Assessment of echocardiography and biomarkers for the extended prediction of cardiotoxicity in patients treated with anthracyclines, taxanes, and trastuzumab.
Assessment of echocardiography and biomarkers for the extended prediction of cardiotoxicity in patients treated with anthracyclines, taxanes, and trastuzumab.
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DOI：
10.1161/circimaging.112.973321
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发表时间：
2012-09-01
期刊：
影响因子：
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通讯作者：
Scherrer-Crosbie M
中科院分区：
文献类型：
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作者：
Sawaya H;Sebag IA;Plana JC;Januzzi JL;Ky B;Tan TC;Cohen V;Banchs J;Carver JR;Wiegers SE;Martin RP;Picard MH;Gerszten RE;Halpern EF;Passeri J;Kuter I;Scherrer-Crosbie M
由于癌症患者存活时间更长，与使用癌症治疗相关的心脏毒性的影响也在加剧。本研究调查了在蒽环类药物、紫杉烷和曲妥珠单抗治疗期间，心肌应变和血液生物标志物的早期改变是否能预测乳腺癌患者发生的心脏毒性。81名新诊断为人类表皮生长因子受体2阳性乳腺癌的妇女，接受蒽环类药物治疗，随后接受紫杉烷和曲妥珠单抗治疗，在癌症治疗期间（共15个月）每3个月使用超声心动图和血液样本进行评估。计算左心室射血分数、收缩峰值纵向、径向和周向心肌应变。同时检测超敏肌钙蛋白I、n端前b型利钠肽和白细胞介素家族成员（ST2）。左心室射血分数在15个月内下降（64±5%至59±6%；P<0.0001）。26名患者（32%,[22%-43%]）出现心脏毒性（心脏审查和评估委员会对曲妥珠单抗的定义）；在这些患者中，5例（6%,[2%-14%]）有心力衰竭症状。蒽环类药物治疗结束时心肌收缩纵向应变峰值和超敏肌钙蛋白I预测心脏毒性的后续发展；左室射血分数、n端前b型利钠肽和ST2无显著相关性。在所有后来发生心力衰竭的患者中，纵向应变<19%。在接受蒽环类药物、紫杉烷和曲妥珠单抗治疗的乳腺癌患者中，在蒽环类药物治疗完成时测量收缩纵向心肌应变和超敏感肌钙蛋白I有助于预测随后的心脏毒性，并可能有助于指导治疗以避免心脏副作用。
Because cancer patients survive longer, the impact of cardiotoxicity associated with the use of cancer treatments escalates. The present study investigates whether early alterations of myocardial strain and blood biomarkers predict incident cardiotoxicity in patients with breast cancer during treatment with anthracyclines, taxanes, and trastuzumab. Eighty-one women with newly diagnosed human epidermal growth factor receptor 2–positive breast cancer, treated with anthracyclines followed by taxanes and trastuzumab were enrolled to be evaluated every 3 months during their cancer therapy (total of 15 months) using echocardiograms and blood samples. Left ventricular ejection fraction, peak systolic longitudinal, radial, and circumferential myocardial strain were calculated. Ultrasensitive troponin I, N-terminal pro–B-type natriuretic peptide, and the interleukin family member (ST2) were also measured. Left ventricular ejection fraction decreased (64 ± 5% to 59 ± 6%; P<0.0001) over 15 months. Twenty-six patients (32%, [22%–43%]) developed cardiotoxicity as defined by the Cardiac Review and Evaluation Committee Reviewing Trastuzumab; of these patients, 5 (6%, [2%–14%]) had symptoms of heart failure. Peak systolic longitudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines treatment predicted the subsequent development of cardiotoxicity; no significant associations were observed for left ventricular ejection fraction, N-terminal pro–B-type natriuretic peptide, and ST2. Longitudinal strain was <19% in all patients who later developed heart failure. In patients with breast cancer treated with anthracyclines, taxanes, and trastuzumab, systolic longitudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines therapy are useful in the prediction of subsequent cardiotoxicity and may help guide treatment to avoid cardiac side-effects.