The role of agtr1 gene a1166c (rs5186) polymorphism in the clinical course of chronic heart failure in patients after coronary artery bypass grafting
Received: 2026-02-22
Published: 2026-06-29
Abstract
The progression of chronic heart failure (CHF) after coronary artery bypass grafting (CABG) remains a pressing issue in cardiac surgery. This review systematizes current data on the impact of the A1166C (rs5186) single nucleotide polymorphism of the angiotensin II type 1 receptor gene (AGTR1) on post-infarction remodeling and surgical revascularization outcomes. The molecular genetic mechanism is considered, in which the transition of adenine to cytosine disrupts the binding of microRNA-155 to the gene’s mRNA, leading to pathological overexpression of AT1R on cell membranes. Under conditions of surgical stress, carrying the mutant C allele is associated with systemic inflammation, endothelial dysfunction, accelerated myocardial fibrosis, an increased risk of graft thrombosis, and the development of atrial fibrillation. Special attention is paid to the pharmacogenetic aspect: the phenomenon of "escape"during ACE inhibitor therapy is described in carriers of the C allele, which makes the prioritized prescription of angiotensin receptor blockers (ARBs/sartans) pathogenetically justified. The clinical significance of genotyping the rs5186 locus for personalizing neurohumoral blockade and improving the long-term prognosis of patients is emphasized.
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