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Background: Capecitabine and other 5-fluorouracil prodrugs are medications widely employed in treating solid tumors, including breast and colorectal cancer. However, they carry a notable risk for cardiotoxicity, including coronary vasospasm, possibly related to their impact on vascular endothelium and smooth muscle. Case Report: We present a case of a 45-year-old male with a pancreatic neuroendocrine tumor who developed exertional chest pain after starting capecitabine. Initial evaluations in the emergency department, including a 12-lead electrocardiogram and cardiac enzymes, were normal, but suspicion for coronary vasospasm persisted due to the temporal relationship with drug initiation and symptom characteristics. A graded exercise test reproduced his symptoms, accompanied by hyperacute peaked T waves and subsequent ST segment elevations in the inferior leads. Coronary angiography revealed patent coronary arteries, rendering provocative testing unnecessary due to a high clinical suspicion of capecitabine-induced vasospasm. Discontinuing the patient's medication was a more efficient approach than continuing additional cardiac workup while the drug was still administered. After multidisciplinary discussion, capecitabine was discontinued, leading to symptom resolution and a negative repeat graded exercise test. Conclusions: This case underscores the potential for capecitabine to induce coronary artery vasospasm, emphasizing the importance of prompt medication cessation. Patients receiving capecitabine therapy and experiencing chest pain should undergo an evaluation with consideration of capecitabine-induced vasospasm in the differential diagnosis. Prompt recognition and medication cessation are critical to prevent serious cardiovascular complications including death. In our patient, discontinuing capecitabine resolved his symptoms, emphasizing the significance of discontinuing the causative drug and seeking alternative chemotherapy regimens. [ABSTRACT FROM AUTHOR]

Acute coronary syndrome (ACS) is a rare cause of chest pain in adolescents and young adults. Kawasaki disease (KD) is an uncommon illness, but coronary artery aneurysms secondary to KD are implicated in approximately 5% of cases of ACS in young adults. Patients with KD may present with catastrophic coronary disease at a young age and thus early recognition of this disease process and lifelong follow-up is essential. Here we discuss a 19-year-old active duty male with no previously recognized medical history who presented with crushing chest pain while deployed. He was diagnosed with an ST elevation myocardial infarction and was found to have a giant aneurysm of the left main coronary artery with obstructive thrombus treated with emergent thrombectomy and balloon angioplasty. He developed cardiogenic shock requiring mechanical circulatory and ventilatory support. After a prolonged recovery and more in-depth history-taking, he was discovered to have been diagnosed with KD as a child without follow-up. Diagnosing ACS in young adults can be challenging, but a history of KD should increase suspicion for coronary disease. This case demonstrates the importance of screening after a childhood diagnosis of KD, specifically when caring for the tactical athlete. It also highlights the impact that social determinants of health can have on patient outcomes. Finally, it demonstrates the importance of communication and coordination between military and civilian medical centers across the globe driving the care of our deployed injured and ill active-duty military personnel., (© The Association of Military Surgeons of the United States 2024. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site–for further information please contact journals.permissions@oup.com.)

When the atrioventricular node is damaged, accessory pathways can perform primary atrioventricular conduction but may spontaneously degrade during childhood. After surgical atrial septal defect repair during infancy, an adolescent male presented with fatigue due to iatrogenic complete atrioventricular node block with a degrading antegrade accessory pathway resulting in symptomatic bradyarrhythmia.