Long-term electrophysiological abnormalities resulting from experimental myocardial infarction in cats.

Myerburg, Robert J.; Gelband, Henry; Nilsson, Kristina; Sung, Ruey J.; Thurer, Richard J.; Morales, A. R.; Bassett, Arthur L.

doi:10.1161/01.res.41.1.73

Cited by 86 publications

(32 citation statements)

References 30 publications

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“…The tissue from patient 3 showed slow response potentials, variable amplitude responses and inexcitable cells, with both normal resting potentials and abnormal resting potentials. Myerburg et al 4 have also described heterogenous electrophysiologic properties in chronic experimental The slow response activity which we observed in human ventricle is similar to that previously reported in human diseased atrial muscle. "3 14 The verapamilsensitive muscle automaticity resembles the calcium and sodium-dependent automaticity described in depolarized guinea pig papillary muscle.…”

Section: The Variable Amplitude Responsesupporting

confidence: 89%

Cellular electrophysiology of human myocardial infarction. 1. Abnormalities of cellular activation.

Jf¹,

Ln²,

Ab³

et al. 1979

Circulation

141

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SUMMARY Ventricular tissues were obtained at the time of operation from 12 patients who underwent aneurysmectomy or mitral valve replacement. The electrophysiologic characteristics of these tissues were determined in a tissue bath using microelectrodes. Normal-appearing action potentials were recorded from surviving Purkinje fibers and ventricular muscle cells within infarcted ventricular tissues. Normal muscle action potential recordings from infarcted tissues were similar to action potentials from noninfarcted papillary muscles, except that the duration of the action potential was significantly longer in the former. In other areas slow response potentials were recorded. These action potentials conducted slowly and were eliminated by verapamil. We observed verapamil-sensitive slow response automaticity, but this did not correlate with ventricular tachycardias, present in three patients. Variable amplitude responses arising from normal resting potentials and characterized by stimulus intensity-dependent changes in action potential amplitude were recorded in tissues from two patients. These potentials had many characteristics similar to the slow response, but were not eliminated by verapamil. We also saw inexcitable cells with both normal and abnormal resting potentials. The heterogeneous electrophysiologic characteristics of these tissues provide a likely substrate for arrhythmias and may be the source of the ectopic ventricular rhythms observed in these patients. cardium 1-60 months after acute myocardial infarction. The observations indicate that both Purkinje fibers and muscle cells survive. We also document persistent electrophysiologic abnormalities in surviving cells of tissues obtained as late as 60 months after infarction. MethodsSpecimens of human ventricular tissue were obtained from 12 patients at the time of cardiac surgery. The patients ranged in age from 37-68 years. Aneurysmectomy was performed for intractable heart failure or ventricular tachycardia. Mitral valve replacement was performed for severe mitral regurgitation. Before surgery, all patients had some degree of chronic congestive heart failure (table 1). Three of the 12 patients had chronic sustained ventricular tachycardia. No patients had evidence of digitalis toxicity. Cardioactive drugs were discontinued at least 24 hours before operation in nine of 12 patients without ventricular tachycardia, but were continued in the three patients with arrhythmia to the time of surgery. Morphine and halothane were used as anesthetics.The tissues were resected promptly at the initiation of cardiopulmonary bypass and were placed in continuously oxygenated, cooled (20-21°C) Tyrode

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Section: The Variable Amplitude Responsesupporting

confidence: 89%

Cellular electrophysiology of human myocardial infarction. 1. Abnormalities of cellular activation.

Jf¹,

Ln²,

Ab³

et al. 1979

Circulation

141

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“…[17][18][19]32 These studies have invariably demonstrated a number of abnormalities, including partial depolarization and a decline in action potential amplitude and maximum upstroke velocity (Vmax). The abnormalities noted in surviving P cell action potentials are the most severe early in the infarction, but tend to reverse or totally normalize in the days and weeks after coronary occlusion.…”

Section: Discussionmentioning

confidence: 99%

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

et al. 1987

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Permanent coronary occlusion produces time-dependent changes in surviving subendocardial cellular properties. We compared the functional alterations in Purkinje (P) and ventricular muscle (VM) activation early (24 hr) and late (4 weeks or greater) after permanent coronary occlusion in an in vitro preparation of canine papillary muscle. High-density extracellular (1 to 2 mm resolution) and selected intracellular recordings were made in five animals early and seven animals late during stimulation of a free-running P strand. Activation patterns of P and VM layers from ischemic and unaffected papillary muscles were compared in the same animal. Average P layer conduction velocity was determined in normal and ischemic regions with the use of a linear array of recording and stimulating electrodes. Purkinje activation was altered little in the early phase of infarction, while healing was associated with a generalized 25% reduction in P layer conduction velocity and localized block and fragmentation of P waveforms. Intracellular recordings at sites of nonsynchronous P activation revealed electrotonic interaction between cell groups. At 24 hr, small groups of VM were present but with abnormal activation patterns in regions of necrosis with fragmented and delayed extracellular waveforms produced by partially uncoupled groups of cells. Local delay and block could be modulated by rate and site of stimulation. After healing, VM activation abruptly stopped at the visual infarct border, marked by a characteristic "end potential." These studies demonstrate important differences in the functional attributes of the P and VM layers studied early and late after coronary occlusion. Alterations in cell-to-cell relationships are likely very important in determining abnormalities of activation in both settings.

