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Renin-Angiotensin-Aldosterone System Inhibitors and COVID-19 Infection or Hospitalization: A Cohort Study
Sascha Dublin1,2, Rod L Walker1, James S Floyd1,2,3
1Kaiser Permanente Washington Health Research Institute, Kaiser Permanente Washington, Seattle, Washington, USA.
Insights
Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) do not increase the risk of COVID-19 infection or hospitalization, regardless of medication dose. These findings support continued use of ACEIs and ARBs for patients.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pharmacology
Background:
- Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are commonly prescribed cardiovascular medications.
- Previous research has raised concerns about potential links between ACEIs/ARBs and increased risk or severity of coronavirus disease 2019 (COVID-19).
- The impact of medication dosage on these potential risks has not been thoroughly investigated.
Purpose of the Study:
- To investigate the association between the use of ACEIs and ARBs and the risk of COVID-19 infection.
- To examine whether medication dose influences the risk of COVID-19 infection or hospitalization.
- To provide evidence-based recommendations for patients taking ACEIs and ARBs during the COVID-19 pandemic.
Main Methods:
- Retrospective cohort study of over 322,000 individuals in a US healthcare system.
- ACEI and ARB use and standardized daily doses were determined from pharmacy data.
- COVID-19 infection and hospitalization data were collected through June 2020; logistic regression was used for analysis.
Main Results:
- No significant association was found between ACEI/ARB use and COVID-19 infection (adjusted OR 0.91; 95% CI 0.74-1.12).
- Medication dose did not alter the risk of infection; adjusted ORs for infection ranged from 0.89 to 0.92 across different dose categories.
- No association was observed between ACEI/ARB use and COVID-19 hospitalization (adjusted OR 0.98; 95% CI 0.63-1.54).
Conclusions:
- Current use of ACEIs and ARBs is not associated with an increased risk of COVID-19 infection or hospitalization.
- These findings support existing clinical guidelines recommending the continuation of ACEIs and ARBs for patients.
- The study provides reassurance regarding the safety of these medications in the context of the COVID-19 pandemic.
Background:
Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) may increase the risk of coronavirus disease 2019 (COVID-19) infection or affect disease severity. Prior studies have not examined risks by medication dose.
Methods:
This retrospective cohort study included people aged ≥18 years enrolled in a US integrated healthcare system for at least 4 months as of 2/29/2020. Current ACEI and ARB use was identified from pharmacy data, and the estimated daily dose was calculated and standardized across medications. COVID-19 infections and hospitalizations were identified through 6/14/2020 from laboratory and hospitalization data. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for race/ethnicity, obesity, and other covariates.
Results:
Among 322,044 individuals, 826 developed COVID-19 infection. Among people using ACEI/ARBs, 204/56,105 developed COVID-19 (3.6 per 1,000 individuals) compared with 622/265,939 without ACEI/ARB use (2.3 per 1,000), yielding an adjusted OR of 0.91 (95% CI 0.74-1.12). For use of <1 defined daily dose (DDD) vs. nonuse, the adjusted OR for infection was 0.92 (95% CI 0.66-1.28); for 1 to <2 DDDs, 0.89 (95% CI 0.66-1.19); and for ≥2 DDDs, 0.92 (95% CI 0.72-1.18). The OR was similar for ACEIs and ARBs and in subgroups by age and sex. 26% of people with COVID-19 infection were hospitalized; the adjusted OR for hospitalization in relation to ACEI/ARB use was 0.98 (95% CI 0.63-1.54), and there was no association with dose.
Conclusions:
These findings support current recommendations that individuals on these medications continue their use.
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Hypertension II: Pathophysiology

