Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts

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Circulation. 1985;72:596-611

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Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts

PI Gardner, PC Ursell, JJ Fenoglio Jr and AL Wit

The electrophysiologic and anatomic basis for fractionated electrograms were investigated in superfused epicardial preparations from infarcted canine hearts. Fractionated bipolar electrograms were frequently recorded in preparations from infarcts 2 weeks to 18 months old but only rarely in preparations from 5-day-old infarcts. The fractionated electrograms were not caused by movement artifacts. They were not associated with depressed transmembrane resting or action potentials (which were found in the 5-day-old infarcts), but rather transmembrane potentials recorded in the vicinity of the bipolar electrodes were normal. Despite the normal transmembrane potentials, activation time in regions where fractionated electrograms occurred was prolonged. However, prolonged activation time by itself did not cause fractionation, since fractionated electrograms were not recorded from normal preparations in which conduction was markedly slowed by a superfusate containing 16 mM potassium and epinephrine. Unipolar electrograms recorded with glass microelectrodes (tip size 1 to 5 microns) showed that activation in regions where fractionated electrograms were recorded was inhomogeneous. Prepotentials were found preceding the upstrokes of some action potentials in regions where double potentials were recorded, suggesting the possibility of electrotonic transmission across high resistance or inexcitable gaps, but no electrotonic potentials were seen in regions with multicomponent fractionated electrograms. Fractionated electrograms were recorded in regions where infarct healing caused wide separation of individual myocardial fibers while distorting their orientation. The anatomic changes probably caused slow and inhomogeneous activation.

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				E. J. Ciaccio, C. Costeas, J. Coromilas, and A. L. Wit Static Relationship of Cycle Length to Reentrant Circuit Geometry Circulation, October 16, 2001; 104(16): 1946 - 1951. [Abstract] [Full Text] [PDF]

				E. J. Ciaccio, A. C. Tosti, and M. M. Scheinman Relationship Between Sinus Rhythm Activation and the Reentrant Ventricular Tachycardia Isthmus Circulation, July 31, 2001; 104(5): 613 - 619. [Abstract] [Full Text] [PDF]

				K.-C. Koch, J. vom Dahl, M. Wenderdel, B. Nowak, W. M. Schaefer, A. Sasse, C. Stellbrink, U. Buell, and P. Hanrath Myocardial viability assessment by endocardial electroanatomic mapping: comparison with metabolic imaging and functional recovery after coronary revascularization J. Am. Coll. Cardiol., July 1, 2001; 38(1): 91 - 98. [Abstract] [Full Text] [PDF]

				T. Wolf, L. Gepstein, U. Dror, G. Hayam, R. Shofti, A. Zaretzky, G. Uretzky, U. Oron, and S. A. Ben-Haim Detailed endocardial mapping accurately predicts the transmural extent of myocardial infarction J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1590 - 1597. [Abstract] [Full Text] [PDF]

				M. J. Schalij, L. Boersma, M. Huijberts, and M. A. Allessie Anisotropic Reentry in a Perfused 2-Dimensional Layer of Rabbit Ventricular Myocardium Circulation, November 21, 2000; 102(21): 2650 - 2658. [Abstract] [Full Text] [PDF]

				L. Gepstein, G. Hayam, S. Shpun, D. Cohen, and S. A. Ben-Haim Atrial Linear Ablations in Pigs : Chronic Effects on Atrial Electrophysiology and Pathology Circulation, July 27, 1999; 100(4): 419 - 426. [Abstract] [Full Text] [PDF]

				D. Li, S. Fareh, T. K. Leung, and S. Nattel Promotion of Atrial Fibrillation by Heart Failure in Dogs : Atrial Remodeling of a Different Sort Circulation, July 6, 1999; 100(1): 87 - 95. [Abstract] [Full Text] [PDF]

				J. E. Saffitz, R. B. Schuessler, and K. A. Yamada Mechanisms of remodeling of gap junction distributions and the development of anatomic substrates of arrhythmias Cardiovasc Res, May 1, 1999; 42(2): 309 - 317. [Full Text] [PDF]