Endocrine Abstracts (2009) 19 P378

Severe dilated cardiomyopathy and hyperthyroidism

K Ashawesh, RN Kulambil Padinjakara, NPN Murthy, S Sankar & A Syed


WISDEM Centre, University Hospital of Coventry and Warwickshire, Coventry, UK.


Introduction: Dilated cardiomyopathy is an uncommon, but well recognized, manifestation of thyrotoxicosis. However, hyperthyroidism presenting with dilated cardiomyopathy is very rare. We describe an unusual case of dilated cardiomyopathy as the initial manifestation of Graves’ hyperthyroidism.

Case: A 61-year-old man of Malaysian origin, with no significant past medical history, was admitted with two month history of worsening shortness of breath, orthopnoea and paroxysmal nocturnal dyspnoea. He denied any other symptoms. Physical examination was unremarkable except for small diffuse goitre and evidence of congestive heart failure. ECG showed atrial flutter with a 2:1 block. Echocardiography revealed severely impaired left ventricular function with dilated cardiomyopathy and moderate pulmonary hypertension. Initial investigations showed normal full blood count, renal and liver functions, C-reactive protein, cardiac enzymes and coagulation screen. Dilated cardiomyopthy screen was negative for Influenza A and B, Psittacosis/LGV, Coxiella burneti (Q fever), Mycoplasma pneuminae and respiratory syncytial virus CF antibody titres, and Enterovirus IgM (EIA). Thyroid function was abnormal, fT3 24.6 pmol/l (2.8–7.1), fT4 70.9 pmol/l (9.0–26.0), TSH 0.02 mU/l (0.35–6.0), with markedly raised thyroid peroxidase antibodies, 600 kIU/l, consistent with Graves’ hyperthyroidism. He was treated with Carbimazole 20 mg od, Frusemide, Digoxine, Bisoprolol, Warfarin and Ramipril and discharged home 8 days post admission. Seven months later, at outpatient follow up, he was clinically euthyroid with normal fT4 17.1 pmol/l and slightly suppressed TSH 0.18 mU/l, on Carbimazole 10 mg od. His heart failure symptoms have improved, and a repeat echocardiography showed normal left ventricular size with moderately impaired left ventricular function (EF of 45%), indicating a significant improvement of his previously severe dilated cardiomyopathy.

Comment: The pathogenesis of systolic dysfunction and congestive heart failure in thyrotoxicosis remains unclear; the action of thyroid hormone on altering gene expression in cardiac cells, and tachycardia associated with thyrotoxicosis, have both been suggested as possible mechanisms. Because it is a potentially reversible cause, thyrotoxicosis should be considered in the differential diagnosis of dilated cardiomyopathy.

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