Cheraghi Mostafa, Nazari Afshin, Souri Faraz
Cardiovascular Research Center, Shahid Rahimi Hospital, Lorestan University of Medical Sciences, Khorramabad, Iran.
Cardiovascular Research Center, Shahid Rahimi Hospital, Lorestan University of Medical Sciences, Khorramabad, Iran.
Pathol Res Pract. 2025 Jul 15;273:156125. doi: 10.1016/j.prp.2025.156125.
Cardiac arrhythmias, a leading cause of morbidity and mortality, have traditionally been linked to structural heart disease and genetic factors. However, growing evidence indicates that the gut microbiota, via its interactions with the cardiovascular system, may also contribute to arrhythmogenesis. The gut-heart axis, involving microbial metabolites, inflammatory signaling, and neural modulation, has emerged as a key regulator of cardiac electrophysiology.
This review summarizes recent preclinical and clinical studies investigating the role of gut microbiota in the pathophysiology of cardiac arrhythmias. We examine mechanisms through which microbial products like short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), and bile acids influence arrhythmic risk, with a focus on their effects on ion channels, inflammation, and autonomic regulation.
Evidence from both animal models and human studies indicates that dysbiosis, or imbalance in the gut microbiome, is associated with an increased risk of arrhythmias, including atrial fibrillation and ventricular tachycardia. Microbial metabolites have been shown to influence cardiac electrophysiology through direct and indirect mechanisms, including immune modulation and autonomic nervous system regulation. Furthermore, microbiome-based interventions, such as dietary changes, probiotics, and fecal microbiota transplantation, show promise in reducing arrhythmic burden.
The gut microbiota's metabolic, inflammatory, and neural connections with the cardiovascular system increasingly suggest its role in arrhythmia risk. Targeting this gut-heart axis could lead to personalized arrhythmia prevention and treatment strategies.
心律失常是发病和死亡的主要原因,传统上一直与结构性心脏病和遗传因素相关。然而,越来越多的证据表明,肠道微生物群通过与心血管系统的相互作用,也可能导致心律失常的发生。涉及微生物代谢产物、炎症信号传导和神经调节的肠-心轴已成为心脏电生理的关键调节因子。
本综述总结了最近调查肠道微生物群在心律失常病理生理学中作用的临床前和临床研究。我们研究了短链脂肪酸(SCFAs)、氧化三甲胺(TMAO)和胆汁酸等微生物产物影响心律失常风险的机制,重点关注它们对离子通道、炎症和自主神经调节的影响。
动物模型和人体研究的证据均表明,肠道微生物群失调或肠道微生物组失衡与心律失常风险增加有关,包括心房颤动和室性心动过速。微生物代谢产物已被证明通过直接和间接机制影响心脏电生理,包括免疫调节和自主神经系统调节。此外,基于微生物组的干预措施,如饮食改变、益生菌和粪便微生物群移植,在减轻心律失常负担方面显示出前景。
肠道微生物群与心血管系统的代谢、炎症和神经联系越来越表明其在心律失常风险中的作用。针对这一肠-心轴可能会产生个性化的心律失常预防和治疗策略。