Changes in myocardial electrical impedance induced by coronary artery occlusion in pigs with and without preconditioning: correlation with local ST-segment potential and ventricular arrhythmias.

BACKGROUND Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by ischemic preconditioning in isolated myocardium. Alterations in myocardial resistivity elicited by ischemia in vivo may influence arrhythmogenesis and local ST-segment changes, but this is not well known. METHODS AND RESULTS Myocardial impedance (resistivity [omega x cm] and phase angle [degrees]), epicardial ST segment, and ventricular arrhythmias were analyzed during 4 hours of coronary artery occlusion in 11 anesthetized open-chest pigs; these were compared with 13 other pigs submitted to a similar coronary occlusion preceded by ischemic preconditioning. Myocardial resistivity rose slowly during the first 34+/-7 minutes of occlusion (237+/-41 to 359+/-59 omega x cm), increased rapidly to 488+/-100 omega x cm at 60 minutes, and reached a plateau value (718+/-266 omega x cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle changes began after 17 minutes of ischemia (-3.0+/-1.6 degrees to -4.2+/-1.2 degrees at 29+/-8 minutes) and evolved faster thereafter (-12.5+/-5.3 degrees at 144+/-56 minutes). Marked changes in myocardial impedance were observed during the reversion of ST-segment elevation that occurred 1 to 4 hours after occlusion, but impedance changes were less apparent during the early ST-segment recovery seen at 15 to 35 minutes of ischemia. The second arrhythmia peak (30+/-5 minutes) coincided with the fast change in tissue impedance, and both were delayed (P<.05) by ischemic preconditioning. CONCLUSIONS A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.

[1]  R Lazzara,et al.  Characterization and Localization of Ventricular Arrhythmias Resulting from Myocardial Ischemia and Infarction , 1974, Circulation research.

[2]  JOHN W. Moore.  Membranes, ions, and impulses , 1976 .

[3]  D. Kleinbaum,et al.  Applied Regression Analysis and Other Multivariate Methods , 1978 .

[4]  D Durrer,et al.  Mechanism and Time Course of S‐T and T‐Q Segment Changes during Acute Regional Myocardial Ischemia in the Pig Heart Determined by Extracellular and Intracellular Recordings , 1978, Circulation research.

[5]  J. Madias.  Electrocardiography in myocardial infarction. , 1979, Journal of electrocardiology.

[6]  R. W. Zmyslinski,et al.  Natural course of the S-T segment and QRS complex in patients with acute anterior myocardial infarction. , 1979, The American journal of cardiology.

[7]  C W Balke,et al.  Two Periods of Early Ventricular Arrhythmia in the Canine Acute Myocardial Infarction Model , 1979, Circulation.

[8]  D Durrer,et al.  Mechanism and time course of the early electrical changes during acute coronary artery occlusion. An attempt to correlate the early ECG changes in man to the cellular electrophysiology in the pig. , 1980, Chest.

[9]  A. Kleber,et al.  Flow of “Injury” Current and Patterns of Excitation during Early Ventricular Arrhythmias in Acute Regional Myocardial Ischemia in Isolated Porcine and Canine Hearts: Evidence for Two Different Arrhythmogenic Mechanisms , 1980, Circulation research.

[10]  D. Durrer,et al.  Tissue Osmolality, Cell Swelling, and Reperfusion in Acute Regional Myocardial Ischemia in the Isolated Porcine Heart , 1981, Circulation research.

[11]  W. Penny.  The deleterious effects of myocardial catecholamines on cellular electrophysiology and arrhythmias during ischaemia and reperfusion. , 1984, European heart journal.

[12]  J. Lowe,et al.  On-line detection of reversible myocardial ischemic injury by measurement of myocardial electrical impedance. , 1987, The Annals of thoracic surgery.

[13]  E Gersing,et al.  Impedance Spectroscopy: a Method for Surveillance of Ischemia Tolerance of the Heart , 1987, The Thoracic and cardiovascular surgeon.

