Model of bipolar electrogram fractionation and conduction block associated with activation wavefront direction at infarct border zone lateral isthmus boundaries.
BACKGROUND
Improved understanding of the mechanisms underlying infarct border zone electrogram fractionation may be helpful to identify arrhythmogenic regions in the postinfarction heart. We describe the generation of electrogram fractionation from changes in activation wavefront curvature in experimental canine infarction.


RESULTS
A model was developed to estimate the extracellular signal shape that would be generated by wavefront propagation parallel to versus perpendicular to the lateral boundary (LB) of the reentrant ventricular tachycardia (VT) isthmus or diastolic pathway. LBs are defined as locations where functional block forms during VT, and elsewhere they have been shown to coincide with sharp thin-to-thick transitions in infarct border zone thickness. To test the model, bipolar electrograms were acquired from infarct border zone sites in 10 canine heart experiments 3 to 5 days after experimental infarction. Activation maps were constructed during sinus rhythm and during VT. The characteristics of model-generated versus actual electrograms were compared. Quantitatively expressed VT fractionation (7.6±1.2 deflections; 16.3±8.9-ms intervals) was similar to model-generated values with wavefront propagation perpendicular to the LB (9.4±2.4 deflections; 14.4±5.2-ms intervals). Fractionation during sinus rhythm (5.9±1.8 deflections; 9.2±4.4-ms intervals) was similar to model-generated fractionation with wavefront propagation parallel to the LB (6.7±3.1 deflections; 7.1±3.8-ms intervals). VT and sinus rhythm fractionation sites were adjacent to LBs ≈80% of the time.


CONCLUSIONS
The results suggest that in a subacute canine infarct model, the LBs are a source of activation wavefront discontinuity and electrogram fractionation, with the degree of fractionation being dependent on activation rate and wavefront orientation with respect to the LB.
Division of Cardiology, Department of Medicine.
Edward J
EJ
Ciaccio
Hiroshi
H
Ashikaga
James
J
Coromilas
Bruce
B
Hopenfeld
Daniel O
DO
Cervantes
Andrew L
AL
Wit
Nicholas S
NS
Peters
Elliot R
ER
McVeigh
Hasan
H
Garan
D000200:Action Potentials; D000818:Animals; D003198:Computer Simulation; D004195:Disease Models, Animal; D004285:Dogs; D022062:Electrophysiologic Techniques, Cardiac; D006327:Heart Block / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006329:Heart Conduction System / Q000473:pathology / Q000503:physiopathology*; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
cardiac electrophysiology; electrical conductivity; electrophysiologic techniques, cardiac; infarction; tachycardia, ventricular