The following is a summary of “Capecitabine-induced-coronary-vasospasm leading to polymorphic ventricular tachycardia and cardiac arrest,” published in the February 2024 issue of Oncology by Kabat et al.

Capecitabine, a pro-drug of 5-fluorouracil, stands as a cornerstone in the treatment regimens for breast and colorectal cancer. While its adverse effects like nausea, vomiting, and fatigue are widely recognized, the incidence of coronary vasospasm represents a lesser-known but significant complication associated with fluoropyrimidine-based therapies, including capecitabine. 

Proposed mechanisms underlying this complication encompass direct endothelium-independent vasoconstriction, activation of protein kinase C, and stimulation of the cyclooxygenase pathway. Herein, the researchers present a compelling case of capecitabine-induced coronary vasospasm culminating in progressive ST elevations, myocardial ischemia, and subsequent polymorphic ventricular tachycardia. These events transpired in a male patient in his early 40s, diagnosed with stage IIIB sigmoid colon cancer, devoid of pre-existing coronary artery disease or cardiovascular risk factors. Prompt intervention involved initiating calcium channel blocker therapy with verapamil to mitigate further coronary vasospasm episodes. 

Following comprehensive discussions prioritizing the patient’s input and values, implantation of a subcutaneous cardioverter-defibrillator was undertaken. Subsequent outpatient follow-up visits revealed the resumption of capecitabine therapy alongside verapamil prophylaxis, with the patient remaining free from subsequent defibrillator shocks. This case underscores the imperative of involving patients in decision-making processes, particularly when addressing unexpected and severe complications, to ensure treatment strategies align with their quality of life and personal preferences.

Source: cardiooncologyjournal.biomedcentral.com/articles/10.1186/s40959-024-00214-4