01-10-2014 | Imaging in Intensive Care Medicine
Thyrotoxic cardiomyopathy with recurrent ventricular fibrillation and multi-organ failure
Published in: Intensive Care Medicine | Issue 10/2014
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A 54-year-old woman presented with giant struma, hyperthyroidism of unknown duration, palpitations and dyspnoea. The ECG showed tachycardia atrial fibrillation. Echocardiography revealed dilatation of the left ventricle, highly reduced systolic function and diffuse hypokinesia. Serum thyroid stimulating hormone (TSH) levels were less than 0.03 µU/ml (physiological range 0.55–4.78 µU/ml), free triiodothyronine (fT3) was 7.32 pg/ml (2.30–4.20 pg/ml) and free thyroxine (fT4) amounted to 1.72 ng/dl (0.89–1.76 ng/dl). Shortly after hospital admission, the patient developed multi-organ failure and recurrent ventricular fibrillation (VF) requiring cardiopulmonary resuscitation. Hemodynamic stabilization could only be achieved by high doses of catecholamines and amiodarone despite hyperthyroidism. Thyrostatic therapy was performed with sodium perchlorate and thiamazole. Subsequently, renal, hepatic and cardiac function improved. After 9 days, mechanical ventilation was terminated. Thyroidectomy was performed on day 11. Thirty-six hours after thyroidectomy, a torsades de pointes tachycardia occurred and was terminated by defibrillation. At that time, ECG revealed QTc interval prolongation (520 ms) possibly caused by amiodarone therapy and/or reduced levels of free calcium (0.85 mmol/l). Coronary artery disease was ruled out by coronary angiography. Cardiovascular magnetic resonance imaging revealed a slightly improved left ventricular ejection fraction of 47 % with pronounced apical akinesia and corresponding transmural scars in this region (Fig. 1a, b; Video 1A and B in the electronic supplementary material), which might be caused by myocardial ischaemia due to severe coronary spasms. As a result of myocardial damage and repeated occurrence of VF, the patient received a subcutaneous implantable defibrillator.×
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