Endocrine Abstracts

Case history: A 69-year-old female was referred acutely from the community with 4 weeks of progressive breathlessness. Initially exertional, she was now also breathless at rest with orthopnoea and paroxysmal nocturnal dyspnoea. She had a background of antibody-positive thyrotoxicosis diagnosed 33 years ago, managed solely in primary care on carbimazole 20 mg, with good compliance. On examination, she was dyspnoeic with an irregularly-irregular tachycardia and fine tremor to the outstretched hands. There was no ophthalmoplegia or palpable goitre. She had fine bibasal crackles with mild bilateral pitting oedema. She reported 10 kg of unintentional weight loss with anorexia over 6 months (BMI 18.5 kg/m2) and 3 months of intermittent palpitations and heat intolerance. Review of community records revealed a suppressed TSH for at least 20 years. The patient reported symptoms of recurrent relapsing thyrotoxicosis. The clinical concern was of acute high-output heart failure on the background of longstanding uncontrolled Graves’. She was admitted for further investigation and management.

Investigations: Admission ECG showed left bundle branch block and atrial fibrillation with rapid ventricular response. Serial troponins were mildly elevated but down-trending (49ng/l to 31ng/l). Pulmonary congestion was seen on chest X-ray. TSH was <0.01mU/l, fT4 >100.0 pmol/l, TSH-receptor-antibody 4.03IU/land thyroperoxidase-antibody 344kunits/l. There was an iron-deficiency anaemia (Hb 100) and no electrolyte abnormalities.

Results and treatment: Carbimazole was up-titrated to 60 mg and she started cholestyramine 1g twice daily, propranolol 40 mg 8-hourly and oral anticoagulation. fT4 fell to 53.9 pmol/l in 96 hours and rate-control was achieved. N-terminal BNP was elevated (5530ng/l). An echocardiogram reported impaired left-ventricular systolic function (35-40%) with a dilated left-atrium, and pulmonary-arterial hypertension (PASP 33mmHg). Biventricular size was normal. She was discussed with cardiology and heart failure secondary to thyrotoxicosis was thought likely. She was diuresed, propranolol switched to bisoprolol, and ramipril up-titrated. At one month, the patient was clinically euthyroid with improved breathlessness and peripheral oedema, but ongoing thyrotoxicosis (fT4 15.9, TSH <0.01) prompted discussions surrounding definitive management.

Discussion: Heart failure in the context of thyrotoxicosis is a spectrum ranging from acute rate-related high-output failure, to congestive cardiac failure and dilated-cardiomyopathy secondary to chronic exposure to a hyperdynamic circulation. The symptom burden of Graves’ thyrotoxicosis usually prompts clinical presentation and thus rapid achievement of disease control. As such, congestive cardiac failure as seen in our patient, is rare. Management focuses on reducing the risk of acute cardiovascular complications and cardio-prognostication, alongside achieving the euthyroid state that can lead to restored cardiac function.