PURPOSE: Previous studies have described a reduction in triiodthyronine (T3) serum levels in patients with cardiac disease. Low T3 has been reported to be a prognostic marker in congestive heart failure. However systematic data on T3 serum levels in patients with pulmonary arterial hypertension are scarce. Therefore this prospective study evaluates the role of T3 in patients with pulmonary arterial hypertension (PAH).
METHODS: In 25 patients with PAH, mean pulmonary artery pressure 46.8±15.6 mmHg, WHO functional class II-III, (12 idiopathic, 8 thrombembolic, 5 associated with interstitial lung disease), thyroid function and respiratory muscle function (maximal inspiratory mouth occlusion pressure (Pimax) and 0.1 s after beginning of inspiration during tidal breathing at rest (P0.1)) were evaluated. Right ventricular function, systolic pulmonary artery pressure (PAP), tricuspid annular plane systolic excursion (TAPSE), Tei Index, systolic strain and strain rate were assessed by echocardiography.
RESULTS: In 18 patients, free T3 serum levels were reduced (1.8 ± 0.3 ng/l, normal range 2.0-4.2 ng/l). In those patients Pimax (5.2±2 kPa) was reduced and the P0.1/Pimax ratio was increased as compared to patients with normal fT3 (0.068±0.0065 vs. 0.022±0.009, p<0.005). There was a moderate correlation between fT3 and Pimax and P0.1/Pimax respectively (r= 0.61 and r=0.54, p<0.001). There was no significant correlation between fT3 and echocardiographic parameters of right ventricular performance.
CONCLUSION: This study provides first evidence of false normal thyroid function in patients with PAH, which might contribute to respiratory muscle dysfunction. The pathomechanisms and the prognostic significance of a “ low T3 syndrome” in PAH need further investigation.
CLINICAL IMPLICATIONS: Noninvasive monitoring of patients with pulmonary arterial hypertension.
DISCLOSURE: Arthur Filusch, None.