Case 1

A 31 year old woman was admitted with pulmonary oedema. Two months earlier she had complained of fatigue, palpitation, and chest discomfort. She had no risk factors for coronary artery disease, had regular menses, and denied smoking or alcohol consumption. There were no symptoms of intercurrent infection.

On physical examination she looked very ill. Her heart rate was 120 beats/min and blood pressure 130/80 mm Hg. She had a small goiter and typical signs of thyrotoxicosis including warm, moist skin and a fine tremor. There was an audible S3 on cardiac auscultation. ECG showed sinus tachycardia, increased voltage, and ST depression in leads I, II , aVL, and V4–6.

Chest radiography was consistent with interstitial pulmonary oedema and moderate cardiomegaly. Echocardiography showed four chamber dilatation and depressed left ventricular (LV) function with an ejection fraction of 34% (fig 1). Routine tests were normal as was erythrocyte sedimentation rate. She had mild anaemia (haemoglobin 115 g/l). Thyroid function tests were available later: thyroid stimulating hormone< 0.2 MU/l (normal range 0.3–4.5), total triiodothyronine 11 pmol/l (normal range 1.0–2.7), and free thyroxine 60 nmol/l (normal range 8.9–24.3).

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Figure 1

Parasternal long axis view (B mode and M mode) showing reduced systolic left ventricular function. End diastolic diameter is 5.0 cm; end systolic diameter is 4.2 cm; estimated ejection fraction is 34%.

She was treated with intravenous frusemide and morphine. As thyroid function test results became available treatment with dexamethasone, propylthiouracil, and potassium iodide solution was added. A few hours later she developed atrial fibrillation, which converted to normal sinus rhythm after a short course of amiodarone treatment. She was discharged on oral propylthiouracil, propranolol, and captopril. One year later thyroid function tests were normal, she was free from any symptoms of heart failure, and continued only propylthiouracil treatment. Repeated echocardiography was normal (fig 2).

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Figure 2

Parasternal long axis view showing normal left ventricular diameter and function. Estimated ejection fraction is 62%.

Case 2

A 46 year old man, who had a history of partial thyroidectomy because of Grave’s disease, was admitted with pulmonary oedema. The clinical and laboratory results were typical of thyrotoxicosis. Following successful treatment of thyrotoxicosis with propylthiouracil and β blockers his left ventricular ejection fraction increased from 34% to 50%. He remains clinically well and euthyroid on maintenance propylthiouracil treatment.

Discussion

The association of thyrotoxicosis and cardiovascular morbidity is well established. There are several cardiac manifestations of thyrotoxicosis, including enlargement of the heart, atrial fibrillation, high output heart failure, hypertrophic cardiomyopathy, anginal syndrome without evidence of coronary artery disease, and sudden death.1-3 The high output state in thyrotoxicosis results from direct enhancement of heart rate and contractility by thyroid hormones, indirectly increasing blood volume and causing peripheral vasodilatation. High output heart failure develops despite increased cardiac performance.3 Low output heart failure is an extremely rare manifestation of thyrotoxicosis. There have been a few recent reports of dilated cardiomyopathy and congestive heart failure, especially in children and elderly patients with apathetic thyrotoxicosis.4 ,5 Most of the patients had complete or near complete recovery of cardiac function after treatment.4 ,5 However, Ebisawa et al reported that cardiomyopathy in patients with thyrotoxicosis may be irreversible even 15 years after successful treatment of their thyrotoxicosis.5 There has also been a report of sudden death in one young patient with thyrotoxicosis and dilated cardiomyopathy.6 There were no specific abnormalities in myocardial biopsy specimens taken from these patients.

We describe two young patient with thyrotoxicosis who developed dilated cardiomyopathy and pulmonary oedema as the first presenting symptom. Patients presenting with heart failure and dilated cardiomyopathy may have thyrotoxicosis as the underlying cause. Treatment of the thyrotoxicosis can restore left ventricular function. Awareness of this possible presentation of thyrotoxicosis may help identify patients with reversible dilated cardiomyopathy.