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Sci Rep . Assessment of the myocardial effects of Bradykinin inhibitors by cardiac magnetic resonance (CMR) in discharged COVID-19 patients

tetano

Editor, Senior Moderator
Sci Rep


. 2025 Aug 11;15(1):29340.
doi: 10.1038/s41598-025-15489-5. Assessment of the myocardial effects of Bradykinin inhibitors by cardiac magnetic resonance (CMR) in discharged COVID-19 patients

Adriana Aparecida Bau[SUP] #[/SUP][SUP] 1 [/SUP], Roberto Schreiber[SUP] #[/SUP][SUP] 2 [/SUP], Eduarda O Z Minin[SUP] 2 [/SUP], Luis Miguel da Silva[SUP] 1 [/SUP], Layde Rosane Paim[SUP] 2 [/SUP], Camila Nicolela Geraldo Martins[SUP] 1 [/SUP], Andréa Coy-Canguçu[SUP] 1 [/SUP], Maria Luiza Moretti[SUP] 2 [/SUP], Marcelo Dantas Tavares de Melo[SUP] 3 [/SUP], Sergio Dertkigil[SUP] 4 [/SUP], Andrei Sposito[SUP] 1 [/SUP], Jose Roberto Matos-Souza[SUP] 1 [/SUP], Wilson Nadruz[SUP] 1 [/SUP], Bruna Bombassaro[SUP] 2 [/SUP], Eli Mansour[SUP] 2 [/SUP], Lício A Velloso[SUP] 2 [/SUP], Michael Jerosch-Herold[SUP] 5 [/SUP], Otávio Rizzi Coelho-Filho[SUP] 6 [/SUP]



Affiliations
Abstract

Myocardial involvement associated with COVID-19 has been linked to worse clinical outcomes. In a recent study, both a bradykinin B2 receptor inhibitor (icatibant acetate) and plasma-derived C1 inhibitor (pdC1INH) led to an improvement in lung computed tomography scores and increased blood eosinophil counts. Nevertheless, the effects of these therapies on COVID-19-associated myocardial involvement remain uncertain. To evaluate the impact of bradykinin inhibitors on myocardial tissue abnormalities in patients with COVID-19. Survivors of COVID-19 treated with either icatibant or pdC1INH as a supplement to standard-care underwent cardiac magnetic resonance (CMR) myocardial tissue characterization with T1/T2 mapping and serum biomarker collection at 30 days and 6 months post-discharge. At 30 days post-discharge, left ventricular ejection fraction (LVEF) was normal across all groups (Standard-care: 62.6 ± 2.7%, pdC1INH: 64.9 ± 7.5%, icatibant: 66.7 ± 4.8%; p = 0.4), with no significant change at 6 months (p = 0.14). However, pdC1INH treatment significantly reduced myocardial T2 (p = 0.005) and intracellular water lifetime (τic) (p = 0.045), indicating reduced myocardial edema and cardiomyocyte hypertrophy. Anemia, affecting 63% of patients 30 days post-discharge, was associated with larger cardiomyocyte size and prolonged hospital stay (p < 0.001). Hemoglobin levels (11.92 ± 2.45 g/dL at discharge vs. 14.66 ± 1.36 g/dL at 6 months) were inversely linked to intracellular water lifetime (τ[SUB]ic[/SUB]) (p < 0.05), suggesting that anemia contributes to myocardial remodeling. This study suggests that pdC1INH may offer potential cardioprotective benefits in COVID-19 patients by reducing myocardial injury and edema, while icatibant showed less favorable effects, and highlights the importance of managing anemia to mitigate myocardial remodeling and improve clinical outcomes.


 
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