Effect of L-thyroxine treatment on left ventricular function in subclinical hypothyroidism

F Franzoni, F Galetta, P Fallahi, L Tocchini, G Merico, L Braccini, M Rossi, A Carpi, A Antonelli, G Santoro
Biomedicine & Pharmacotherapy 2006, 60 (8): 431-6
Aim of this study was to investigate the effects of thyroxine treatment on myocardial regional left ventricular (LV) systolic and diastolic function in patients with subclinical hypothyroidism (SH) by tissue Doppler imaging (TDI). Forty-two patients (29 women and 13 men; mean age 52.2+/-15.1 years) with SH, as judged by elevated serum thyroid-stimulating hormone (TSH) levels (>3.6 mIU/l; range, 3.8-12.0) and free thyroid hormones (FT4 and FT3) within the normal range, and 30 euthyroid volunteers (21 women and nine men; mean age 50.4+/-17.1 years) underwent standard echocardiography and TDI-derived early (Em) and late (Am) diastolic velocities, systolic (Sm) velocity, and isovolumetric relaxation time (IVRTm). Patients were randomly assigned to receive or not L-thyroxine replacement therapy. All patients returned after 6 months to repeat thyroid function tests and the evaluation of all parameters. No significant differences were seen in the Sm peak between SH and control groups. Respect to controls, SH patients exhibited a lower Em, a higher Am, and, subsequently, a reduced Em/Am ratio of both lateral wall (LW) and interventricular septum (IVS) (P<0.001 for both). The IVRTm was distinctly longer in SH patients, as compared to controls (P<0.001). At 6 months, L-thyroxine-treated patients showed a significant increase of Em (P<0.01) and a subsequent increase of the Em/Am ratio (P<0.01), whereas IVRTm significantly reduced (P<0.05). No significant change in any of these parameters was observed in the untreated group. Our data suggest that SH is associated with a subtle, reversible impairment of myocardial function. TDI analysis detects and extends these functional defects by displaying alterations in regional myocardial function. L-T4 replacement therapy should be advised for these patients with the aim to correct preclinical cardiac dysfunction and prevent the development of clinically significant myocardial dysfunction.

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