Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD, 21287, USA.
MTA-SE Cardiovascular Imaging Research Group, Heart and Vascular Center, Semmelweis University, 68 Városmajor str, Budapest, 1122, Hungary.
Eur Radiol. 2021 May;31(5):2756-2767. doi: 10.1007/s00330-021-07755-7. Epub 2021 Mar 3.
To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans.
We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: -100-350HU), low-attenuation noncalcified (LA-NCP: -100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes.
There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0-19.4] mm/year vs. 4.9 [IQR: 1.5-18.3] mm/year, p = 0.14), LA-NCP (0.2 [IQR: 0.0-1.6] mm/year vs. 0.2 [IQR: 0.0-0.9] mm/year, p = 0.07) or CP volumes (0.3 [IQR: 0.0-3.4] mm/year vs. 0.1 [IQR: 0.0-3.2] mm/year, p = 0.30). Multivariately, HIV infection was not associated with NCP (-6.9mm, CI: [-32.8-19.0], p = 0.60), LA-NCP (-0.1mm, CI: [-2.6-2.4], p = 0.92), or CP volumes (-0.3mm, CI: [-9.3-8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes (p > 0.05 for all).
The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume.
• Human immunodeficiency virus-infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.
在对非裔美国人的一项纵向研究中，评估 HIV 感染是否直接或间接促进冠状动脉疾病（CAD）体积进展。
我们从 2004 年 5 月至 2015 年 8 月期间一项前瞻性流行病学研究的 1429 名心血管无症状参与者中随机选择了 300 名患有亚临床 CAD 的个体（210 名男性；年龄：48.0±7.2 岁；226 名 HIV 感染，174 名可卡因使用者）。个体在两个时间点接受冠状动脉 CT 血管造影（平均随访：4.0±2.3 年）。我们量化了非钙化（NCP：-100-350HU）、低衰减非钙化（LA-NCP：-100-30HU）和钙化斑块（CP：≥351HU）体积。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斑块体积的影响。
HIV 感染和未感染个体在 NCP（8.7[IQR：3.0-19.4]mm/年 vs. 4.9[IQR：1.5-18.3]mm/年，p=0.14）、LA-NCP（0.2[IQR：0.0-1.6]mm/年 vs. 0.2[IQR：0.0-0.9]mm/年，p=0.07）或 CP 体积（0.3[IQR：0.0-3.4]mm/年 vs. 0.1[IQR：0.0-3.2]mm/年，p=0.30）方面的年度进展率没有显著差异。多变量分析显示，HIV 感染与 NCP（-6.9mm，CI：[-32.8-19.0]，p=0.60）、LA-NCP（-0.1mm，CI：[-2.6-2.4]，p=0.92）或 CP 体积（-0.3mm，CI：[-9.3-8.6]，p=0.96）无关。然而，ASCVD 风险的每增加一个百分点和可卡因使用的每增加一年都会显著增加 HIV 感染个体的总斑块、NCP 和 CP 体积，但不会增加 HIV 未感染个体的总斑块、NCP 和 CP 体积。重要的是，HIV 相关药物对斑块体积均无影响（p＞0.05）。
HIV 感染个体的危险因素的更深远的不良影响可能解释了这些人 CAD 的加速进展，因为 HIV 感染与任何冠状动脉斑块体积均无独立相关性。
HIV 感染个体可能存在相似的亚临床冠状动脉疾病，因为感染与冠状动脉斑块体积无关。
然而，心血管危险因素和非法药物使用可能对 HIV 感染个体的动脉粥样硬化进展产生更深远的影响，这可能解释了这些人 CAD 的加速进展。
然而，通过严格的预防和戒除非法药物，这些个体可能会经历与未感染个体相似的心血管结局。
