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Cardiac hypertrophy as a result of long-term thyroxine therapy and thyrotoxicosis
G W Ching1, J A Franklyn, T J Stallard
1Department of Cardiovascular Medicine, University of Birmingham, Queen Elizabeth Hospital.
Insights
Long-term thyroxine treatment can cause left ventricular hypertrophy without affecting heart rate or blood pressure. Further studies are needed to assess cardiovascular risk in patients on long-term thyroid hormone therapy.
Area of Science:
- Cardiology
- Endocrinology
- Thyroid Research
Background:
- Thyroid hormone replacement therapy is common.
- The cardiovascular effects of long-term thyroxine treatment require further elucidation.
- Thyrotoxicosis significantly impacts cardiovascular function.
Purpose of the Study:
- To investigate the long-term effects of thyroxine treatment on cardiac function and autonomic indices.
- To compare these effects with findings in patients with thyrotoxicosis.
- To assess changes before and during antithyroid drug treatment for thyrotoxicosis.
Main Methods:
- Cross-sectional and longitudinal study designs.
- Inclusion of patients on long-term thyroxine, patients with thyrotoxicosis, and controls.
- Utilized 24-hour ambulatory monitoring, echocardiography, and autonomic function tests.
Main Results:
- Long-term thyroxine treatment led to a significant increase in left ventricular mass index (18.4%) without altering heart rate, blood pressure, or systolic function.
- Thyroxine treatment and thyrotoxicosis did not affect autonomic function tests.
- Untreated thyrotoxicosis caused increased blood pressure, heart rate, and improved cardiac function, all reversible with treatment.
Conclusions:
- Left ventricular hypertrophy in patients on long-term thyroxine suggests a direct trophic effect of thyroid hormone on the heart.
- The development of left ventricular hypertrophy necessitates further research into cardiovascular risk.
- Cardiovascular changes in thyrotoxicosis are reversible with appropriate treatment.
Objectives:
To define the effects of long-term thyroxine treatment upon heart rate, blood pressure, left ventricular systolic function, and left ventricular size, as well as indices of autonomic function, and to compare findings with those in patients with thyrotoxicosis before and during treatment.
Design:
Cross sectional study of patients prescribed thyroxine long term (n = 11), patients with thyrotoxicosis studied at presentation (n = 23), compared with controls (n = 25); longitudinal study of patients with thyrotoxicosis studied at presentation and serially 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-term thyroxine treatment in doses that reduced serum thyrotrophin to below normal had no effect on blood pressure, heart rate, left ventricular systolic function or stroke volume index, but was associated with an 18.4% increase in left ventricular mass index (mean (SEM) 101.9 (3.09) g/m2 v controls 86.1 (4.61), P < 0.01). Thryoxine treatment, like thyrotoxicosis, had no effect on tests of autonomic function. Untreated thyrotoxicosis resulted in pronounced changes in systolic and diastolic blood pressure and an increase in heart rate during waking and sleep. Patients with thyrotoxicosis at presentation had an increase in left 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/m2 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/m2); all changes were corrected within 2 months by antithyroid drugs.
Conclusions:
The development of left ventricular hypertrophy in patients receiving thyroxine in the absence of significant changes in heart rate, blood pressure, and left ventricular systolic function is consistent with a direct trophic effect of thyroid hormone on the myocardium. The presence of left ventricular hypertrophy determines that further studies are essential to assess cardiovascular risk in patients taking thyroxine long term.