Drozd Daniel R, Kitahata Mari M, Althoff Keri N, Zhang Jinbing, Gange Stephen J, Napravnik Sonia, Burkholder Greer A, Mathews William C, Silverberg Michael J, Sterling Timothy R, Heckbert Susan R, Budoff Matthew J, Van Rompaey Stephen, Delaney Joseph A C, Wong Cherise, Tong Weiqun, Palella Frank J, Elion Richard A, Martin Jeffrey N, Brooks John T, Jacobson Lisa P, Eron Joseph J, Justice Amy C, Freiberg Matthew S, Klein Daniel B, Post Wendy S, Saag Michael S, Moore Richard D, Crane Heidi M
*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.
J Acquir Immune Defic Syndr. 2017 Aug 15;75(5):568-576. doi: 10.1097/QAI.0000000000001450.
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.
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.
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.
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.
既往针对HIV感染者心血管疾病（CVD）的研究受到限制，无法验证并区分动脉粥样硬化性1型心肌梗死（T1MI）与其他事件。我们旨在确定北美艾滋病队列协作研究与设计（NA-ACCORD）参与者中T1MI的发病率以及传统因素和HIV特异性因素所致风险，并将调整后的发病率（IR）与社区动脉粥样硬化风险（ARIC）队列的一般人群进行比较。
我们确定并判定了1995年至2014年期间纳入7个NA-ACCORD队列的个体中的新发心肌梗死。我们使用泊松回归计算了T1MI的IR、调整发病率比（aIRR）以及风险因素的95%置信区间。我们比较了NA-ACCORD中T1MI的aIRR与ARIC中的aIRR。
在29169名HIV感染者中，T1MI的IR为每1000人年2.57（2.30至2.86），与ARIC参与者相比，aIRR显著更高[1.30（1.09至1.56）]。在仅限于HIV感染者且包括传统CVD风险因素的多变量分析中，T1MI的发生率随CD4计数降低而增加[≥500个细胞/μL：参照；350 - 499个细胞/μL：aIRR = 1.32（0.98至1.77）；200 - 349个细胞/μL：aIRR = 1.37（1.01至1.86）；100 - 199个细胞/μL：aIRR = 1.60（1.09至2.34）；<100个细胞/μL：aIRR = 2.19（1.44至3.33）]。仅在排除CD4时，与可检测到的HIV RNA相关的风险[<400拷贝/mL：参照；≥400拷贝/mL：aIRR = 1.36（1.06至1.75）]显著增加。
HIV感染者中T1MI的较高发病率以及与较低CD4计数和可检测到的HIV RNA相关的风险增加表明，早期抑制性抗逆转录病毒治疗以及积极管理传统CVD风险因素对于最大程度降低心肌梗死风险是必要的。
