Case Presentation: A 62-year-old male with a history of colon cancer status post partial colectomy and initiation of Capecitabine two days prior presented to the emergency department with one day of severe episodic chest pain radiating to the back. The chest pain was increasing in frequency and relieved by sublingual nitroglycerin. He denied any prior history of similar chest pain or coronary artery disease. Upon admission, he experienced another episode of chest pain, and an accompanying electrocardiogram (ECG) demonstrated clear ST-segment elevations in inferolateral leads. He received another dose of nitroglycerin and repeat ECGs showed dynamic changes, first with inferolateral ST-segment depressions followed by a return to baseline. Cardiology recommended loading with aspirin and beginning a heparin drip. Later, he experienced another episode of chest pain and ST elevations on ECG, which was now unrelieved by nitroglycerin, so an intravenous nitroglycerin drip was initiated. Throughout this, he had only mildly elevated high-sensitivity troponin, peaking at 82 ng/L. Given his ST changes, cardiology classified him as a true ST-elevation myocardial infarction (STEMI), and he was emergently taken for a coronary angiogram, which revealed no evidence of obstructive coronary artery disease (CAD). He was ultimately diagnosed with Capecitabine-induced coronary vasospasm. Capecitabine was discontinued, and he was started on nifedipine. He has had no recurrence of chest pain or vasospastic symptoms.
Discussion: Fluoropyrimidines, namely 5-fluorouracil (5-FU), are known to cause cardiotoxicity, including coronary vasospasm. However, this is less frequently reported with its pro-drug Capecitabine, a chemotherapeutic agent used to treat colorectal and breast cancers. While this association may be more recognized among oncologists, it remains less recognized in other fields, such as hospital medicine and cardiology. Coronary vasospasm itself is a rarer presentation of cancer-therapeutics related cardiotoxicity, occurring less frequently than heart failure or hypertension. This case highlights an important rare and underrecognized presentation of a medication toxicity that can mimic emergent life-threatening conditions such as acute coronary syndromes, including frank STEMI as described. In reported cases, coronary vasospasm typically occurs within the first week of therapy initiation, which we saw here as well. Clinicians should consider this diagnosis in patients recently initiated on Capecitabine who present to the hospital with new-onset chest pain, particularly when dynamic ECG changes are present. It remains a diagnosis of exclusion and requires a coronary angiogram to rule out obstructive atherosclerotic CAD. Management of Capecitabine-induced coronary vasospasm involves discontinuation of the drug and initiation of a dihydropyridine calcium-channel blocker.
Conclusions: Capecitabine-induced coronary vasospasm is an underrecognized cardiotoxicity that can mimic life-threatening cardiac conditions, including STEMI. While coronary angiogram is still required in these patients to rule out CAD, recognition of this adverse effect of Capecitabine is important for timely and appropriate management.