Abstract

Case Description: A 49-year-old male with recent diagnosis of rectal cancer presented to ED for chest tightness, which had never experienced before. He had started Capecitabine for chemotherapy three days before. The patient had no history of CV disease or risk factors, was a never smoker and never used illicit substances. He is a SWAT/police officer who runs an 8-minute mile every morning without problems. In ED, was initially chest pain free. ECG with 1 mm ST segment depressions in V1 - V3. Five hours later, developed chest tightness again, and ECG revealed diffuse ST-elevations. Was started on nitroglycerin drip and admitted for monitoring. His chest tightness and ST segment elevations resolved completely. High-sensitivity troponin T was initially 37, and down trended to 27 over 4 hours. He was transitioned to long-acting Nifedipine. The chest tightness did not recur and was discharged with discontinuation of Capecitabine. Outpatient CTA of coronary arteries and echocardiogram were normal. A diagnosis of coronary artery vasospasm secondary to Capecitabine was confirmed. Discussion: Coronary artery vasospasm is the most common cardiotoxic effect of Capecitabine. It happens more frequently during the first three doses and can occur in patients with no hx of CV risk factors. The management consists of discontinuation of the medication. Long-acting CCB can be used for prevention. CTA of coronaries can be used to assess patients at low-to-intermediate risk of CAD.

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