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      Increased Risk of Myocardial Infarction in HIV-Infected Individuals in North America Compared to the General Population

      research-article
      , MD, MSc 1 , , MD, MPH 1 ,   , PhD 2 , , MS 2 , , PhD 2 , , PhD 3 , , MD 4 , , MD 5 , , MPH, PhD 6 , , MD 7 , , MD, MPH, PhD 8 , , MD 9 , , PhD 1 , , PhD, MSc 8 , 2 , 2 , , MD 10 , , MD 11 , 12 , , MD, MPH 13 , , MD 14 , , ScD 2 , , MD 3 , , MD, PhD 15 , , MD, MSc 7 , , MD 16 , , MD 17 , , MD 4 , , MD 17 , , MD, MPH 1
      Journal of acquired immune deficiency syndromes (1999)
      HIV, cardiovascular disease, myocardial infarction, MI, CVD

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          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 to the general population Atherosclerosis Risk in Communities (ARIC) cohort.

          Methods

          We ascertained and adjudicated incident MIs among individuals enrolled in seven NA-ACCORD cohorts between 1995–2014. We calculated incidence rates (IR), 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[2.30–2.86] per 1000 person-years, and the aIRR was significantly higher compared with participants in ARIC (1.30[1.09–1.56]). 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[0.98–1.77]; 200–349 cells/μL: aIRR=1.37[1.01–1.86]; 100–199 cells/μL: aIRR=1.60[1.09–2.34]; <100 cells/μL: aIRR=2.19[1.44–3.33]). Risk associated with detectable HIV RNA (<400 copies/mL: ref; ≥400 copies/mL: aIRR=1.36 [1.06–1.75]) 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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          Author and article information

          Journal
          100892005
          21821
          J Acquir Immune Defic Syndr
          J. Acquir. Immune Defic. Syndr.
          Journal of acquired immune deficiency syndromes (1999)
          1525-4135
          1944-7884
          24 May 2017
          15 August 2017
          15 August 2018
          : 75
          : 5
          : 568-576
          Affiliations
          [1 ]Department of Medicine, University of Washington School of Medicine, Seattle, WA
          [2 ]Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
          [3 ]Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC
          [4 ]Department of Medicine, University of Alabama School of Medicine, Birmingham, AL
          [5 ]Department of Medicine, University of California San Diego, San Diego, CA
          [6 ]Kaiser Permanente Division of Research, Oakland, CA
          [7 ]Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN
          [8 ]Department of Epidemiology, University of Washington School of Public Health, Seattle, WA
          [9 ]Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA
          [10 ]Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
          [11 ]Department of Medicine, George Washington University School of Medicine, Washington, District of Columbia
          [12 ]Department of Clinical Investigations, Whitman Walker Health, Washington, District of Columbia
          [13 ]Department of Epidemiology & Biostatistics, University of California San Francisco, San Francisco, CA
          [14 ]Division of HIV/AIDS Prevention, National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, GA
          [15 ]Department of Medicine, Yale School of Public Health, New Haven, CT
          [16 ]Department of Infectious Diseases, San Leandro Medical Center, CA
          [17 ]Department of Medicine, Johns Hopkins University, Baltimore, MD
          Author notes
          Author for Correspondence and Reprint Requests: Daniel R. Drozd, MD, MSc, University of Washington, Division of Allergy & Infectious Diseases, Box 359931, 325 9 th Avenue, Seattle, WA 98104, Phone: 206.685.7791, Facsimile: 206.744.3694, ddrozd@ 123456uw.edu
          Article
          PMC5522001 PMC5522001 5522001 nihpa875840
          10.1097/QAI.0000000000001450
          5522001
          28520615
          8356fcf7-0145-493e-8d1e-0d1e5897b0e3
          History
          Categories
          Article

          MI,CVD,HIV,cardiovascular disease,myocardial infarction
          MI, CVD, HIV, cardiovascular disease, myocardial infarction

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