Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA; Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Can J Cardiol. 2019 Mar;35(3):270-279. doi: 10.1016/j.cjca.2018.11.029. Epub 2018 Dec 4.
Understanding why persons with human immunodeficiency virus (HIV) have accelerated atherosclerosis and its sequelae, including coronary artery disease (CAD) and myocardial infarction, is necessary to provide appropriate care to a large and aging population with HIV. In this review, we delineate the diverse pathophysiologies underlying HIV-associated CAD and discuss how these are implicated in the clinical manifestations of CAD among persons with HIV. Several factors contribute to HIV-associated CAD, with chronic inflammation and immune activation likely representing the primary drivers. Increased monocyte activation, inflammation, and hyperlipidemia present in chronic HIV infection also mirror the pathophysiology of plaque rupture. Furthermore, mechanisms central to plaque erosion, such as activation of toll-like receptor 2 and formation of neutrophil extracellular traps, are also abundant in HIV. In addition to inflammation and immune activation in general, persons with HIV have a higher prevalence than uninfected persons of traditional cardiovascular risk factors, including dyslipidemia, hypertension, insulin resistance, and tobacco use. Antiretroviral therapies, although clearly necessary for HIV treatment and survival, have had varied effects on CAD, but newer generation regimens have reduced cardiovascular toxicities. From a clinical standpoint, this mix of risk factors is implicated in earlier CAD among persons with HIV than uninfected persons; whether the distribution and underlying plaque content of CAD for persons with HIV differs considerably from uninfected persons has not been definitively studied. Furthermore, the role of cardiovascular risk estimators in HIV remains unclear, as does the role of traditional and emerging therapies; no trials of CAD therapies powered to detect clinical events have been completed among persons with HIV.
了解为什么人类免疫缺陷病毒 (HIV) 感染者会加速动脉粥样硬化及其后果，包括冠心病 (CAD) 和心肌梗死，对于为大量老龄化的 HIV 感染者提供适当的护理是必要的。在这篇综述中，我们描述了与 HIV 相关的 CAD 的多种病理生理学，并讨论了这些病理生理学如何与 HIV 感染者的 CAD 临床表现相关。有几个因素导致了与 HIV 相关的 CAD，慢性炎症和免疫激活可能是主要的驱动因素。慢性 HIV 感染中存在的单核细胞激活、炎症和高脂血症也反映了斑块破裂的病理生理学。此外，斑块侵蚀的核心机制，如 toll 样受体 2 的激活和中性粒细胞细胞外陷阱的形成，在 HIV 中也很丰富。除了一般的炎症和免疫激活外，HIV 感染者比未感染者更常见传统心血管危险因素，包括血脂异常、高血压、胰岛素抵抗和吸烟。抗逆转录病毒疗法虽然对 HIV 的治疗和生存是必要的，但对 CAD 的影响各不相同，但新一代的方案减少了心血管毒性。从临床角度来看，这种危险因素的混合导致了 HIV 感染者比未感染者更早出现 CAD；HIV 感染者的 CAD 的分布和潜在斑块内容是否与未感染者有很大的不同，尚未得到明确的研究。此外，心血管风险评估器在 HIV 中的作用仍不清楚，传统和新兴疗法的作用也是如此；尚未完成针对 HIV 感染者的 CAD 治疗的临床试验，以检测临床事件。
