Pulmonary vein isolation in patients with paroxysmal atrial fibrillation is associated with regional cardiac sympathetic denervation

Christian Wenning, Philipp S Lange, Christoph Schülke, Alexis Vrachimis, Gerold Mönnig, Otmar Schober, Lars Eckardt, Michael Schäfers, Christian Wenning, Philipp S Lange, Christoph Schülke, Alexis Vrachimis, Gerold Mönnig, Otmar Schober, Lars Eckardt, Michael Schäfers

Abstract

Background: Circumferential pulmonary vein isolation (PVI) is the cornerstone of the current state-of-the-art management of atrial fibrillation (AF). However, the precise mechanisms behind AF relapses post PVI are still unknown. Since the activity of the autonomous nervous system is crucial in triggering paroxysmal AF, we hypothesized that PVI is associated with changes of cardiac sympathetic activity.

Methods: Sixteen patients with paroxysmal AF underwent cardiac iodine-123-meta-iodobenzylguanidine (123I-mIBG) planar cardiac imaging and single-photon emission computed tomography with low-dose computed tomography (SPECT/CT) for attenuation correction before and 4 weeks after PVI. The heart-to-mediastinum ratio (H/M ratio), washout rate (WR), regional myocardial uptake, and regional washout were analyzed.

Results: The late H/M ratio was unchanged by PVI (pre, 2.9 ± 0.5 vs. post, 2.7 ± 0.6, p = 0.53). Four of the 16 patients (25%) displayed regional deficits before PVI. After PVI, regional deficits were present in ten patients (62.5%) with newly emerging deficits localized in the inferolateral wall. In a 6-month follow-up, four out of the ten patients (40%) with regional 123I-mIBG defects suffered from a recurrence of AF, while only one of the six patients (16.7%) without a regional 123I-mIBG defect experienced a recurrence.

Conclusion: A significant number of patients with paroxysmal AF show regional cardiac sympathetic innervation deficits at baseline. In addition, PVI is associated with newly emerging defects. The presence of regional sympathetic denervation after PVI may correlate with the risk of AF relapses.

Figures

Figure 1
Figure 1
Mean late H/M ratios and global WRs. Late H/M ratios (A) and global WR (B) before and after PVI indicate no changes in global sympathetic innervation.
Figure 2
Figure 2
Example of a patient with a new innervation defect after PVI. Short axis slices of the left ventricle 15 min and 4 h after 123I-mIBG injection before and after PVI. Regional late innervation deficit/increased regional washout after PVI affecting the basal inferolateral wall (white arrow). Increasing SDS (summed defect score) but Stable H/M ratio.
Figure 3
Figure 3
Development of the SDS (summed defect score) in the individual patients (pre-PVI versus post PVI).
Figure 4
Figure 4
Quantitative 17-segmental analysis. Quantitative 17-segmental analysis of the late 123I-mIBG uptake (left) and washout (right) of the left ventricle before (A) and after (B) PVI. Values are expressed as mean regional uptake in comparison to the regional maximum uptake and segmental washout (%). Significantly reduced uptake and increased regional washout after PVI (mean values after PVI compared with mean values before PVI) in the basal inferior and basal lateral segments (C).
Figure 5
Figure 5
Number of relapses in patients without (1/6) and with (4/10) innervation deficits post PVI.

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