Abstract
The association between angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB) and the risk of mortality in hospitalized patients with severe coronavirus disease 2019 (COVID-19) was investigated. This retrospective cohort study was performed in all hospitalized patients with COVID-19 in tertiary hospitals in Daegu, Korea. Patients were classified based on whether they received ACE-I or ARB before COVID-19 diagnosis. The analysis of the primary outcome, in-hospital mortality, was performed using the Cox proportional hazards regression model. Of 130 patients with COVID-19, 30 (23.1%) who received ACE-I or ARB exhibited an increased risk of in-hospital mortality (adjusted hazard ratio, 2.20; 95% confidence interval [CI], 1.10–4.38; P = 0.025). ACE-I or ARB was also associated with severe complications, such as acute respiratory distress syndrome (ARDS) (adjusted odds ratio [aOR], 2.58; 95% CI, 1.02–6.51; P = 0.045) and acute kidney injury (AKI) (aOR, 3.06; 95% CI, 1.15–8.15; P = 0.026). Among the patients with ACE-I or ARB therapy, 8 patients (26.7%) used high equivalent doses of ACE-I or ARB and they had higher in-hospital mortality and an increased risk of ARDS and AKI (all, P < 0.05). ACE-I or ARB therapy in patients with severe COVID-19 was associated with the occurrence of severe complications and increased in-hospital mortality. The potentially harmful effect of ACE-I or ARB therapy may be higher in patients who received high doses.
Highlights
The outbreak of coronavirus disease 2019 (COVID-19) spread worldwide from Wuhan, China, initiating the second pandemic of the twenty-first century[1,2,3]
We report the association between Renin–angiotensin system (RAS) blockade therapy and the risk of in-hospital mortality or severe complications such as acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) in patients with severe COVID-19 and compare the outcomes according to the doses of RAS blockade
Among the laboratory indices on admission, white blood cell (WBC) count and creatinine were higher among ACE inhibitor (ACE-I) or Ang II receptor blocker (ARB) medication patients, and estimated glomerular filtration rate was lower in ACE-I or ARB medication patients than nonmedication patients
Summary
The outbreak of coronavirus disease 2019 (COVID-19) spread worldwide from Wuhan, China, initiating the second pandemic of the twenty-first century[1,2,3]. The binding of the spike protein to ACE2 results in ACE2 downregulation, prohibiting the main function of ACE2 to degrade angiotensin (Ang) II to Ang 1–7. This contributes to lung injury because the increased Ang stimulates Ang receptor 1 to enhance pulmonary vascular permeability[9,10]. Renin–angiotensin system (RAS) blockades, such as ACE inhibitor (ACE-I) or Ang II receptor blocker (ARB), increase ACE2 expression and could enhance the entry of SARS-CoV-2 into target c ells[11,12]. ACE-I and ARB may block the excessive Ang-mediated Ang II type 1 receptor activation caused by SARS-CoV-2 and protect the infected patients against acute lung injury[13]. We report the association between RAS blockade therapy and the risk of in-hospital mortality or severe complications such as acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) in patients with severe COVID-19 and compare the outcomes according to the doses of RAS blockade
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