Treatment with angiotensin II in COVID-19 patients may not be beneficial
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Treatment with angiotensin II in COVID-19 patients may not be beneficial Susanne Rysz1,2, Francesca Campoccia Jalde2,3, Anders Oldner2,3, Lars I. Eriksson2,3, Johan Lundberg4,5 and Malin Jonsson Fagerlund2,3* Dear Editor, We read with great interest the recent article by Zangrillo et al. regarding infusion of angiotensin II (ANGII) in COVID-19 [1], stating that ANGII vasopressor treatment may be logical in the setting of COVID-19 patients requiring vasopressor support. The authors refer to the ATHOSIII trial as support for the use of ANGII in catecholamine-resistant vasodilatory shock despite the known concern for thrombotic and infectious complications associated with ANGII [2]. In addition, the authors suggest to use ANGII in COVID-19 patients recently exposed to angiotensin-converting enzyme inhibitors. We believe that both these statements raise some concern. SARS-CoV-1 downregulates ACE2 with a subsequent increase in ANGII levels creating a disruption akin to over activating the renin-angiotensin-aldosterone system (RAAS) [3]. In a recent COVID-19 case series, ANGII
levels were markedly elevated and linearly associated with viral load and lung injury [4]. Moreover, in a prepublished report currently under journal review, infusion of ANGII in a porcine model rapidly (within hours) induced a clinical syndrome closely reflecting the one seen in COVID-19 patients, including histological changes in the lungs with severe thickening of the alveolar walls, possible hyaline membranes, and clotting of vessels, as previously reported in the human COVID-19 phenotype [5]. We suggest that much of the pathophysiology in ICU patients with COVID-19 is potentially driven by a loss of the inhibition of the RAAS, causing supranormal concentrations of ANGII [5]. In our opinion, the use of ANGII in COVID-19 patients is therefore at present most questionable. Rather, we propose further evaluation of a plausible contributing mechanism of RAAS behind pathophysiology seen in COVID-19.
Authors’ response
Alberto Zangrillo, Giovanni Landoni, Luigi Beretta, Federica Morselli, Ary Serpa Neto and Rinaldo Bellomo We thank Dr. Rysz and colleagues for their correspondence [6]. In response, we note that their concerns about the increased risk of thrombosis and infection with angiotensin II have no statistical substance. In addition, for objectivity, other adverse effects would also have to be This comment refers to the article available at https://doi.org/10.1186/ s13054-020-02928-0. * Correspondence: [email protected] 2 Function Perioperative Medicine and Intensive Care, Karolinska University Hospital, Stockholm, Sweden 3 Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden Full list of author information is available at the end of the article
similarly considered, such as a 34% reduction in adverse effects leading to discontinuation compared to placebo, or the 34% reduction in respiratory adverse events, or the absolute 6.4% reduction in serious adverse events compared to plac
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