Abstract

A special role in the formation of atrial fibrillation in patients with arterial hypertension is played by diseases of the thyroid gland. In any form of hypothyroidism, vascular tone increases, hypervolemia is formed, which leads to changes in blood pressure, myocardial dystrophy and the development of AF. The development and progression of AF affects the lack of thyroid hormones: TH suppresses aldosterone synthesis and stimulates the secretion of atrial and cerebral natriuretic peptide. Therefore, hypothyroidism develops hyperaldosteronism and decreases the content of natriuretic hormone in the blood, which leads to hypervolemia. Atrophic processes in cardiomyocytes are exacerbated by intracellular potassium deficiency, which is caused by hyper aldosteronism characteristic of all types of hypothyroidism. TG plays the role of physiological antagonists of antidiuretic hormone, and their deficiency leads to increased water reabsorption and increases the likelihood of the formation of a volume-dependent form of hypertension, the effect on the endothelium of the cell, releasing vasoactive substances and reducing the sensitivity of adrenoreceptors to the action of catecholamines. In hypothyroidism, almost all soft tissues, including the vascular wall, accumulate in an excessive amount of glycosaminoglycans, which ' ions and water, which leads to swelling of the vascular wall, reduction of nitric oxide production and narrowing of the lumen of arteries and veins. Hyperproduction of thyroliberin, which leads to a decrease in dopaminergic activity of the brain. In addition, hypothyroidism causes thickening of the basement membrane of capillaries and the diffusion of oxygen through their wall is disturbed. The effect of hypothyroidism and drugs used in its treatment on AF is ambiguous. The authors disagree about the course of AF and the frequency of relapse, the risk of complications of AF. All this indicates the need to continue research in this direction.

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