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Abstract：
To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET).
We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio (TBRmax). The independent relationships between HIV status and both TBRmax and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD).
Unadjusted mean TBRmax in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-TBRmax in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001).
In patients with high cardiovascular risk, HIV status was an independent predictor of increased TBRmax in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels.
We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio (TBRmax). The independent relationships between HIV status and both TBRmax and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD).
Unadjusted mean TBRmax in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-TBRmax in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001).
In patients with high cardiovascular risk, HIV status was an independent predictor of increased TBRmax in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels.
摘要：
通过18F-氟脱氧葡萄糖（18F-FDG）-正电子发射断层扫描（PET）评估，比较HIV感染者（PLWH）和未感染人群之间的动脉炎症（AI）。
我们前瞻性招募了20名PLWH患者和20名未感染患者，他们没有已知的心血管疾病和至少3种传统的心血管危险因素。所有患者均接受胸部和颈部的18F-FDG-PET/计算机断层扫描（CT）。还确定了与炎症和动脉粥样硬化相关的生物标志物。主要结果是升主动脉（AA）的AI，测量为平均最大目标背景比（TBRmax）。通过调整体重指数的多元线性回归评估HIV状态与TBRmax和生物标志物之间的独立关系，肌酐,他汀类药物治疗,和动脉粥样硬化心血管10年估计风险（ASCVD）。
AA中未调整的平均TBRmax略高于PLWH（2.07;IQR1.97,2.32]），但与未感染人群（2.01;IQR1.85,2.16]）相比，差异无统计学意义（P=0.18）。在多变量分析中，PLWH在AA中具有平均log-TBRmax升高的独立风险(coef=0.12;95CI0.01,0.22;P=0.032)。HIV感染与白细胞介素-10的较高值独立相关(coef=0.83;95CI0.34,1.32;P=.001),干扰素-γ（系数。=0.90；95CI0.32，1.47；P=.003），和血管细胞粘附分子-1（VCAM-1）（coef。=0.75；95CI：0.42，1.08，P<.001）。
在心血管风险高的患者中，HIV状况是AA患者TBRmax升高的独立预测因子。PLWH还增加了IFN-γ的独立风险，IL-10和VCAM-1水平。
我们前瞻性招募了20名PLWH患者和20名未感染患者，他们没有已知的心血管疾病和至少3种传统的心血管危险因素。所有患者均接受胸部和颈部的18F-FDG-PET/计算机断层扫描（CT）。还确定了与炎症和动脉粥样硬化相关的生物标志物。主要结果是升主动脉（AA）的AI，测量为平均最大目标背景比（TBRmax）。通过调整体重指数的多元线性回归评估HIV状态与TBRmax和生物标志物之间的独立关系，肌酐,他汀类药物治疗,和动脉粥样硬化心血管10年估计风险（ASCVD）。
AA中未调整的平均TBRmax略高于PLWH（2.07;IQR1.97,2.32]），但与未感染人群（2.01;IQR1.85,2.16]）相比，差异无统计学意义（P=0.18）。在多变量分析中，PLWH在AA中具有平均log-TBRmax升高的独立风险(coef=0.12;95CI0.01,0.22;P=0.032)。HIV感染与白细胞介素-10的较高值独立相关(coef=0.83;95CI0.34,1.32;P=.001),干扰素-γ（系数。=0.90；95CI0.32，1.47；P=.003），和血管细胞粘附分子-1（VCAM-1）（coef。=0.75；95CI：0.42，1.08，P<.001）。
在心血管风险高的患者中，HIV状况是AA患者TBRmax升高的独立预测因子。PLWH还增加了IFN-γ的独立风险，IL-10和VCAM-1水平。
