk factors are necessary to maximally reduce MI risk.
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