Heart failure in thyrotoxicosis, an approach to management.

hyperthyroidism [3]. Of these 57% had pre-existing Case history ischaemic, hypertensive or valvular heart disease. There are reports of patients with thyrotoxic heart failure An 80-year-old female was admitted in extremis. Her respiratory rate was 50 min; she was sweaty and pale, with associated with a cardiomyopathy, in whom no additional cause could be found [5, 6]. Some authors have proposed a pulse rate of 155 beats min. There was a history of increasing shortness of breath and orthopnoea in the preceding that there is a specific thyrotoxic cardiomyopathy, with reduced myocardial function in the hyperthyroid state, days, but none of chest pain. She was taking nifedipine 20 mg twice daily for hypertension. Her bowel habit was normal and reversible after treatment [7, 8]. However, this is not supported by data from invasive monitoring studies which her weight was said to be stable. The electrocardiogram showed sinus tachycardia with absence of ‘R’ waves in the have demonstrated increased myocardial contractility and cardiac index at rest in patients with hyperthyroidism septal leads. A chest radiograph demonstrated pulmonary oedema. The biochemical investigations were normal. whether symptoms of cardiac failure were present or not [2, 8]. There is an inability to increase cardiac output further in There was an initial symptomatic response to frusemide 100 mg i.v. , but atrial fibrillation, with a ventricular rate of response to exercise, but this is due primarily to the high output state rather than myocardial depression. Moreover 170 beats min developed subsequently. Digoxin 500 mg i.v. was administered and intravenous heparin was comchanges at the molecular level suggest adaptations to enhance myocardial performance in hyperthyroidism. There is an menced. The heart rate remained uncontrolled and the patient was unwell. Chemical cardioversion was attempted increase in mRNA coding for contractile elements [9] and for the sarcoplasmic reticulum Ca ATPase [10]. Left with amiodarone 300 mg i.v. over 1 h and subsequent infusion. By the following morning the rhythm had reverted ventricular mass increases [11] and diastolic function, assessed by trans-mitral Doppler echocardiography is enhanced [12]. to sinus and the symptoms of cardiac failure had resolved. However, by the third hospital day fast atrial fibrillation Furthermore, cardiac failure in hyperthyroidism is not associated with any histopathological change [13]. For all of had returned, with recurrence of pulmonary oedema. At this time thyroid function tests from the time of admisthese reasons hyperthyroid cardiomyopathy has not been demonstrated convincingly. sion became available and revealed thyrotoxicosis: TSH<0.08 mU l; T4 47.8 pmol l . A cardiac enzyme series was normal over 3 days. In light of the recurrent atrial Role of the sympathetic nervous system dysrhythmia in the context of proven thyrotoxicosis, propranolol 20 mg orally three times daily was commenced. The role of the sympathetic nervous system in the pathophysiolology of hyperthyroidism is unclear. This The rate and rhythm were controlled and heart failure did not recur. The echocardiogram in sinus rhythm showed uncertainty complicates both our understanding of the disease and, as will be discussed, the formulation of a good left ventricular function with septal hypokinesis. Carbimazole 20 mg once daily was added and the patient targeted approach to treatment. The clinical spectrum of symptoms (including tachycardia, tremor and anxiety) was anticoagulated with warfarin. She was discharged, well, on the seventh hospital day. On outpatient review, at suggests that, in addition to any effect of thyroid hormone itself, there is also a hyperadrenergic state. This impression 2 weeks, there had been no recurrence of heart failure. is reinforced by the dramatic reversal of these symptoms after the administration of b-adrenoceptor antagonists [14]. Discussion Despite this, the concentrations of catecholamines in both plasma [15] and urine [16] are normal or low in hyperPathophysiology thyroidism. An alternative explanation is that sensitivity to catecholamines is enhanced. Increased numbers of The haemodynamic features of hyperthyroidism are due to functional alterations in both the peripheral circulation and b-adrenoceptors have been reported in rat heart [17] and human muscle and adipose tissue in hyperthyroidism [18]. the myocardium. There is an increase in total blood volume and a decrease in systemic vascular resistance [1]. These There is also a greater increase in plasma cAMP concentration in response to insulin induced hypoglycaemia in hyperthyroid effects increase preload and decrease afterload and are accompanied by an increase in heart rate and myocardial patients than in normal controls [19], suggestive of enhanced b-adrenergic responsiveness. By contrast, there is no increase contractility [2]. The result is a high output cardiac state. Overt heart failure in hyperthyroidism occurs in 6–19% in the metabolic or haemodynamic sensitivity to infused adrenaline [18, 20]. of unselected patients [3, 4], the incidence increasing with age. However, on systematic enquiry Sandler & Wilson elicited cardiac symptoms in 33% of patients treated for Atrial tachyarrhythmias