Background: Hyperthyroidism secondary to Graves’ disease commonly causes tachycardia and may result in pulmonary hypertension and high output cardiac failure. There is limited information regarding the effect of treatment with anti-thyroid drugs on cardiac function using modern echocardiographic techniques
Methods: Eight patients with Graves' hyperthyroidism diagnosed on the basis of thyroid function tests and TSH receptor antibody titre, aged 22-64 years of age, five males and three females, underwent comprehensive transthoracic echocardiography at three time points, immediately prior to commencement of carbimazole, 2 weeks after commencement of carbimazole, and 6 months or more after commencement of carbimazole when euthyroid, along with assessment of functional exercise capacity and quality of life. Exercise capacity was assessed using the six-minute walk distance, and quality of life was assessed by SF36v2.
Results: There was evidence of hyperdynamic right ventricular function as measured by peak systolic velocity of the free wall of the tricuspid annulus (RVs’), tricuspid annular plane systolic excursion (TAPSE) and right ventricular ejection fraction (RVEF), which normalised after resolution of thyrotoxicosis. There was no measurable pulmonary hypertension in any of the cases. Cardiac output was significantly lower in the euthyroid compared to the thyrotoxic state. A higher baseline thyroid-stimulating hormone (TSH)-receptor antibody (TRAb) corresponded to a greater improvement in exercise capacity and physical quality of life on resolution of the hyperthyroidism.
Conclusion: Graves’ hyperthyroidism causes a hyperdynamic right ventricle which normalises on restoration to the euthyroid state.