PMC:7534795 / 104520-105999 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7534795","sourcedb":"PMC","sourceid":"7534795","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7534795","text":"Importantly, evidence demonstrating upregulation and enhanced activity of ACE2 suggested it will facilitate the infectivity of SARS-CoV-2 (South, Diz, \u0026 Chappell, 2020). Accordingly, some researchers proposed that ACE inhibitors and ARBs should be discontinued in COVID-19 patients (Diaz, 2020; Esler \u0026 Esler, 2020). However, in addition to the direct effects on cardiac ACE2 other mechanisms such as triggering a cytokine storm will markedly contribute to SARS-CoV-2-induced injury (Chen, Li, Chen, Feng, \u0026 Xiong, 2020). A recent study conducted by Yang et al., demonstrated COVID-19 patients with hypertension using ACE inhibitors/ARBs had lower mortality rates than hypertensive COVID-19 patients that were not on ACE inhibitors/ARBs (Yang et al., 2020). Moreover, Mancia et al. examined 6272 patients and found no association between RAAS inhibitor use and susceptibility or development of COVID-19 (Mancia, Rea, Ludergnani, Apolone, \u0026 Corrao, 2020). In that sense, a published statement by American Heart Association (AHA), the American College of Cardiology (ACC) and the Heart Failure Society of America strongly recommended continuation of ACE inhibitor/ARBs (Zhang, Zhu, Cai, et al., 2020). Together, these data suggest therapies targeting ACE and Ang II do not appear to increase the likelihood of SARS-CoV-2 infection, but may have a role in abrogating the inflammatory response and vasoconstriction that contributes to the clinical deterioration in COVID-19 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