Your browser doesn't support javascript.
loading
Atherosclerosis Vindicated: A Case of Chest Pain Due to Capecitabine-Induced Coronary Artery Spasm.
Thomesen, Kaitlyn; Kisling, Adam; Conte, Lisa; Park, Dean; Gallagher, Robert.
Affiliation
  • Thomesen K; Internal Medicine Residency Program, National Capital Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA.
  • Kisling A; Department of Cardiology, National Capital Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA.
  • Conte L; Department of Cardiology, National Capital Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA.
  • Park D; Department of Hematology and Oncology, National Capital Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA.
  • Gallagher R; Department of Cardiology, National Capital Consortium, Walter Reed National Military Medical Center, Bethesda, MD, USA.
Am J Case Rep ; 25: e941759, 2024 Jan 13.
Article in En | MEDLINE | ID: mdl-38217283
ABSTRACT
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Coronary Vasospasm / Atherosclerosis Type of study: Diagnostic_studies Limits: Humans / Male / Middle aged Language: En Journal: Am J Case Rep / The American journal of case reports Year: 2024 Document type: Article Affiliation country: Estados Unidos Country of publication: Estados Unidos

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Coronary Vasospasm / Atherosclerosis Type of study: Diagnostic_studies Limits: Humans / Male / Middle aged Language: En Journal: Am J Case Rep / The American journal of case reports Year: 2024 Document type: Article Affiliation country: Estados Unidos Country of publication: Estados Unidos