蒽环类药物引起的心血管毒性:心力衰竭协会和国际心脏肿瘤学会风险评分的验证。
Anthracycline-induced cardiovascular toxicity: validation of the Heart Failure Association and International Cardio-Oncology Society risk score.
发表日期:2024 Aug 06
作者:
Borja Rivero-Santana, Jesús Saldaña-García, Juan Caro-Codón, Pilar Zamora, Pedro Moliner, Amparo Martínez Monzonis, Eduardo Zatarain, Carlos Álvarez-Ortega, Pilar Gómez-Prieto, Sonia Pernas, Isabel Rodriguez, Antonio Buño Soto, Rosalía Cadenas, Patricia Palacios Ozores, Sara Pérez Ramírez, María Merino Salvador, Silvia Valbuena, Lucía Fernández Gasso, Victor Juárez, Andrea Severo, Belén Terol, Teresa de Soto Álvarez, Olaia Rodríguez, María Brion, José González-Costello, Miguel Canales Albendea, José R González-Juanatey, Raúl Moreno, José López-Sendón, Teresa López-Fernández
来源:
EUROPEAN HEART JOURNAL
摘要:
基线心血管毒性风险分层在心脏肿瘤学中至关重要。心力衰竭协会 (HFA) 和国际心脏肿瘤学会 (ICOS) 评分旨在评估这种风险,但缺乏现实生活中的验证。本研究验证了蒽环类药物引起的心血管毒性的 HFA-ICOS 评分。CARDIOTOX 登记处 (NCT02039622) 中接受蒽环类药物治疗的患者根据 HFA-ICOS 评分进行分层。主要终点是有症状或中度至重度无症状癌症治疗相关心功能障碍 (CTRCD),次要终点是全因死亡率和心血管死亡率。该分析包括 1066 名患者(平均年龄 54 ± 14 岁;81.9% 为女性;24.5% 为女性)。 % ≥65 岁)。根据HFA-ICOS标准,571例患者(53.6%)被归类为低风险,333例(31.2%)为中度风险,152例(14.3%)为高风险,10例(0.9%)为极高风险。中位随访时间为 54.8 个月(四分位数范围 24.6-81.8)。共有 197 名患者 (18.4%) 死亡,718 名患者 (67.3%) 发展为 CTRCD(有症状:n = 45;中度至重度无症状:n = 24;轻度无症状:n = 649)。随着 HFA-ICOS 评分的增加,有症状或中度至重度症状 CTRCD 的发生率和全因死亡率显着增加 [风险比 28.74,95% 置信区间 (CI) 9.33-88.5; P < .001,风险比 7.43,95% CI 3.21-17.2; P < .001) 对于极高危患者。该预测模型在预测症状方面表现出良好的校准(Brier 评分 0.04,95% CI 0.03-0.05)和辨别力(曲线下面积 0.78,95% CI 0.70-0.82;Uno 的 C 统计量 0.78,95% CI 0.71-0.84)或 12 个月时重度/中度无症状 CTRCD。HFA-ICOS 评分可根据心血管毒性风险对患者进行有效分类,并显示出对高风险蒽环类药物相关心血管毒性和全因死亡率的强大预测能力。© 作者 2024。由牛津大学出版社代表欧洲心脏病学会出版。版权所有。如需商业重复使用,请联系 reprints@oup.com 获取转载和转载的翻译权。所有其他权限都可以通过我们网站文章页面上的权限链接通过我们的 RightsLink 服务获得 - 如需了解更多信息,请联系journals.permissions@oup.com。
Baseline cardiovascular toxicity risk stratification is critical in cardio-oncology. The Heart Failure Association (HFA) and International Cardio-Oncology Society (ICOS) score aims to assess this risk but lacks real-life validation. This study validates the HFA-ICOS score for anthracycline-induced cardiovascular toxicity.Anthracycline-treated patients in the CARDIOTOX registry (NCT02039622) were stratified by the HFA-ICOS score. The primary endpoint was symptomatic or moderate to severe asymptomatic cancer therapy-related cardiac dysfunction (CTRCD), with all-cause mortality and cardiovascular mortality as secondary endpoints.The analysis included 1066 patients (mean age 54 ± 14 years; 81.9% women; 24.5% ≥65 years). According to the HFA-ICOS criteria, 571 patients (53.6%) were classified as low risk, 333 (31.2%) as moderate risk, 152 (14.3%) as high risk, and 10 (0.9%) as very high risk. Median follow-up was 54.8 months (interquartile range 24.6-81.8). A total of 197 patients (18.4%) died, and 718 (67.3%) developed CTRCD (symptomatic: n = 45; moderate to severe asymptomatic: n = 24; and mild asymptomatic: n = 649). Incidence rates of symptomatic or moderate to severe symptomatic CTRCD and all-cause mortality significantly increased with HFA-ICOS score [hazard ratio 28.74, 95% confidence interval (CI) 9.33-88.5; P < .001, and hazard ratio 7.43, 95% CI 3.21-17.2; P < .001) for very high-risk patients. The predictive model demonstrated good calibration (Brier score 0.04, 95% CI 0.03-0.05) and discrimination (area under the curve 0.78, 95% CI 0.70-0.82; Uno's C-statistic 0.78, 95% CI 0.71-0.84) for predicting symptomatic or severe/moderate asymptomatic CTRCD at 12 months.The HFA-ICOS score effectively categorizes patients by cardiovascular toxicity risk and demonstrates strong predictive ability for high-risk anthracycline-related cardiovascular toxicity and all-cause mortality.© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.