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Am J Physiol Heart Circ Physiol 279: H1737-H1747, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1737-H1747, October 2000

Endocardial activation during ventricular fibrillation in normal and failing canine hearts

Gordon L. Pierpont1,2, Sumeet S. Chugh1,2, John A. Hauck3, and Charles C. Gornick1,2

1 Minneapolis Veterans Administration Medical Center, Minneapolis 55417; 2 University of Minnesota, Minneapolis 55455; and 3 Endocardial Solutions Incorporated, St. Paul, Minnesota 55113

Because congestive heart failure (CHF) promotes ventricular fibrillation (VF), we compared VF in seven dogs with CHF induced by combined myocardial infarction and rapid ventricular pacing to VF in six normal dogs. A noncontact, multielectrode array balloon catheter provided full-surface real-time left ventricular (LV) endocardial electrograms and a dynamic color-coded display of endocardial activation projected onto a three-dimensional model of the LV. Fast Fourier transform (FFT) analysis of virtual electrograms showed no difference in peak or centroid frequency in CHF dogs compared with normals. The average number of simultaneous noncontiguous wavefronts present during VF was higher in normals (2.4 ± 1.0 at 10 s of VF) than in CHF dogs (1.3 ± 1.0, P < 0.005) and decreased in both over time. The wavefront "turnover" rate, estimated using FFT of the noncontiguous wavefront data, did not differ between normals and CHF and did not change over 5 min of VF. Thus the fundamental frequency characteristics of VF are unaltered by CHF, but dilated abnormal ventricles sustain fewer active wavefronts than do normal ventricles.

arrhythmia; ventricular arrhythmias; cardiomyopathy


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T. H. Everett IV, E. E. Wilson, S. Foreman, and J. E. Olgin
Mechanisms of Ventricular Fibrillation in Canine Models of Congestive Heart Failure and Ischemia Assessed by In Vivo Noncontact Mapping
Circulation, September 13, 2005; 112(11): 1532 - 1541.
[Abstract] [Full Text] [PDF]


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