Key result
Severe COVID-19 was associated with elevated angiotensin II levels (114 vs 58 pmol/L) and a significantly lower angiotensin II:I ratio (1.6 vs 2.6) compared to non-severe COVID-19.
Population
159 patients hospitalized with COVID-19, stratified by disease severity (severe, n = 76; non-severe: n = 83)
Design
Cohort
Authors
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Elevated classical RAS metabolites in severe COVID-19 largely reflect RAS inhibitor use; leaves open whether targeted modulation improves outcomes.
Observational (n=159)
Yes
Absolute Event Rate: 114% vs 58%
p-value: p=<0.05
Angiotensin II is elevated in severe COVID-19 but is markedly influenced by RAS inhibitors and driven by overall RAS activation rather than just ACE2 downregulation.
Reindl‐Schwaighofer et al. (2022) conducted an observational in COVID-19 (n=159). Severe COVID-19 vs. Non-severe COVID-19 was evaluated on Angiotensin II levels (pmol/L) (p=<0.05). Severe COVID-19 was associated with elevated angiotensin II levels (114 vs 58 pmol/L) and a significantly lower angiotensin II:I ratio (1.6 vs 2.6) compared to non-severe COVID-19.
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