Endocrine Abstracts

A middle age barrister admitted via accident and emergency department with the history of dyspnoea on exersion, orthopnoea,palpitation, weight loss and significantly reduced exercise tolerance to an extent he was not able to walk more than few metres. He had been investigated for tuberculosis and treated for chronic alcohol excess in the past, there was no history of ischaemic heart disease. He was not on any regular medication.

Clinical examination revealed irregular and fast pulse rate (170 beats/min), he looked emaciated and had bilateral pitting leg odema, raised jugular venous pressure, tremor of outstretched hands. Mild enlargement of thyroid gland and there was no eye signs.

Investigations revealed normal renal function, mildly raised alkaline phosphatase otherwise normal liver function test. TFT revealed completely suppressed TSH (<0.01 mU/l) and significantly raised Free T4 (62.2 pmol/l).

ECG confirmed fast atrial fibrillation and chest X-ray showed sings of pulmonary odema. Echocardiography showed marked bi-atrial dilatation, severe tricuspid regurgitation, moderate Mitral regurgitation. Moderately dilated right ventricle and global systolic dysfunction.

He was treated with 60 mg of carbimazole, B-Blocker, digoxin and diuretics, ACE inhibitor and low molecular weight heparin.

After a week his symptoms improved and discharged. Six weeks later his symptoms improved remarkably and TFT was within normal limit. Heart failure medication stopped.

Three months after initial presentation he had repeat echocardiography, which showed that all cardiac chambers were within normal dimension with normal systolic function and he only noted to have mild tricuspid regurgitation.

Thyrotoxicosis seemed to be directly responsible for the development of sustained tachycardia – induced cardiomyopathy causing severe heart failure.

Although thyrotoxic cardiomyopathy relatively uncommon, this aetiology should not be overlooked in patients with thyrotoxicosis and heart failure.

This case shows that hyperthyroidism by itself can cause a reversible cardiomyopathy.