Excitable gap in canine fibrillating ventricular myocardium: Effect of subacute and chronic myocardial infarction

Introduction: The existence of an excitable gap during ventricular fibrilla tion (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. Methods and Results: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction, Experimental infarction w as produced by left anterior descending coronary ligation. The excitable ga p was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites usi ng recordings from a 112-electrode plaque sutured to the epicardial surface of the left ventricle, The excitable gap also was correlated to local elec trophysiologic and anatomic properties. The excitable gap using the wavefro nt propagation method and shortest activation method was significantly long er in subacute infarction dogs (48 +/- 17 msec and 37 +/- 18 msec, respecti vely) and chronic infarction dogs (41 +/- 14 msec and 35 +/- 14 msec, respe ctively) than normal dogs (32 +/- 13 msec and 30 +/- 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activatio n method, respectively. The excitable gap correlated better with local vent ricular refractoriness determined using the wavefront propagation method th an with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacu te infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. Conclusion: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction, These finding have implications for understanding the pathop hysiology of VF and targeting antiarrhythmic therapies.