Thyrotoxicosis: A Primary Cause of Arrhythmias and Acute Heart Failure

Abstract

Thyrotoxicosis results from excessive thyroid hormone and may occur in Graves’ disease, multinodular goiter, and thyroiditis. The association of hyperthyroidism with the worsening of pre-existing heart disease is very well recognized. Additionally, hyperthyroidism can also cause primary cardiac disease including arrhythmias and congestive heart failure. We present a 65-year-old female with a past medical history of intermittent palpitations who came to the emergency department with shortness of breath and bilateral lower extremity swelling. Physical exam revealed an anxious woman with bilateral proptosis, jugular venous distention, bibasilar crackles, and bilateral lower extremity edema. Laboratory data was significant for a brain natriuretic peptide level of 1,930. Chest x-ray revealed vascular congestion. Transthoracic echocardiogram showed an ejection fraction of 63% and diastolic dysfunction. She was admitted and received diuretics for acute heart failure. She developed atrial fibrillation with a rapid ventricular response, managed with a diltiazem infusion and anticoagulation. This event prompted thyroid evaluation which showed a thyroid-stimulating hormone (TSH) of 0.01mU/L, elevated free T4 at 3.37ng/dl, free T3 at 5.8pg/ml, positive Thyroid-stimulating immunoglobulins (TSI) 473%, and thyroid peroxidase (TPO) antibodies 158U/ml. Her symptoms improved after treatment with methimazole. The heart is susceptible to hyperthyroidism due to multiple thyroid hormone receptors on cardiac myocytes causing high sympathetic stimulation from an increased number of myocardial beta-cell receptors. Atrial fibrillation occurs in 10 to 20% of patients with hyperthyroidism and is prevalent among the elderly population. People 60 years and above with a low serum thyrotropin concentration are at a threefold higher risk of developing atrial fibrillation in the subsequent decade. Complications such as cerebrovascular accidents occur in about 14% of cases. About 6% of thyrotoxic individuals develop heart failure secondary to a tachycardia mediated mechanism, leading to an increased level of cytosolic calcium during diastole. This causes reduced ventricular contractility and diastolic dysfunction, often associated with tricuspid regurgitation. Graves’ disease is an autoimmune process characterized by hyperthyroidism due to circulating autoantibodies. TSI binds to and activates thyrotropin receptors, causing the increased synthesis of thyroid hormones. If left untreated, Graves’ disease can lead to severe thyrotoxicosis. Clinicians should be aware of this disease association and ensure thorough clinical investigation, prompt diagnosis, and treatment of thyrotoxicosis to avert these life-threatening events.