Division of Cardiology, University Magna Graecia, Catanzaro.
Division of Infectious and Tropical Diseases, 'Magna Graecia' University of Catanzaro, Catanzaro, Italy.
J Cardiovasc Med (Hagerstown). 2021 May 1;22(5):329-334. doi: 10.2459/JCM.0000000000001160.
Coronavirus disease 2019 (COVID-19) is caused by the novel coronavirus first identified in Wuhan, China. The global number of confirmed cases of COVID-19 has surpassed 28,285,700 with mortality that appears higher than for seasonal influenza. About 20% of COVID-19 patients have experienced cardiac involvement and myocardial infarction in patients infected with SARS-CoV-2 had a worse prognosis. Furthermore, the widespread use of antiviral drugs can be linked to a worsening of heart function. Arrhythmias and hypertension have also been reported in patients with Covid-19. On the other hand, previous cardiac diseases are present in 30% of patients infected with SARS-CoV-2. There is uncertainty in the use of ace inhibitors and angiotensin II (Ang II) antagonists in the COVID-19 era. The mechanism of action of SARS-CoV-2 has been elucidated. It has been demonstrated that angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for the new coronavirus SARS-CoV-2 and it is required for host cell entry and subsequent viral replication. The effect of the SARS-CoV-2 infection is the downregulation of ACE2 that may contribute to the severity of lung pathologies as well as the cardiac function. ACE2, a homolog of ACE, is a monocarboxypeptidase that converts Ang II into angiotensin 1-7 (Ang 1-7) that with its vasodilatory, antifibrotic, antihypertrophic effects counterbalances the negative effects of Ang II. On the other hand, angiotensin-converting enzyme inhibitors (ACEi) and AT1R blockers have been shown to upregulate the expression of ACE2. Based on the mechanism of action of SARS-CoV-2, the use of renin angiotensin system (RAS) inhibitors was questioned although all scientific societies did not recommend discontinuation when clinically recommended. The BRACE CORONA, a phase 4, randomized study tested two strategies: temporarily stopping the ACE inhibitor/angiotensin receptor blockers (ARB) for 30 days versus continuing ACE inhibitors/ARBs in patients who were taking these medications chronically and were hospitalized with a confirmed diagnosis of COVID-19 was also discussed. Therefore, the goal of this review is to summarize recent laboratory and clinical investigations concerning the use of ACEi and ARBs during the COVID-19 pandemic. The available data, based also on a randomized trial, suggest that ACEIs or ARBs, when clinically indicated, should be regularly used in the COVID-19 era.
2019 年冠状病毒病（COVID-19）是由最初在中国武汉发现的新型冠状病毒引起的。全球确诊的 COVID-19 病例数已超过 2828.57 万，死亡率似乎高于季节性流感。约 20%的 COVID-19 患者出现心脏受累，感染 SARS-CoV-2 的患者心肌梗死预后更差。此外，广泛使用抗病毒药物会导致心脏功能恶化。COVID-19 患者也有报道出现心律失常和高血压。另一方面，在感染 SARS-CoV-2 的患者中，有 30%存在既往心脏病。在 COVID-19 时代，使用血管紧张素转换酶抑制剂（ACEI）和血管紧张素 II（Ang II）拮抗剂存在不确定性。SARS-CoV-2 的作用机制已经阐明。已证明血管紧张素转换酶 2（ACE2）是新型冠状病毒 SARS-CoV-2 的细胞受体，宿主细胞进入和随后的病毒复制都需要 ACE2。SARS-CoV-2 感染的影响是 ACE2 的下调，这可能导致肺部病变以及心脏功能的严重程度。ACE2 是 ACE 的同源物，是一种单羧肽酶，可将 Ang II 转化为血管紧张素 1-7（Ang 1-7），其血管扩张、抗纤维化、抗肥厚作用可抵消 Ang II 的负面影响。另一方面，血管紧张素转换酶抑制剂（ACEi）和 AT1R 阻滞剂已被证明可上调 ACE2 的表达。基于 SARS-CoV-2 的作用机制，尽管所有科学学会都没有建议在临床上推荐时停止使用，但肾素血管紧张素系统（RAS）抑制剂的使用受到质疑。BRACE CORONA 是一项 4 期、随机研究，测试了两种策略：对于长期服用 ACEI/ARB 且确诊 COVID-19 住院的患者，暂时停用 ACEI/ARB 30 天与继续服用 ACEI/ARB 相比。还讨论了这种策略。因此，本综述的目的是总结最近有关 COVID-19 大流行期间使用 ACEi 和 ARB 的实验室和临床研究。基于随机试验的可用数据表明，在 COVID-19 时代，当临床上需要时，ACEIs 或 ARBs 应常规使用。
