CONGRESS ABSTRACT

Introduction: Mesalazine (5-ASA) is a cornerstone therapy for ulcerative colitis (UC), but rarely can cause immune-mediated cardiotoxicity (myocarditis/pericarditis/myopericarditis), usually within weeks of starting induction. CMR is pivotal to confirm myocardial/pericardial involvement and guide follow-up. Case: A 28-year-old man with UC presented with acute pericarditic chest pain (worse supine/deep inspiration, better upright), without syncope, palpitations, or relevant dyspnea. One week earlier he had been discharged after an intestinal flare and started mesalazine 3 g/day plus systemic steroids (tapering). He also reported a recent febrile rhinitis episode. Initial work-up: Hemodynamically stable, afebrile, no heart failure signs. ECG was normal (no ST elevation or PR depression). Labs showed isolated troponin elevation (200 pg/mL) with normal CRP/ESR. Differential included viral myocarditis, extra-intestinal IBD involvement, and 5-ASA adverse reaction. Echo/CMR: Transthoracic echo showed a small pericardial effusion, no tamponade, preserved systolic function. Acute CMR confirmed preserved biventricular function, small effusion, myocardial edema (T2/T2-mapping) and a non-ischemic LGE pattern (subepicardial, inferolateral, non-coronary distribution) with associated pericardial enhancement—consistent with acute myopericarditis. Management and outcome: Given the compatible timing, lack of systemic inflammation, negative virology, and imaging findings, mesalazine-related cardiotoxicity was considered highly likely. Mesalazine was permanently discontinued and class avoidance recommended; steroids were continued with a revised taper and an alternative non-5-ASA maintenance strategy planned (immunomodulator/biologic according to phenotype). Symptoms resolved and troponin normalized. Follow-up: At 1 month, off mesalazine, the patient was asymptomatic with normal labs; repeat CMR showed regression of myocardial edema and complete resolution of pericarditis signs. Conclusion: 5-ASA myopericarditis may present with normal ECG and negative inflammatory markers; troponin and CMR are key for diagnosis and follow-up. In recently treated IBD patients, pericarditic chest pain with troponin rise should promptly raise suspicion of drug-induced cardiotoxicity and trigger early multidisciplinary management.