Atrial fibrillation in hypertrophic cardiomyopathy - A contemporary mini-review.
Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheorese
Hypertrophic cardiomyopathy (HCM) represents the most common genetically inherited cardiovascular disorder and a leading cause of heart failure and sudden cardiac death. Atrial fibrillation (AF) is the most common arrhythmia encountered in HCM patients, primarily due to the process of left atrium dilatation and remodeling. Its presence typically leads to progressive functional decline, increased frequency of heart failure hospitalizations, and increased thromboembolic risk. In this mini-review, we summarize the contemporary data on AF pathophysiology, risk factors, and management in HCM patients suffering from AF.
Gut microbiota dysbiosis promotes age-related atrial fibrillation by lipopolysaccharide and glucose-induced activation of NLRP3-inflammasome.
Zhang Yun,Zhang Song,Li Bolin,Luo Yingchun,Gong Yongtai,Jin Xuexin,Zhang Jiawei,Zhou Yun,Zhuo Xiaozhen,Wang Zixi,Zhao Xinbo,Han Xuejie,Gao Yunlong,Yu Hui,Liang Desen,Zhao Shiqi,Sun Danghui,Wang Dingyu,Xu Wei,Qu Guangjin,Bo Wanlan,Li Dan,Wu Yue,Li Yue
AIMS:Ageing is the most significant contributor to the increasing prevalence of atrial fibrillation (AF). The gut microbiota dysbiosis is involved in age-related diseases. However, whether the aged-associated dysbiosis contributes to age-related AF is still unknown. Direct demonstration that the aged gut microbiota is sufficient to transmit the enhanced AF susceptibility in a young host via microbiota-intestinal barrier-atria axis has not yet been reported. This study aimed to determine whether gut microbiota dysbiosis affects age-related AF. METHODS AND RESULTS:Herein, by using a faecal microbiota transplantation (FMT) rat model, we demonstrated that the high AF susceptibility of aged rats could be transmitted to a young host. Specially, we found the dramatically increased levels of circulating lipopolysaccharide (LPS) and glucose led to the up-regulated expression of NOD-like receptor protein (NLRP)-3 inflammasome, promoting the development of AF, which depended on the enhanced atrial fibrosis in recipient host. Inhibition of inflammasome by a potent and selective inhibitor of the NLRP3 inflammasome, MCC950, resulted in a lower atrial fibrosis and AF susceptibility. Then, we conducted cross-sectional clinical studies to explore the effect of ageing on the altering trends with glucose levels and circulating LPS among clinical individuals in two China hospitals. We found that both of serum LPS and glucose levels were progressively increased in elderly patients as compared with those young. Furthermore, the ageing phenotype of circulating LPS and glucose levels, intestinal structure and atrial NLRP3-inflammasome of rats were also confirmed in clinical AF patients. Finally, aged rats colonized with youthful microbiota restored intestinal structure and atrial NLRP3-inflammasome activity, which suppressed the development of aged-related AF. CONCLUSIONS:Collectively, these studies described a novel causal role of aberrant gut microbiota in the pathogenesis of age-related AF, which indicates that the microbiota-intestinal barrier-atrial NLRP3 inflammasome axis may be a rational molecular target for the treatment of aged-related arrhythmia disease.
Inflammasome Signaling in Atrial Fibrillation: JACC State-of-the-Art Review.
Journal of the American College of Cardiology
As the most prevalent form of arrhythmia, atrial fibrillation (AF) increases the risk of heart failure, thromboembolism, and stroke, contributing to the raising mortality and morbidity in patients with cardiovascular diseases. Despite the multifaceted nature of AF pathogenesis and complexity of AF pathophysiology, a growing body of evidence indicates that the NLRP3 inflammasome activation contributes to onset and progression of AF. Herein, the authors aim at reviewing the current literature on the role of inflammasome signaling in AF pathogenesis, and novel therapeutic options in the management of AF.
Emerging Roles of Inflammasomes in Cardiovascular Diseases.
Frontiers in immunology
Cardiovascular diseases are known as the leading cause of morbidity and mortality worldwide. As an innate immune signaling complex, inflammasomes can be activated by various cardiovascular risk factors and regulate the activation of caspase-1 and the production and secretion of proinflammatory cytokines such as IL-1β and IL-18. Accumulating evidence supports that inflammasomes play a pivotal role in the progression of atherosclerosis, myocardial infarction, and heart failure. The best-known inflammasomes are NLRP1, NLRP3, NLRC4, and AIM2 inflammasomes, among which NLRP3 inflammasome is the most widely studied in the immune response and disease development. This review focuses on the activation and regulation mechanism of inflammasomes, the role of inflammasomes in cardiovascular diseases, and the research progress of targeting NLRP3 inflammasome and IL-1β for related disease intervention.