Maciej Kabat, Roma Padalkar, Sara Hazaveh, Vladimir Joseph, David Feigenblum, Sean Sadikot
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In this report, we present a case of capecitabine-induced coronary vasospasm leading to progressive, focal ST-elevations, myocardial ischemia, and subsequently polymorphic ventricular tachycardia. These events were captured on telemetry, in a male in his early 40s, diagnosed with stage IIIB sigmoid colon cancer. Notably, the patient had no pre-existing coronary artery disease or other cardiovascular risk factors. Upon diagnosis, the patient was initiated on a calcium channel blocker, verapamil, to mitigate further coronary vasospasm events. After thorough discussions that prioritized the patient's input and values, an implantable cardioverter-defibrillator was placed subcutaneously. Following discharge, the patient restarted capecitabine therapy along with verapamil prophylaxis and did not experience any subsequent shocks from his ICD as assessed during his outpatient follow-up visits. 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引用次数: 0
摘要
卡培他滨是 5-氟尿嘧啶的原研药,常用于治疗乳腺癌和结直肠癌。其副作用包括恶心、呕吐、腹泻、乏力、食欲不振和骨髓抑制,这些副作用已得到广泛认可。然而,冠状动脉血管痉挛是以氟嘧啶为基础的疗法(如卡培他滨)的一种不太常见但却很重要的并发症。这种不良反应并发症的拟议机制包括直接的内皮依赖性血管收缩、激活蛋白激酶 C 和激活环氧化酶途径。在本报告中,我们介绍了一例卡培他滨诱导的冠状动脉血管痉挛导致进行性、局灶性 ST 抬高、心肌缺血以及随后的多形性室性心动过速的病例。这些事件是通过遥测技术捕捉到的,患者是一名 40 岁出头的男性,被诊断为乙状结肠癌 IIIB 期。值得注意的是,患者之前没有冠状动脉疾病或其他心血管风险因素。确诊后,患者开始服用钙通道阻滞剂维拉帕米,以减轻进一步的冠状动脉血管痉挛事件。经过充分讨论并优先考虑患者的意见和价值观后,皮下植入了植入式心律转复除颤器。出院后,患者重新开始了卡培他滨治疗和维拉帕米预防治疗,根据门诊随访评估,ICD 没有再发生电击。本病例强调了让患者参与决策过程的必要性,尤其是在处理意外和严重并发症时,以确保治疗符合患者的生活质量和个人偏好。
Capecitabine-induced-coronary-vasospasm leading to polymorphic ventricular tachycardia and cardiac arrest.
Capecitabine, a pro-drug of 5-fluorouracil, is commonly used in the treatment of breast and colorectal cancer. Its side effects, including nausea, vomiting, diarrhea, fatigue, loss of appetite, and bone marrow suppression, are well recognized. However, coronary vasospasm represents a less commonly recognized but significant complication of fluoropyrimidine-based therapies such as capecitabine. Proposed mechanisms for this adverse effect complication include direct endothelium-independent vasoconstriction, activation of protein kinase C, and activation of the cyclooxygenase pathway. In this report, we present a case of capecitabine-induced coronary vasospasm leading to progressive, focal ST-elevations, myocardial ischemia, and subsequently polymorphic ventricular tachycardia. These events were captured on telemetry, in a male in his early 40s, diagnosed with stage IIIB sigmoid colon cancer. Notably, the patient had no pre-existing coronary artery disease or other cardiovascular risk factors. Upon diagnosis, the patient was initiated on a calcium channel blocker, verapamil, to mitigate further coronary vasospasm events. After thorough discussions that prioritized the patient's input and values, an implantable cardioverter-defibrillator was placed subcutaneously. Following discharge, the patient restarted capecitabine therapy along with verapamil prophylaxis and did not experience any subsequent shocks from his ICD as assessed during his outpatient follow-up visits. This case emphasizes the need to involve patients in decision-making processes, especially when managing unexpected and serious complications, to ensure treatments align with their quality of life and personal preferences.