When Thyrotoxicosis Mimics Stemi: A Caso of Acute Myocarditis With Non-Obstructive Coronary Arteries

Background The association between hyperthyroidism and acute myocarditis has been already reported in literature; however, this case presents an unusual scenario without classical hyperthyroidism symptoms or infective myocarditis features, in which the coexistence with thyrotoxicosis suggests a possible but unproven relationship. Case presentation A 26–year–old male presented with acute chest pain: he denied fever, recent infections or prodromal viral symptoms. ECG performed by emergency medical services showed inferior ST–segment elevation with reciprocal anterior ST depression. Therefore, cath–lab was activated; urgent coronary angiography revealed no significant coronary stenosis (Figure 1). Early echocardiography showed preserved systolic function without wall motion abnormalities. Laboratory tests revealed markedly abnormal cardiac biomarkers (hs–TnT peak 3,138 ng/L and elevated CK–MB and CPK) with normal inflammatory markers. Thyroid tests showed nearly suppressed TSH and markedly elevated thyroid hormones (TSH 0.002 mUI/L; fT3 67 pmol/L). Endocrinology consultation prompted further assessment: neck ultrasound demonstrated a normally structured thyroid gland and thyroid autoantibodies (anti–TPO, TRAb, anti–Tg) were negative. The biochemical trend and clinical context made destructive thyroiditis and iodine–induced hyperthyroidism unlikely. Screening for catecholamine excess, porphyria, metabolic and rheumatologic disorders was negative. Further diagnostic assessments are ongoing to investigate a possible underlying endocrinological syndrome. During hospitalization, the patient experienced recurrent chest/epigastric pain with limited response to analgesics; serial ECGs showed dynamic ST–segment elevation with recurrent troponin rises (Figure 3). Cardiac magnetic resonance demonstrated mildly reduced ejection fraction (44%), diffuse myocardial edema and subepicardial late gadolinium enhancement with a ring–like apical pattern, consistent with acute myocarditis(Figure 2). Guideline–directed therapy for ventricular dysfunction and thyrostatic treatment were initiated, with initial improvement. The patient was discharged with indication for strict follow–up; however, subsequent clinical evolution could not be assessed due to loss to follow–up. Conclusion This case supports the relevance of a structured diagnostic approach in STEMI–like presentations with non–obstructive coronary arteries and suggests a possible association between thyrotoxicosis and acute myocarditis.