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“…The animals were monitored for at least 8 wk after the operation. This time period was chosen because: (a) Bassett and Gelband (2) have shown in cats that the hypertrophic response of the right ventricle to chronic pulmonary banding occurs by 2 1 days postbanding; (b) Marcus et al (22) have shown in cats that with intermittent pulmonary artery banding, right ventricular hypertrophy occurs primarily within the 1st wk, but does not change after 4 wk; (c) Myerburg et al (26) considered an experimental myocardial infarction "chronic" after 7 days; (d) in our preliminary studies, we monitored two animals in each group for 12 weeks. There were no significant differences between weeks 8 and 12.…”

Section: Chronic Stimulation and Recording Protocolmentioning

confidence: 99%

“…This was performed 30 min after the heart rate returned to control values following isoproterenol infusion. Using the method of Myerburg et al (26), the vagus nerve was stimulated (10 timesls; stimulus strength, 10 V; pulse duration, 0.10 s) with a Grass model S4 stimulator. Stimulation was then continued until sinus arrest or complete AV block occurred, allowing unmasking of the subsidiary "escape" pacemaker.…”

Section: Chronic Stimulation and Recording Protocolmentioning

confidence: 99%

“…Because of this uncertainty, an animal model was sought in which complete tigate the mechanism of any ventricular dysrhythmias observed in association with ventriculotomy, right ventricular hypertension, or the combination. The majority of prior work on the electrophysiologic effects of fibrosis, hypertrophy, and stretch have been on either anesthetized animals or in the tissue bath (1,2,19,26,27,33). In the present model, chronically instrumented, nonsedated animals were used in an attempt to model more closely the clinical situation.…”

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Ventricular Dysrhythmias after Congenital Heart Surgery: a Canine Model

Garson

1984

Pediatr Res

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ABSTRACT. To examine the possible mechanisms of ventricular dysrhythmias in the presence of right ventricular hypertension and following ventriculotomy, we instrumented 6-month-old puppies. There were four groups: 1) six animals served as controls (instrumentation only); 2) six animals underwent ventriculotomy only; 3) six animals underwent pulmonary artery banding with a pneumatic vessel occluder to produce right ventricular hypertension; 4) six animals had both ventriculotomy and right ventricular hypertension. Each week for 8 wk, 24-h electrocardiograms and electrophysiologic studies were performed with the animals awake and unsedated. We attempted to induce ventricular dysrhythmias with premature extrastimuli, rapid pacing, isoproterenol, and vagal stimulation. electrocardiogram, there were no chronic spontaneous ventricular dysrhythmias in any control or ventriculotomy animal, but were present in 5 of 6 right ventricular hypertension animals and 6 of 6 ventriculotomy and right ventricular hypertension animals. At electrophysiology study, no ventricular dysrhythmias were induced in the control or ventriculotomy animals but in the right ventricular hypertension group, 5 of 6 had accelerated ventricular escape and 2 of 6 had induced ventricular dysrhythmias; in the ventriculotomy and right ventricular hypertension group, 5 of 6 had accelerated ventricular escape and the same 5 of 6 had induced ventricular dysrhythmias including two with sustained ventricular tachycardia. In four animals, the coupling interval to the dysrhythmia was dependent upon the preceding cycle, a feature of triggered activity. In In a long term follow-up of patients who had had intracardiac repair of tetralogy of Fallot, 10.3% had premature ventricular contractions found on routine electrocardiogram taken more than 1 month postoperatively, and 38% of those with premature ventricular contractions died suddenly between 3 months and 10 years postoperatively. Of the patients with premature ventricular contractions, 88% had a postoperative right ventricular systolic pressure of 60 mm Hg or more, and all had a right ventricular end diastolic pressure of 8 mm Hg or more. All of the patients who died suddenly had prior premature ventricular contractions, a right ventricular systolic pressure of at least 70 mm Hg, and a right ventricular end diastolic pressure of at least 10 mm Hg (1 1). These data have been confirmed by other investigators, and have been extended to other patients with right ventricular outflow obstruction and interventricular communication (7,9,10). On the basis of these findings, we have hypothesized a relationship between elevated right ventricular systolic pressure and end diastolic pressure, ventricular dysrhythmias, and sudden death (1 3). This may not be the only mechanism for late sudden death after tetralogy repair. Some patients may die from late complete AV block (37). However, two of these patients that later died suddenly had complete information regarding hemodynamics, dysrhythmia, and electrophysiology. Because of...

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Long-term electrophysiological abnormalities resulting from experimental myocardial infarction in cats.

Cited by 86 publications

References 30 publications

Cellular electrophysiology of human myocardial infarction. 1. Abnormalities of cellular activation.

Cellular electrophysiology of human myocardial infarction. 1. Abnormalities of cellular activation.

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

Ventricular Dysrhythmias after Congenital Heart Surgery: a Canine Model

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