Vasospastic Angina Following Capecitabine Initiation: A Rare but Serious Cardiotoxic Effect

BACKGROUND Fluoropyrimidines are widely used chemotherapy agents in the treatment of solid tumors, particularly colorectal cancer (CRC). The cardiotoxic effect most commonly associated with 5-fluorouracil (5-FU) is coronary vasospasm, which typically occurs within the first hours or days following administration and can present with a spectrum of manifestations ranging from stable angina to acute coronary syndrome with hemodynamic instability. Capecitabine, a prodrug of 5-FU, has less defined cardiovascular side effects. CASE REPORT A 66-year-old man with lower rectal adenocarcinoma, receiving capecitabine, presented with chest pain and diaphoresis 48 h after starting therapy. Initial electrocardiogram (ECG) showed new biphasic T waves. During evaluation, he developed recurrent chest pain and hyperacute T waves in repeat ECG. Nitroglycerin relieved symptoms and normalized ECG changes. Suspecting high-risk Non-ST Elevation Acute Coronary Syndrome, he was admitted and underwent coronary angiography, which showed no obstructive coronary disease. However, acetylcholine provocation induced severe focal vasospasm with corresponding symptoms and ischemic ECG changes, confirming vasospastic angina. Echocardiography revealed normal left ventricular function. Capecitabine was discontinued, and the patient was treated with calcium channel blockers and nitrates. He was discharged after five days and remained symptom-free at follow-up. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians should suspect fluoropyrimidine-induced cardiotoxicity in patients with chest pain after starting capecitabine, even without cardiac risk factors. Early recognition, drug discontinuation, and vasodilator therapy are critical to prevent serious complications and ensure timely cardiology-oncology coordination.