Circulation, Vol 76, 860-874, Copyright © 1987 by American Heart Association
MG Kienzle, RC Tan, BM Ramza, ML Young and RW Joyner
Permanent coronary occlusion produces time-dependent changes in surviving
subendocardial cellular properties. We compared the functional alterations
in Purkinje (P) and ventricular muscle (VM) activation early (24 hr) and
late (4 weeks or greater) after permanent coronary occlusion in an in vitro
preparation of canine papillary muscle. High-density extracellular (1 to 2
mm resolution) and selected intracellular recordings were made in five
animals early and seven animals late during stimulation of a free-running P
strand. Activation patterns of P and VM layers from ischemic and unaffected
papillary muscles were compared in the same animal. Average P layer
conduction velocity was determined in normal and ischemic regions with the
use of a linear array of recording and stimulating electrodes. Purkinje
activation was altered little in the early phase of infarction, while
healing was associated with a generalized 25% reduction in P layer
conduction velocity and localized block and fragmentation of P waveforms.
Intracellular recordings at sites of nonsynchronous P activation revealed
electrotonic interaction between cell groups. At 24 hr, small groups of VM
were present but with abnormal activation patterns in regions of necrosis
with fragmented and delayed extracellular waveforms produced by partially
uncoupled groups of cells. Local delay and block could be modulated by rate
and site of stimulation. After healing, VM activation abruptly stopped at
the visual infarct border, marked by a characteristic "end potential."
These studies demonstrate important differences in the functional
attributes of the P and VM layers studied early and late after coronary
occlusion. Alterations in cell-to-cell relationships are likely very
important in determining abnormalities of activation in both settings.
ARTICLES
Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction
Department of Internal Medicine, University of Iowa, Iowa City.
This article has been cited by other articles:
![]() |
A. O Verkerk, M. W Veldkamp, R. Coronel, R. Wilders, and A. C.G van Ginneken Effects of cell-to-cell uncoupling and catecholamines on Purkinje and ventricular action potentials: implications for phase-1b arrhythmias Cardiovasc Res, July 1, 2001; 51(1): 30 - 40. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Wilders, E. E. Verheijck, R. W. Joyner, D. A. Golod, R. Kumar, A. C. G. van Ginneken, L. N. Bouman, and H. J. Jongsma Effects of Ischemia on Discontinuous Action Potential Conduction in Hybrid Pairs of Ventricular Cells Circulation, March 30, 1999; 99(12): 1623 - 1629. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C.G. van Ginneken, and W. N. Goolsby Experimental Model for an Ectopic Focus Coupled to Ventricular Cells Circulation, August 15, 1996; 94(4): 833 - 841. [Abstract] [Full Text] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1987 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |