Why the study?
Excessive sympathetic activity aggravates arrhythmogenic processes in AF and leads to β1-adrenoreceptor desensitization, which may be reflected in changes in ADRB1 gene expression.
Does ablation alter the expression of the β1-adrenoreceptor gene (ADRB1) in patients with different forms of atrial fibrillation?
Does ablation alter the expression of the β1-adrenoreceptor gene (ADRB1) in patients with different forms of atrial fibrillation?
Ablation for atrial fibrillation induces dynamic, form-specific changes in β1-adrenoreceptor gene expression, potentially reflecting autonomic nervous system remodeling.
Atrial fibrillation (AF) is one of the most frequent cardiac arrhythmias and leads to heart failure. Excessive sympathetic activity aggravates arrhythmogenic processes at the cellular and tissue levels. Hypersympathicotonia leads to desensitization of β1-adrenoreceptors (β1-AR), negative regulation develops until the synthesis of new receptors stops. Desensitization processes may be indirectly reflected in an increase or decrease in the expression of the ADRB1 gene encoding β1-AR. The level of relative expression of the β1-AP ADRB1 gene in leukocytes of 52 patients with different forms of AF was analyzed in dynamics: before treatment, 3 days, 3 and 12 months after ablation. Before ablation, expression was reduced in patients with persistent AF compared to groups with other forms of AF (р = 0.026). The study of dynamics revealed a significant decrease in the level of expression in patients with paroxysmal AF at the point of 3 days compared with the level before ablation (p = 0.003), with a further increase in values to the baseline at the point of 12 months (p = 0.021) relative to the point of 3 days. In patients with persistent AF, the expression level significantly increased 3 months after ablation (p = 0.046) compared to the level before surgery. Patients with long-term persistent AF after ablation had a tendency to decrease expression.
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Popova et al. (2024) studied this question.
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