Abbreviations:
AF = atrial fibrillation
AWT = atrial wall thickness
CE-MRA = contrast-enhancement magnetic resonance angiography
CT = computed tomography
LA = left atrium
LAA = left atrial appendage
LGE-MRI = late-gadolinium enhanced magnetic resonance imaging
MRs = meandering rotors
MWs = multiple wavelets
NPAs = non-passively activated areas
PAs = passively activated areas
PV = pulmonary vein
PVI = pulmonary vein isolation
RA = right atrium
ROC = receiver operating characteristic
SD = standard deviation
3D = three-dimensional
%NP = non-passively activated ratio
Introduction
Pulmonary vein isolation (PVI) is a well-established ablation strategy for paroxysmal atrial fibrillation (AF), but it is much less effective in persistent AF patients.1 Late-gadolinium enhanced magnetic resonance imaging (LGE-MRI) has been reported to detect myocardial fibrosis. Furthermore, the progression of atrial fibrosis after catheter ablation may be associated with AF recurrence.2 It has been previously reported that AF drivers are observed in patchy LGE areas but not in dense LGE areas, in computer simulation models.3 That shows the importance of a qualitative and quantitative analysis of the LGE areas. Recently, the modulation of the AF drivers has been proposed as one of the effective ablation strategies for persistent AF.4 To evaluate the location of AF drivers precisely, a novel phase mapping system (ExTRa MappingTM; Nihon Kohden, Japan) has been developed.5 ExTRa Mapping is a phase map based on myocardial action potentials, which has been validated by high-resolution optical membrane potential mapping in an animal study.6 We previously reported that AF drivers detected by the ExTRa Mapping were frequently found in heterogenous LGE areas assessed by LGE-MRI in persistent AF patients. However, some of them were also found in lesser LGE areas.7 This has implied that there are other possible structural factors associated with AF drivers. A previous computer simulation study demonstrated the role of the atrial wall thickness (AWT) as a substrate for AF drivers and marker for the identification of AF driver locations in patient-specific atria, and the AWT gradients acted as anchoring points for AF drivers in the absence of fibrosis.8 However, such an effect of the AWT on AF drivers has not been fully verified in humans. The aim of this study was to evaluate the impact of the AWT in lesser LGE areas on AF drivers in persistent AF patients.
Methods