Metabolism Unit, Endocrine Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, 5 LON 207, Boston, MA, 02114, USA.
Cardiac MR PET CT Program, Division of Cardiology and Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Curr HIV/AIDS Rep. 2019 Oct;16(5):371-380. doi: 10.1007/s11904-019-00458-1.
People with HIV (PHIV) with access to modern antiretroviral therapy (ART) face a two-fold increased risk of heart failure as compared with non-HIV-infected individuals. The purpose of this review is to consider evolving risks, mechanisms, and preventive considerations pertaining to heart failure among PHIV.
While unchecked HIV/AIDS has been documented to precipitate heart failure characterized by overtly reduced cardiac contractile function, ART-treated HIV may be associated with either heart failure with reduced ejection fraction (HFrEF) or with heart failure with preserved ejection fraction (HFpEF). In HFpEF, a "stiff" left ventricle cannot adequately relax in diastole-a condition known as diastolic dysfunction. Diastolic dysfunction, in turn, may result from processes including myocardial fibrosis (triggered by hypertension and/or immune activation/inflammation) and/or myocardial steatosis (triggered by metabolic dysregulation). Notably, hypertension, systemic immune activation, and metabolic dysregulation are all common conditions among even those PHIV who are well-treated with ART. Of clinical consequence, HFpEF is uniquely intransigent to conventional medical therapies and portends high morbidity and mortality. However, diastolic dysfunction is reversible-as are contributing processes of myocardial fibrosis and myocardial steatosis. Our challenges in preserving myocardial health among PHIV are two-fold. First, we must continue working to realize UNAIDS 90-90-90 goals. This achievement will reduce AIDS-related mortality, including cardiovascular deaths from AIDS-associated heart failure. Second, we must work to elucidate the detailed mechanisms continuing to predispose ART-treated PHIV to heart failure and particularly HFpEF. Such efforts will enable the development and implementation of targeted preventive strategies.
与未感染 HIV 的个体相比，接受现代抗逆转录病毒疗法 (ART) 的 HIV 感染者 (PHIV) 心力衰竭的风险增加了一倍。本综述的目的是考虑 PHIV 心力衰竭的不断变化的风险、机制和预防注意事项。
虽然未经治疗的 HIV/AIDS 已被证明可引发心力衰竭，其特征为明显降低的心脏收缩功能，但接受 ART 治疗的 HIV 可能与射血分数降低的心力衰竭 (HFrEF) 或射血分数保留的心力衰竭 (HFpEF) 相关。在 HFpEF 中，“僵硬”的左心室在舒张期不能充分放松——这种情况称为舒张功能障碍。舒张功能障碍反过来可能是由多种过程引起的，包括心肌纤维化（由高血压和/或免疫激活/炎症触发）和/或心肌脂肪变性（由代谢失调触发）。值得注意的是，高血压、全身免疫激活和代谢失调在接受 ART 充分治疗的 PHIV 中都是常见的情况。HFpEF 的临床后果是独特的，对常规医学治疗无效，并预示着高发病率和死亡率。然而，舒张功能障碍是可以逆转的——心肌纤维化和心肌脂肪变性的过程也是如此。我们在 PHIV 中保护心肌健康面临着双重挑战。首先，我们必须继续努力实现 UNAIDS 90-90-90 目标。这一成就将降低与艾滋病相关的死亡率，包括因艾滋病相关性心力衰竭导致的心血管死亡。其次，我们必须努力阐明继续使接受 ART 治疗的 PHIV 易患心力衰竭特别是 HFpEF 的详细机制。这些努力将使我们能够制定和实施有针对性的预防策略。
