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Abstract <p>The neurotransmitter acetylcholine (ACh) is known for itsdualistic effects: it promotes regeneration in structural cardiovasculardisorders and increases arrhythmia susceptibility, as has been widelydescribed for the ventricles. Atrial fibrillation (AF) is a multifactorialarrhythmia associated with increased parasympathetic tone and postmenopausalestrogen deficiency, which further leads to changes in cardiac fatmorphology and function. We estimated the structural remodelingof the left and right atria (LA, RA) and cardiac adipose tissuein a rat model of ACh-CaCl<sub>2</sub>-induced AF under6-weeks estrogen deficiency (AF+OVX). Sham-operated rats (Ctr),rats with ACh-CaCl<sub>2</sub>-induced AF developedwithout estrogen deficiency (AF), and rats with bilateral ovariectomy(OVX) were used to verify the morphological changes observed inthe AF+OVX model. In both AF and AF+OVX, atria showed signs of myocardial dystrophy—adecrease in LA cardiomyocyte length (in the AF group) and width(in the AF+OVX group). In the AF and AF+OVX, we observed reducedcellularity in the RA without changes in collagen content as wellas cardiac adipose tissue or leptin production. OVX rats did notshow changes in atrial morphology, nor in cardiac adipose tissue.In the AF and AF+OVX groups, we found a smoothing of interatrialdifferences in morphology which were present in the Ctr group andpersisted in the OVX group. We conclude that the atrial morphologyis less sensitive to estrogen deficiency compared with cholinergicoverload-triggered AF, leading to a significant atrial remodelingin minimal terms. However, we prognosticate an increased impactof estrogen deficiency if pathology prolongs.</p>

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Adverse Cardiac Structural Remodelling Induced by Cholinergic Atrial Fibrillation Regardless of Estrogen Deficiency in Rats

  • 期刊论文

  • 发表日期：

    2025年7月1日

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  • Е. А. Mukhlynina,
  • X. A. Butova,
  • T. A. Myachina,
  • D. A. Kuznetsov,
  • R. A. Simonova,
  • D. V. Shchepkin

摘要

Abstract

The neurotransmitter acetylcholine (ACh) is known for itsdualistic effects: it promotes regeneration in structural cardiovasculardisorders and increases arrhythmia susceptibility, as has been widelydescribed for the ventricles. Atrial fibrillation (AF) is a multifactorialarrhythmia associated with increased parasympathetic tone and postmenopausalestrogen deficiency, which further leads to changes in cardiac fatmorphology and function. We estimated the structural remodelingof the left and right atria (LA, RA) and cardiac adipose tissuein a rat model of ACh-CaCl2-induced AF under6-weeks estrogen deficiency (AF+OVX). Sham-operated rats (Ctr),rats with ACh-CaCl2-induced AF developedwithout estrogen deficiency (AF), and rats with bilateral ovariectomy(OVX) were used to verify the morphological changes observed inthe AF+OVX model. In both AF and AF+OVX, atria showed signs of myocardial dystrophy—adecrease in LA cardiomyocyte length (in the AF group) and width(in the AF+OVX group). In the AF and AF+OVX, we observed reducedcellularity in the RA without changes in collagen content as wellas cardiac adipose tissue or leptin production. OVX rats did notshow changes in atrial morphology, nor in cardiac adipose tissue.In the AF and AF+OVX groups, we found a smoothing of interatrialdifferences in morphology which were present in the Ctr group andpersisted in the OVX group. We conclude that the atrial morphologyis less sensitive to estrogen deficiency compared with cholinergicoverload-triggered AF, leading to a significant atrial remodelingin minimal terms. However, we prognosticate an increased impactof estrogen deficiency if pathology prolongs.