Rose Kathleen A M, Vera Jaime H, Drivas Peter, Banya Winston, Keenan Niall, Pennell Dudley J, Winston Alan
*Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom; †Section of Infectious Diseases, Department of Medicine, Imperial College London, London, United Kingdom; and ‡Division of Medicine, Brighton and Sussex Medical School, United Kingdom.
J Acquir Immune Defic Syndr. 2016 Apr 15;71(5):514-21. doi: 10.1097/QAI.0000000000000900.
Premature atherosclerosis has been observed among HIV-infected individuals with high cardiovascular risk using one-dimensional ultrasound carotid intima-media thickness. We evaluated the assessment of HIV-infected individuals with low traditional cardiovascular disease risk using cardiovascular magnetic resonance, which allows three-dimensional assessment of the carotid artery wall.
Carotid cardiovascular magnetic resonance was performed in 33 HIV-infected individuals (cases) (19 male, 14 female), and 35 HIV-negative controls (20 male, 15 female). Exclusion criteria included smoking, hypertension, hyperlipidemia (total cholesterol/HDL ratio > 5) or family history of premature atherosclerosis. Cases were stable on combination antiretroviral therapy with plasma HIV-1 RNA <50 copies per milliliter. Using computer modeling, the arterial wall, lumen, and total vessel volumes were calculated for a 4-cm length of each carotid artery centered on the bifurcation. The wall/outer-wall ratio (W/OW), an index of vascular thickening, was compared between the groups.
Cases had a median CD4 cell count of 690 cells per microliter. Mean (±SD) age and 10-year Framingham coronary risk scores were similar for cases and controls (45.2 ± 9.7 years versus 46.9 ± 11.6 years and 3.97% ± 3.9% versus 3.72% ± 3.5%, respectively). W/OW was significantly increased in cases compared with controls (36.7% versus 32.5%, P < 0.0001); this was more marked in HIV-infected females. HIV status was significantly associated with increased W/OW after adjusting for age (P < 0.0001). No significant association between antiretroviral type and W/OW was found-W/OW lowered comparing abacavir to zidovudine (P = 0.038), but statistical model fits poorly.
In a cohort of treated HIV-infected individuals with low measurable cardiovascular risk, we have observed evidence of premature subclinical atherosclerosis.
使用一维超声颈动脉内膜中层厚度,已在具有高心血管风险的HIV感染者中观察到过早出现动脉粥样硬化。我们使用心血管磁共振成像对传统心血管疾病风险较低的HIV感染者进行评估,该技术能够对颈动脉壁进行三维评估。
对33例HIV感染者(病例组)(19例男性,14例女性)和35例HIV阴性对照者(20例男性,15例女性)进行颈动脉心血管磁共振成像检查。排除标准包括吸烟、高血压、高脂血症(总胆固醇/高密度脂蛋白比值>5)或过早发生动脉粥样硬化的家族史。病例组接受联合抗逆转录病毒治疗病情稳定,血浆HIV-1 RNA<50拷贝/毫升。使用计算机建模,以颈动脉分叉为中心,计算每条颈动脉4厘米长度的动脉壁、管腔和总血管体积。比较两组间血管增厚指数壁/外壁比值(W/OW)。
病例组CD4细胞计数中位数为每微升690个细胞。病例组和对照组的平均(±标准差)年龄及10年弗明汉姆冠心病风险评分相似(分别为45.2±9.7岁对46.9±11.6岁,3.97%±3.9%对3.72%±3.5%)。与对照组相比,病例组的W/OW显著升高(36.7%对32.5%,P<0.0001);在感染HIV的女性中更为明显。校正年龄后,HIV感染状态与W/OW升高显著相关(P<0.0001)。未发现抗逆转录病毒药物类型与W/OW之间存在显著关联——与齐多夫定相比,阿巴卡韦使W/OW降低(P = 0.038),但统计模型拟合不佳。
在一组经治疗且可测量的心血管风险较低的HIV感染者中,我们观察到了过早出现亚临床动脉粥样硬化的证据。