überlebensquote nach akutem experimentellem Coronarverschluß in Abhängigkeit von Spontankollateralen des Herzens

Meesmann, W.; Schulz, F; Schley, Gunnar; Adolphsen, P

doi:10.1007/bf02048758

Cited by 45 publications

(12 citation statements)

References 38 publications

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“…ischaemic control 29 Possible Mechanisms of the Acute Ischemia-Induced Ventricular Arrhythmiasthe occlusion of a main coronary artery may vary between 0 and 100% depending upon the preexisting collateralization. They also pointed out that although the preexisting collaterals are not able to prevent myocardial ischemia in dogs, collateral flow attenuates rapid development of inhomogeneity and electrical instability of heart [64]. In contrast, in pigs which have a poor collateral system, more than 50% of the animals develop VF during phase 1A and about one-third during phase 1B [65].…”

Section: Mechanisms Of Generation Of Phase 1b Arrhythmiasmentioning

confidence: 94%

“…These species differences can be associated with the extent of functionally effective preexisting collaterals which influence the time of appearance and severity of arrhythmias following sudden coronary artery occlusion [63]. Meesmann and colleagues [64] showed in 1970s that in dogs the rate of mortality within 1 h after Fig. 29.3 Changes in gap junction permeability and in connexin 43 (Cx43) phosphorylation, determined at the end of a 60-min coronary artery occlusion in the nonischemic control (NC), in the ischemic control (IC) and in the preconditioned (PC) heart samples.…”

Section: Mechanisms Of Generation Of Phase 1b Arrhythmiasmentioning

confidence: 99%

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Possible Mechanisms of the Acute Ischemia-Induced Ventricular Arrhythmias: The Involvement of Gap Junctions

Végh

Papp

2011

Heart Rate and Rhythm

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The problem of sudden cardiac death (SCD) from ventricular fibrillation (VF) during coronary artery occlusion or reperfusion, outside the hospital setting, is still the biggest challenge that clinical cardiology faces. More than half of SCDs can be attributed to sudden VF. As drug therapy has proved to be largely ineffective except in the hospital setting, understanding the underlying mechanisms that lead to these life-threatening ventricular arrhythmias is crucial for developing novel therapeutic strategies.Several experimental models -from cells to in situ animal models -are available for exploring the dynamic changes during the acute phase of myocardial ischemia that are responsible for the occurrence of the accompanying severe, often fatal, ventricular arrhythmias. The dynamic nature of ischemia development can be discussed by considering its several aspects. With respect to associated arrhythmias, four phases of the ischemic events are distinguished within the first hour. The sequence of these changes is time-dependent. Studies in large animals showed that after commencement of occlusion, the rapidly developing and progressing ischemic changes give rise to an early phase of arrhythmias (phase 1A) which, in anesthetized dogs, is apparent between 3 and 8 min of start of ischemia [1]. This is followed by a restoration of normal rhythm (compensatory phase) during which the ionic changes become balanced, and electrophysiological parameters seem to return to normal [2]. This phase might be of particular importance as changes during this short (5 min) period directly contribute to the next event (phase 1B) of arrhythmias. Phase 1B lasts from 15 to 30 min of ischemia and is more severe than phase 1A arrhythmias, often terminating in sudden VF [3,4]. After this period, if ischemia is maintained, a "healing over" process starts during which the dying cells are sharply demarcated from the viable ones by interrupting the electrical and metabolic

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Section: Mechanisms Of Generation Of Phase 1b Arrhythmiasmentioning

confidence: 94%

Section: Mechanisms Of Generation Of Phase 1b Arrhythmiasmentioning

confidence: 99%

Possible Mechanisms of the Acute Ischemia-Induced Ventricular Arrhythmias: The Involvement of Gap Junctions

Végh

Papp

2011

Heart Rate and Rhythm

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“…2). It has been reported that canine hearts, which have few collateral channels demonstrable by coronary angiography, develop a higher incidence of ventricular fibrillation following acute coronary occlusion than hearts with multiple collateral channels (Meesman et al, 1970). Furthermore, porcine hearts, which have only a minimally functioning coronary collateral circulation (Schaper, 1971;Fedor et al, 1978;Most et al, 1978), show a 75% incidence of ventricular fibrillation following acute occlusion of the proximal left anterior descending coronary artery (Downar et al, 1977).…”

Section: Conduction Abnormalities and Arrhythmiasmentioning

confidence: 99%

“…It has been shown that the volume of collateral blood flow to the ischemic myocardium is inversely related to the depression in amplitude of bipolar electrograms recorded from the subepicardium and subendocardium and to the increase in duration of subepicardial electrograms (Ruffy et al, 1979). Furthermore, ventricular fibrillation following acute coronary artery occlusion in the dog has been reported to occur only in those animals that have a limited number of preexisting collateral channels (Meesman et al, 1970).…”

mentioning

confidence: 99%

The interruption of collateral blood flow to the ischemic canine myocardium by embolization of a coronary artery with latex: effects on conduction delay and ventricular arrhythmias.

Euler¹,

Prood²,

Spear³

et al. 1981

Circulation Research

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“…Another study on this topic, published in 1970, described a similar experiment in dogs. The researchers acutely occluded the LAD or the LCX in 69 dogs [8]. Occlusion of the LCX was associated with an approximately 50% risk of VF and mortality compared to occlusion of the LAD.…”

Section: Early Researchmentioning

confidence: 99%

Sudden Cardiac Arrest during Acute Coronary Occlusion – Who Is at Risk?

Meier

Seiler

2010

Cardiology

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Many people with acute myocardial infarction die from sudden cardiac arrest before reaching the hospital. The current clinical understanding of the mechanisms and risk factors surrounding sudden cardiac death is limited. However, 2 factors related to sudden death, namely the occluded coronary vessel (right coronary, left circumflex, or left anterior descending artery) and the extent of collateral circulation, are of potential relevance. Recent data suggest that the risk differs between the different coronary arteries and that coronary collateral circulation seems to have an important protective ‘antiarrhythmic’ effect. This editorial will address possible mechanisms and potential implications in clinical practice.

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überlebensquote nach akutem experimentellem Coronarverschluß in Abhängigkeit von Spontankollateralen des Herzens

Cited by 45 publications

References 38 publications

Possible Mechanisms of the Acute Ischemia-Induced Ventricular Arrhythmias: The Involvement of Gap Junctions

Possible Mechanisms of the Acute Ischemia-Induced Ventricular Arrhythmias: The Involvement of Gap Junctions

The interruption of collateral blood flow to the ischemic canine myocardium by embolization of a coronary artery with latex: effects on conduction delay and ventricular arrhythmias.

Sudden Cardiac Arrest during Acute Coronary Occlusion – Who Is at Risk?

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