Brener Michael, Ketlogetswe Kerunne, Budoff Matthew, Jacobson Lisa P, Li Xiuhong, Rezaeian Panteha, Razipour Aryabod, Palella Frank J, Kingsley Lawrence, Witt Mallory D, George Richard T, Post Wendy S
aJohns Hopkins University School of Medicine, Baltimore, Maryland bLos Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California cJohns Hopkins Bloomberg School of Public Health, Baltimore, Maryland dNorthwestern University, Chicago, Illinois eUniversity of Pittsburgh, Pittsburgh, Pennsylvania, USA. *Michael Brener and Kerunne Ketlogetswe contributed equally to this work.
AIDS. 2014 Jul 17;28(11):1635-44. doi: 10.1097/QAD.0000000000000116.
Cytokines released by epicardial fat are implicated in the pathogenesis of atherosclerosis. HIV infection and antiretroviral therapy have been associated with changes in body fat distribution and coronary artery disease. We sought to determine whether HIV infection is associated with greater epicardial fat and whether epicardial fat is associated with subclinical coronary atherosclerosis.
We studied 579 HIV-infected and 353 HIV-uninfected men aged 40-70 years with noncontrast computed tomography to measure epicardial adipose tissue (EAT) volume and coronary artery calcium (CAC). Total plaque score (TPS) and plaque subtypes (noncalcified, calcified, and mixed) were measured by coronary computed tomography angiography in 706 men.
We evaluated the association between EAT and HIV serostatus, and the association of EAT with subclinical atherosclerosis, adjusting for age, race, and serostatus and with additional cardiovascular risk factors and tested for modifying effects of HIV serostatus.
HIV-infected men had greater EAT than HIV-uninfected men (P=0.001). EAT was positively associated with duration of antiretroviral therapy (P=0.02), specifically azidothymidine (P<0.05). EAT was associated with presence of any coronary artery plaque (P=0.006) and noncalcified plaque (P=0.001), adjusting for age, race, serostatus, and cardiovascular risk factors. Among men with CAC, EAT was associated with CAC extent (P=0.006). HIV serostatus did not modify associations between EAT and either CAC extent or presence of plaque.
Greater epicardial fat volume in HIV-infected men and its association with coronary plaque and antiretroviral therapy duration suggest potential mechanisms that might lead to increased risk for cardiovascular disease in HIV.
心外膜脂肪释放的细胞因子与动脉粥样硬化的发病机制有关。HIV感染和抗逆转录病毒疗法与身体脂肪分布变化及冠状动脉疾病相关。我们试图确定HIV感染是否与更多的心外膜脂肪有关，以及心外膜脂肪是否与亚临床冠状动脉粥样硬化有关。
我们对579名40 - 70岁感染HIV的男性和353名未感染HIV的男性进行了研究，通过非增强计算机断层扫描测量心外膜脂肪组织（EAT）体积和冠状动脉钙化（CAC）。在706名男性中通过冠状动脉计算机断层扫描血管造影测量总斑块评分（TPS）和斑块亚型（非钙化、钙化和混合）。
我们评估了EAT与HIV血清学状态之间的关联，以及EAT与亚临床动脉粥样硬化之间的关联，对年龄、种族和血清学状态进行了调整，并纳入了其他心血管危险因素，并测试了HIV血清学状态的修饰作用。
感染HIV的男性比未感染HIV的男性有更多的EAT（P = 0.001）。EAT与抗逆转录病毒治疗的持续时间呈正相关（P = 0.02），特别是与齐多夫定（P < 0.05）。在对年龄、种族、血清学状态和心血管危险因素进行调整后，EAT与任何冠状动脉斑块的存在（P = 0.006）和非钙化斑块（P = 0.001）有关。在有CAC的男性中，EAT与CAC程度有关（P = 0.006）。HIV血清学状态并未改变EAT与CAC程度或斑块存在之间的关联。
感染HIV的男性心外膜脂肪体积更大，且其与冠状动脉斑块及抗逆转录病毒治疗持续时间的关联提示了可能导致HIV感染者心血管疾病风险增加的心外膜脂肪相关机制。
