A 20-year-old Caucasian male was admitted to the emergency department of an external secondary care hospital after he collapsed with syncopation while he watched a football match in the stadium. He had lost consciousness for less than a minute. Two years before he was diagnosed to have hypothyroidism, and the prescribed medication consisted of low dose levothyroxine and, for unknown reasons, low dose of carbimazole, potentially because of high TRAb titers. He was, however, taking his medication irregularly. Upon hospital admission he complained of increasing fatigue over the last two months. Dyspnea, chest pain, weight gain and stool irregularity were denied as well as symptoms and signs of previous viral infection in the last months. At arrival, the patient was awake and amenable, without showing any signs of alcohol consumption. His body temperature was 35.8  C, heart rate was 52 bpm and the blood pressure was 80/40 mmHg. The physical examination was otherwise unremarkable. His initial electrocardiography (ECG) showed sinus bradycardia without atrioventricular block and ST-segment abnormalities. Echocardiography in the emergency department demonstrated impaired cardiac contractility with ejection fraction (LVEF) of 38 % and a pericardial effusion with maximal thickness of 15 mm without hemodynamic relevance. All valves were well visualized and appeared to be normal. Initial laboratory findings revealed a TSH level of over 100 mIU/L, therefore the patient was moved to our hospital in face of imminent myxedema coma. We confirmed hypothyroidism with reduced levels of plasma free thyroxine (fT4, < 3.9 pmol/L, see Table 1 for reference ranges) and plasma free triiodothyronine (fT3, 2.4 pmol/L) associated with massive rise in plasma thyrotropin (TSH, 108 mIU/L). Creatin kinase (CK) was 437 U/L (normal < 172) and CK-MB was 34 U/l (normal < 24). However, troponin I and BNP concentrations were low. Serum electrolytes, complete blood count, and basal levels of cortisol and ACTH were normal. The patient was transferred to the ICU, where treatment with intravenous infusion of levothyroxine (500 mug over the first 24 h) was commenced. ECG monitoring revealed an intermittent atrioventricular block type Mobitz 2 (Fig. 1). In order to evaluate the pericardial effusion and the impaired left ventricular ejection fraction, magnetic resonance imaging was performed, which confirmed the echocardiographic findings. A potential peri-myocarditis was susptected because of the increased signal intensity in the epicardial layer, suggesting local edema, in the T2-weighted and late gadolinium enhancement images (Fig. 2 and Additional file 1). Therefore, to rule out a peri-myocarditis, serologic studies, including parvovirus-B19, streptococcus, influenza-virus, mycoplasma, adenovirus, enterovirus, herpes virus type 6 and cytomegalovirus were performed, which did not support the diagnosis.
Titres of three subtypes of anti-thyroid antibodies were elevated, suggesting hypothyroid Graves' disease with Hashimoto component (TgAb > 2000 U/mL, TPO-Ab > 3000 U/mL, TRAb 5,9 U/mL). After 3 days the intravenous levothyroxine therapy was terminated and oral substitution continued with a daily dose of 150 mug for 7 days, followed by 125 mug daily. After 7 days an echocardiography revealed normal LVEF and the pericardial effusion had vanished. When peripheral euthyroidism was achieved after 9 days, 24-h Holter ECG monitoring demonstrated regression of the bradycardiac episodes, however an intermittent atrioventricular block Mobitz type 2 during the night remained. A pacemaker was not considered because of a rise in the cardiac frequency during training. In a follow-up MRI investigation after 3 weeks, the initially increased signal intensity in the epicardial layer in T2-weighted and late gadolinium enhancement images had been dissolved (Fig. 3 and Additional file 2). Cardiac output had improved to 6.0 L/min from formerly 3.2 L/min (Table 1).