BTK抑制剂启动后的心房颤动负担和临床结果
Atrial fibrillation burden and clinical outcomes following BTK inhibitor initiation
影响因子:13.40000
分区:医学1区 Top / 血液学1区 肿瘤学2区
发表日期:2024 Oct
作者:
John Alan Gambril, Sanam M Ghazi, Stephen Sansoterra, Mussammat Ferdousi, Onaopepo Kola-Kehinde, Patrick Ruz, Adam S Kittai, Kerry Rogers, Michael Grever, Seema Bhat, Tracy Wiczer, John C Byrd, Jennifer Woyach, Daniel Addison
摘要
Bruton的酪氨酸激酶抑制剂（BTKI）对B细胞恶性肿瘤具有显着的功效，但与心脏毒性（包括心房颤动（AF））相关。与BTKI相关的AF的负担，严重性以及含义是未知的。利用2009 - 2020年从BTKI启动的大量连续B细胞恶性患者，我们确定了具有延长的卧床节律监测的患者。 BTKI生机后的主要结果是AF负担。次要结果包括心室心律失常负担和其他心律不齐。观察到的事件 - AF率和下一代BTKI的负担与ibrutinib进行了比较。多变量回归定义了节奏措施与重大不良心脏事件（MACE）和死亡率之间的关联。有98例BTKI治疗的患者[38.8％的下一代BTKI，14.3％的前AF]，监测28,224 h。中位持续时间为34个月。在平均持续时间为12天的监测中，有72.4％的人出现心律不齐（16.3％AF-AF，其他SVT 31.6％，心室心动过速14.3％）。 14.3％的AF负担很高。艾布鲁替尼和下一代BTKI的AF-Burden相似。没有单一的抗心律失常疗法阻止与BTKI相关的AF。然而，与心律失常负担减轻有关的抗心律失常起始（p = 0.009）。在对传统心血管危险因素的多变量模型中，与BTKI后AF-BORDED的增加有关。在随访中，与MACE（HR 3.12，P = 0.005）和死亡率（HR 2.97，P = 0.007）相关的高AF负担。在BTKI治疗的患者中，高AF负担预后可以预测未来的MACE和死亡率风险。
Abstract
Bruton's tyrosine kinase inhibitors (BTKi) have dramatic efficacy against B-cell malignancies, but link with cardiotoxicity, including atrial fibrillation (AF). Burden, severity, and implications of BTKi-related AF are unknown. Leveraging a large-cohort of consecutive B-cell malignancy patients initiated on BTKi from 2009-2020, we identified patients with extended ambulatory rhythm monitoring. The primary outcome was AF burden after BTKi-initiation. Secondary outcomes included ventricular arrhythmia burden and other arrhythmias. Observed incident-AF rates and burden with next-generation BTKi's were compared to ibrutinib. Multivariable regression defined association between rhythm measures and major adverse cardiac events (MACE), and mortality. There were 98 BTKi-treated patients [38.8% next-generation BTKi's, 14.3% prior-AF], with 28,224 h of monitoring. Median duration BTKi-use was 34 months. Over mean duration 12 days monitoring, 72.4% developed arrhythmias (16.3% incident-AF, 31.6% other SVTs, 14.3% ventricular tachycardia). 14.3% had high AF-burden. AF-burden was similar between ibrutinib and next-generation BTKi's. No single antiarrhythmic-therapy prevented BTKi-related AF. However, antiarrhythmic initiation associated with reduction in arrhythmic burden (P = 0.009). In a multivariable model accounting for traditional cardiovascular risk factors, prior-AF associated with increased post-BTKi AF-burden. In follow-up, high AF burden associated with MACE (HR 3.12, P = 0.005) and mortality (HR 2.97, P = 0.007). Among BTKi-treated patients, high AF burden prognosticates future MACE and mortality risk.