Enhanced arrhythmogenic potential induced by renal autonomic nerve stimulation: Role of renal artery catheter ablation

Renal artery catheter ablation has been reported as a possible therapeutic option for drug-refractory ventricular arrhythmias (VAs) associated with structural heart diseases. To further clarify its therapeutic background, we examined the relationship between electrical nerve stimulation (ENS)–induce...

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Veröffentlicht in:Heart rhythm 2020-01, Vol.17 (1), p.133-141
Hauptverfasser: Chinushi, Masaomi, Saitoh, Osamu, Sugai, Ayari, Oikawa, Ayaka, Watanabe, Junya, Furushima, Hiroshi
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Sprache:eng
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Zusammenfassung:Renal artery catheter ablation has been reported as a possible therapeutic option for drug-refractory ventricular arrhythmias (VAs) associated with structural heart diseases. To further clarify its therapeutic background, we examined the relationship between electrical nerve stimulation (ENS)–induced blood pressure (BP) elevation and occurrence of VAs by using an acute canine model of renal artery ablation. Using a decapolar electrode catheter, ENS was successively applied from the distal, mid, and proximal segments of the renal artery in 8 beagles. The same ENS was repeated after accomplishment of radiofrequency ablation at the ostial site of the renal artery by using an irrigation catheter. Before ablation, ENS increased BP from 140 ± 11/77 ± 11 to 167 ± 20/98 ± 16 mm Hg and heart rate from 100 ± 21 to 131±33 beats/min as well as induced VAs in 20 of the 45 ENS applications. Occurrence of VAs was associated with a greater magnitude of sympathetic nerve augmentation, and VAs were more frequently observed by ENS at the distal (67%) rather than mid/proximal segments of the renal artery (33%). Renal artery ablation was accomplished without any angiographic stenosis, and ENS-induced BP elevation, heart rate acceleration, and VAs occurrence were attenuated not only at the close segment (proximal) but also at the remote segments (mid/distal) of the renal artery. The renal autonomic nerves are considered as one of the therapeutic targets for suppression of frequent VAs because its activation has arrhythmogenic potential and induces premature ventricular beats.
ISSN:1547-5271
1556-3871
DOI:10.1016/j.hrthm.2019.07.029