Prevalence of echocardiographic criteria for the diagnosis of pulmonary hypertension in patients with Graves’ disease: Before and after antithyroid treatment

• Published in: Journal of endocrinological investigation Vol. 34; no. 8; pp. e229 - e234
• Main Authors: Suk, J. H., Cho, K. I., Lee, S. H., Lee, H. G., Kim, S. M., Kim, T. I., Kim, M. K., Shong, Y. K.
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.09.2011
• Subjects: Adolescent; Adult; Aged; Antithyroid Agents - therapeutic use; Echocardiography; Endocrinology; Female; Graves Disease - blood; Graves Disease - complications; Graves Disease - drug therapy; Humans; Hypertension, Pulmonary - diagnosis; Hypertension, Pulmonary - diagnostic imaging; Hypertension, Pulmonary - etiology; Male; Medicine; Medicine & Public Health; Metabolic Diseases; Methimazole - therapeutic use; Middle Aged; Original Articles; Thyroid Hormones - blood; Young Adult; Graves’ disease; pulmonary hypertension
• ISSN: 0391-4097; 1720-8386
• DOI: 10.3275/7573

Background: Right-sided heart failure with clinical manifestation is only occasionally seen in patients with Graves’ disease (GD). Recent studies revealed that pulmonary hypertension (PHT) detected by echocardiography was not rare in patients with GD. We performed this study to investigate the prevalence of PHT in patients with GD before and after antithyroid treatment, and to assess potential mechanisms from the relationship with clinical and echocardiographic features. Subjects and methods: Serial echocardiographic examinations were performed in 64 patients with newly diagnosed GD before and after antithyroid treatment to measure cardiac factors, such as pulmonary artery systolic pressure (PAPs), cardiac output, total vascular resistance, left ventricular filling pressure and right ventricular (RV) function. PHT was defined as PAPs of at least 35 mmHg. Results: The prevalence of PHT in untreated GD patients was 44% (28 out of 64 patients). The presence of systemic hypertension was associated with PHT, especially with pulmonary venous hypertension. GD patients with PHT showed reduced RV function represented by higher RV myocardial performance index without difference of pulmonary vascular resistance, RV wall thickness and peak systolic velocity of free wall side of tricuspid annulus. Follow-up echocardiography was performed in 20 out of 28 GD patients with PHT, and PHT disappeared in all except one patient. Conclusion: PHT is a frequent and reversible complication in patients with GD. Our study suggests that PHT in GD may not be related to underlying autoimmune process and increased pulmonary blood flow from thyrotoxicosis might contributes to the pathogenesis of PHT related to GD.