Alterations in the transmural gradient of ventricular repolarization with different pacing sites in normal and heart failure canines.
- Author:
Tao WANG
1
;
Zhan-Qi PANG
1
;
Xue-Qi LIN
1
;
Bo-Wen SONG
1
;
Zhuo-Ran LI
1
;
Shi-Jun LI
1
;
Yun-Long XIA
2
Author Information
1. Department of Cardiology, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian 116033, China.
2. First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. yunlong_xia@126.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Arrhythmias, Cardiac;
Dogs;
Heart;
Heart Failure;
Heart Ventricles;
Humans;
Myocardium
- From:
Acta Physiologica Sinica
2020;72(4):419-425
- CountryChina
- Language:English
-
Abstract:
Alterations of the transmural gradient of repolarization may contribute to the increase of transmural dispersion of repolarization and ventricular arrhythmias. The transmural gradient of repolarization may play an important role in sudden death associated with left ventricular epicardial pacing. To investigate the changes of transmural gradient dispersion of ventricular repolarization with different pacing sites in heart failure (HF) canines, 8 mongrel dogs were randomized into healthy group and HF group (n = 4). We mapped the monophasic action potential duration (MAPD) in the subendocardial, subepicardial and mid-myocardial layers of the left ventricle (LV) in canines of healthy and HF groups during right atrium (RA) pacing, right ventricular apical endocardial (RV) pacing, left ventricular lateral epicardial (LV) pacing and biventricular (Biv) pacing respectively. The results showed that in the healthy group, the MAPDs were significantly different among the three layers during RA pacing (all P < 0.05). The MAPD was longer in the mid-myocardial layer compared with those in the subepicardial and subendocardial layers during RV, LV or Biv pacing (P < 0.05). However, there was no significant difference in MAPD between the subendocardial and subepicardial layers during RV, LV or Biv pacing (P > 0.05). In the HF group, the MAPDs in all three layers were prolonged compared with those in the same locations in the healthy group (all P < 0.05). However, there were no differences in MAPD among the three layers during RA, RV, LV or Biv pacing (all P > 0.05). By MAP recording with our new mapping electrode, we found a transmural MAPD gradient among the three layers of the LV during RA pacing and the gradient between the subendocardial and subepicardial layers vanished during RV, LV or Biv pacing in healthy dogs. In contrast, there was no transmural MAPD gradient during RA, RV, LV or Biv pacing in HF dogs. These results are helpful to understand the mechanism of ventricular arrhythmias in patients with HF.
