Bharaj Inderjeet Singh, Brar Ajit Singh, Kahlon Jasraj, Singh Anmol, Hotwani Priya, Kumar Vikash, Sohal Aalam, Batta Akash
Department of Internal Medicine, Abrazo Health Network, Glendale, AZ 85308, United States.
Department of Internal Medicine, Michigan State University at Hurley Medical Center, Flint, MI 48503, United States.
World J Cardiol. 2025 Jun 26;17(6):106147. doi: 10.4330/wjc.v17.i6.106147.
Metabolic dysfunction-associated steatotic liver disease (MASLD) significantly contributes to cardiovascular morbidity, with cardiovascular disease being the leading cause of mortality among affected individuals. Atrial fibrillation (AF), the most common cardiac arrhythmia, is frequently observed in patients with MASLD. While shared metabolic risk factors such as obesity, diabetes, dyslipidemia, and hypertension are implicated, underlying pathophysiological mechanisms that include systemic inflammation, oxidative stress, insulin resistance, endothelial dysfunction, and activation of the renin-angiotensin-aldosterone system (RAAS) are proposed to play significant part in the increased risk of AF in MASLD. The aim is to review the pathogenesis linking MASLD and AF. A comprehensive literature review was conducted, focusing on studies that explore the epidemiology, pathogenesis, and clinical implications of MASLD and AF. Databases searched included PubMed, Scopus, and Web of Science, with keywords such as "metabolic associated steatotic liver disease", "non fibrotic metabolic associated steatohepatitis", "Nonalcoholic fatty liver disease", "metabolic syndrome", "atrial fibrillation", "antifibrotic therapies", "pathogenesis", and "cardiovascular risk". Chronic low-grade inflammation and oxidative stress in MASLD contribute to atrial structural and electrical remodeling, fostering an arrhythmogenic substrate. Insulin resistance, a hallmark of MASLD, exacerbates metabolic dysfunction and promotes atrial fibrosis. Dysregulated lipid metabolism and gut microbiota alterations further compound cardiovascular risk. Aldosterone dysregulation and systemic inflammation stemming from RAAS activation contributes to the shared pathophysiology. The severity of MASLD does not seem to directly influence the risk of AF, suggesting that even early stages of liver disease can increase susceptibility to this arrhythmia. Effective management of MASLD requires targeted risk-factor modification strategies, including weight management, glycemic control, and pharmacological interventions. A multidisciplinary approach is essential for comprehensive assessment and management of MASLD patients, with a focus on cardiovascular risk assessment and arrhythmia prevention. Future research should explore the impact of emerging MASLD therapeutic agents on the incidence and recurrence of cardiac arrhythmias. Early detection and comprehensive management of MASLD and AF are crucial to mitigate the dual burden of these conditions.
代谢功能障碍相关脂肪性肝病(MASLD)显著增加心血管疾病的发病率,心血管疾病是该病患者的主要死亡原因。心房颤动(AF)是最常见的心律失常,在MASLD患者中经常出现。虽然肥胖、糖尿病、血脂异常和高血压等共同的代谢风险因素与之相关,但包括全身炎症、氧化应激、胰岛素抵抗、内皮功能障碍以及肾素-血管紧张素-醛固酮系统(RAAS)激活在内的潜在病理生理机制被认为在MASLD患者发生AF风险增加中起重要作用。目的是综述连接MASLD和AF的发病机制。进行了全面的文献综述,重点关注探索MASLD和AF的流行病学、发病机制及临床意义的研究。检索的数据库包括PubMed、Scopus和科学网,关键词有“代谢相关脂肪性肝病”、“非纤维化代谢相关脂肪性肝炎”、“非酒精性脂肪性肝病”、“代谢综合征”、“心房颤动”、“抗纤维化治疗”、“发病机制”和“心血管风险”。MASLD中的慢性低度炎症和氧化应激导致心房结构和电重构,形成致心律失常基质。胰岛素抵抗是MASLD的一个标志,会加剧代谢功能障碍并促进心房纤维化。脂质代谢失调和肠道微生物群改变进一步增加心血管风险。RAAS激活导致的醛固酮失调和全身炎症促成了共同的病理生理过程。MASLD的严重程度似乎并不直接影响AF风险,这表明即使是肝病早期也会增加对这种心律失常的易感性。有效管理MASLD需要有针对性的风险因素修正策略,包括体重管理、血糖控制和药物干预。多学科方法对于全面评估和管理MASLD患者至关重要,重点是心血管风险评估和心律失常预防。未来的研究应探索新兴的MASLD治疗药物对心律失常发生率和复发率的影响。早期发现和全面管理MASLD和AF对于减轻这些疾病的双重负担至关重要。