Department of Radiology, Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Department of Health Economics, School of Business Studies, Stralsund University of Applied Sciences, Stralsund, Germany.
Clin Infect Dis. 2023 Dec 15;77(12):1676-1686. doi: 10.1093/cid/ciad419.
Pericoronary adipose tissue (PCAT) may influence plaque development through inflammatory mechanisms. We assessed PCAT density, as a measure of pericoronary inflammation, in relationship to coronary plaque among people with human immunodeficiency virus (HIV [PWH]) and to a matched control population.
In this baseline analysis of 727 participants of the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) Mechanistic Substudy, we related computed tomography-derived PCAT density to presence and extent (Leaman score) of coronary artery disease (CAD), noncalcified plaque, coronary artery calcium (CAC), and vulnerable plaque features using multivariable logistic regression analyses. We further compared the PCAT density between PWH and age, sex, body mass index, CAC score, and statin use-matched controls from the community-based Framingham Heart Study (N = 464), adjusting for relevant clinical covariates.
Among 727 REPRIEVE participants (age 50.8 ± 5.8 years; 83.6% [608/727] male), PCAT density was higher in those with (vs without) coronary plaque, noncalcified plaque, CAC >0, vulnerable plaque, and high CAD burden (Leaman score >5) (P < .001 for each comparison). PCAT density related to prevalent coronary plaque (adjusted odds ratio [per 10 HU]: 1.44; 95% confidence interval, 1.22-1.70; P < .001), adjusted for clinical cardiovascular risk factors, body mass index, and systemic immune/inflammatory biomarkers. Similarly, PCAT density related to CAC >0, noncalcified plaque, vulnerable plaque, and Leaman score >5 (all P ≤ .002). PCAT density was greater among REPRIEVE participants versus Framingham Heart Study (-88.2 ± 0.5 HU versus -90.6 ± 0.4 HU; P < .001).
Among PWH in REPRIEVE, a large primary cardiovascular disease prevention cohort, increased PCAT density independently associated with prevalence and severity of coronary plaque, linking increased coronary inflammation to CAD in PWH.
冠状动脉周围脂肪组织（PCAT）可能通过炎症机制影响斑块的发展。我们评估了 PCAT 密度，作为冠状动脉周围炎症的一种衡量标准，以评估其与人类免疫缺陷病毒（HIV [PWH]）患者和匹配的对照人群中冠状动脉斑块的关系。
在预防 HIV 血管事件的随机试验（REPRIEVE）机制子研究的 727 名参与者的这项基线分析中，我们使用多变量逻辑回归分析，将计算机断层扫描（CT）得出的 PCAT 密度与冠状动脉疾病（CAD）的存在和程度（Leaman 评分）、非钙化斑块、冠状动脉钙（CAC）和易损斑块特征联系起来。我们还比较了 PWH 和年龄、性别、体重指数、CAC 评分和他汀类药物使用匹配的社区弗雷明汉心脏研究（Framingham Heart Study）（N=464）中 PCAT 密度的差异，调整了相关的临床协变量。
在 727 名 REPRIEVE 参与者中（年龄 50.8±5.8 岁；83.6%[608/727]为男性），与无冠状动脉斑块、无非钙化斑块、CAC>0、易损斑块和高 CAD 负荷（Leaman 评分>5）的患者相比，PCAT 密度更高（每种比较的 P<.001）。PCAT 密度与现患冠状动脉斑块相关（每增加 10HU 的调整优势比[per 10 HU]：1.44；95%置信区间，1.22-1.70；P<.001），调整了临床心血管危险因素、体重指数和全身免疫/炎症生物标志物。同样，PCAT 密度与 CAC>0、非钙化斑块、易损斑块和 Leaman 评分>5 相关（所有 P≤.002）。REPRIEVE 参与者的 PCAT 密度高于弗雷明汉心脏研究（-88.2±0.5HU 与-90.6±0.4HU；P<.001）。
在 REPRIEVE 中，一个大型的主要心血管疾病预防队列中的 PWH 中，PCAT 密度的增加与冠状动脉斑块的患病率和严重程度独立相关，这将增加的冠状动脉炎症与 PWH 中的 CAD 联系起来。
