Abstract
Background: Excess thyroid hormone alters the hemodynamics of the heart and vascular system resulting in a hyper-dynamic circulatory state which can lead to thyrotoxic heart disease. Clinical case: A 48-year-old male presented to the hospital with several days of rapid heart rate and weakness. He denied prior medical history, medication or supplement intake. Pertinent exam revealed a very thin, hoarse gentleman with shallow breathing and obvious hand tremors; heart exam with irregular rate and tachycardia, absent peripheral edema and bibasilar crackles bilaterally. EKG was consistent with atrial fibrillation with rapid ventricular response. Lab work revealed a pro-BNP of 4000 and positive D-dimer. CTA-Thorax was consistent with CHF with cardiomegaly, large pleural effusions, pulmonary edema and an incidental finding of thyromegaly. Echocardiogram revealed global LV hypokinesis with Ejection Fraction of 10-15%. TSH was <0.005, free Thyroxine >8.00, and Triiodothyronine was 27.04. Thyroid ultrasound showed heterogeneous enlarged gland with hypervascularity and no focal nodules. Graves’ Disease was confirmed with thyroid stimulating Immunoglobulin of 507. Methimazole and hydrocortisone were initiated along with Metoprolol and digoxin for rate control. Thyroid hormone has significant impact on cardiac function, structure and the vascular system. In the vasculature, T3 works to decrease systemic vascular resistance via direct vasodilatation. The decrease in SVR activates RAAS resulting in retention of sodium and fluid. Thyroid hormone also stimulates erythropoiesis which results in an increase in blood volume and stroke volume. In the heart, T3 enters the myocyte via specific transport proteins and via transcription-and non-transcription-mediated effects, increases contractility and relaxation of the cells. Given the increased metabolism, low SVR and increase in total blood volume, this creates a high cardiac output state. Untreated high-output state leads to ventricular dilatation, persistent tachycardia and eventual heart failure. Thus, prompt diagnosis and treatment of cardiac dysfunction is key. Of most importance is correction of thyroid dysfunction with either anti-thyroid medication, radioactive iodine ablation or thyroidectomy. This can possibly reverse and “cure” patient’s systolic heart failure. Conclusion: We present a case of thyrotoxicosis -induced cardiomyopathy with left ventricular ejection fraction of 10% secondary to undiagnosed Graves disease and emphasize the importance of thyroid disease as a possible cause of systolic heart failure. References: Riaz K, Forker AD, Isley WL, Hamburg MS, McCullough PA. (2007). Hyperthyroidism: A “Curable” Cause of Congestive Heart Failure - Three Case Reports and a Review of the Literature. Congestive Heart Failure.2007; 9: 40-46