Review links metabolic syndrome to 1.5 to 2 times higher atrial fibrillation risk

In recent years, atrial fibrillation (AF) has emerged as one of the most prevalent cardiac arrhythmias with escalating global incidence. Characterized by complex pathophysiology and unfavorable clinical outcomes, AF has become a focal point in cardiovascular research. Concurrently, metabolic syndrome (MetS)—a clinical constellation encompassing obesity, insulin resistance or impaired glucose metabolism, hypertension, and dyslipidemia—has evolved into a major global public health challenge. Accumulating clinical evidence indicates that MetS confers a 1.5–2 times increased risk of AF development compared with the general population, underscoring intricate pathophysiological interconnections between these conditions. Although conventional perspectives attribute this association primarily to obesity and hypertension, emerging research implicates multifactorial mechanisms including myocardial fibrosis, atrial electrical-structural remodeling, systemic inflammation, oxidative stress, adipokine dysregulation, and autonomic nervous system dysfunction. Nevertheless, the association of MetS with AF remains incompletely understood, with ongoing debates regarding the independent contributions and synergistic interactions of individual metabolic components in modifying atrial substrate. This review synthesizes current epidemiological evidence, explores the molecular mechanisms of the MetS and AF interfaces, and evaluates recent advances in clinical intervention strategies, with the aim of informing early preventive approaches and precision therapeutics.