Endocrine Division, Program in Nutritional Metabolism, Massachusetts General Hospital, 55 Fruit St 5LON 207, Boston, MA 02114, USA.
Curr HIV/AIDS Rep. 2012 Sep;9(3):200-5. doi: 10.1007/s11904-012-0123-y.
HIV + patients face a heightened risk of cardiovascular disease (CVD), which cannot be fully explained by traditional risk factors or antiretroviral therapy (ART)-related cardiotoxicity. Increasing evidence suggests a significant contribution of HIV-specific immune dysregulation to atherosclerosis. HIV-specific immune dysregulation may have the following atherogenic effects: 1) activation of endothelial and immune cells; 2) enhancement of the percentage of circulating atherogenic immune cell subsets; and 3) modification of lipid function. Efforts are underway to link immune dysregulation markers with validated CVD endpoints and to identify genetic predispositions for HIV-induced atherogenesis. Moreover, immune suppressants are under evaluation in HIV + patients to attempt modification of immune-mediated CVD risk. Taken together, these studies will enhance understanding of CVD risk stratification and reduction strategies in HIV.
HIV+ 患者面临心血管疾病(CVD)的风险增加,这不能完全用传统的危险因素或抗逆转录病毒治疗(ART)相关的心脏毒性来解释。越来越多的证据表明,HIV 特异性免疫失调对动脉粥样硬化有重要贡献。HIV 特异性免疫失调可能具有以下致动脉粥样硬化作用:1)激活内皮细胞和免疫细胞;2)增加循环致动脉粥样硬化免疫细胞亚群的百分比;3)修饰脂质功能。目前正在努力将免疫失调标志物与经过验证的 CVD 终点联系起来,并确定 HIV 诱导的动脉粥样形成的遗传易感性。此外,免疫抑制剂正在 HIV+患者中进行评估,以尝试改变免疫介导的 CVD 风险。综上所述,这些研究将增强对 HIV 患者 CVD 风险分层和降低策略的理解。