Nonhomogeneous electrophysiological changes and the bimodal distribution of early ventricular arrhythmias during acute coronary artery occlusion

Horacek, Th; Neumann, Martin; Mutius, S. Von; Budden, M.; Meesmann, W.

doi:10.1007/bf01908383

Cited by 34 publications

(16 citation statements)

References 43 publications

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“…We report a significant prolongation of LV APD90 in the control group, coupled with increased beat-to-beat variation in MAP duration. Both of these characteristics, indicative of peri-infarct ischaemia and increased arrhythmogenesis [13][14][15], were eliminated in GH-treated rats.…”

Section: Discussionmentioning

confidence: 91%

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Growth hormone decreases phase II ventricular tachyarrhythmias during acute myocardial infarction in rats

et al. 2007

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GH (growth hormone) administration during acute MI (myocardial infarction) ameliorates subsequent LV (left ventricular) dysfunction. In the present study, we examined the effects of such treatment on arrhythmogenesis. A total of 53 Wistar rats (218+/-17 g) were randomized into two groups receiving two intraperitoneal injections of either GH (2 international units/kg of body weight; n=26) or normal saline (n=27), given at 24 h and 30 min respectively, prior to MI, which was generated by left coronary artery ligation. A single-lead ECG was recorded for 24 h post-MI, using an implanted telemetry system. Episodes of VT (ventricular tachyarrhythmia) and VF (ventricular fibrillation) during the first hour (phase I) and the hours following (phase II) MI were analysed. Monophasic action potential was recorded from the lateral LV epicardium at baseline and 24 h post-MI, and APD90 (action duration at 90% of repolarization) was measured. Infarct size was calculated 24 h post-MI. Infarct size and phase I VT+VF did not differ significantly between groups, but phase II hourly duration of VT+VF episodes was 82.8+/-116.6 s/h in the control group and 18.3+/-41.2 s/h in the GH group (P=0.0027), resulting in a lower arrhythmic (P=0.016) and total (P=0.0018) mortality in GH-treated animals. Compared with baseline, APD90 was prolonged significantly 24 h post-MI in the control group, displaying an increased beat-to-beat variation, but remained unchanged in the GH group. We conclude that GH decreases phase II VTs during MI in the rat. This finding may have implications in cardiac repair strategies.

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Section: Discussionmentioning

confidence: 91%

“…We hypothesized that the cardioprotective effects of early GH administration may decrease VT (ventricular tachyarrythmia) during acute MI. We tested this hypothesis in a rat model, which exhibits a high frequency of VTs, with a time course corresponding to that seen in humans [12,13].…”

Section: Introductionmentioning

confidence: 99%

Growth hormone decreases phase II ventricular tachyarrhythmias during acute myocardial infarction in rats

et al. 2007

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“…Most studies have used either the dog or the pig, the subject having been reviewed from the point ofview of these two species by several investigators Lazzara et al, 1978;Janse, 1982;Horacek et al, 1984). By comparison, the early ischaemia-induced electrical changes in the rat myocardium have been studied only rarely, (Budden et al, 1981;Mertz & Kaplan, 1982).…”

Section: Discussionmentioning

confidence: 99%

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Northover

1986

British J Pharmacology

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1 The hearts of anaesthetized, artificially ventilated rats were exposed, and the left coronary artery occluded. The diastolic threshold voltage for stimulation (DTV), the duration of the bipolar electrogram (DBE) and the functional refractory period (FRP) of the ischaemic area were measured at minute intervals for an hour after occlusion. 2 Coronary occlusion caused a rise in DTV, a prolongation of the DBE and a biphasic change in the FRP, with an initial prolongation phase (1-4 min) followed by a decline to below pre-occlusion values (5-15 min). 3 Episodes ofventricular tachyarrhythmia (VT) were most frequent during the period 5-15 min after the onset of occlusion of the coronary artery. This coincided with the period when FRP was minimal and the difference between DBE and FRP was maximal. 4 Pretreatment of rats with sulphinpyrazone (2.5-40mgkg-') or indomethacin (5-20mgkg-') protected against the episodes of coronary occlusion-induced VT and against the associated decline in FRP of the ischaemic muscle. Sulphinpyrazone was more effective than indomethacin in this respect and a combination of the two drugs was approximately as effective as sulphinpyrazone alone. 5 It was concluded that sulphinpyrazone protects rats against coronary occlusion-induced episodes of VT by reducing the risk of ventricular action potential re-entry. This effect is probably due to protection against the ischaemia-induced shortening of the myocardial FRP.

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“…Actually, this immediate rise of [K+]e in the isehemie myoeardium correlates with inhomogeneous electrophysiological alterations which finally lead to the early VA (24). *) Preliminary results were presented at the International Symposium on Calcium entry blockers and tissue protection, Rome, 1984, at the 59th Meeting of the Deutsche Physiologische Gesellschaft, Dortmund, 1984, at the 50th meeting of the Deutsche Gesellschaft ffir Herz-und Kreislaufforschung, Mannheim, 1984, and at the IXth European Congress of Cardiology, Dfisseldorf, 1984. It has been known since 1968 (27) that the pretreatment of dogs with the calcium antagonist verapamil reduces the incidence of ischemia-induced arrhythmias.…”

Section: Introductionmentioning

confidence: 97%

Effects of the calcium antagonist gallopamil on the increase of myocardial extracellular potassium activity during LAD occlusion in dogs

Budden¹,

Kirchengast²,

Zhang³

et al. 1987

Basic Res Cardiol

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It has been implied that the increase of myocardial extracellular potassium activity [( K+]e) in the early stage of acute myocardial ischemia is a major cause of the increased likelihood of arrhythmia after acute coronary artery occlusion. There is also experimental evidence that some calcium antagonists reduce the occurrence of ischemia-induced early ventricular arrhythmias. In order to clarify the antiarrhythmic effect of gallopamil during the early phase of acute LAD occlusion, the influence of this calcium antagonist on the time course of [K+]e during acute ischemia was measured in open-chest anesthetized dogs using a K+-selective surface multielectrode. The regional myocardial blood flow was determined with 9 micron radioactive tracer microspheres. After application of gallopamil (bolus 25 micrograms/kg and infusion 2.5 micrograms/kg.min for 30 min) the maximal and mean rate of rise of [K+]e as well as the plateau of [K+]e reached during ischemia were significantly diminished compared with the control occlusions. 90 min after gallopamil, the rate of rise of [K+]e as well as the plateau of [K+]e reached were still significantly reduced, but 180 min after the gallopamil application, no significant differences between the time course of [K+]e and that of the two control occlusions could be found. Gallopamil significantly elevated myocardial blood flow in the non-ischemic area, but did not influence blood flow in the ischemic region. While collateral perfusion remains unchanged, the slowed and reduced increase of myocardial [K+]e during acute coronary artery occlusion may be an important component of the antiarrhythmic effect of gallopamil during early ischemia.

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Nonhomogeneous electrophysiological changes and the bimodal distribution of early ventricular arrhythmias during acute coronary artery occlusion

Cited by 34 publications

References 43 publications

Growth hormone decreases phase II ventricular tachyarrhythmias during acute myocardial infarction in rats

Growth hormone decreases phase II ventricular tachyarrhythmias during acute myocardial infarction in rats

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Effects of the calcium antagonist gallopamil on the increase of myocardial extracellular potassium activity during LAD occlusion in dogs

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