2020
DOI: 10.1016/j.rccar.2020.04.005
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COVID-19 and ACE -inhibitors and angiotensin receptor blockers-: The need to differentiate between early infection and acute lung injury

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Cited by 10 publications
(9 citation statements)
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“… 144 There has been initial concern about the safety of angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs), related to the intensification of ACE2 receptor expression, which could be associated with an increased risk of SARS-CoV-2 infection. 145 However, ACE2 receptors may protect against acute respiratory distress syndrome (ARDS) in COVID-19 patients 145 and more recent studies suggest that the use of renin-angiotensin-aldosterone system inhibitors is not associated with increased risk of severe forms of COVID-19. 146 , 147 …”
Section: Discussionmentioning
confidence: 99%
“… 144 There has been initial concern about the safety of angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs), related to the intensification of ACE2 receptor expression, which could be associated with an increased risk of SARS-CoV-2 infection. 145 However, ACE2 receptors may protect against acute respiratory distress syndrome (ARDS) in COVID-19 patients 145 and more recent studies suggest that the use of renin-angiotensin-aldosterone system inhibitors is not associated with increased risk of severe forms of COVID-19. 146 , 147 …”
Section: Discussionmentioning
confidence: 99%
“…Conversely, the increase in the ACE2 receptor expression could be associated with a reduction of the severity of Acute Respiratory Distress Syndrome (ARDS) [32]. In this regard, ACE2 metabolizes the vasoconstrictor peptide angiotensin II to produce angiotensin 1-7, which is involved in reducing inflammation, tissue damage, and pulmonary edema [33]. Ongoing clinical studies would provide information on the effectiveness of ATV in preventing or mitigating these effects in patients with COVID-19 [34, 35].…”
Section: Discussionmentioning
confidence: 99%
“…Although downregulation in ACE 2 with COVID-19 is reported in many studies and was previously confirmed in 2002 with SARS-CoV as well [ 10 ] yet, it is questionable by other studies that states that ACE 2 are still functioning despite being attached to the S protein of SARS-CoV-2, questioning the role of RAS dysregulated mechanism in stroke and COVID-19 [ 11 ] and that cytokine surge secondary to the virus infection may over express ACE 2 rather than down regulate it and this facilitates more viral entry to cells [ 12 ].…”
Section: Main Textmentioning
confidence: 99%