Myocardial electrical impedance mapping of ischemic sheep hearts and healing aneurysms.
BACKGROUND
This study was designed to examine the bulk electrical properties of myocardium and their variation with the evolution of infarction after coronary occlusion. These properties may be useful in distinguishing between normal, ischemic, and infarcted tissue on the basis of electrophysiological parameters.


RESULTS
The electrical impedance of myocardial tissue was studied in a sheep model of infarction. The animal model involved a one-stage ligation of the left anterior descending and second diagonal arteries at a point 40% of the distance from the apex to the base. By use of a four-electrode probe, an epicardial mapping system was developed that allowed for cardiac cycle gated and signal-averaged measurements. Subthreshold current (15 microA) was injected through two of the electrodes at frequencies of 1, 5, and 15 kHz and the induced potential measured with the other two electrodes. Epicardial maps of the left ventricle were obtained during acute infarction and at 1-, 2-, and 6-week intervals after occlusion. Results showed the average specific impedance of the myocardium before infarction to be 158 +/- 26 omega-cm independent of location on the epicardium. By 60 minutes after coronary occlusion, the specific impedance had increased by 199% (p < 0.005, n = 9); it remained elevated for up to 4 hours. One week after infarction, the specific impedance decreased to 59% of the control value (p < 0.025, n = 8). Six weeks after occlusion, the specific impedance remained low at 57% of that of the noninfarcted tissue (p < 0.005, n = 9). The phase angle of the complex impedance was also measured and revealed similar changes. The hydroxyproline content of the tissue was assayed to assess infarct healing.


CONCLUSIONS
In this animal model, impedance is a bulk electrical property of tissue that varies with the evolution of myocardial infarction. Impedance mapping revealed significantly different values for normal, ischemic, and infarcted tissue and may prove useful in better defining the electrophysiological characteristics of such tissue.
Fallert
M A
MA
Department of Medicine, University of Pennsylvania, Philadelphia.
Mirotznik
M S
MS
Downing
S W
SW
Savage
E B
EB
Foster
K R
KR
Josephson
M E
ME
Bogen
D K
DK
D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004553:Electric Conductivity; D004594:Electrophysiology / Q000379:methods; D006321:Heart / Q000503:physiopathology*; D006322:Heart Aneurysm / Q000503:physiopathology*; D006909:Hydroxyproline / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D008863:Microspheres; D008962:Models, Theoretical; D009206:Myocardium / Q000378:metabolism; D012756:Sheep; D013997:Time Factors
D006909:Hydroxyproline