Introduction: Vasospastic angina is a clinical entity characterized by resting thoracic pain with ischemia ST segment modifications on electrocardiogram. Approxi-mately 2% of unstable angina pectoris clinical presen-tations are patients with pure vasospastic angina, more frequently young adults, men, smokers.In the context of increasing usage of oncological medication, we draw attention to a new category of trigger factors of coro-nary spasm: cytotoxic medication.
Methods: We will present the clinical case of a 63-year-old, hypertensive, obese, with stage 4 rectosigmoid adenocarcinoma, treated with chemotherapy (Capecitabine 500mg x7pills/day for 14 days) symptomatic on day 7 of treatment with retrosternal pain. During chest pain, electrocardiogram recorded transient elevation of ST segment (2-3 mm in lateral territory), followed by an immediate rise of Troponin I. Under conventional treatment and with non-cardiological medication wi-thdrawal, the patient becomes asymptomatic. The ove-rall assessment of the patient was performed through bio-humoral balance, ECG, transthoracic echocardio-graphy. The evaluation of ischemia after stabilization was initially performed by exercise testing on the cycle-ergometer, followed by coronarography.
Results: Intercritical electrocardiogram recorded si-nus rhythm 60 bpm; QRS Axis -20°; without ischemic changes. The echocardiographic exam reveals concen-tric hypertrophy of the left ventricle, with a globally preserved systolic function, grade I diastolic dysfunc-tion, with no segmental kinetics disorder. Exercise testing at the cycle ergometer was negative for angina pectoris and myocardial ischemia. Coronary angiogra-phy found an isolated focal stenosis (50%) on a small diagonal artery. The clinical and bio-humoral profile of the patient (male, elderly, hypertensive, obese, dyslipi-demic) along with the recently episode of ischemic in-stability would suggest the typical pattern of significant coronary atherosclerotic lesions.
Conclusions: Surprisingly, the patient did not develop pain or ischemia during the stress test, and the coro-narography did not detect significant hemodynamic lesions. Corroborating clinical, paraclinical and anam-nestic information, we considered that the transient se-vere myocardial ischemia was the result of coronay va-sospasm. We reviewed the oncological treatment of the patient who included Capecitabine.The sudden disap-pearance of the clinical picture after cessation of Cape-citabine and history of vasospasm reported in patients using this treatment has strengthened the hypothesis of iatrogenic vasospasm. Between January 2009 and June 2019, 21 cases of coronary vasospasm caused by Cape-citabine were reported in the english literature (Sear-ched on Pubmed, Keywords: capecitabine, vasospasm).