代谢功能障碍相关的脂肪变性肝病和心房颤动:发病机制综述。

IF 2.8 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Inderjeet Singh Bharaj, Ajit Singh Brar, Jasraj Kahlon, Anmol Singh, Priya Hotwani, Vikash Kumar, Aalam Sohal, Akash Batta
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引用次数: 0

摘要

代谢功能障碍相关的脂肪变性肝病(MASLD)与心血管疾病的发病率有显著关系,心血管疾病是患者死亡的主要原因。房颤(AF)是MASLD患者中最常见的心律失常。虽然共同的代谢危险因素如肥胖、糖尿病、血脂异常和高血压都有关联,但潜在的病理生理机制,包括全身性炎症、氧化应激、胰岛素抵抗、内皮功能障碍和肾素-血管紧张素-醛固酮系统(RAAS)的激活,被认为在MASLD中AF风险增加中起重要作用。目的是回顾MASLD和房颤的发病机制。我们进行了全面的文献综述,重点探讨MASLD和房颤的流行病学、发病机制和临床意义。检索数据库包括PubMed、Scopus和Web of Science,检索关键词为“代谢性脂肪性肝病”、“非纤维化代谢性脂肪性肝炎”、“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的慢性低度炎症和氧化应激有助于心房结构和电重构,促进心律失常的底物。胰岛素抵抗,MASLD的标志,加剧代谢功能障碍和促进心房纤维化。脂质代谢失调和肠道菌群改变进一步加剧了心血管风险。由RAAS激活引起的醛固酮失调和全身性炎症有助于共同的病理生理。MASLD的严重程度似乎并不直接影响AF的风险,这表明即使是早期肝脏疾病也会增加对这种心律失常的易感性。MASLD的有效管理需要有针对性的风险因素调整策略,包括体重管理、血糖控制和药物干预。多学科方法对MASLD患者的综合评估和管理至关重要,重点是心血管风险评估和心律失常预防。未来的研究应探讨新出现的MASLD治疗药物对心律失常发生率和复发的影响。早期发现和综合管理MASLD和AF对于减轻这些疾病的双重负担至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Metabolic-dysfunction associated steatotic liver disease and atrial fibrillation: A review of pathogenesis.

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.

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来源期刊
World Journal of Cardiology
World Journal of Cardiology CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
3.30
自引率
5.30%
发文量
54
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