Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology #301, Baltimore, MD, 21287, USA.
MTA-SE Cardiovascular Imaging Research Group, Heart and Vascular Center, Semmelweis University, 68 Városmajor str., Budapest, Hungary, 1122.
Sci Rep. 2021 Nov 30;11(1):23110. doi: 10.1038/s41598-021-02556-w.
Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). 300 African Americans with asymptomatic CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV-infected) who underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years) were randomly selected from 1429 participants of a prospective epidemiological study between May 2004 and August 2015. We calculated Agatston-scores, number of coronary plaques and segment stenosis score (SSS). Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use on CAD. There was no significant difference in annual progression rates between HIV-infected and-uninfected regarding Agatston-scores (10.8 ± 25.1/year vs. 7.2 ± 17.8/year, p = 0.17), the number of plaques (0.2 ± 0.3/year vs. 0.3 ± 0.5/year, p = 0.11) or SSS (0.5 ± 0.8/year vs. 0.5 ± 1.3/year, p = 0.96). Multivariately, HIV-infection was not associated with Agatston-scores (8.3, CI: [- 37.2-53.7], p = 0.72), the number of coronary plaques (- 0.1, CI: [- 0.5-0.4], p = 0.73) or SSS (- 0.1, CI: [- 1.0-0.8], p = 0.84). ASCVD risk scores and years of cocaine-use significantly increased all CAD outcomes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-medications were associated with any of the CAD outcomes. HIV-infection is not directly associated with CAD and therefore HIV-infected are not destined to have worse CAD profiles. However, HIV-infection may indirectly promote CAD progression as risk factors may have a more prominent role in the acceleration of CAD in these patients.
我们的目的是评估人类免疫缺陷病毒（HIV）感染是否直接或间接促进了冠状动脉疾病（CAD）的临床特征进展。2003 年 5 月至 2015 年 8 月期间，从一项前瞻性流行病学研究的 1429 名参与者中随机选择了 300 名无症状 CAD 的非裔美国人（210 名男性；年龄：48.0±7.2 岁；226 名 HIV 感染），他们在两个时间点接受了冠状动脉 CT 血管造影（平均随访：4.0±2.3 年）。我们计算了 Agatston 评分、冠状动脉斑块数量和节段狭窄评分（SSS）。线性混合模型用于评估 HIV 感染、动脉粥样硬化性心血管疾病（ASCVD）风险和可卡因使用年限对 CAD 的影响。在 Agatston 评分（10.8±25.1/年 vs. 7.2±17.8/年，p=0.17）、斑块数量（0.2±0.3/年 vs. 0.3±0.5/年，p=0.11）或 SSS（0.5±0.8/年 vs. 0.5±1.3/年，p=0.96）方面，HIV 感染与未感染患者之间的年进展率没有显著差异。多变量分析显示，HIV 感染与 Agatston 评分（8.3，CI：[-37.2-53.7]，p=0.72）、冠状动脉斑块数量（-0.1，CI：[-0.5-0.4]，p=0.73）或 SSS（-0.1，CI：[-1.0-0.8]，p=0.84）均无相关性。ASCVD 风险评分和可卡因使用年限显著增加了 HIV 感染者所有的 CAD 结局，但在 HIV 未感染者中没有增加。重要的是，HIV 药物与任何 CAD 结局均无关。HIV 感染与 CAD 没有直接关系，因此 HIV 感染者的 CAD 情况不一定更差。然而，HIV 感染可能会间接促进 CAD 的进展，因为危险因素在这些患者中可能会更显著地加速 CAD 的发展。
