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Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation.
J Am Coll Cardiol. 2005 Jun 07; 45(11):1878-86.JACC

Abstract

OBJECTIVES

This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF).

BACKGROUND

The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown.

METHODS

In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness.

RESULTS

Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p </=0.05. The fewest number of APDs from the RSPV required to induce AF during AG stimulation was as follows: control (no stimulation) 7 +/- 4, 2.4 V; 3 +/- 1, p </=0.05. In seven dogs, lidocaine (2%, 0.4 cc), a neuronal blocker, was injected into the fat pad, resulting in the loss of AF inducibility in six of seven dogs at the same AG stimulation levels. Three of seven dogs showed AF inducibility only with AG stimulation >/=9.3 V.

CONCLUSIONS

The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.

Authors+Show Affiliations

Scherlag BJ
Cardiac Arrhythmia Research Institute, Oklahoma University Medical Center, Oklahoma City, Oklahoma, USA. bejamin-scherlag@ouhsc.edu
Yamanashi W
No affiliation info available
Patel U
No affiliation info available
Lazzara R
No affiliation info available
Jackman WM
No affiliation info available

MeSH

AnimalsAtrial FibrillationDogsElectrocardiographyElectrophysiologic Techniques, CardiacGanglia, AutonomicPulmonary Veins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15936622

Clinical Trial Links

First Line Radiofrequency Ablation Versus Antiarrhythmic Drugs for Atrial Fibrillation Treatment (The RAAFT Study)

Citation

Scherlag, Benjamin J., et al. "Autonomically Induced Conversion of Pulmonary Vein Focal Firing Into Atrial Fibrillation." Journal of the American College of Cardiology, vol. 45, no. 11, 2005, pp. 1878-86.
Scherlag BJ, Yamanashi W, Patel U, et al. Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation. J Am Coll Cardiol. 2005;45(11):1878-86.
Scherlag, B. J., Yamanashi, W., Patel, U., Lazzara, R., & Jackman, W. M. (2005). Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation. Journal of the American College of Cardiology, 45(11), 1878-86.
Scherlag BJ, et al. Autonomically Induced Conversion of Pulmonary Vein Focal Firing Into Atrial Fibrillation. J Am Coll Cardiol. 2005 Jun 7;45(11):1878-86. PubMed PMID: 15936622.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation. AU - Scherlag,Benjamin J, AU - Yamanashi,William, AU - Patel,Utpal, AU - Lazzara,Ralph, AU - Jackman,Warren M, PY - 2004/08/17/received PY - 2005/01/10/revised PY - 2005/01/11/accepted PY - 2005/6/7/pubmed PY - 2005/6/25/medline PY - 2005/6/7/entrez SP - 1878 EP - 86 JF - Journal of the American College of Cardiology JO - J Am Coll Cardiol VL - 45 IS - 11 N2 - OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p </=0.05. The fewest number of APDs from the RSPV required to induce AF during AG stimulation was as follows: control (no stimulation) 7 +/- 4, 2.4 V; 3 +/- 1, p </=0.05. In seven dogs, lidocaine (2%, 0.4 cc), a neuronal blocker, was injected into the fat pad, resulting in the loss of AF inducibility in six of seven dogs at the same AG stimulation levels. Three of seven dogs showed AF inducibility only with AG stimulation >/=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF. SN - 0735-1097 UR - https://www.unboundmedicine.com/medline/citation/15936622/Autonomically_induced_conversion_of_pulmonary_vein_focal_firing_into_atrial_fibrillation_ DB - PRIME DP - Unbound Medicine ER -