[14]  D. Hearse,et al.  Preconditioning of ischemic myocardium: reperfusion-induced arrhythmias. , 1987, The American journal of physiology.

[15]  A. Kleber,et al.  Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. , 1987, Circulation research.

[16]  A. Noma,et al.  Dependence of junctional conductance on proton, calcium and magnesium ions in cardiac paired cells of guinea‐pig. , 1987, The Journal of physiology.

[17]  A. Bardají,et al.  Ventricular arrhythmias and local electrograms after chronic regional denervation of the ischemic area in the pig heart. , 1989, Journal of the American College of Cardiology.

[18]  W. Cascio,et al.  Passive electrical properties, mechanical activity, and extracellular potassium in arterially perfused and ischemic rabbit ventricular muscle. Effects of calcium entry blockade or hypocalcemia. , 1990, Circulation research.

[19]  K. Kamiya,et al.  ATP directly affects junctional conductance between paired ventricular myocytes isolated from guinea pig heart. , 1990, Circulation research.

[20]  A. Schoenenberger,et al.  Effects of anaesthesia on acute ischaemic arrhythmias and epicardial electrograms in the pig heart in situ. , 1990, Cardiovascular research.

[21]  R. Kloner,et al.  Effect of preconditioning ischemia on reperfusion arrhythmias after coronary artery occlusion and reperfusion in the rat. , 1991, Circulation research.

[22]  S. Komori,et al.  Protective effect of preconditioning on reperfusion induced ventricular arrhythmias of isolated rat hearts. , 1991, Cardiovascular research.

[23]  Y. Li,et al.  Cardioprotective effects of ischaemic preconditioning are not mediated by prostanoids. , 1992, Cardiovascular research.

[24]  T. Opthof,et al.  Reperfusion arrhythmias in isolated perfused pig hearts. Inhomogeneities in extracellular potassium, ST and TQ potentials, and transmembrane action potentials. , 1992, Circulation research.

[25]  A. Kleber,et al.  Propagation of Electrical Activity in Ischemic and Infarcted Myocardium as the Basis of Ventricular Arrhythmias , 1992 .

[26]  P. Steendijk,et al.  The four-electrode resistivity technique in anisotropic media: theoretical analysis and application on myocardial tissue in vivo , 1993, IEEE Transactions on Biomedical Engineering.

[27]  F. Spelman,et al.  Quantitative in vivo measurements of inner ear tissue resistivities. I. In vitro characterization , 1993, IEEE Transactions on Biomedical Engineering.

[28]  K R Foster,et al.  Myocardial Electrical Impedance Mapping of Ischemic Sheep Hearts and Healing Aneurysms , 1993, Circulation.

[29]  P. Corr,et al.  Inhibition of gap junctional conductance by long-chain acylcarnitines and their preferential accumulation in junctional sarcolemma during hypoxia. , 1993, Circulation research.

[30]  H. Tan,et al.  Ischaemic preconditioning delays ischaemia induced cellular electrical uncoupling in rabbit myocardium by activation of ATP sensitive potassium channels. , 1993, Cardiovascular research.

[31]  J. Downey,et al.  Conscious rabbits become tolerant to multiple episodes of ischemic preconditioning. , 1994, Circulation research.

[32]  A. Bardají,et al.  ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone. , 1995, Circulation.

[33]  W. Cascio,et al.  The Ib phase of ventricular arrhythmias in ischemic in situ porcine heart is related to changes in cell-to-cell electrical coupling. Experimental Cardiology Group, University of North Carolina. , 1995, Circulation.

[34]  W. Cascio,et al.  Correlation of ischemia-induced extracellular and intracellular ion changes to cell-to-cell electrical uncoupling in isolated blood-perfused rabbit hearts. Experimental Working Group. , 1996, Circulation.

[35]  M J Janse,et al.  Intracellular Ca2+, intercellular electrical coupling, and mechanical activity in ischemic rabbit papillary muscle. Effects of preconditioning and metabolic blockade. , 1996, Circulation research.