Jericó Carlos, Knobel Hernando, Calvo Nahum, Sorli María L, Guelar Ana, Gimeno-Bayón Juan L, Saballs Pere, López-Colomés José L, Pedro-Botet Juan
Department of Medicine, Hospital del Mar, Barcelona, Spain.
Stroke. 2006 Mar;37(3):812-7. doi: 10.1161/01.STR.0000204037.26797.7f. Epub 2006 Jan 26.
Whether or not combination antiretroviral therapy (CART) alone directly contributes to accelerating atherosclerosis in HIV-infected patients has not been studied in depth. This study aimed to ascertain the relationship between this therapy and subclinical carotid atherosclerosis according to cardiovascular risk.
Sixty-eight HIV-infected patients with < or =1 cardiovascular risk factors and 64 with > or =2 risk factors completed the study protocol consisting of clinical, laboratory, and vascular evaluation by carotid high-resolution B-mode ultrasonography. Univariate and multivariate logistic regression analyses were performed with the presence of subclinical carotid atherosclerosis, defined by carotid intima-media thickness >0.8 mm or the presence of plaque being the dependent variable.
Among the 132 enrolled patients, 93 (70.5%) were on CART and 39 (29.5%) had never been on antiretroviral therapy. In accordance with cardiovascular risk stratification, subclinical carotid atherosclerosis was found in 26.6% (17 of 64 patients) of the very low-risk group (10-year coronary risk <5%), 35.3% (12 of 34 patients) of the low-risk group (10-year coronary risk between 5% and 9%) and 76.5% (26 of 34 patients) of the moderate/high-risk group (10-year coronary risk > or =10%). Thus, 55 (41.7%) of the 132 HIV-infected patients had subclinical carotid atherosclerosis, and independent variables associated with carotid atherosclerosis (odds ratio; 95% CI) were: CART exposure (10.5; 2.8 to 39) and 10-year coronary risk > or =10% (4.2; 1.5 to 12). In very low coronary risk patients (<5%), age (per 10-year increment: 4.01; 1.12 to 14.38), systolic blood pressure (per unit mm Hg 1.07; 1.01 to 1.14), and CART exposure (8.65; 1.54 to 48.54) were independently associated with subclinical carotid atherosclerosis.
CART should be considered a strong, independent predictor for the development of subclinical atherosclerosis in HIV-infected patients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy.
单纯联合抗逆转录病毒疗法（CART）是否直接促使HIV感染患者动脉粥样硬化加速尚未得到深入研究。本研究旨在根据心血管风险确定该疗法与亚临床颈动脉粥样硬化之间的关系。
68例有≤1个心血管危险因素的HIV感染患者和64例有≥2个危险因素的患者完成了研究方案，包括临床、实验室检查以及通过颈动脉高分辨率B型超声进行血管评估。以颈动脉内膜中层厚度>0.8mm或存在斑块定义亚临床颈动脉粥样硬化，将其作为因变量进行单因素和多因素逻辑回归分析。
在132例入组患者中，93例（70.5%）接受CART治疗，39例（29.5%）从未接受过抗逆转录病毒治疗。根据心血管风险分层，极低风险组（10年冠心病风险<5%）中26.6%（64例中的17例）存在亚临床颈动脉粥样硬化，低风险组（10年冠心病风险在5%至9%之间）中35.3%（34例中的12例）存在，中/高风险组（10年冠心病风险≥10%）中76.5%（34例中的26例）存在。因此，132例HIV感染患者中有55例（41.7%）存在亚临床颈动脉粥样硬化，与颈动脉粥样硬化相关的独立变量（比值比；95%可信区间）为：接受CART治疗（10.5；2.8至39）和10年冠心病风险≥10%（4.2；1.5至12）。在冠心病风险极低的患者（<5%）中，年龄（每增加10岁：4.01；1.12至14.38）、收缩压（每单位mmHg 1.07；1.01至1.14）以及接受CART治疗（8.65；1.54至48.54）与亚临床颈动脉粥样硬化独立相关。
无论已知的主要心血管危险因素以及该疗法引起的致动脉粥样硬化代谢异常如何，CART都应被视为HIV感染患者发生亚临床动脉粥样硬化的一个强有力的独立预测因素。
