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

Taresh Taneja, George Horvath, Darlene K. Racker, Jeffrey Goldberger, Alan Kadish

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Excitable Gap in Infarcted Canine Myocardium. Introduction: The existence of an excitable gap during ventricular fibrillation (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 was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112-electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 ± 17 msec and 37 18 msec, respectively) and chronic infarction dogs (41 ± 14 msec and 35 ± 14 msec, respectively) 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 activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute 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 pathophysiology of VF and targeting antiarrhythmic therapies.

Original languageEnglish (US)
Pages (from-to)708-715
Number of pages8
JournalJournal of Cardiovascular Electrophysiology
Issue number6
StatePublished - 2001
Externally publishedYes


  • Electrophysiology
  • Excitable gap
  • Fibrillation
  • Infarction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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