Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD, USA.
Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Baltimore, MD, USA.
Adv Exp Med Biol. 2021;1318:243-261. doi: 10.1007/978-3-030-63761-3_15.
Hypertension has been listed in several case series and retrospective cohorts as a potential risk factor for the incidence and severity of the new coronavirus (SARS-CoV-2)-associated disease (COVID-19). The debate is noteworthy because almost one billion people around the globe are estimated to have hypertensive diseases, according to the Global Burden of Disease study. Considering the SARS-CoV-2's high infectivity rates, a possible interaction between COVID-19 and hypertension is worrisome. Additionally, antihypertensive drugs, especially the renin-angiotensin-aldosterone system (RAAS) inhibitors, could also influence the natural course of COVID-19 infection. Not only can these associations hold from an epidemiologic standpoint, a mechanistic scenario possibly exists. Hypertension and antihypertensive drugs can increase the expression of transmembrane angiotensin-converting enzyme (ACE)-2 receptors, the entry target of the viruses, thus facilitating infectivity. On the other hand, an increase in ACE-2 could be protective considering the anti-inflammatory, antithrombotic effects of the ACE-2-angiotensin 1-7/Mas pathway. So far, little is known about the whole picture. Observational studies appear to indicate at least a twofold increased risk of mortality for hypertensive patients with COVID-19; however, the previous and continued use of RAAS inhibitors may be protective in this subgroup of patients. The scarcity of randomized clinical trials precludes evidence-based decision-making. At least one randomized study in a non-specified sub-analysis demonstrated no relationship between an angiotensin-converting enzyme inhibitor and incidence or severity of the disease. It is reflected mainly by observational studies and, therefore, by international cardiology societies' guidelines, which state that antihypertensive drugs, particularly RAAS inhibitors, should not be discontinued unless necessary on a case-by-case basis.
高血压已在多个病例系列和回顾性队列研究中被列为新型冠状病毒（SARS-CoV-2）相关疾病（COVID-19）发病和严重程度的潜在危险因素。这场争论引人关注，因为根据全球疾病负担研究，估计全球有近 10 亿人患有高血压病。考虑到 SARS-CoV-2 的高传染性，COVID-19 与高血压之间可能存在相互作用，令人担忧。此外，降压药物，尤其是肾素-血管紧张素-醛固酮系统（RAAS）抑制剂，也可能影响 COVID-19 感染的自然病程。这些关联不仅从流行病学角度来看是成立的，而且可能存在一种机制性的情况。高血压和降压药物可增加跨膜血管紧张素转换酶（ACE）-2 受体的表达，而 ACE-2 受体是病毒的进入靶点，从而促进了感染性。另一方面，ACE-2 的增加可能具有保护作用，因为 ACE-2-血管紧张素 1-7/Mas 途径具有抗炎、抗血栓作用。到目前为止，人们对全貌知之甚少。观察性研究似乎表明，COVID-19 高血压患者的死亡率增加了至少两倍；然而，在这组患者中，RAAS 抑制剂的既往和持续使用可能具有保护作用。随机临床试验的缺乏使得基于证据的决策变得困难。至少有一项非特定亚组分析的随机研究表明，血管紧张素转换酶抑制剂与疾病的发生率或严重程度之间没有关系。这主要反映在观察性研究中，因此，也反映在国际心脏病学会的指南中，这些指南指出，除非有特殊情况，否则不应停止使用降压药物，特别是 RAAS 抑制剂。
