In the human embryo, the thyroid gland develops at about 3-4 weeks gestation from the pharyngeal floor. It then migrates to the front of the neck. It consists of two connected lobes and the lower two thirds of the lobes are joined by connective tissue called the isthmus. The thyroid gland secretes three hormones: two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) as well as a peptide hormone called calcitonin. 
In children, T3 and T4 are crucial for growth and development, and in adults, they are responsible for regulation of the intrinsic metabolic rate and protein synthesis. T3 and T4 secretion is regulated by thyroid- stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus. 
Hyperthyroidism is the overproduction of thyroid hormones. It has many causes: multinodular goitre, toxic adenomas, thyroiditis, excessive ingestion of iodine, pituitary adenomas and Graves' disease. The overall prevalence of hyperthyroidism is approximately 1.3 percent and increases to 4 to 5 percent in older women. The male to female prevalence ratio is 1:5 and hyperthyroidism is also more prevalent in smokers. 
Grave’s disease causes up to 80% of hyperthyroidism. It is an autoimmune condition where the main autoantigen is the thyroid-stimulating hormone (TSH) receptor (TSHR). Lymphocytes from the thyroid tissue of patients affected by Grave’s disease secrete thyroid autoantibodies, including thyrotropin receptor antibodies (TRAb). The presence of TRAb is very sensitive and specific for Grave’s disease and is used to determine therapy. [3,4]. Grave’s disease is also associated with other autoimmune conditions such as pernicious anaemia and immune thrombocytopenia. [1-4]
Thyrotoxicosis is the clinical syndrome resulting from hyperthyroidism and often the terms are used interchangeably. The clinical manifestations of Grave’s disease are those of hyperthyroidism, a diffuse goitre as well specific orbitopathy and dermopathy. The pathogenesis, diagnosis and treatment of the latter two conditions are beyond the scope of this article and our patient did not have any of those. [1-4]
Clinical features of hyperthyroidism include: warm skin, lid lag, breathlessness due to increased ventilatory drive; respiratory muscle weakness and pulmonary hypertension, cachexia due to an increased metabolic rate, osteoporosis due to thyroid hormones stimulating bone resorption, normochromic, normocytic anaemia due to an increase in plasma volume, behavioural and personality changes such as psychosis, agitation, and depression and lastly cardiovascular problems which we will describe further. 
The cardiotoxic effects of hyperthyroidism are well described with an estimated epidemiology of between 12% to 68%. Thyrotoxic heart failure (THF) is due to myocardial damage due to the toxicity of abundant serum free T3 and T4. This causes altered energy synthesis by cardiomyocytes (oxidative phosphorylation glycolysis), impaired intracellular metabolism and protein synthesis) and defective myofibril contractile function . Typical manifestations include left ventricular hypertrophy and systolic dysfunction (up to 47%), sinus or atrial tachycardias (up to 90%), dilated cardiomyopathy (estimated at 1%), pulmonary hypertension (29% in subclinical thyrotoxicosis and 39.6% in overt thyrotoxicosis) and diastolic dysfunction.  LV systolic dysfunction is reversible with treatment in around two third of patients. 
There are 3 recognised stages to THF: 1. Hyperkinetic phase with preserved ventricular function (“high output heart failure), 2. Normo-kinetic phase in which there is reversible myocardial hypertrophy and diastolic dysfunction (heart failure with preserved ejection fraction or HFpEF) and 3. The hypokinetic stage characterized by systolic dysfunction and cardiac chamber dilatation (heart failure with reduced ejection fraction or HFrEF). THF is more common in elderly patients with other cardiovascular co-morbidities but younger patients without cardiovascular pathology can high output failure with myocardial hyper- contractility, as did our patient. This subgroup may still go on to develop HFrEF in a dilated cardiomyopathy phenotype particular in untreated chronic severe thyrotoxicosis. HFrEF is associated with significantly worse prognosis than HFpEF , although this could be less generalisable to THF where there is a clear reversible cause. Decompensation of heart failure can occur with intercurrent illness such as infections.
We surmise that our patient already had a propensity to develop thyroid disease (as she had pernicious anaemia already) and had been hyperthyroid for some time. The pneumonia caused her decompensation and admission to hospital. Fortunately, her cardiac involvement was in the hyperdynamic or high-output phase and her cardiac function returned to normal with early treatment.
Treatment of THF is well established. [7,10,11] The normalisation of the circulating thyroid hormones can take some time and thus any symptoms and signs of THF must be managed in the interim. In patients with THF, with or without structural heart disease, beta blockers such as propranolol, bisoprolol or metoprolol are recommended until a euthyroid state has been achieved. Propranolol is usually used first line as it is non-cardioselective and inhibits peripheral conversion of T4 to T3 as well as its cardiac effects. Beta blockers lower heart rate and reduce contractility (negative chronotropic and inotropic effects), but can also directly treat arrhythmias by increase AV node refractory period and reducing excitability of ectopic foci. They have significant prognostic benefit in LV systolic dysfunction (HFrEF).  Diuretics can help in overloaded states [10,13]. Our patient clinically improved on propranolol, the dose of which was slowly reduced over time.
Suppression of thyroid hormones can be done with anti-thyroid drugs, radioactive iodine or thyroidectomy. Carbimazole is a pro-drug and is converted to methimazole after absorption. Methimazole prevents thyroid peroxidase enzyme from iodinating and coupling of tyrosine residues on thyroglobulin to reduce the production of T3 and T4. Carbimazole is associated with significant side effects most notably bone marrow suppression leading to neutropenia and agranulocytosis. Should this happen, patients are normally swapped onto propylthiouracil which inhibits the formation of T3 and T4 by blocking the enzyme thyroperoxidase. This happened with our patient.
Her reassuring convalescent CMR and the resolution of her pleural effusions would suggest that all of her intial clinical and echocardiographic features of heart failure were due to acute thyroid-related heart dysfunction and not underlying cardiac disease. The persistence of hyperdynamic ventricular function on CMR at two months suggests that thyroid control is not yet fully established.
Radioactive iodine induces hypothyroidism and has high success rates but imposes significant limitations on patients. Patients who receive radioiodine can expose their home and household contacts via saliva, urine, or radiation from their body. They should avoid sharing cups or utensils, sleeping in the same bed with another adult, pregnant woman, infant, or child, sexual contact and close contact with children and pregnant women. Pregnancy should also be delayed for four to six months.  Our patient declined this because of her job and the fact that she could not isolate herself. She is now considering thyroidectomy as a definitive management option and continues under regular follow up.