Increased wave break during ventricular fibrillation in the epicardial border zone of hearts with healed myocardial infarction.
BACKGROUND
The action potential duration (APD) restitution hypothesis of wave break during ventricular fibrillation (VF) in the epicardial border zone (EBZ) of hearts with chronic myocardial infarction is unknown.


RESULTS
VF was induced by rapid pacing, and the EBZ with the two adjoining sites (right ventricle and lateral left ventricle) were sequentially mapped in random order in 7 open-chest anesthetized dogs 6 to 8 weeks after left anterior descending artery occlusion and in 4 control dogs. At each site, 3 seconds of VF was mapped with 477 bipolar electrodes 1.6 mm apart. The number of wave fronts and approximate entropy were significantly (P:<0.01) higher in the EBZ than all other sites in both groups independent of the rate of invasion of new wave fronts and epicardial breakthroughs. The higher wavelet density in the EBZ was caused by increased (P:<0.01) incidence of spontaneous wave breaks. There was no difference between the two groups in either reentry period (80 episodes) or VF cycle length. Reentry in the EBZ had a smaller core perimeter, slower rotational speed, and a small or no excitable gap (P:<0.01), often causing termination after one rotation. The dynamic monophasic action potential duration restitution curve in the EBZ had longer (P:<0.01) diastolic intervals, over which the slope was >1. Connexin43-positive staining was significantly (P:<0.01) and selectively reduced in the EBZ.


CONCLUSIONS
A selective increase in wave break and alteration of reentry occur in the EBZ during VF in hearts with healed myocardial infarction. Increased wave break in the EBZ is compatible with the action potential duration restitution hypothesis.
Ohara
T
T
Division of Cardiology, Cedars-Sinai Research Institute, the Departments of Medicine and Pathology, UCLA School of Medicine, Los Angeles, CA, USA.
Ohara
K
K
Cao
J M
JM
Lee
M H
MH
Fishbein
M C
MC
Mandel
W J
WJ
Chen
P S
PS
Karagueuzian
H S
HS
D000200:Action Potentials; D000818:Animals; D018031:Connexin 43 / Q000378:metabolism; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D008297:Male; D008871:Microvilli / Q000502:physiology; D009203:Myocardial Infarction / Q000503:physiopathology*; D010496:Pericardium / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000503:physiopathology*
D018031:Connexin 43