Characterized by lack of evidence of structural heart disease or any secondary causes of atrial fibrillation (AF), “lone AF” is used to represent a unique subtype of AF among young individuals aged less than 60 years. Although the longstanding definition has been proposed for years, the diagnostic criteria for “lone AF” remain ambiguous. As more contributing factors causing AF are recognized gradually, the validity of the term “lone AF” is in question. Despite advances in the past few decades, the mechanism of AF remains poorly understood, particularly in the absence of other structural changes. It is generally accepted that three essential electrophysiological elements (trigger, substrate, and modulators) contribute to the initiation and maintenance of lone AF. In addition, the role of microRNAs and genomic variations in the pathogenesis of lone AF has been also gaining attention. Some changes in relevant biomarker levels have also been proven to correlate with lone AF. Accumulating insights into the pathogenesis of lone AF strongly suggest coexistent disorders in patients with lone AF. Consequently, the growing evidence of these numerous and diverse pathogenic mechanisms and factors related to lone AF inevitably raises the question of whether the term “lone AF” is a meaningful category. The classification of lone AF as a separate identity has not lead to any unique clinical management. In this review, we update knowledge of definition, mechanisms, genetics, biomarkers, and clinical management of “lone AF.” With this comprehensive review, we suggest that the term “lone AF” should be abandoned for its futility.
- clinical management
- lone atrial fibrillation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine