Introduction Hyperthyroidism causes circulatory alterations, including elevated heart rate and atrial automaticity, which can result in conditions such as Atrial Fibrillation (AF) and heart failure, ultimately leading to increased mortality rates. Even though euthyroid is achieved through medication, cardiovascular symptoms may persist. Additional research into factors linked to persistent AF is required to decide on the appropriate anticoagulant therapy.

Case Presentation A 66-year-old Malay man with hypertension, dyslipidaemia, and Thyrotoxic Atrial Fibrillation (TAF) due to Grave's disease for five years was presented to the emergency department after two failed radioactive iodine treatments and thyroid gland surgery. He reported periodic palpitations, dyspnoea, and left chest pain. The electrocardiogram (ECG) revealed rapid ventricular AF and uncontrolled elevated blood pressure. Thyroid function tests were normal (T4 = 14.21, TSH = 4.78). The patient was referred to cardiology for assessment and cardiac ablation. In another case, a 34-year-old woman with Graves' disease and AF, despite taking bisoprolol, presented to the emergency department with frequent palpitations and dizziness but no chest pain. Correspondingly, the ECG showed AF. Her thyroid function tests were normal (T4 = 15.21, TSH = 3.56). She was treated for symptomatic AF, and elevated troponin levels prompted a cardiology referral for assessment and cardiac ablation.

Discussion Thyroid hormones affect cardiovascular function, predisposing individuals to AF even after achieving euthyroid. The thromboembolic risk in TAF is mitigated by oral anticoagulants. Treatment for TAF involves antithyroid medications to restore euthyroid and rate and rhythm control. Wong et al., (2017) identified an unexpected relationship between decreased free thyroxine levels and chronic AF. TAF carries a high thromboembolic risk even after achieving euthyroid, necessitating anticoagulants, and ongoing monitoring to prevent a recurrence. In cases of symptomatic AF that do not respond to medication, AF ablation is performed by using catheters to deliver energy (radiofrequency, cryoenergy, or pulsed field) to create lesions that block abnormal electrical impulses and prevent them from triggering AF.

Conclusion The management of AF caused by hyperthyroidism requires collaboration between endocrinology and cardiology specialists. Thus, prompt diagnosis and personalised treatment, including achieving biochemical euthyroid, anticoagulant therapy, and potentially definitive treatment with ablation, can improve prognosis and reduce complications.