Bau Adriana Aparecida, Schreiber Roberto, Minin Eduarda O Z, da Silva Luis Miguel, Paim Layde Rosane, Martins Camila Nicolela Geraldo, Coy-Canguçu Andréa, Moretti Maria Luiza, de Melo Marcelo Dantas Tavares, Dertkigil Sergio, Sposito Andrei, Matos-Souza Jose Roberto, Nadruz Wilson, Bombassaro Bruna, Mansour Eli, Velloso Lício A, Jerosch-Herold Michael, Coelho-Filho Otávio Rizzi
Discipline of Cardiology, School of Medical Science, Hospital das Clínicas, University of Campinas, UNICAMP, Rua Vital Brasil, 251-Cidade Universitária "Zeferino Vaz", Campinas, São Paulo, CEP:13083-888, Brasil.
Department of Internal Medicine, School of Medical Sciences, University of Campinas, São Paulo, Brazil.
Sci Rep. 2025 Aug 11;15(1):29340. doi: 10.1038/s41598-025-15489-5.
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) (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.
与新型冠状病毒肺炎（COVID-19）相关的心肌受累与更差的临床结局有关。在最近一项研究中，缓激肽B2受体抑制剂（醋酸艾替班特）和血浆源性C1抑制剂（pdC1INH）均使肺部计算机断层扫描评分得到改善，并使血液嗜酸性粒细胞计数增加。然而，这些疗法对COVID-19相关心肌受累的影响仍不确定。为了评估缓激肽抑制剂对COVID-19患者心肌组织异常的影响。接受醋酸艾替班特或pdC1INH作为标准治疗补充的COVID-19幸存者在出院后30天和6个月接受了心脏磁共振（CMR）心肌组织特征分析，采用T1/T2映射法，并收集血清生物标志物。出院后30天，所有组的左心室射血分数（LVEF）均正常（标准治疗组：62.6±2.7%，pdC1INH组：64.9±7.5%，醋酸艾替班特组：66.7±4.8%；p = 0.4），6个月时无显著变化（p = 0.14）。然而，pdC1INH治疗显著降低了心肌T2（p = 0.005）和细胞内水寿命（τic）（p = 0.045），表明心肌水肿减轻和心肌细胞肥大减轻。贫血影响了出院后30天63%的患者，与更大的心肌细胞大小和更长的住院时间相关（p < 0.001）。血红蛋白水平（出院时为11.92±2.45 g/dL，6个月时为14.66±1.36 g/dL）与细胞内水寿命（τ）呈负相关（p < 0.05），表明贫血促进心肌重塑。这项研究表明，pdC1INH可能通过减少心肌损伤和水肿为COVID-19患者提供潜在的心脏保护益处，而醋酸艾替班特的效果较差，并强调了管理贫血以减轻心肌重塑和改善临床结局的重要性。
