Dyhl-Polk Anne, Schou Morten, Vistisen Kirsten K, Sillesen Anne-Sophie, Bojesen Stig E, Faber Jens, Vaage-Nilsen Merete, Nielsen Dorte L
Department of Oncology, Herlev-Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark.
Department of Cardiology, Herlev-Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Acta Oncol. 2025 Jul 2;64:837-847. doi: 10.2340/1651-226X.2025.43089.
Treatment with fluoropyrimidines can lead to cardiotoxicity. For 5-fluorouracil, silent myocardial ischemia and effort-related myocardial ischemia have been demonstrated. We investigated the incidence of myocardial ischemia and clinical cardiotoxicity during treatment with capecitabine, a pro-drug of 5-fluorouracil.
We included patients with breast- or colorectal cancer, who received first-time treatment with capecitabine. Holter recording, clinical evaluation, 12-lead electrocardiogram, and measurement of plasma cardiac troponin I and copeptin were performed before and during treatment.
A total of 42 patients with breast cancer and 39 with colorectal cancer were included. Seven patients (9%) experienced clinical cardiotoxicity; five with unstable angina, one with dyspnoea, ST elevations and anterolateral hypokinesia, and one with cardiac arrest. Six patients (8%) had myocardial ischemia on Holter recording during treatment. Among these were two with clinical cardiotoxicity, and four (5.0%) with silent myocardial ischemia. More patients had myocardial ischemia on Holter recording during treatment compared to before, but the difference was not statistically significant (1st cycle: p = 0.22, 3rd/4th cycle: p = 0.50). Plasma copeptin increased during 1st cycle (p = 0.004), while cardiac troponin I remained unchanged (p = 0.92). More patients had non-sustained ventricular tachycardia during 1st cycle of treatment than before (p = 0.020).
Treatment with capecitabine was associated with an incidence of myocardial ischemia of 8%, an incidence of clinical cardiotoxicity of 9%, and an increase in plasma copeptin and the frequency of non-sustained ventricular tachycardia episodes. Increases in cardiac troponin I were rare. The incidence of myocardial ischemia was lower than previously reported for 5-fluorouracil.
氟嘧啶治疗可导致心脏毒性。对于5-氟尿嘧啶,已证实存在无症状性心肌缺血和劳力性心肌缺血。我们调查了5-氟尿嘧啶前体药物卡培他滨治疗期间心肌缺血和临床心脏毒性的发生率。
我们纳入了首次接受卡培他滨治疗的乳腺癌或结直肠癌患者。在治疗前及治疗期间进行动态心电图记录、临床评估、12导联心电图检查以及血浆心肌肌钙蛋白I和 copeptin的测定。
共纳入42例乳腺癌患者和39例结直肠癌患者。7例患者(9%)出现临床心脏毒性;5例为不稳定型心绞痛,1例伴有呼吸困难、ST段抬高和前外侧运动减弱,1例发生心脏骤停。6例患者(8%)在治疗期间动态心电图记录显示有心肌缺血。其中2例有临床心脏毒性,4例(5.0%)为无症状性心肌缺血。与治疗前相比,更多患者在治疗期间动态心电图记录显示有心肌缺血,但差异无统计学意义(第1周期:p = 0.22,第3/4周期:p = 0.50)。血浆copeptin在第1周期升高(p = 0.004),而心肌肌钙蛋白I保持不变(p = 0.92)。与治疗前相比,更多患者在第1周期治疗期间出现非持续性室性心动过速(p = 0.020)。
卡培他滨治疗与8%的心肌缺血发生率、9%的临床心脏毒性发生率以及血浆copeptin升高和非持续性室性心动过速发作频率增加相关。心肌肌钙蛋白I升高罕见。心肌缺血发生率低于先前报道的5-氟尿嘧啶。