Cardiovascular system disorder is one of the key complications of thyrotoxicosis. R. Kraus suggested the hyperthyroid heart term in 1899. Myocardial dystrophy is observed in hyperthyroid heart, which develops under the influence of two main mechanisms. Firstly, persistent hyperfunction of the cardiac muscle in presence of activation of the sympathetic part of the autonomic nervous system is noted. Secondly, thyroxine and triiodothyronine have direct toxic effect on myocardium. There are 3 stages of heart remodeling in patients with thyrotoxicosis in clinical cardiology: hyperkinetic, normally kinetic and hypokinetic. The signs of hyperthyroid heart must be distinguished from toxico-allergic myocarditis, rheumatic defects of the valvular heart apparatus and other variants of metabolic cardiomyopathies for differential diagnosis. Drug therapy is aimed at achieving euthyroid state and maximum possible cardiac symptoms relief. Comprehensive treatment includes the following groups of medications: beta-adrenergic blocking agents, antiarrhythmics, diuretics and anticoagulants. Non-selective blockers, which contribute to the elimination of tachycardia and other types of arrhythmias, are prescribed to the majority of patients. It is necessary to achieve persistent euthyroidism, in which arrhythmia can be eliminated and the risk of cardiovascular crises can be reduced, to prevent the complications of thyrotoxicosis. The disease outcome directly depends on the success of thyrotoxicosis cause treatment, patient’s compliance, timeliness of cardiac pathology diagnosis.