Protracted ventricular tachcardia induced by premature stimulation of the canine heart after coronary artery occlusion and reperfusion.
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Histological studies on all infarcts showed that, after permanent occlusion, necrosis was uniform; after temporary occlusions, viable myocardium survived in the necrotic region, and salvaged myocardial fibers may provide reentrant pathways, causing long-lasting tachycardia.Abstract:
The effects of premature ventricular stimuli were studied in two groups of dogs with infarcts, one group subjected to permanent occlusion of the left anterior descending coronary artery and the other to temporary occlusion for 2 hours. In dogs with permanent occlusion, spontaneous ventricular arrhythmias occurred after 3-6 hours. In 13 dogs with temporary occlusion, ventricular arrhythmias occurred immediately after reperfusion and then persisted. In five dogs with temporary occlusion, ventricular arrhythmias did not occur spontaneously until 13-15 hours after occlusion. On days 2-9 after surgery, after sinus rhythm had returned, the ventricles of each awake dog were stimulated. After permanent occlusion, premature stimuli occurring on the T wave usually induced from one to 10 repetitive responses on days 2-4. Protracted ventricular tachycardia (lasting greater than 10 seconds) was induced in only two of 10 dogs. The response to premature stimuli was similar after temporary occlusion when ventricular arrhythmias did not occur spontaneously until 13-15 hours after occlusion. Protracted tachycardia was not induced. In the dogs with temporary occlusion, which initially had continuous arrhythmias, premature stimuli occurring on the T wave on days 3-5 after surgery induced both repetitive responses and protracted ventricular tachycardia. Stimuli applied to the ventricles during tachycardia terminated it. Histological studies on all infarcts showed that, after permanent occlusion, necrosis was uniform; after temporary occlusion, viable myocardium survived in the necrotic region. These salvaged myocardial fibers may provide reentrant pathways, causing long-lasting tachycardia.read more
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References
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Journal ArticleDOI
The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs.
TL;DR: The results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog.
Journal ArticleDOI
The effect of coronary occlusion on myocardial contraction
Robert Tennant,Carl J. Wiggers +1 more
TL;DR: Desc descriptions of a technique and of a type of optical myograph suitable for such studies and an analysis of the changes in optical myograms which follow clamping of a large coronary vessel are concerned.
Journal ArticleDOI
Delayed Development of Ventricular Ectopic Rhythms following Experimental Coronary Occlusion
TL;DR: Following aseptic occlusion of the anterior descending artery of the dog's heart ectopic ventricular tachycardia develops after a latency of four and one-half to eight hours, and persists for two to four days.
Journal ArticleDOI
Recurrent sustained ventricular tachycardia. 1. Mechanisms.
TL;DR: It is concluded that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia.
Journal ArticleDOI
Quantitative assessment of the extent of myocardial infarction in the conscious dog by means of analysis of serial changes in serum creatine phosphokinase activity
TL;DR: The method described is useful for accurate assessment of infarct size in the conscious animal and for detection of modification of infArct size produced by pharmacologic interventions.