Cilj: naglasiti teške nuspojave kapecitabina i spriječiti pogrešnu dijagnozu u bolesnika s
akutnim koronarnim sindromom (AKS). Metode: prikazujemo slučaj 74-godišnje bolesnice s adenokarcinomom
gušterače koja je u bolnicu primljena s kliničkom slikom AKS-a induciranim uporabom kapecitabina.
Primljena je u hitnu službu zbog epizode pritiska u prsima. Liječenje oralnim kapecitabinom
(2500 mg na dan) započeto je 72 sata prije prijema. Imala je elektrokardiografske (EKG) promjene
i pozitivne biokemijske markere miokardne ishemije (uključujući visokoosjetljivi kardijalni troponin
T; hs-cTnT) te je premještena u Koronarnu jedinicu. Hitna kateterizacija srca i koronarna angiografija
dokazale su odsutnost koronarne bolesti srca (KBS). Trideset sati nakon otpusta bolesnica se vratila
u hitnu službu s istim simptomima dva sata nakon uzimanja 1000 mg kapecitabina. Razrješenje boli
nakon primjene nitrata, normalizacija EKG-a i razina hs-cTnT zajedno s dokazanom odsutnošću KBSa
isključili su AKS. Zaključak: prikazana je bolesnica imala vazospazam koronarnih arterija induciran
liječenjem kapecitabinom u odsutnosti prethodnog KBS-a. Daljnja primjena kapecitabina mora biti
prekinuta kako bi se izbjegao rizik od njegovih kardiotoksičnih nuspojava.Aim: To emphasize the severe adverse effects of capecitabine and prevent misdiagnosis
in patients with acute coronary syndrome. Methods: We present the case of a 74-year-old woman with
pancreatic adenocarcinoma who presented to the hospital with capecitabine-induced acute coronary
syndrome. She was admitted to the Emergency Department (ED) because of a squeezing chest pain
episode. Treatment with oral capecitabine (2500 mg daily) was initiated 72 hours before admission.
The patient had electrocardiographic (ECG) changes and positive biochemical markers for myocardial
ischemia (including HS-troponin T) and was transferred to the coronary intensive care unit. Urgent
cardiac catheterization was performed and showed no coronary artery disease (CAD). Thirty hours after
discharge, the patient presented to the ED with the same symptoms arising two hours after taking
1000 mg of capecitabine. The resolution of chest pain after using nitrates, normalization of ECG, and
HS troponin T levels combined with the proven absence of CAD ruled out acute coronary syndrome in
our patient. Conclusion: Our patient had capecitabine-induced coronary vasospasm in the absence of
pre-existing CAD. Further use of capecitabine had to be discontinued to avoid the risk of cardiotoxicity
