Cardiac hypertrophy as a result of long-term thyroxine therapy and thyrotoxicosis.

Abstract

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/m' v controls 86-1 (4.61), P < 0.01). Thyroxine 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 (1P66)% 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) mu/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)

The Evaluation of Left Ventricular Hypertrophy in Hypertensive Patients with Subclinical Hyperthyroidism

“…Eleven of 17 subjects in group I were affected by multinodular goiter and the other 6 were affected by solitary thyroid nodule. Stable endogenous subclinical hyperthyroidism diagnosis was confirmed in all 17 patients of group I by screening for antithyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies once and by measuring TSH, fT 4 and fT 3 twice more within the following two months. Three dimensional ultrasound examination of thyroid tissue was performed for all subjects.…”

“…It has been demonstrated that exogenous subclinical hyperthyroidism, in which patients treated with TSHsuppressive doses of levothyroxine, may affect the heart as in subjects with overt hyperthyroidism, but it remains controversial whether endogenous subclinical hyperthyroidism affects the heart [3][4][5].…”

“…Subclinical hyperthyroidism can be the result of the same causes of overt clinical hyperthyroidism but patients with subclinical hyperthyroidism do not usually show specific symptoms and signs of hyperthyroidism [1,2]. It has been demonstrated that exogenous subclinical hyperthyroidism, in which patients treated with TSHsuppressive doses of levothyroxine, may affect the heart as in subjects with overt hyperthyroidism, but it remains controversial whether endogenous subclinical hyperthyroidism affects the heart [3][4][5].Situations in which thyroid hormones were increased have been shown to stimulate myocardial hypertrophy. Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity and mortality.…”

Thyrotoxic Cardiomyopathy

“…On the one hand, some authors found the increase in left ventricular myocardium mass in both overt (Nixon et al, 1979;Auer et al, 2001;Dorr et al, 2005;Marcisz et al, 2006) and subclinical (Ching et al, 1996;Biondi, 1999Biondi, , 2000Auer, 2001) thyrotoxicosis. On the other hand, there are not enough studies considering LVH occurrence in thyrotoxicosis and factors contributing its development, geometry type (eccentric or concentric), and reversibility.…”

“…The main manifestations of thyrotoxic cardiomyopathy (TCMP) are left ventricular hypertrophy (LVH) (Ching et al, 1996, Dorr et al, 2005, heart rhythm disturbances (usually, atrial fibrillation (AF)) (Dunn et al, 1986;Frost et al, 2004), dilation of the heart chambers and heart failure (HF) (Dougherty & Craige, 1973;Siu et al, 2007), pulmonary hypertension (PH) (Chu et al, 2002;Rubin & Badesch, 2006), and diastolic dysfunction. Epidemiology data on TCMP are currently lacking.…”