To do or not to do: Angiotensin converting enzyme inhibitors/angiotensin receptor blocker in COVID-19 elderly patients

Naga Venkata Rama Krishna Vura, Rashi Sandooja, Amena Firoz
2021
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative organism of coronavirus disease-19 (COVID-19) is tied to the 2020 pandemic that originally began at the end of December 2019 in Wuhan, Hubei province, China. Epidemiological studies have shown that SARS-CoV-2 is known to cause increased mortality in adults beyond the sixth decade of life; similar findings were noticed consistently across the orb; the reason for the differential clinical severity remains murky. The
more » ... prevalence of cardiovascular disease (CVD), hypertension, and diabetes mellitus in older adults infected with COVID-19 are linked to deteriorating the prognosis. The majority of the older adults are known to be taking either angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEl/ARBs) for various aforementioned causes. SARS-CoV-2 uses its viral spike glycoprotein ectodomain to bind the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry into the human cells (Walls et al, 2020) . Preclinical studies have suggested that the renin-angiotensin-aldosterone system (RAAS) inhibitors may increase ACE2 expression, raising concerns regarding their safety in patients with COVID-19. This issue sparked a debate regarding the use of ACEl/ARBs because of the association between ACE2 and SARS-CoV-2. We review recent research to provide evidence-based recommendations amid Covid-19 in older adults using ACEI/ARBs. Renin-Angiotensin System (RAS) The initial rate-controlling step in RAS is renin. Renin is responsible for hydrolyzing angiotensinogen to angiotensin I. Angiotensin I is further converted to angiotensin II by angiotensin-converting enzyme (ACE1). Angiotensin II binds and activates angiotensin II receptor type 1, this activates downstream pro-inflammatory actions, including vasoconstriction and cell proliferation, responsible for acute lung injury seen in COVID-19 patients. ACE2 physiologically counters RAAS activation by metabolizing angiotensin II to angiotensin1-7 and angiotensin I to angiotensin1-9. Angiotensin1-9 binds to the Mas receptor which leads to anti-inflammatory and vasodilation. Both ACE1 and ACE2 are members of the ACE family of dipeptidyl carboxydipeptidases (Bavishi et al., 2020) . ACE2 is predominantly expressed in alveolar epithelium,
doi:10.17179/excli2021-3821 fatcat:rucdkgnhlbhxljxuerwlcxmmey