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The aim of this work was to study the role of hypovolemia on pathogenesis of arterial hypertension (AH) in patients with primary hypothyroidism (PH) and specification of indirect signs indicative of increased circulating blood volume. 217patients with PH and AH (mean age 53.3 yr) received substitution therapy with sodium levothyroxin and standard hypotensive therapy with ACE inhibitors. All the patients allocated to 3 groups were examined by 24 hour Holter monitoring and measurement of serum TSH and free T4. Group 1 (n = 74) were patients with compensated PH, group 2 (n = 57) comprised patients with subclinical hypothyroidism, group 3 (n = 86) were patients with decompensated hypothyroidism. The latter group was dominated by non-dippers, the patients showed elevated systolic and diastolic AD, its small reduction and high variability at night time. These clinical and functional signs are supposed to reflect hypovolemia in patients with PH and concomitant AH.

Aim: To examine disturbances of cardiac rhythm and effects of autonomic nervous system on cardiovascular system in hypothyrosis patients as shown by circadian ECG monitoring., Material and Methods: A total of 171 patients with primary hypothyrosis (11 males, 160 females, mean age 56.2 +/- 4.8 years) were examined with circadian ECG monitoring. The patients were divided into two groups by the degree of hypothyrosis compensation. Group 1 (n = 87) had primary hypothyrosis in decompensation (TTH 14.78 +/- 1.3 mIU/l), group 2 (n = 84) had compensated hypothyrosis treated with sodium levothyroxin as replacement therapy (TTH 1.32 +/- 0.3 mIU/l)., Results: It was found that group 1 patients have bradycardia, subnormal circadian index, prolonged corrected interval Q-T, inhibition of atrioventricular conduction, increased number of supra- and ventricular extrasystoles, predominance of the parasympathetic autonomic nervous system in regulation of heart rhythm., Conclusion: Decompensated hypothyrosis is accompanied with significant disorders of cardiac activity and imbalance of autonomic nervous system which are corrected in hypothyrosis compensation.

The purpose of the investigation was to study the effects of hypothyroidism on the 24-hour profile of arterial pressure (AP). One hundred and fifty-one patients (mean age 52 +/- 3.2 years) with primary hypothyroidism and concomitant arterial hypertension were examined; the patients received substitutive therapy (levothyroxine sodium) and standard hypotensive therapy (ACE inhibitors and indapamide). Twenty-four-hour AP monitoring was performed; the level of thyrotropic hormone was measured by immune enzyme assay. The patients were distributed into two groups according their thyroid status. Group 1 consisted of 72 patients with compensated hypothyroidism; 79 patients with decompensated hypothyroidism constituted group 2. The study found the following facts about patients with decompensated hypothyroidism: higher systolic AP, high variability of nocturnal AP, insufficient decrease in AP during day hours, and accelerated morning AP increase. The results suggest that hypothyroidism has significant effects on the 24-hour AP profile, and its decompensation lowers the efficacy of hypotensive therapy.