Format

Send to

Choose Destination
See comment in PubMed Commons below
Auton Neurosci. 2013 Mar;174(1-2):54-60. doi: 10.1016/j.autneu.2013.01.004. Epub 2013 Jan 31.

Effects of low-intensity atrial ganglionated plexi stimulation on ventricular electrophysiology and arrhythmogenesis.

Author information

1
Department of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, PR China.

Abstract

BACKGROUND:

Atrial ganglionated plexi (GP) have been shown to modulate sinus rate, atrioventricular conduction and atrial electrophysiology. The aim of this study was to investigate the effect of low-intensity GP stimulation (GPS) on ventricular electrophysiological properties in normal heart and on ventricular arrhythmogenesis after acute myocardial ischemia (AMI) in canine.

METHODS AND RESULTS:

Thirty-nine dogs were assigned into the normal heart group (n=12) and the acute myocardial ischemia (AMI) group (n=27, 12 in control and 15 in low-intensity GPS). In the normal heart group, ventricular effective refractory period (ERP), dynamic restitution and electrical alternans were measured at baseline and after 6-hour low-intensity GPS. In the AMI group, the incidence of ventricular arrhythmias was determined during 1-hour recording after AMI was induced. In the normal heart, 6-hour low-intensity GPS significantly prolonged ventricular ERP and action potential duration (APD) at each site (all P<0.05) but did not change their spatial dispersions when compared with baseline. Low-intensity GPS also caused an upward shift of ventricular restitution curves in each site but did not change the slope of restitution curves. APD alternans after low-intensity GPS occurred at longer pacing cycle length at each site when compared with baseline (all P<0.05). In the AMI heart, the incidence of ventricular arrhythmias in low-intensity GPS group was significantly lower than that in control group (P<0.05).

CONCLUSIONS:

Low-intensity GPS induces no increase in the risk of ventricular arrhythmias in the normal heart as well as protects against ventricular arrhythmogenesis during AMI.

PMID:
23375649
DOI:
10.1016/j.autneu.2013.01.004
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center