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

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 (τic) (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.