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[ACE-inhibitors, angiotensin receptor blockers and severe acute respiratory syndrome caused by coronavirus].
G Ital Cardiol (Rome). 2020 May; 21(5):321-327.GI

Abstract

Some Authors recently suggested that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) should be discontinued, even temporarily, given the current pandemic of SARS-CoV-2 virus. The suggestion is based on the hypothesis that ACE-inhibitors and ARBs may favor the entry and diffusion of SARS-CoV-2 virus into the human cells. ACE-inhibitors and ARBs may increase the expression of ACE2 receptors, which are the sites of viral entry into the human organism. ACE2 receptors are ubiquitous, although they are extremely abundant on the cell surface of type 2 pneumocytes. Type 2 pneumocytes are small cylindrical alveolar cells located in close vicinity to pulmonary capillaries and responsible for the synthesis of alveolar surfactant, which is known to facilitate gas exchanges. The increased expression of ACE2 for effect of ACE-inhibitors and ARBs can be detected by increased production of angiotensin1-7 and mRNA related to ACE2. There is the fear that the increased expression of ACE2 induced by ACE-inhibitors and ARBs may ultimately facilitate the entry and diffusion of the SARS-CoV-2 virus. However, there is no clinical evidence to support this hypothesis. Furthermore, available data are conflicting and some counter-intuitive findings suggest that ARBs may be beneficial, not harmful. Indeed, studies conducted in different laboratories demonstrated that ACE2 receptors show a down-regulation (i.e. the opposite of what would happen with ACE-inhibitors and ARBs) for effect of their interaction with the virus. In animal studies, down-regulation of ACE2 has been found as prevalent in the pulmonary areas infected by virus, but not in the surrounding areas. In these studies, virus-induced ACE2 down-regulation would lead to a reduced formation of angiotensin1-7 (because ACE2 degrades angiotensin II into angiotensin1-7) with consequent accumulation of angiotensin II. The excess angiotensin II would favor pulmonary edema and inflammation, a phenomenon directly associated with angiotensin II levels, along with worsening in pulmonary function. Such detrimental effects have been blocked by ARBs in experimental models. In the light of the above considerations, it is reasonable to conclude that the suggestion to discontinue ACE-inhibitors or ARBs in all patients with the aim of preventing or limiting the diffusion of SARS-CoV-2 virus is not based on clinical evidence. Conversely, experimental studies suggest that ARBs might be useful in these patients to limit pulmonary damage through the inhibition of type 1 angiotensin II receptors. Controlled clinical studies in this area are eagerly awaited. This review discusses facts and theories on the potential impact of ACE-inhibitors and ARBs in the setting of the SARS-CoV-2 pandemic.

Authors+Show Affiliations

Fondazione Umbra Cuore e Ipertensione-ONLUS e S.C. Cardiologia, Ospedale S. Maria della Misericordia, Perugia.Dipartimento di Medicina, Università degli Studi, Perugia.Fondazione Umbra Cuore e Ipertensione-ONLUS e S.C. Cardiologia, Ospedale S. Maria della Misericordia, Perugia.S.C. Cardiologia, Ospedale "G. Mazzoni", Ascoli Piceno.Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese; Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientifici Maugeri, IRCCS, Tradate (VA).

Pub Type(s)

