Abstract
Atrial fibrillation (AF) is the most prevalent arrhythmia in the general population. There is a close association between chronic kidney disease (CKD) and AF. In recent years, attention has been focused on the relationship between AF and uremic toxins, including indoxyl sulfate (IS). Several animal studies have shown that IS promotes the development and progression of AF. IS has been shown to cause fibrosis and inflammation in the myocardium and exacerbate AF by causing oxidative stress and reducing antioxidative defense. Administration of AST-120, an absorbent of uremic toxins, decreases uremic toxin-induced AF in rodents. We have recently reported that patients with a higher serum IS level exhibit a higher rate of AF recurrence after catheter ablation, with serum IS being a significant predictor of AF recurrence. In this review, we discuss the possible mechanisms behind the AF-promoting effects of uremic toxins and summarize the reported clinical studies of uremic toxin-induced AF.
Highlights
Atrial fibrillation (AF) is a common and chronic cardiovascular condition
An association between chronic kidney disease (CKD) and AF has been described, and several studies have revealed the complex relationship between CKD and AF
We focused on the causative association between uremic toxins and AF
Summary
Atrial fibrillation (AF) is a common and chronic cardiovascular condition. AF requires expensive health monitoring and treatment because AF patients have an increased risk of stroke, sudden death, heart failure, unplanned hospital admissions, and other complications [1,2,3,4]. The management of AF has substantially advanced, with significant developments in the past few decades, the contributing factors and mechanisms promoting AF are still unclear. An association between chronic kidney disease (CKD) and AF has been described, and several studies have revealed the complex relationship between CKD and AF. We focused on the causative association between uremic toxins and AF
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