Endocrine Abstracts (2009) 20 P131

Regression of pulmonary arterial hypertension after treatment of hyperthyroidism

Ana Rosa Quidute1, Joyce Paiva1, Virgínia Fernandes1, Clarisse Ponte1, Rejane Magalhães1, Renan Montenegro1, Ana Gardênia Farias2, Carlos Roberto Rodrigues Sobrinho2,4 & Renan Montenegro Júnior1,3


1Endocrinology and Diabetes Service, Walter Cantídio University Hospital, Federal University of Ceará, Fortaleza, Ceará, Brazil; 2Cardiology Service, Walter Cantídio University Hospital, Federal University of Ceará, Fortaleza, Ceará, Brazil; 3Comunity Health Department, Faculty of Medicine, Federal University of Ceará, Fortaleza, Ceará, Brazil; 4Clinical Medicine Department, Faculty of Medicine, Federal University of Ceará, Fortaleza, Ceará, Brazil.


Several pathological processes contribute to the development and progression of pulmonary arterial hypertension (PAH), which is a disorder with high morbidity and mortality rates. However, although cardiac manifestations are common in hyperthyroidism (HT), they have been seldom described in association with HT. Thus, the objective of this study was to evaluate echocardiographic parameters in patients with Graves Disease (GD) during uncontrolled hyperthyroidism and after its reversion with radioactive iodine therapy. We evaluate prospectively six patients with GD, (41.0±14.6 years), of whom four were female. The PAH was defined using Systolic Pulmonary Arterial Pressure (SPAP) ≥30 mmHg. The SPAP was determined by measuring the average of the regurgitation flow through the tricuspid valve (Bernoulli’s equation). Tricuspid insufficiency (TI) was classified as mild, moderate and severe. In the initial evaluation these six patients had suppressed TSH, raised free T4 (5.4±0.9 ng/dl) and raised T3 (431.8±137.0 ng/dl). In the initial evaluation all the patients had raised SPAP (61.0±9.7 mmHg), 16.6% (1/6) had severe TI, 66.6% (4/6) moderate TI and 16.6% (1/6) mild TI, and five patients had severe manifestations of right cardiac insufficiency. After the normalization of thyroid function they all presented a reversal of the PAH (PSAP 30.83±3.06 mmHg) and mild TI. There was no correlation between the free T4 and SPAP during HT (r=0.00621; P<0.05). This data suggests an association between hyperthyroidism and PAH. The observation of this abnormality in patients with hyperthyroidism as well as its regression after euthyroidism reestablishment demonstrate the importance of systematic echocardiographic evaluation of hyperthyroid patients, especially of those who present right cardiac insufficiency.

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