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A case of chemoradiotherapy-associated cardiotoxicity that developed into acute heart failure with progressive subendocardial fibrosis

机译:一例与放化疗相关的心脏毒性反应发展为急性心力衰竭并进行性心内膜下纤维化

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摘要

We describe the case of a 61-year-old Japanese woman who developed acute heart failure 5 years after chemoradiotherapy for breast cancer. The patient received less than the cardiotoxic dose of docetaxel, epirubicin, cyclophosphamide, and fluorouracil and experienced no cardiovascular complications in the 5 years between the onset of chemoradiotherapy and the onset of acute heart failure. Cardiac catheterization was performed and elevation of end diastolic pressure of both ventricles was observed. Endomyocardial biopsy showed progressive replacement fibrosis in the subendocardium. Normal thickness of the right endocardium is <20 μm. Surprisingly, our patient had a fibrous subendocardium that was 100–200 μm thick. Ultrastructural abnormalities similar to those observed in anthracycline cardiotoxicity were evident on electron micrographs. This case report demonstrates the unique pathophysiology of heart failure in a patient who received less than the cardiotoxic dose of antineoplastic agents. Recent protocols have decreased the dosage of cardiotoxic agents; however, even these reduced doses might not be safe for all Japanese individuals and may cause subclinical cardiovascular damage and late-onset heart failure. Clinicians should monitor cancer survivors carefully, even if antineoplastic agents were administered under the cardiotoxic dose.<>Learning objective: Intensive chemotherapy is commonly used to treat cancer patients. Recent protocols have decreased the dose of cardiotoxic agents; however, even these reduced doses might not be safe and may cause subclinical cardiovascular damage and late-onset heart failure. Clinicians should monitor cancer survivors carefully, even if antineoplastic agents were administered under the toxic dose.>
机译:我们描述了一名61岁的日本妇女在乳腺癌放化疗后5年出现急性心力衰竭的案例。该患者接受的化疗药物剂量低于多西他赛,表柔比星,环磷酰胺和氟尿嘧啶,并且在放化疗和急性心力衰竭发作之间的5年内没有发生心血管并发症。进行了心脏导管检查,观察到两个心室的舒张末期压力升高。心内膜活检显示心内膜下进行性置换纤维化。右心内膜的正常厚度为<20μm。令人惊讶的是,我们的患者的纤维内膜下层厚度为100-200μm。在电子显微照片上明显可见与蒽环类药物心脏毒性相似的超微结构异常。该病例报告证明了接受少于抗肿瘤剂心脏毒性剂量的患者心力衰竭的独特病理生理。最近的方案减少了心脏毒性剂的剂量。但是,即使这些减少的剂量对所有日本人来说也不是安全的,并且可能导致亚临床心血管损害和迟发性心力衰竭。即使抗肿瘤药是在心脏毒性剂量下给药,临床医生也应仔细监测癌症幸存者。 strong>学习目标:密集化疗通常用于治疗癌症患者。最近的方案已经减少了心脏毒性剂的剂量。但是,即使这些减少的剂量也可能并不安全,并且可能导致亚临床心血管损害和迟发性心力衰竭。即使抗肿瘤药以毒性剂量给药,临床医生也应仔细监测癌症幸存者。

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