Thyroid dysfunction is associated with characteristic changes in heart rate and arrhythmias. Thyroid hormones act through genomic and non-genomic effects on myocytes and influence contractility, relaxation and action potential duration through avariety of mechanisms. Atrial fibrillation is the most common arrhythmia associated with thyroid dysfunction, it occurs in both euthyroidism and hyperthyroidism in clear association with T4 levels. Mechanistically, in the hyperthyroid state, increased automaticity and triggered activity, together with ashortened refractory period and slowing of the conduction speed, lead to the initiation and maintenance of multiple intraatrial reentry circuits. Influences from the autonomic nervous system and hemodynamics controlled by thyroid hormones act as modulators for arrhythmias, which are promoted by acorresponding substrate (significant impact of comorbidities). Concerning therapy, in addition to treating hyperthyroidism, the initial therapeutic focus is on adequate rate control and anticoagulation in patients with ahigh risk of thromboembolism. Ablation of atrial fibrillation can be considered later on, although there is an increased likelihood of recurrence compared to patients without hyperthyroidism.Prolongation of the QT interval and increase in QT dispersion are involved in the formation of ventricular arrhythmias. Epidemiological data suggest an association of elevated T4 levels with ventricular arrhythmias and sudden cardiac death. However, this seems to be mainly relevant for patients with underlying cardiac disease (e.g. ICD users).