Pulmonary Arterial Hypertension in Patients with Hyperthyroid Graves’ Disease and Toxic Multinodular Goiter

source: Endocrine Society

year: 2017

authors: Gabriel Fenteany, Taiga Inoue, Gul Bahtiyar, Shaul Fishman, Alan Scott Sacerdote

A number of case reports and small series have been published suggesting an association between hyperthyroidism and pulmonary artery hypertension (PAH), although such an association is not widely appreciated among endocrinologists, cardiologists, or pulmonologists. Some authors have speculated that PAH in this setting is autoimmune in origin and, thus, likely to occur in Graves’ disease, but unlikely to occur in non-autoimmune hyperthyroidism.

We evaluated 24 patients with hyperthyroid Graves’ disease (GD) — confirmed by the combination of hyperthyroidism with increased titers of thyroid-stimulating immunoglobulin (TSIG) or thyroid peroxidase (TPO) antibody or thyroglobulin antibody — and 3 patients with antibody-negative toxic multinodular goiter (TMG with trans-thoracic 2-D echocardiography while they were hyperthyroid. In a smaller number of patients (3), we were able to repeat their echocardiograms when their hyperthyroidism had either much improved or they had actually become euthyroid. The cardiologist reading the echocardiograms was blinded as to their thyroid status. 54.2 % of the patients with GD and 100% of the patients with TMG had PAH. In the patients with repeat echocardiograms, mean pulmonary artery pressure dropped from 35.8 to 24.3 mmHg. One, previously reported patient closed a patent foramen ovale in association with amelioration of her hyperthyroidism and PAH. 

We conclude that PAH is common in both GD and TMG. The observation that it was present in a larger percentage of TMG patients than GD patients suggests that the phenomenon is more likely related to hyperthyroidism itself or to upper airway obstruction related to the goiter than to autoimmunity. Future studies involving patients with thyrotoxic adenoma, TSH-dependent hyperthyroidism, and athyreotic patients with iatrogenic hyperthyroidism would be of interest in clarifying the etiology of this common association.