ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 OC2.7

Impact of resistance to thyroid hormone on the cardiovascular system in adult humans

Melania Pulcrano1, Deborah Mannavola2, Emiliano A Palmieri3, Irene Campi2, Michele Ciulla2, Riccardo Michi2, Serena Ippolito1, Gaetano Lombardi1, Bernadette Biondi1 & Paolo Beck-Peccoz2

1Department of Clinical and Molecular Endocrinology and Oncology, University ‘Federico II’, Naples, Italy; 2Department of Medical Sciences, University of Milan, Fondazione Policlinico IRCCS, Milan, Italy; 3Division of Cardiology, Centro Traumatologico Ospedaliero, Naples, Italy.

Background: Resistance to thyroid hormone (RTH) is an inherited condition of reduced tissue responsiveness to thyroid hormone (TH), biochemically characterized by elevated serum TH concentrations, with inappropriate, non-suppressed thyrotropin levels (TSH). It is caused by point mutations in the ligand binding domain of the TH receptor (TR) β gene, and the mutant TR interferes with the function of the normal TRs (dominant negative effect). The clinical manifestations of RTH are highly variable and the impact of RTH on the cardiovascular system has been poorly investigated.

Aim: We compare the cardiovascular characteristics of 16 patients with RTH with those of euthyroid healthy controls to define the cardiovascular involvement in RTH syndrome.

Patients and methods: Sixteen RTH patients (8 males; age: 32±12 years, range: 19–63) and 16 controls (9 males; age: 33±5 years, range: 24–42) were included in the analysis. For each patient, clinical data (age, gender, body mass index, blood pressure, heart rate, cardiovascular symptoms) and assessment of thyroid status were recorded. An echocardiographic evaluation was performed by a single investigator, blinded to the subject’s clinical data.

Results: RTH patients did not show cardiovascular symptoms (palpitations, dyspnea at rest and after exercise). Heart rate was comparable to the control group whereas arterial pressure was higher than controls. RTH patients showed mean interventricular septum diastolic thickness (IST) and mean left ventricular posterior wall diastolic thickness (LVPWT), significantly lower than the controls with consequent significant decrease of the mean LV mass and LV mass indexed by body surface area. RTH patients also showed abnormalities of myocardial relaxation as indicated by the significant increase of peak-A and consequent reduction of E/A ratio. Finally, in RTH patients, systemic vascular resistance was significantly increased compared to those of the control group.

Conclusions: Our results suggest an altered and inefficient cardiovascular action of TH in RTH patients.