PDF(Pubmed)
Abstract：
BACKGROUND Capecitabine and other 5-fluorouracil prodrugs are medications widely employed in treating solid tumors, including breast and colorectal cancer. However, they carry a notable risk for cardiotoxicity, including coronary vasospasm, possibly related to their impact on vascular endothelium and smooth muscle. CASE REPORT We present a case of a 45-year-old male with a pancreatic neuroendocrine tumor who developed exertional chest pain after starting capecitabine. Initial evaluations in the emergency department, including a 12-lead electrocardiogram and cardiac enzymes, were normal, but suspicion for coronary vasospasm persisted due to the temporal relationship with drug initiation and symptom characteristics. A graded exercise test reproduced his symptoms, accompanied by hyperacute peaked T waves and subsequent ST segment elevations in the inferior leads. Coronary angiography revealed patent coronary arteries, rendering provocative testing unnecessary due to a high clinical suspicion of capecitabine-induced vasospasm. Discontinuing the patient\'s medication was a more efficient approach than continuing additional cardiac workup while the drug was still administered. After multidisciplinary discussion, capecitabine was discontinued, leading to symptom resolution and a negative repeat graded exercise test. CONCLUSIONS This case underscores the potential for capecitabine to induce coronary artery vasospasm, emphasizing the importance of prompt medication cessation. Patients receiving capecitabine therapy and experiencing chest pain should undergo an evaluation with consideration of capecitabine-induced vasospasm in the differential diagnosis. Prompt recognition and medication cessation are critical to prevent serious cardiovascular complications including death. In our patient, discontinuing capecitabine resolved his symptoms, emphasizing the significance of discontinuing the causative drug and seeking alternative chemotherapy regimens.
摘要：
背景技术卡培他滨和其他5-氟尿嘧啶前药是广泛用于治疗实体瘤的药物。包括乳腺癌和结肠直肠癌.然而,它们具有明显的心脏毒性风险，包括冠状动脉痉挛,可能与它们对血管内皮和平滑肌的影响有关。病例报告我们介绍了一例45岁男性胰腺神经内分泌肿瘤，在开始卡培他滨后出现劳力性胸痛。急诊科的初步评估，包括12导联心电图和心肌酶，是正常的，但是，由于与药物起始和症状特征的时间关系，仍然怀疑冠状动脉痉挛。分级运动测试再现了他的症状，伴有超急性峰值T波和随后的下导联ST段抬高。冠状动脉造影显示冠状动脉未闭,由于临床高度怀疑卡培他滨引起的血管痉挛，因此无需进行挑衅性测试。停止患者的药物治疗是比继续额外的心脏检查更有效的方法。经过多学科的讨论，卡培他滨停药,导致症状解决和阴性重复分级运动测试。结论本病例强调卡培他滨可能诱发冠状动脉血管痉挛，强调迅速停止用药的重要性。接受卡培他滨治疗并经历胸痛的患者应在鉴别诊断中考虑卡培他滨引起的血管痉挛进行评估。及时识别和停药对于预防包括死亡在内的严重心血管并发症至关重要。在我们的病人身上，停止卡培他滨缓解了他的症状，强调停止致病药物和寻求替代化疗方案的重要性。
