Voß Fabian, Nienhaus Fabian, Pietrucha Saskia, Ruckhäberle Eugen, Fehm Tanja, Melz Tobias, Cramer Mareike, Haberkorn Sebastian M, Flögel Ulrich, Westenfeld Ralf, Scheiber Daniel, Jung Christian, Kelm Malte, Polzin Amin, Bönner Florian
Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Hospital Düsseldorf, Moorenstr. 5, 40225, Düsseldorf, Germany.
Division of Gynecology, Medical Faculty, University Hospital Düsseldorf, Düsseldorf, Germany.
Cardiooncology. 2024 Jul 16;10(1):43. doi: 10.1186/s40959-024-00244-y.
Cancer therapy-related cardiac dysfunction (CTRCD) is a dreaded complication of anthracycline therapy. CTRCD most frequently appears in patients with cardiovascular risk factors (CVR) or known cardiovascular disease. However, limited data exist on incidence and course of anthracycline-induced CTRCD in patients without preexisting risk factors. We therefore aimed to longitudinally investigate a cohort of young women on anthracycline treatment due to breast cancer without cardiovascular risk factors or known cardiovascular disease (NCT03940625).
We enrolled 59 women with primary breast cancer and scheduled anthracycline-based therapy, but without CVR or preexisting cardiovascular disease. We conducted a longitudinal assessment before, immediately and 12 months after cancer therapy with general laboratory, electrocardiograms, echocardiography and cardiovascular magnetic resonance (CMR), including myocardial relaxometry with T1, T2 and extracellular volume mapping. Every single patient experienced a drop in CMR-measured left ventricular ejection fraction (LVEF) of 6 ± 3% immediately after cancer therapy. According to the novel definition 32 patients (54.2%) developed CTRCD after 12 months defined by reduction in LVEF, global longitudinal strain (GLS) and/or biomarkers elevation, two of them were symptomatic. Global myocardial T2 relaxation times as well as myocardial mass increased coincidently with a decline in wall-thickening. While T2 values and myocardial mass normalized after 12 months, LVEF and GLS remained impaired.
In every single patient anthracyclines induce a decline of myocardial contractility, even among patients without pre-existing risk factors for CTRCD. Our data suggest to thoroughly evaluate whether this may lead to an increased risk of future cardiovascular events.
癌症治疗相关的心脏功能障碍（CTRCD）是蒽环类药物治疗可怕的并发症。CTRCD最常出现在有心血管危险因素（CVR）或已知心血管疾病的患者中。然而，关于无既往危险因素的患者中蒽环类药物所致CTRCD的发生率和病程的数据有限。因此，我们旨在对一组因乳腺癌接受蒽环类药物治疗且无心血管危险因素或已知心血管疾病的年轻女性进行纵向研究（NCT03940625）。
我们纳入了59例原发性乳腺癌且计划接受蒽环类药物治疗，但无CVR或既往心血管疾病的女性。我们在癌症治疗前、治疗即刻及治疗后12个月进行了纵向评估，包括一般实验室检查、心电图、超声心动图和心血管磁共振（CMR），其中CMR包括用T1、T2和细胞外容积成像进行心肌弛豫测量。每例患者在癌症治疗后即刻CMR测量的左心室射血分数（LVEF）均下降了6±3%。根据新定义，32例患者（54.2%）在12个月后发生了CTRCD，定义为LVEF降低、整体纵向应变（GLS）降低和/或生物标志物升高，其中2例有症状。整体心肌T2弛豫时间以及心肌质量随着室壁增厚的下降而同时增加。虽然T2值和心肌质量在12个月后恢复正常，但LVEF和GLS仍受损。
即使在无CTRCD既往危险因素的患者中，蒽环类药物也会导致每例患者心肌收缩力下降。我们的数据表明，应全面评估这是否可能导致未来心血管事件风险增加。
