Effects of Thyroid Replacement Therapy on Arterial Blood Pressu
Effects of Thyroid Replacement Therapy on Arterial Blood Pressu
Background. Hypothyroidism is frequently accompanied by cardiac dysfunction, increased vascular resistance, and a greater prevalence of hypertension. Treatment of hypothyroidism may lead to normalization of blood pressure, although some patients may exhibit sustained hypertension. The mechanism of this condition may be the alterations in aortic stiffness.
Methods. Aortic stiffness was studied in 30 patients who never received treatment for hypertension or hypothyroidism, 15 patients with normal blood pressure and hypothyroidism, and 15 patients with hypertension and normal thyroid function. Thirty healthy age- and sex-matched subjects with normal thyroid function served as control subjects. Aortic diameter evaluated by M-mode echocardiography and blood pressure measured by a sphygmomanometer were used to calculate aortic stiffness index.
Results. Patients with high blood pressure and hypothyroidism, those with normal blood pressure and hypothyroidism, and those with hypertension and normal thyroid function showed increased aortic stiffness index (18.8 ± 6.4, 11.7 ± 3.5, and 19.2 ± 5.3 vs 9.5 ± 2.7; P < .001) compared with control subjects. In 15 patients with hypertension and hypothyroidism, levothyroxine therapy showed only a small decrease in blood pressure (151/105 ± 9/9 mm Hg, group A). The remaining 15 patients showed complete normalization of blood pressure (118/83 ± 8/3 mm Hg, group B). Aortic stiffness index was increased in group A compared with group B both before and after treatment (before, 24.0 ± 4.1 vs 13.7 ± 3.2; and after, 22.3 ± 4.2 vs 11.1 ± 2.9; P < .001 for both comparisons). Felodipine was given to patients in group A after levothyroxine was administered, resulting in normalization of blood pressure and a significant decrease of aortic stiffness index (P < .001). Aortic stiffness index was decreased in patients with hypothyroidism and hypertension after administration of levothyroxine (9.5 ± 2.2; P < .001) and felodipine (14.5 ± 7.5; P < .001) therapy, respectively. Percent changes in systolic blood pressure showed a significant correlation with percent changes in aortic stiffness index in all patients (r = 0.65, P < .001). After multivariate adjustment, aortic stiffness index (odds ratio = 1.9932; confidence interval = 1.1481 to 3.4605) was significantly associated with incomplete normalization of blood pressure.
Conclusions. Patients with hypertension and hypothyroidism have increased aortic stiffness. Aortic stiffness is decreased in all patients, whereas hypertension is completely reversible in 50% of patients by hormone replacement therapy. Sustained hypertension may be due to increased aortic stiffness.
The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiovascular function in patients with hypothyroidism. In patients with hypothyroidism, a true enhanced incidence of hypertension (increased peripheral vascular resistance) has been found. The reported prevalence of hypertension in hypothyroidism varies between 0% and 50%. Hypothyroidism has been identified as a cause of hypertension in 3% of patients with high blood pressure. Patients with hypothyroidism have a 3-fold increased prevalence of hypertension, usually diastolic. In addition, hypercholesterolemia and impairment of fatty acid mobilization are associated with myxedema and present additional risk factors for the development of atherosclerotic cardiovascular disease.
Thyroid hormone replacement therapy in patients with high blood pressure and hypothyroidism do not always successfully decrease the blood pressure. The pathogenesis and the exact mechanism of sustained hypertension in spite of pharmaceutical normal thyroid function have not been delineated. Impairment of the aortic elastic properties may be the cause for the incomplete normalization of blood pressure in patients with hypothyroidism and hypertension. But no study has examined the elastic properties of the aorta before and after hormone replacement therapy in patients with hypothyroidism and high blood pressure.
The aim of this study was to investigate the reversibility of arterial hypertension and of the impairment in aortic stiffness as measured by echocardiography after restoration of normal thyroid function in patients with hypertension and hypothyroidism. Furthermore, we examined any possible relation between aortic stiffness and the response of blood pressure to levothyroxine.
