TY - JOUR
T1 - Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction
AU - Hanich, Robert F.
AU - Levine, Joseph H.
AU - Prood, Charles
AU - Weiss, James L.
AU - Callans, David J.
AU - Spear, Joseph F.
AU - Moore, E. Neil
N1 - Funding Information:
From the Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia; and Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore. Supported by grants HL-33593 and HL-28393 and by the W. W. Smith Charitable Trust. Dr. Hanich was a recipient of a postdoctoral fellowship from the American Heart Association, Maryland Affiliate. Received for publication June 22, 1992; accepted Aug. 1, 1992. Reprint requests: E. Neil Moore, DVM, PhD, Suite 201E, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce St., Philadelphia, PA 19104. 4/l/42145
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1993/1
Y1 - 1993/1
N2 - 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. Depspite 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.
AB - 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. Depspite 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.
UR - http://www.scopus.com/inward/record.url?scp=0027472214&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027472214&partnerID=8YFLogxK
U2 - 10.1016/0002-8703(93)90052-B
DO - 10.1016/0002-8703(93)90052-B
M3 - Article
C2 - 8417523
AN - SCOPUS:0027472214
SN - 0002-8703
VL - 125
SP - 23
EP - 32
JO - American heart journal
JF - American heart journal
IS - 1
ER -