Characterization and consistency of interactions of triggers and substrate at the onset of paroxysmal atrial fibrillation.
OBJECTIVE
Initiating mechanisms of atrial fibrillation (AF) remain poorly understood, involving complex interaction between triggers and the atrial substrate. This study sought to classify the transitional phenomena, hypothesizing that there is consistency within and between patients in trigger-substrate interaction during transition to AF.


RESULTS
Non-contact left atrial (LA) mapping was performed in 17 patients undergoing ablation for paroxysmal AF. All had spontaneous ectopy. Left atrial activation from the first ectopic to established AF was examined offline to characterize the initiating and transitional sequence of activation. In 57 fully mapped spontaneous AF initiations in 8 patients, all involved interaction of pulmonary venous/LA triggers with a septopulmonary line of block (SP-LOB) also evident in sinus rhythm, by 4 different transitional mechanisms characterized by (i) continuous focal firing: AF resulted from fragmentation of each ectopic wavefront through gaps in the SP-LOB and persisted only while focal firing continued (n = 18/32%) (ii) transient focal firing, wavefront fragmentation at the SP-LOB produced wavelet re-entry that persisted after cessation of an initiating ectopic source (n = 12/21%), (iii) of two separate interacting ectopic foci (n = 15/26%), or from (iv) transiently stable macroreentry (n = 12/21%), around the SP-LOB extending to the LA roof, resulting in progressive wavefront fragmentation. It was found that 79 ± 22% of each of the initiations in individual patients showed the same triggering mechanism.


CONCLUSIONS
Onset of paroxysmal AF can be described by discrete mechanistic categories, all involving interaction of ectopic activity with a common SP-LOB. Within/between-patient consistency of initiations suggests constancy of the interacting triggers and substrate, and supports the concept of mechanistically tailored treatment.
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.|Royal Brompton & Harefield NHS Foundation Trust, London, UK.
David G
DG
Jones
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.|Royal Brompton & Harefield NHS Foundation Trust, London, UK.
Vias
V
Markides
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.
Anthony W C
AWC
Chow
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.
Richard J
RJ
Schilling
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.
Prapa
P
Kanagaratnam
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.|Royal Brompton & Harefield NHS Foundation Trust, London, UK.
Tom
T
Wong
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.
D Wyn
DW
Davies
St Mary's Hospital, Imperial College NHS Trust, London, UK.|Imperial College London, London, UK.
Nicholas S
NS
Peters
D000200:Action Potentials; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D017115:Catheter Ablation; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology* / Q000601:surgery; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D013997:Time Factors
Atrial fibrillation; Mapping; Mechanisms; Substrate; Triggers