Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Baltimore, MD, 21287, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD, 21279, USA.
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD, 21279, USA.
Atherosclerosis. 2022 Jul;353:33-40. doi: 10.1016/j.atherosclerosis.2022.04.019. Epub 2022 Apr 25.
People living with HIV (HIV+) are surviving longer due to effective antiretroviral therapy. Cardiovascular disease is a leading cause of non-AIDS related clinical events. We determined HIV-related factors associated with coronary artery stenosis progression.
We performed serial coronary CT angiography among HIV+ and HIV-uninfected (HIV-) men in the Multicenter AIDS Cohort Study. The median inter-scan interval was 4.5 years. Stenosis was graded as 0, 1-29, 30-49, 50-69 or ≥70%. Progression was defined as an increase ≥2 categories. Suppressed HIV infection was consistent viral loads <50 copies/mL allowing 1 "blip" <500 copies/mL, otherwise considered viremic. Multivariable Poisson regression analysis assessed adjusted associations between HIV serostatus and viremia with coronary stenosis progression.
The sample included 310 HIV+ (31% viremic) and 234 HIV- men. The median age was 53 years, 30% Black and 23% current smokers. Viremic men were 2.3 times more likely to develop coronary stenosis progression than HIV- men (adjusted RR 2.30; 95% CI, 1.32-4.00, p = 0.003), with no difference in progression between HIV+ suppressed and HIV- men (RR 1.10; 95% CI, 0.70-1.74, p = 0.67). There was a progressive increase in adjusted relative risk with greater viremia (p = 0.03). Men with >1 viral load >500 copies/ml demonstrated greatest stenosis progression (RR 3.01; 95% CI, 1.53-4.92, p = 0.001 compared with HIV- men). Suppressed HIV+ men with suboptimal antiretroviral adherence had greater stenosis progression (RR 1.91; 95% CI 1.12-3.24, p = 0.02) than HIV + suppressed men with optimal adherence.
Coronary artery stenosis progression was associated with suboptimal HIV RNA suppression and antiretroviral therapy adherence. Effective ongoing HIV virologic suppression and antiretroviral therapy adherence may mitigate risk for coronary disease events among people living with HIV.
由于有效的抗逆转录病毒治疗,HIV 感染者(HIV+)的生存时间更长。心血管疾病是导致非艾滋病相关临床事件的主要原因。我们确定了与冠状动脉狭窄进展相关的 HIV 相关因素。
我们在艾滋病多中心队列研究中对 HIV+和未感染 HIV(HIV-)的男性进行了连续冠状动脉 CT 血管造影。两次扫描之间的中位间隔时间为 4.5 年。狭窄程度分为 0、1-29、30-49、50-69 或≥70%。进展定义为增加≥2 个类别。抑制性 HIV 感染是指病毒载量持续<50 拷贝/mL,允许出现 1 次<500 拷贝/mL 的“尖峰”,否则视为病毒血症。多变量泊松回归分析评估了 HIV 血清状态和病毒血症与冠状动脉狭窄进展之间的调整关联。
样本包括 310 名 HIV+(31%病毒血症)和 234 名 HIV-男性。中位年龄为 53 岁,30%为黑人,23%为当前吸烟者。病毒血症男性发生冠状动脉狭窄进展的可能性是 HIV-男性的 2.3 倍(调整后的 RR 2.30;95%CI,1.32-4.00,p=0.003),而 HIV+抑制和 HIV-男性之间的进展无差异(RR 1.10;95%CI,0.70-1.74,p=0.67)。随着病毒载量的增加,调整后的相对风险呈递增趋势(p=0.03)。病毒载量>1 次>500 拷贝/ml 的男性显示出最大的狭窄进展(RR 3.01;95%CI,1.53-4.92,p=0.001 与 HIV-男性相比)。抗逆转录病毒治疗依从性不佳的抑制性 HIV+男性的狭窄进展程度大于依从性良好的 HIV+抑制男性(RR 1.91;95%CI,1.12-3.24,p=0.02)。
冠状动脉狭窄进展与 HIV RNA 抑制不佳和抗逆转录病毒治疗依从性差有关。有效的持续 HIV 病毒学抑制和抗逆转录病毒治疗依从性可能会降低 HIV 感染者发生冠心病事件的风险。