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

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• 作者：Bo He¹ ; Zhibing Lu¹ ; Wenbo He ; Liu Wu ; Bing Huang ; Lilei Yu ; Bo Cui ; Xiaorong Hu ; Hong Jiang ; ^{jianghong58@gmail.com}
• 关键词：Ganglionated plexi stimulation ; Ventricular electrophysiology ; Acute myocardial ischemia
• 刊名：Autonomic Neuroscience
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：174
• 期：1-2
• 页码：54-60
• 全文大小：597 K

文摘

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.