TY - JOUR
T1 - Should we abandon the term 〝lone atrial fibrillation〞?
AU - Lin, Kai bin
AU - Marine, Joseph E.
AU - Calkins, Hugh
AU - Nazarian, Saman
AU - Wei, Meng
AU - Huang, Dong
AU - Li, Jing bo
N1 - Funding Information:
The present study was supported by grants from the National Natural Science Foundation of China (NSFC, no. 81571363 and no. 81871102 ), Shanghai Pujiang Talent Project (no. 17PJD029 ) to Dr. Dong Huang, and National Natural Science Foundation of China (NSFC, no. 81770282 ) to Dr. Meng Wei.
Publisher Copyright:
© 2019 Hellenic Society of Cardiology
PY - 2019/7/1
Y1 - 2019/7/1
N2 - 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.
AB - 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.
KW - biomarker
KW - clinical management
KW - genetics
KW - lone atrial fibrillation
KW - mechanism
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U2 - 10.1016/j.hjc.2019.04.005
DO - 10.1016/j.hjc.2019.04.005
M3 - Review article
C2 - 31004765
AN - SCOPUS:85065248659
SN - 1109-9666
VL - 60
SP - 216
EP - 223
JO - Hellenic Journal of Cardiology
JF - Hellenic Journal of Cardiology
IS - 4
ER -