Widespread use of contemporary antiretroviral therapy globally has transformed HIV disease into a chronic illness associated with excess risk for disorders of the heart and circulatory system. Current clinical care and research has focused on improving HIV-related cardiovascular disease outcomes, survival, and quality of life. In high-income countries, emphasis on prevention of atherosclerotic coronary artery disease over the past decade, including aggressive management of traditional risk factors and earlier initiation of antiretroviral therapy, has reduced risk for myocardial infarction among persons living with human immunodeficiency virus-1 infection. Still, across the globe, persons living with human immunodeficiency virus-1 infection on effective antiretroviral therapy treatment remain at increased risk for ischemic outcomes such as myocardial infarction and stroke relative to the persons without HIV. Unique features of HIV-related cardiovascular disease, in part, include the pathogenesis of coronary disease characterized by remodeling ectasia and unusual plaque morphology, the relative high proportion of type 2 myocardial infarction events, abnormalities of the aorta such as aneurysms and diffuse aortic inflammation, and HIV cerebrovasculopathy as a contributor to stroke risk. Literature over the past decade has also reflected a shift in the profile and prevalence of HIV-associated heart failure, with a reduced but persistent risk of heart failure with reduced ejection fraction and a growing risk of heart failure with preserved ejection fraction. Cardiac magnetic resonance imaging and autopsy data have emphasized the central importance of intramyocardial fibrosis for the pathogenesis of both heart failure with preserved ejection fraction and the increase in risk of sudden cardiac death. Still, more research is needed to better characterize the underlying mechanisms and clinical phenotype of HIV-associated myocardial disease in the current era. Across the different cardiovascular disease manifestations, a common pathogenic feature is that HIV-associated inflammation working through different mechanisms may amplify underlying pathology because of traditional risk and other host factors. The prevalence and phenotype of individual cardiovascular disease manifestations is ultimately influenced by the degree of injury from HIV disease combined with the profile of underlying cardiometabolic factors, both of which may differ substantially by region globally.

中文翻译：

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HIV 感染者的心血管疾病：全球背景下发病机制和临床表现的新见解

当代抗逆转录病毒疗法在全球范围内的广泛使用已将 HIV 疾病转变为与心脏和循环系统疾病风险过高相关的慢性疾病。目前的临床护理和研究重点是改善与 HIV 相关的心血管疾病的结果、生存和生活质量。在高收入国家，过去十年强调预防动脉粥样硬化性冠状动脉疾病，包括积极管理传统危险因素和及早开始抗逆转录病毒治疗，降低了人类免疫缺陷病毒 1 感染者发生心肌梗死的风险。尽管如此，在全球范围内，与未感染 HIV 的人相比，接受有效抗逆转录病毒疗法治疗的 1 型人类免疫缺陷病毒感染者发生心肌梗塞和中风等缺血性后果的风险仍然增加。HIV 相关心血管疾病的独特特征部分包括以重塑扩张和异常斑块形态为特征的冠状动脉疾病的发病机制、相对较高比例的 2 型心肌梗死事件、主动脉异常如动脉瘤和弥漫性主动脉炎症，和 HIV 脑血管病是导致中风风险的一个因素。过去十年的文献也反映了 HIV 相关心力衰竭的概况和患病率的变化，射血分数降低的心力衰竭风险降低但持续存在，而射血分数保留的心力衰竭风险增加。心脏磁共振成像和尸检数据强调了心肌内纤维化对于射血分数保留的心力衰竭和心源性猝死风险增加的发病机制的核心重要性。尽管如此，仍需要更多的研究来更好地描述当前时代 HIV 相关心肌病的潜在机制和临床表型。在不同的心血管疾病表现中，一个共同的致病特征是通过不同机制起作用的 HIV 相关炎症可能由于传统风险和其他宿主因素而放大潜在的病理学。