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Coronary sinus pacing prevents induction of atrial fibrillation
P Papageorgiou1, F Anselme, C J Kirchhof
1Harvard-Thorndike Institute of Electrophysiology, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass 02215, USA.
Insights
Distal coronary sinus pacing prevents atrial fibrillation (AF) induction by high right atrial extrastimuli. This simpler pacing approach limits conduction delays, suppressing reentry crucial for AF development.
Area of Science:
- Electrophysiology
- Cardiac Pacing
- Arrhythmia Mechanisms
Background:
- Atrial fibrillation (AF) is a common arrhythmia often caused by reentry circuits.
- Previous studies suggest dual-site or biatrial pacing can reduce AF incidence.
- The role of specific pacing sites in preventing AF induction remains an area of investigation.
Purpose of the Study:
- To investigate if distal coronary sinus (CSd) pacing can prevent AF induction by high right atrial (HRA) premature atrial depolarizations (APDs).
- To test the hypothesis that CSd pacing mitigates conduction delays associated with AF inducibility.
Main Methods:
- Programmed electrical stimulation was performed using HRA and CSd pacing in 13 patients.
- Bipolar recordings were obtained from multiple atrial sites.
- Extrastimuli were delivered to assess AF inducibility under different pacing conditions.
Main Results:
- Atrial fibrillation was reproducibly induced by HRA APDs during HRA pacing.
- AF was not induced when HRA APDs were delivered during CSd pacing.
- CSd pacing significantly prolonged the APD coupling interval at the posterior triangle of Koch compared to HRA pacing.
Conclusions:
- Distal coronary sinus pacing effectively suppresses AF inducibility by HRA APDs.
- CSd pacing limits prematurity and local conduction delay at the posterior triangle of Koch, preventing reentry.
- This suggests CSd pacing is a potential strategy to prevent AF.
Background:
Atrial fibrillation (AF) is due to reentry, and its incidence has been shown to decrease after dual-site atrial or biatrial pacing. We investigated whether a simpler pacing approach via the distal coronary sinus (CSd) could eliminate AF inducibility by high right atrial (HRA) extrastimuli (APDs). We based our hypothesis on our previous observation that AF inducibility by HRA APDs was associated with conduction delays to the posterior triangle of Koch, whereas AF was never induced with CSd APDs, which were associated with minimal intra-atrial conduction delays.
Methods And Results:
Programmed electrical stimulation was performed from the high right atrium and CSd, and bipolar recordings were obtained from the high right atrium, His bundle, posterior triangle of Koch, and coronary sinus. In 13 patients (age, 44+/-18 years), AF was reproducibly induced with a critically timed HRA APD (220+/-22 ms) delivered during HRA pacing. AF was not induced in any of the patients when HRA APDs were delivered during CSd pacing at the same critical coupling intervals. Coronary sinus APDs delivered during HRA pacing also were not associated with AF induction. The APD coupling interval measured at the posterior triangle of Koch during CSd pacing was significantly prolonged compared with the one measured during HRA pacing and AF induction (381+/-58 versus 263+/-37 ms; P<.0001).
Conclusions:
We propose that CSd pacing suppresses the propensity of HRA APDs to induce AF by limiting their prematurity at the posterior triangle of Koch and not allowing local conduction delay and local reentry to occur.