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      Could renin–angiotensin–aldosterone system inhibitors be used for hypertensive patients with coronavirus disease 2019?

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      a , b , a , b , a , b
      Journal of Hypertension
      Lippincott Williams & Wilkins

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          Abstract

          Coronavirus disease 2019 (COVID-19) has reached pandemic proportions. Angiotensin-converting enzyme 2 (ACE2) in type II alveolar epithelial cells is the key factor that binds the spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing COVID-19. Recently, Esler and Esler [1] suggested that administration of AT1-blocking (ARB) drugs during the COVID-19 pandemic may be harmful because upregulation of ACE2 caused by ARB agents can accelerate virus replication and transmission. However, another perspective indicates that renin–angiotensin–aldosterone system (RAAS) inhibitors may be useful for treating COVID-19 patients with hypertension. RAAS inhibitors such as ACE inhibitor and ARB have been reported to increase myocardial ACE2 expression [2]. Whether RAAS inhibitors can be used in COVID-19 patients with hypertension remains controversial, and the following points must be considered: first, will administration of RAAS inhibitors increase the chance of virus infection? Second, will acute lung injury be exacerbated by using RAAS inhibitors? Third, will the side effects of these drugs such as coughing accelerate virus spread? Cardiovascular disease was the most common comorbidity in patients with COVID-19 and RAAS inhibitors were frequently administered to these patients, particularly to those with hypertension and congestive heart failure. However, there is no evidence that RAAS inhibitors increase the risk of SARS-CoV-2 infection. Moreover, Liu et al.[3] found that exacerbated lung injury was linearly associated with markedly elevated levels of angiotensin II (Ang II) in plasma samples from patients with COVID-19. Thus, RAAS inhibitors may be repurposed to treat COVID-19 by its virtue of decreasing Ang II production via inhibiting ACE1 activity or suppressing Ang II function by blocking the Ang II receptor type 1. Consistent with this, other studies have confirmed that RAAS inhibition attenuates acute lung injury and sepsis induced by SARS [4]. In contrast, although myocardial ACE2 levels were increased by lisinopril and losartan by up to 4.7-fold and 2.8-fold, respectively, RAAS inhibitors may have different effects on type II alveolar epithelial cells [4]. Overall, administration of RAAS inhibitors has not been shown to promote SARS-CoV-2 infection or exacerbate lung injury. Furthermore, RAAS inhibitors are generally well tolerated, and side effects such as coughing and angioneurotic edema are typically mediated by increasing bradykinin levels [5]. Patients may change drugs early if they are sensitive to any side effects. Moreover, patients administered RAAS inhibitors for a long time may have better tolerance to increased bradykinin levels. In these patients, RAAS inhibitors will not increase the incidence of coughing, which is known to cause virus transmission. In summary, there is no evidence that RAAS inhibitors are harmful to patients with COVID-19. These drugs are first-line antihypertensive agents and have significant protective effects on the heart and kidney. Thus, patients administered RAAS inhibitors for a long time may not need to change to different antihypertensive agents. However, considering the potential side effects of RAAS inhibitors in patients with COVID-19, these drugs may not be the first choice for patients with emerging hypertension during the course of COVID-19. Additional clinical evidence is needed to confirm these inferences. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.

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          Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury

          The outbreak of the 2019-nCoV infection began in December 2019 in Wuhan, Hubei province, and rapidly spread to many provinces in China as well as other countries. Here we report the epidemiological, clinical, laboratory, and radiological characteristics, as well as potential biomarkers for predicting disease severity in 2019-nCoV-infected patients in Shenzhen, China. All 12 cases of the 2019-nCoV-infected patients developed pneumonia and half of them developed acute respiratory distress syndrome (ARDS). The most common laboratory abnormalities were hypoalbuminemia, lymphopenia, decreased percentage of lymphocytes (LYM) and neutrophils (NEU), elevated C-reactive protein (CRP) and lactate dehydrogenase (LDH), and decreased CD8 count. The viral load of 2019-nCoV detected from patient respiratory tracts was positively linked to lung disease severity. ALB, LYM, LYM (%), LDH, NEU (%), and CRP were highly correlated to the acute lung injury. Age, viral load, lung injury score, and blood biochemistry indexes, albumin (ALB), CRP, LDH, LYM (%), LYM, and NEU (%), may be predictors of disease severity. Moreover, the Angiotensin II level in the plasma sample from 2019-nCoV infected patients was markedly elevated and linearly associated to viral load and lung injury. Our results suggest a number of potential diagnosis biomarkers and angiotensin receptor blocker (ARB) drugs for potential repurposing treatment of 2019-nCoV infection. Electronic Supplementary Material Supplementary material is available for this article at 10.1007/s11427-020-1643-8 and is accessible for authorized users.
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            Can angiotensin receptor-blocking drugs perhaps be harmful in the COVID-19 pandemic?

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              Renin Angiotensin Aldosterone System Inhibitors in Hypertension: Is There Evidence for Benefit Independent of Blood Pressure Reduction?

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                Author and article information

                Journal
                J Hypertens
                J. Hypertens
                JHYPE
                Journal of Hypertension
                Lippincott Williams & Wilkins
                0263-6352
                1473-5598
                06 May 2020
                06 May 2020
                : 10.1097/HJH.0000000000002474
                Affiliations
                [a ]Institute of Cardiovascular Disease, China Three Gorges University
                [b ]Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei Province, China
                Author notes
                Correspondence to Dr Hui Wu, MD, PhD, Department of Cardiology, Yichang Central People's Hospital, Yichang 443003, Hubei Province, China. Tel: +86 151 7183 3889; e-mail: wuhui@ 123456ctgu.edu.cn
                Article
                JH-D-20-00257
                10.1097/HJH.0000000000002474
                7236847
                32371813
                f1b01bd0-92d9-40af-9508-ea5634e0383b
                Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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