title: Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction.
abstract: Previous investigators have hypothesized that myocardial "stunning" may result either from a primary impairment in excitation or from electromechanical dissociation. Thrombolytic therapy and angioplasty have increased the importance of understanding the electrophysiologic effects of brief ischemia followed by reperfusion. We investigated the electrophysiologic properties of mechanically dysfunctional stunned myocardium in 18 dogs anesthetized with pentobarbital (30 mg/kg, intravenously administered). After thoracotomy, the proximal anterior descending coronary artery was occluded for 15 minutes, which was followed by 20 minutes of reperfusion. At baseline, peak ischemia, and 20 minutes of reperfusion, local electrogram durations, activation times, and refractory periods were measured from 12 standardized sites within the ischemic and border zones. Echocardiographic percentage of systolic wall thickening confirmed normal preischemic and markedly reduced postischemic function in the investigated region. Despite the marked electrophysiologic abnormalities observed in the ischemic zone during ischemia, mean electrogram duration, calculated conduction velocity, and mean effective refractory period after 20 minutes of reperfusion had returned almost to baseline values 39.2 +/- 11.5 msec versus 37.2 +/- 12.1 msec, 0.65 +/- 0.15 m/sec versus 0.68 +/- 0.15 m/sec, and 134 +/- 14 msec versus 131 +/- 8 msec, respectively. Corresponding mean values within the ischemic border zone were similarly close to baseline values after reperfusion. There was no significant difference in local heterogeneity (coefficient of variation) within the ischemic or border zone after reperfusion versus baseline values. Although the postischemic electrophysiologic status returned to normal, systolic thinning and dyskinesis persisted in the region of measurement. The contractile dysfunction that results from reperfusion-induced injury can thus occur in the setting of apparent excitation-contraction uncoupling.
authors.affiliation: Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.
authors.forename: R F
authors.initials: RF
authors.lastname: Hanich
authors.forename: J H
authors.initials: JH
authors.lastname: Levine
authors.forename: C
authors.initials: C
authors.lastname: Prood
authors.forename: J L
authors.initials: JL
authors.lastname: Weiss
authors.forename: D J
authors.initials: DJ
authors.lastname: Callans
authors.forename: J F
authors.initials: JF
authors.lastname: Spear
authors.forename: E N
authors.initials: EN
authors.lastname: Moore
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004285:Dogs; D004452:Echocardiography; D004562:Electrocardiography / Q000295:instrumentation / Q000379:methods / Q000706:statistics & numerical data; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000453:epidemiology / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000453:epidemiology / Q000503:physiopathology*; D012032:Refractory Period, Electrophysiological / Q000502:physiology; D013599:Systole / Q000502:physiology*; D013997:Time Factors