The reduced levels of angiotensin converting enzyme (ACE) 2 associated with cardiovascular disease and increasing age lead to a higher susceptibility to greater disease severity in COVID-19. A viewpoint published online in JAMA Cardiology hypothesises that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binding to ACE2 acutely exaggerates the proinflammatory background created by lower levels of ACE 2 in this subpopulation, predisposing them to greater COVID-19 disease severity and mortality.Authors Majd AlGhatrif (National Institute on Aging, National Institutes of Health, and Department of Medicine, Johns Hopkins School of Medicine, Baltimore, USA) and colleagues write: “This hypothesis is in line with the evidence of a protective role of angiotensin II antagonism against sepsis-associated acute lung injury, and supports continuing therapy with ACEIs/ARBs [angiotensin-converting enzyme inhibitors/angiotensin receptor blockers] and, more so, urgently calls for expanding ongoing trials treating patients with severe COVID-19 with RAS [renin angiotensin system] interventions to examine the role of these interventions in preventing lethal lung complications of COVID-19 as cases surge around the world.”

 

 

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