Abstract
This article is devoted to the effect of the renin-angiotensin-aldosterone system on the development and maintenance of atrial fibrillation on patients with arterial hypertension. It is noted that the adverse effects of the renin-angiotensin-aldosterone system end products, angiotensin II and aldosterone, can be caused not only by their hyperproduction, but also by the activation of the transforming growth factor β1 initiated by them. This cytokine initiates the process of fibrosis in the left atrium, which is a substrate of arrhythmia. The article features the results of multicenter clinical trial demonstrating the effectiveness of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and mineralocorticoid receptor antagonists in the prevention of atrial fibrillation. The review includes the analysis of the effect of polymorphic variants of the angiotensin-converting enzyme gene ((I/D) ACE), the angiotensin II receptor gene type 1 ((A1166C) AGTR1), the aldosterone synthase gene (C/T (-344) CYP11B2) and the gene of the transforming growth factor β1 (G/C (+915) TGFB1) on the development of arterial hypertension and atrial fibrillation, as well as on the effectiveness of therapy with renin-angiotensin-aldosterone system blocking drugs.
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