The major electrophysiological changes during the first 10 min of myocardial ischemia caused by complete obstruction of a coronary artery are a reduction in membrane potential, a decrease in action ...potential amplitude and upstroke velocity, and a prolongation of recovery of excitability following an action potential. Conduction velocity in the direction parallel to the long axis of myocardial fibers (VL) and in the transverse direction (VT) in normal myocardium are in the order of 40 cm/s and 20 cm/s respectively. During ischemia, conduction velocity decreases and lowest values for VL are in the order of 20 cm/s, for VT around 10 cm/s, before the ischemic tissue becomes inexcitable. Calculated dimensions of a possible re-entrant circuit in acutely ischemic myocardium (the product of refractory period and conduction velocity) are in the order of 7 to 8 cm. Re-entrant circuits of such dimensions were indeed demonstrated by simultaneous recording of 125 extracellular potentials from the epicardial surface of the ventricles during spontaneously occurring ventricular arrhythmias after coronary occlusion. Previous studies provided evidence that premature ventricular depolarization which initiate re-entry originated in the subendocardium, and the present experiments confirmed this. Destruction of the subendocardium of isolated, Langendorff perfused canine hearts, including the Purkinje system, by intracavitary application of phenol, did not, however, abolish ectopic activity during either ischemia or reperfusion, although the nature of the arrhythmias during ischemia was different from those in intact hearts. Coupling intervals of ectopic beats were longer in phenol-treated hearts than in intact hearts, but the site of origin of initial ectopic beats leading to ventricular tachycardia could not be determined. Re-entrant circuits with revolution times in the order of 340 to 400 ms accounted for the slow tachycardias observed in phenol-treated hearts. In contrast to intact hearts, these tachycardias never degenerated into ventricular fibrillation, indicating that an intact Purkinje system may be a necessary requirement for ventricular fibrillation to occur during acute, regional myocardial ischemia.
Early Electrophysiologic Changes in Acute Ischemia.
Introduction:
The purpose of this study was to match changes in conduction velocity, refractoriness, and wavelength during acute regional ischemia ...with initiation of ventricular fibrillation.
Methods and Results:
In 30 isolated, Langendorff‐perfused pig hearts we measured refractory period duration and conduction velocity in ventricular myocardium during the first minutes of regional ischemia in an attempt to determine the minimal changes in these parameters related to the occurrence of ventricular fibrillation (VF). In addition, we wanted to evaluate whether wavelength, i.e., the product of conduction velocity and refractory period, was a useful parameter to predict the occurrence of arrhythmias, as has been shown to be the case for atrial arrhythmias.
1
The refractory period increased significantly after 1 minute of ischemia at basic cycle length and after one and two premature beats. Longitudinal and transverse conduction velocities varied with ischemic time. Compared to the preocclusion value, the longitudinal conduction velocity decreased significantly, but only after 2 minutes of ischemia and at basic cycle length. Wavelength was the least sensitive parameter for ischemia: neither in the longitudinal nor in the transverse direction did it change significantly even during 5 minutes of ischemia. VF was never induced by applying a single premature stimulus within the ischemic area. It occurred in 33% of the occlusions when three successive premature stimuli were delivered from within the ischemic zone, and in 100% when they were applied to the nonischemic myocardium. Whenever fibrillation was induced, it occurred within 3 minutes following coronary occlusions. Wavelength, neither before nor after coronary occlusion, could predict whether VF would occur. The only difference between hearts that fibrillated by stimulation of the ischemic myocardium and those that did not was that, in the first group, the refractory period at the site of stimulation prolonged significantly less than in the no‐VF group. Since electrophysiologic changes within the ischemic zone are inhomogeneous,
2
an attempt was made to measure simultaneously at 52 sites the onset of inhomogeneity by determining the average interval between local depolarization during VF. This so‐called VF interval is an index of local refractoriness.
3
The coefficient of variation of the VF interval, taken as an index of spatial dispersion in refractoriness, increased significantly 1 minute after occlusion in the border zone and 2 minutes after occlusion in the central ischemic area.
Conclusion:
In conclusion, wavelength is not a useful parameter to predict the occurrence of VF in hearts with regional ischemia because of the inhomogeneity in refractoriness, which develops within 2 minutes of ischemia. VF occurs when hearts are stimulated from sites with relatively short refractory periods, either within or outside the ischemic zone. (
J Cardiovasc Electrophysiol, Vol. 3, pp. 128–140, April 1992
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