Early Arrhythmias and Primary Ventricular Fibrillation after Acute Myocardial Ischaemia in Relation to Pre-existing Coronary Collaterals

Meesmann, W.

doi:10.1007/978-1-349-06260-7_6

Cited by 35 publications

(17 citation statements)

References 31 publications

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“…This is important, because the size of the ischemic area determines the frequency of ventricular arrhythmias. For example, the dog has a large variation in preexisting collateral flow, and, depending on the degree of collateral flow, the incidence of arrhythmias may vary from zero to 100% after occlusion of a major coronary artery (28).…”

Section: Discussionmentioning

confidence: 99%

Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats

Lujan

Chen

DiCarlo³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Lujan HL, Chen Y, DiCarlo SE. Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemiainduced ventricular tachycardia in conscious rats. Am J Physiol Heart Circ Physiol 296: H1364 -H1372, 2009. First published March 13, 2009 doi:10.1152/ajpheart.01286.2008.-Midthoracic spinal cord injury is associated with ventricular arrhythmias that are mediated, in part, by enhanced cardiac sympathetic activity. Furthermore, it is well known that sympathetic neurons have a lifelong requirement for nerve growth factor (NGF). NGF is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, we tested the hypothesis that paraplegia is associated with an increased cardiac NGF content, sympathetic tonus, and susceptibility to ischemia-induced ventricular tachyarrhythmias. Intact and paraplegic (6 -9 wk posttransection, T5 spinal cord transection) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, and a snare was placed around the left main coronary artery. Following recovery, the susceptibility to ventricular arrhythmias (coronary artery occlusion) was determined in intact and paraplegic rats. In additional groups of matched intact and paraplegic rats, cardiac nerve growth factor content (ELISA) and cardiac sympathetic tonus were determined. Paraplegia, compared with intact, increased cardiac nerve growth factor content (2,146 Ϯ 286 vs. 180 Ϯ 36 pg/ml, P Ͻ 0.05) and cardiac sympathetic tonus (154 Ϯ 4 vs. 68 Ϯ 4 beats/min, P Ͻ 0.05) and decreased the ventricular arrhythmia threshold (3.6 Ϯ 0.2 vs. 4.9 Ϯ 0.2 min, P Ͻ 0.05). Thus altered autonomic behavior increases the susceptibility to ventricular arrhythmias in paraplegic rats. cardiovascular risks; arrhythmia OUR LABORATORY RECENTLY DOCUMENTED that T 5 spinal cord transection (T 5 X) increased the susceptibility to ischemiareperfusion-induced sustained ventricular tachycardia (25). The increased susceptibility to the life-threatening arrhythmia was prevented with cardiac ␤

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Section: Discussionmentioning

confidence: 99%

Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats

Lujan

Chen

DiCarlo³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…29.3). 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.…”

Section: Mechanisms Of Generation Of Phase 1b Arrhythmiasmentioning

confidence: 98%

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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“…The first period, called phase la, occurs between 2 and 10 minutes after coronary occlusion; the second period, phase Ib, occurs approximately 12 to 30 minutes after occlusion 4 ). The previous experimental evidence suggests that la arrhythmia is predominantly caused by reentry due to inhomogeneous delayed conduction 3 -7), and Ib arrhythmia is linked to the release of endogeneous catecholamines which induce abnormal automaticity21), as well as the slow and inhomogeneous conduction caused by electrical cell to cell uncoupling 22 ). Thus, it is probable that biphasic changes of both the number of peaks and the duration of wavelet transform would reflect inhomogeneous conduction delay due to the changes in transmembrane action potential immediately following coronary occlusion, i.e., la phase, and due to the changes superimposed by cell-to-cell uncoupling in Ib phase.…”

Section: Discussionmentioning

confidence: 99%

Estimation of Microinhomogeneity of Conduction Impairment by Wavelet Analysis During Early Phase of Myocardial Ischemia in Pigs

Furukawa

Maehara

Saito

et al. 2006

FJMS

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Ventricular fibrillation (VF) is most frequent in the very early phase in acute coronary occlusion, and is triggered by the re-entrant mechanism in this phase. An inhomogeneous conduction in the ischemic myocardium would be substrates for re-entry. The aim of this study was to examine the relationship between the severity of irregularities of the QRS complex and VF. Eleven pigs were analyzed, and the heart was fixed in the pericardial cradle. Ag-AgCI bipolar electrodes were fixed on the epicardium in ischemic and non-ischemic regions. The proximal portion of the left anterior descending coronary artery was occluded for one hour. Electrocardiograms (ECGs) were continuously recorded on a magnetic tape, and wavelet analysis was performed on signal-averaged ECG (25 beats) every 60 sec after the experiment. The number of local maxima (N) and the duration between the first and the last local maximum (D) were automatically measured. Nand D significantly increased in the ischemic area, but not in the non-ischemic area. Nand D increased approximately twofold just before the occurrence of VF in 8 fibrillated pigs (p < 0.01, each). There were significant positive linear relationships between the rate of increase in Nand D to VF and basal heart rate before coronary occlusion (r = 0.90, P < 0.01 in N, r = 0.84, P < 0.01 in D at 160 Hz). These results suggest that there would be a threshold inhomogeneous conduction for the occurrence of VF and an increase in heart rate would accelerate the inhomogeneous conduction in acute myocardial ischemia.

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Early Arrhythmias and Primary Ventricular Fibrillation after Acute Myocardial Ischaemia in Relation to Pre-existing Coronary Collaterals

Cited by 35 publications

References 31 publications

Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats

Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats

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

Estimation of Microinhomogeneity of Conduction Impairment by Wavelet Analysis During Early Phase of Myocardial Ischemia in Pigs

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