Amiodarone is an antiarrhythmic drug, class III, used for the treatment and prevention of life threatening supraventricular and ventricular tachyarrhythmias, atrial fibrillation (AF) and maintenance of sinus rhythm (1). It is a lipophilic molecule that accumulates in the myocardium, adipose tissue, skeletal muscles and thyroid gland. The effects of amiodarone on the thyroid tissue can be seen as early as a few weeks after starting treatment, while amiodarone and its metabolites demonstrate direct toxicity to cultured thyroid cells, or up to several months after its discontinuation (2). Long term use is associated with a number of side effects, including thyroid dysfunction (both hypo and hyperthyroidism), which is due to amiodarone's high iodine content and its direct toxic effect on the thyroid (3). The effects of amiodarone on thyroid function can be divided into those effects that are intrinsic properties of the drug and those that are due to iodine. Amiodarone-induced hyperthyroidism (AIT) is more common in iodine-deficient regions of the world, whereas amiodarone-induced hypothyroidism (AIH) is usually seen in iodine-sufficient areas. In the most European countries, the proportion of AIT (75%) is higher compared to AIH (25%), whereas in North America, where iodine intake is high, the proportion of AIH (66%) is higher compared to that of AIT (34%) (4). Amiodarone-induced thyrotoxicosis develops in 3% of amiodarone-treated patients in North America (5). Recent reviews of the literature noted that hypothyroidism occurs in 5–10% (6). AIH occurring especially in women with thyroid autoantibodies prior to treatment. Previous study in Netherlands showed an incidence between 6 and 6.9% for AIH (7). The relative high prevalence of thyroid autoantibodies, especially in women, the wide range of known triggers, and slow onset of autoimmune thyroid disease make this process difficult to associate with environmental agents, eventhough environmental exposures are subtle and can occur over a long period of time. Additionally, most individuals are exposed to multiple environmental toxins, and the combination of factors may also be significant for effects on the thyroid function. The presence of thyroid autoantiboides is s known risk factor for the development of autoimmune thyroid disease (8). Amiodarone is widely used in adults with congenital heart diseases (CHD) for decades. Previous studies suggested that low-dose amiodarone (≤ 200 mg/day) is useful and effective for decreasing the frequency of tachyarrhythmia in patients with CHD and has a low incidence of side effects (9).
Ebstein anomaly is a rare disease, accounting for < 1% of all cases of CHD (0.3–0.6%), characterized by tricuspid valve hypoplasia with apically displaced septal and posterior leaflets, which may induce severe tricuspid regurgitation and dilation of the “atrialized” portion of the right ventricle (10). Malformation in Ebstein’s anomaly may range from only minimal displacement of the septal and posterior leaflets to an imperforate membrane or muscular shelf between the inlet and trabecular zones of the right ventricle. Hemodynamic abnormalities are dependent on the severity of the lesion. In mild Ebstein anomaly, tricuspid valve function is close to normal. In moderate to severe forms, with each atrial contraction the blood is propelled into the atrialized right ventricule. With ventricular contraction, blood is forced back into the right atrium (11). Prevoius studies noted that only 5% of patients survive beyond the fifth decade (12). Patients usually present with symptoms associated with heart failure due to the dilated and atrialized right ventricle compressing the left ventricle and, additionally, reducing preload for the left heart (13). The therapeutic approach of Ebstein anomaly in elderly is very discutable, because the operative indication of asymptomatic Ebstein's anomaly in adult patients has not been clearly defined (14). Eventhough operative repair of Ebstein's anomaly is indicated usually during younger age, medical management may be used to manage some of the symptoms of heart failure and arrhythmias, especially in NYHA classes I and II. Surgery is indicated when the patient’s symptoms progress to NYHA class III or IV, increasing cyanosis becomes evident, or if paradoxical embolism occurs (15). A large cohort Study from Mayo clinic demonstrated good benefits from surgery, and better postoperative outcomes in NYHA functional classes I and II (in 40% of patients) (16).