Hypertension, most commonly diastolic, is increased in patients with hypothyroidism because of increased peripheral vascular resistance. Hypertension is caused by hypothyroidism in 3 percent of patients with high blood pressure. Hypercholesterolemia and an increase in fatty acids are also associated with low thyroid function, thus increasing the risk of cardiovascular disease. Thyroid hormone supplementation does not always lower blood pressure. This failure of treatment may be related to impaired aortic elasticity and stiffness. Dernellis and Panaretou examined the effect of thyroid hormone supplementation in patients with hypothyroidism and hypertension. They also investigated the effect of treatment on aortic stiffness in these patients and the relationship between this factor and the blood pressure response.

Thirty patients with elevated blood pressure, primary hypothyroidism, normal coronary arteries, and no other major disease made up the study group. The three comparison groups consisted of (1) patients with hypothyroidism and normal blood pressure, (2) patients with hypertension and normal thyroid function, and (3) patients with neither high blood pressure nor hypothyroidism. All patients with hypothyroidism were treated with increasing doses of levothyroxine until a euthyroid state was achieved, as determined by thyroid-function testing. Patients who remained hypertensive after normalization of thyroid hormone function were given felodipine. Patients who had hypertension but not hypothyroidism were treated with felodipine alone. Aortic stiffness was determined using echocardiographic aortic diameter measurements at differing times in the cardiac cycle.

Participants with hypertension and hypothyroidism had increased aortic stiffness. Treatment with thyroid hormone normalized blood pressure in 15 of the 30 participants in the hypothyroid-hypertensive study group, while aortic stiffness decreased among the entire group. When the 15 participants whose blood pressures did not normalize with hormone supplementation were then treated with felodipine, blood pressure was normalized in all, along with a further decrease in aortic stiffness. Aortic stiffness also decreased in the subjects in the comparison groups when thyroid function and blood pressure were normalized. Systolic blood pressure correlated with changes in aortic stiffness, confirming that a large percentage of the changes in systolic blood pressure resulted from changes in aortic stiffness.

The authors conclude that hypothyroidism causes aortic stiffness and hypertension (usually diastolic). Thyroid hormone therapy decreases aortic stiffness, promoting decreased blood pressure in about 50 percent of these patients. Antihypertensive treatment further improves aortic elasticity and can decrease blood pressure among patients with hypertension and hypothyroidism whose blood pressure does not drop as thyroid function is normalized.