Journal Article

Language

ita

PubMed ID

32310915

Citation

Verdecchia, Paolo, et al. "[ACE-inhibitors, Angiotensin Receptor Blockers and Severe Acute Respiratory Syndrome Caused By Coronavirus]." Giornale Italiano Di Cardiologia (2006), vol. 21, no. 5, 2020, pp. 321-327.
Verdecchia P, Reboldi G, Cavallini C, et al. [ACE-inhibitors, angiotensin receptor blockers and severe acute respiratory syndrome caused by coronavirus]. G Ital Cardiol (Rome). 2020;21(5):321-327.
Verdecchia, P., Reboldi, G., Cavallini, C., Mazzotta, G., & Angeli, F. (2020). [ACE-inhibitors, angiotensin receptor blockers and severe acute respiratory syndrome caused by coronavirus]. Giornale Italiano Di Cardiologia (2006), 21(5), 321-327. https://doi.org/10.1714/3343.33127
Verdecchia P, et al. [ACE-inhibitors, Angiotensin Receptor Blockers and Severe Acute Respiratory Syndrome Caused By Coronavirus]. G Ital Cardiol (Rome). 2020;21(5):321-327. PubMed PMID: 32310915.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [ACE-inhibitors, angiotensin receptor blockers and severe acute respiratory syndrome caused by coronavirus]. AU - Verdecchia,Paolo, AU - Reboldi,Gianpaolo, AU - Cavallini,Claudio, AU - Mazzotta,Giovanni, AU - Angeli,Fabio, PY - 2020/4/21/entrez PY - 2020/4/21/pubmed PY - 2020/4/23/medline SP - 321 EP - 327 JF - Giornale italiano di cardiologia (2006) JO - G Ital Cardiol (Rome) VL - 21 IS - 5 N2 - Some Authors recently suggested that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) should be discontinued, even temporarily, given the current pandemic of SARS-CoV-2 virus. The suggestion is based on the hypothesis that ACE-inhibitors and ARBs may favor the entry and diffusion of SARS-CoV-2 virus into the human cells. ACE-inhibitors and ARBs may increase the expression of ACE2 receptors, which are the sites of viral entry into the human organism. ACE2 receptors are ubiquitous, although they are extremely abundant on the cell surface of type 2 pneumocytes. Type 2 pneumocytes are small cylindrical alveolar cells located in close vicinity to pulmonary capillaries and responsible for the synthesis of alveolar surfactant, which is known to facilitate gas exchanges. The increased expression of ACE2 for effect of ACE-inhibitors and ARBs can be detected by increased production of angiotensin1-7 and mRNA related to ACE2. There is the fear that the increased expression of ACE2 induced by ACE-inhibitors and ARBs may ultimately facilitate the entry and diffusion of the SARS-CoV-2 virus. However, there is no clinical evidence to support this hypothesis. Furthermore, available data are conflicting and some counter-intuitive findings suggest that ARBs may be beneficial, not harmful. Indeed, studies conducted in different laboratories demonstrated that ACE2 receptors show a down-regulation (i.e. the opposite of what would happen with ACE-inhibitors and ARBs) for effect of their interaction with the virus. In animal studies, down-regulation of ACE2 has been found as prevalent in the pulmonary areas infected by virus, but not in the surrounding areas. In these studies, virus-induced ACE2 down-regulation would lead to a reduced formation of angiotensin1-7 (because ACE2 degrades angiotensin II into angiotensin1-7) with consequent accumulation of angiotensin II. The excess angiotensin II would favor pulmonary edema and inflammation, a phenomenon directly associated with angiotensin II levels, along with worsening in pulmonary function. Such detrimental effects have been blocked by ARBs in experimental models. In the light of the above considerations, it is reasonable to conclude that the suggestion to discontinue ACE-inhibitors or ARBs in all patients with the aim of preventing or limiting the diffusion of SARS-CoV-2 virus is not based on clinical evidence. Conversely, experimental studies suggest that ARBs might be useful in these patients to limit pulmonary damage through the inhibition of type 1 angiotensin II receptors. Controlled clinical studies in this area are eagerly awaited. This review discusses facts and theories on the potential impact of ACE-inhibitors and ARBs in the setting of the SARS-CoV-2 pandemic. SN - 1972-6481 UR - https://www.unboundmedicine.com/medline/citation/32310915/[ACE_inhibitors_angiotensin_receptor_blockers_and_severe_acute_respiratory_syndrome_caused_by_coronavirus]_ L2 - https://doi.org/10.1714/3343.33127 DB - PRIME DP - Unbound Medicine ER -