Abstract

<h3>Conflict of Interest</h3> Dr. O’Hare has been the recipient of educational grants from Daiichi Sankyo and Johnson and Johnson Medical Ltd. during the course of this study. <h3>Background</h3> The complex pathogenesis of atrial fibrillation (AF) remains unclear. A key concept is that for AF to be sustained, both a trigger and an atrial substrate capable of perpetuating the arrhythmia are required. Pathological remodelling in the atria can be observed after only a few minutes of high atrial rate, with the chronicity of these changes being directly related to the duration of the episodes of high atrial rate. This underpins the often-quoted axiom ‘AF begets AF’. Increased atrial fibrosis in patients with AF has been observed in both histological and non-invasive studies using LGE-CMR atrial imaging. Reduced atrial conduction velocity (CV) has been observed in fibrotic areas, which may propagate AF as more wavefronts can be sustained in the atria. It is unclear if reduced atrial CV is a prerequisite for AF, or if it develops after the initial periods of arrhythmia. The use of 3D electro-anatomical mapping (EAM) has led to advancement in the accuracy of intra-cardiac CV measurement and investigations into the mechanism for reduced CV. <h3>Hypothesis</h3> We hypothesised that left atrial CV plays a key role in the AF disease process and investigation into atrial CV may improve understanding into the pathogenesis and clinical course of AF. METHODS A systematic review was performed to assess current published evidence. This informed the design of a retrospective study to calculate CV from the left atrial local activation time (LAT) electro-anatomical maps of 90 paroxysmal AF (PAF) and 90 persistent AF (PsAF) patients presenting for first time PVI. Following this, pathological mechanisms were assessed by looking at the associations between left atrial CV determined from EAMs and 3D atrial LGE-CMR in 96 patients. Finally, a pilot study was designed and undertaken to investigate if atrial CV at rest, and at varying heart rates with exercise can be measured non-invasively with the use of electrocardiographic imaging (ECGI) and CMR. <h3>Results</h3> There was no statistical difference in the left atrial CV of patients with PAF compared to PsAF (0.68 m/s vs 0.69 m/s respectively, p-value = 0.70). Left atrial CV did not predict recurrence of AF in the first year after PVI. (Figure 1) Regional analysis of 3D atrial LGE-CMR in 96 patients, found significant variation in the distribution of fibrosis, however fibrosis burden was not significantly correlated with either overall or regional CV. (Figure 2). A pilot study using ECGI with CMR imaging was able to non-invasively measure bi-atrial CV during rest and three exercise stages. CV restitution properties were not demonstrated in this healthy cohort in heart rates up to 150bpm. <h3>Conclusions</h3> Reduced atrial CV is a common finding in AF, however CV is similar in patients with PAF and PsAF in sinus rhythm during PVI. Alterations in CV did not correspond to fibrosis detected on atrial LGE-CMR, suggesting that pathological changes other than fibrotic remodelling account for the reduction in CV seen in these patients.

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