CARDIAC-HYPERTROPHY AS A RESULT OF LONG-TERM THYROXINE THERAPY AND THYROTOXICOSIS

Citation
Gw. Ching et al., CARDIAC-HYPERTROPHY AS A RESULT OF LONG-TERM THYROXINE THERAPY AND THYROTOXICOSIS, HEART, 75(4), 1996, pp. 363-368
Citations number
34
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
HEARTACNP
ISSN journal
13556037
Volume
75
Issue
4
Year of publication
1996
Pages
363 - 368
Database
ISI
SICI code
1355-6037(1996)75:4<363:CAAROL>2.0.ZU;2-5
Abstract
Objectives-To define the effects of long-term thyroxine treatment upon heart rate, blood pressure, left ventricular systolic function, and l eft ventricular size, as well as indices of autonomic function, and to compare findings with those in patients with thyrotoxicosis before an d during treatment. Design-Cross sectional study of patients prescribe d thyroxine long term (n = 11), patients with thyrotoxicosis studied a t presentation (n = 23), compared with controls (n = 25); longitudinal study of patients with thyrotoxicosis studied at presentation and ser ially after beginning antithyroid drug treatment (n = 23). Methods-24 h ambulatory monitoring of pulse and blood pressure, echocardiography, forearm plethysmography, and autonomic function tests. Results-Long-t erm thyroxine treatment in doses that reduced serum thyrotrophin to be low normal had no effect on blood pressure, heart rate, left ventricul ar systolic function or stroke volume index, but was associated with a n 18.4% increase in left ventricular mass index (mean (SEM) 101.9 (3.0 9) g/m(2) v controls 86.1 (4.61), P < 0.01). Thyroxine treatment, like thyrotoxicosis, had no effect on tests of autonomic function. Untreat ed thyrotoxicosis resulted in pronounced changes in systolic and diast olic blood pressure and an increase in heart rate during waking and sl eep. Patients with thyrotoxicosis at presentation had an increase in l eft ventricular systolic function (ejection fraction 70.5 (1.66)% v 65 .4 (1.79), P < 0.01; fractional shortening 40.4 (1.54)% v 35.6 (1.46), P < 0.01), increased stroke volume index (45.9 (2.4) ml/m(2) v 36.6 ( 1.7), P < 0.001), and an increase in forearm blood flow, and decrease in vascular resistance. They had a similar degree of left ventricular hypertrophy to that associated with thyroxine treatment (99.3 (4.03) g /m(2)); all changes were corrected within 2 months by antithyroid drug s. Conclusions-The development of left ventricular hypertrophy in pati ents receiving thyroxine in the absence of significant changes in hear t rate, blood pressure, and left ventricular systolic function is cons istent with a direct trophic effect of thyroid hormone on the myocardi um. The presence of left ventricular hypertrophy determines that furth er studies are essential to assess cardiovascular risk in patients tak ing thyroxine long term.