**12. Treatment**

Recent treatment options for Graves' hyperthyroidism include antithyroid drugs, radioactive iodine, and surgery. In addition β-adrenergic blockade is targeted to blockade cathecolamine discharge. The cardiovascular symptoms stimulated by hyperthyroidism resolve after an adequate treatment regardless of utilizing radioactive iodine or antithyroid drug. Hyperthyroidism may exaggerate preexisting cardiovascular diseases by increasing demand for myocardial oxygen, contractility and heart rate. In such circumstances, silent coronary artery disease, angina or compensated heart failure and even endothelial dysfunction develop [114]. Tachycardia control by using β-blockers should be added into treatment in the management of heart failure. Nevertheless, possible contraindications have to be considered in each individuals. Furosemide may aid to reduce volume overload. However, requirement of more Na-K-ATPase in the myocardium due to İncreased blood volume (distribution) in euthyroid heart failure patients result in relative resistance to digoxin [77]**.** Beta blockers, especially propranolol and atenolol aid to control palpitations by decelerating the heart rate in case of sinus tachycardia [115]. Although, all types of calcium channel blockers are utilized in the management of newly emerged atrial fibrillation, in the presence of thyrotoxicosis, intravenous administration increase adverse effects. The vasodilator and negative inotrope effects of these drugs may cause hypotension and even cardiovascular collapse [116]. Further precautions are required in case of atrial fibrillation, marked palpitations, or severe tachycardia [7, 92].

In case of heart failure resisting despite the heart rate decelerated, or if the patient is in advanced age, or has diagnosed or suspected preexisting heart disease, or has hypertension standard treatment protocols should be applied. In occasional conditions such as hyperthyroidism or thyroid storm requires close cardiovascular monitoring and management of other comorbidities (infection, trauma, acute psychiatric illness) [92, 117]. The efficacy of anticoagulant drugs has been less investigated into correctable causes of AF such as hyperthyroidism. Our clinical routine tends to initiate antithrombotic agents as in general population. After euthyroid state established, and in the documented absence of AF during at least three months, terminating the anticoagulant therapy should be concluded. However, the patients should be kept in close follow-up with routine intervals in terms of heart rate. Although, some clinics demand further documentation, 24 hours of continuous monitoring without AF and the absence of any sign and symptoms regarding AF is sufficient to terminate anticoagulant therapy in our protocol. However, two clinicians decide whether to discontinue anticoagulant treatment according to CHA2DS2-VASc score, regardless of rhythm.