Background. Hypothyroidism is frequently accompanied by cardiac dysfunction, increased vascular resistance, and a greater prevalence of hypertension. Treatment of hypothyroidism may lead to normalization of blood pressure, although some patients may exhibit sustained hypertension. The mechanism of this condition may be the alterations in aortic stiffness.
Methods. Aortic stiffness was studied in 30 patients who never received treatment for hypertension or hypothyroidism, 15 patients with normal blood pressure and hypothyroidism, and 15 patients with hypertension and normal thyroid function. Thirty healthy age- and sex-matched subjects with normal thyroid function served as control subjects. Aortic diameter evaluated by M-mode echocardiography and blood pressure measured by a sphygmomanometer were used to calculate aortic stiffness index.
Results. Patients with high blood pressure and hypothyroidism, those with normal blood pressure and hypothyroidism, and those with hypertension and normal thyroid function showed increased aortic stiffness index (18.8 ± 6.4, 11.7 ± 3.5, and 19.2 ± 5.3 vs 9.5 ± 2.7; P < .001) compared with control subjects. In 15 patients with hypertension and hypothyroidism, levothyroxine therapy showed only a small decrease in blood pressure (151/105 ± 9/9 mm Hg, group A). The remaining 15 patients showed complete normalization of blood pressure (118/83 ± 8/3 mm Hg, group B). Aortic stiffness index was increased in group A compared with group B both before and after treatment (before, 24.0 ± 4.1 vs 13.7 ± 3.2; and after, 22.3 ± 4.2 vs 11.1 ± 2.9; P < .001 for both comparisons). Felodipine was given to patients in group A after levothyroxine was administered, resulting in normalization of blood pressure and a significant decrease of aortic stiffness index (P < .001). Aortic stiffness index was decreased in patients with hypothyroidism and hypertension after administration of levothyroxine (9.5 ± 2.2; P < .001) and felodipine (14.5 ± 7.5; P < .001) therapy, respectively. Percent changes in systolic blood pressure showed a significant correlation with percent changes in aortic stiffness index in all patients (r = 0.65, P < .001). After multivariate adjustment, aortic stiffness index (odds ratio = 1.9932; confidence interval = 1.1481 to 3.4605) was significantly associated with incomplete normalization of blood pressure.
Conclusions. Patients with hypertension and hypothyroidism have increased aortic stiffness. Aortic stiffness is decreased in all patients, whereas hypertension is completely reversible in 50% of patients by hormone replacement therapy. Sustained hypertension may be due to increased aortic stiffness.
The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiovascular function in patients with hypothyroidism. In patients with hypothyroidism, a true enhanced incidence of hypertension (increased peripheral vascular resistance) has been found. The reported prevalence of hypertension in hypothyroidism varies between 0% and 50%. Hypothyroidism has been identified as a cause of hypertension in 3% of patients with high blood pressure. Patients with hypothyroidism have a 3-fold increased prevalence of hypertension, usually diastolic. In addition, hypercholesterolemia and impairment of fatty acid mobilization are associated with myxedema and present additional risk factors for the development of atherosclerotic cardiovascular disease.
Thyroid hormone replacement therapy in patients with high blood pressure and hypothyroidism do not always successfully decrease the blood pressure. The pathogenesis and the exact mechanism of sustained hypertension in spite of pharmaceutical normal thyroid function have not been delineated. Impairment of the aortic elastic properties may be the cause for the incomplete normalization of blood pressure in patients with hypothyroidism and hypertension. But no study has examined the elastic properties of the aorta before and after hormone replacement therapy in patients with hypothyroidism and high blood pressure.
The aim of this study was to investigate the reversibility of arterial hypertension and of the impairment in aortic stiffness as measured by echocardiography after restoration of normal thyroid function in patients with hypertension and hypothyroidism. Furthermore, we examined any possible relation between aortic stiffness and the response of blood pressure to levothyroxine.
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