Time course of electrical fibrillation threshold during brief periods of myocardial ischemia and the genesis of fibrillation: Role of calcium

Timour, Quadiri; Aupetit, Jean‐François; Chevrel, Guillaume; Loufoua-Moundanga, J; Omar, S.; Faucon, G

doi:10.1007/bf00877408

Cited by 6 publications

(5 citation statements)

References 10 publications

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“…The present study showed that transient regional LV myocardial ischemia caused a significant reduction in VFT and an increase in DFT. With respect to the changes in VFT, our findings are consistent with previous studies 8,9 . With respect to the DFT, however, the results of previous studies have been mixed.…”

Section: Discussionsupporting

confidence: 91%

Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold

Anastasiou-Nana¹,

Tsagalou²,

Charitos³

et al. 2005

Pacing Clinical Electrophis

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Section: Discussionsupporting

confidence: 91%

Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold

Anastasiou-Nana¹,

Tsagalou²,

Charitos³

et al. 2005

Pacing Clinical Electrophis

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“…A factor which contributes to the development of ischaemia‐induced fibrillation is a decrease in EFT. A gradual exponential decline of EFT, from normal to near 0 mA, has been associated with triggering of fibrillation (Timour et al , 1994). However, the repetition of ischaemia periods at brief intervals for the monitoring of EFT from normal level to the occurrence of fibrillation might be criticized, since ‘preconditioning’ due to previous ischaemia has been claimed to protect against the arrhythmogenic effect of a subsequent ischaemia (Hagar et al , 1991; Vegh et al , 1992).…”

Section: Discussionmentioning

confidence: 99%

“…With wide diastolic impulses, fibrillation needs relatively high intensity to be triggered under normal conditions (Figure 2). The intensity required for fibrillation declines first rapidly, then more slowly in an exponential way (Timour et al , 1994), with the increase in duration of the ischaemia periods and falls down to near 0 mA. At this time, impulses of 0.3–0.4 mA intensity and 100 ms duration and even increasingly shorter, down to a few milliseconds, become sufficient to initiate fibrillation.…”

Section: Methodsmentioning

confidence: 99%

Ischaemia‐induced loss or reversal of the effects of the class I antiarrhythmic drugs on vulnerability to fibrillation

Aupetit

Loufoua-Moundanga

Faucon

et al. 1997

British J Pharmacology

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1 In the last decade, a number of clinical observations have questioned the ecacy of certain class I antiarrhythmic drugs against ischaemia-induced ventricular ®brillation. The eects of three drugs of this class, disopyramide (Ia), lignocaine (Ib) and¯ecainide (Ic) on the vulnerability to ®brillation during experimental ischaemia were investigated. 2 The study was carried out in anaesthetized, open-chest pigs (n=8 for each of the drugs, in addition to the control group, n=6). Vulnerability to ®brillation was evaluated by measuring electrical ®brillation threshold (EFT) by means of stepwise increased intensity of wide (100 ms) diastolic impulses applied to the ischaemic tissue at a 180 beats min 71 rate. Monophasic action potential (MAP) duration and conduction time in the ischaemic region were also measured. 3 EFT determinations were performed before and during periods of ischaemia induced by complete occlusion of the left anterior descending coronary artery near its origin. Ischaemic periods of increasing duration (30, 60, 90, 120, 150 s) were induced to determine the electrophysiological changes, of EFT especially, leading to ®brillation. 4 In the absence of ischaemia, all three drugs, administered by intravenous route (1 mg kg 71 plus 0.04 mg kg 71 min 71 ) increased EFT to a similar extent (from approximately 7 to 10 mA), despite a 25% prolongation of conduction time. 5 During ischaemia, none of the drugs prevented the fall in EFT towards 0 mA, resulting in spontaneous ®brillation. After 30 s of ischaemia, they no longer had any capacity for raising EFT and, after 60, 90 and 120 s of ischaemia, the decrease in EFT was exacerbated. This accelerated reduction in EFT shortened the time to onset of ®brillation (after 120 s of ischaemia, 62.5% of ®brillations with ecainide instead of 12.5 under control conditions, 75% instead of 25 with lignocaine and 50% instead of 25 with disopyramide). The reduction in MAP duration due to ischaemia was also signi®cantly accelerated (at 60 s, 178+5 ms instead of 192+4 with¯ecainide, 175+3 ms instead of 194+5 with lignocaine and 180+5 ms instead of 196+3 with disopyramide) and the slowing of conduction was made worse (prolongation of conduction time by 70% instead of 50). 6 In conclusion, the anti®brillatory properties normally manifested by these drugs are ®rst suppressed, then inverted by ischaemia, depending on oxygen debt varying with severity and duration of ischaemia.

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“…The duration of these periods was however gradually increased (30, 60, 90, 120 s, etc. ) to follow the decline in electrical fibrillation threshold in the course of a coronary occlusion [18]. However, in order to evaluate the changes in vulnerability to fibrillation due to pharmacological agents, the reproducibility of results in the absence of drug was to be previously established.…”

Section: Preparation Of the Animalsmentioning

confidence: 99%

“…A factor of inducing fibrillation such as ischaemia has long been known to decrease EFT. More precisely, EFT undergoes a decline of exponential type from normal to minor values which do not exceed those of pacing threshold [18]: fibrillation is triggered by the fall in EFT to this level, since the natural stimuli, sufficient to pace the heart like pacing stimuli, will result in fibrillation in the same way.…”

Section: Validity Of Eft For the Appraisal Of Vulnerability To Fibrilmentioning

confidence: 99%

Cardiac β-adrenoceptor activation and ventricular fibrillation under normal and ischaemic conditions

Bui‐Xuan

Freysz

et al. 1996

Cardiovascular Research

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Tachycardia produced by activation of atrial adrenoceptors decreases EFT in the healthy heart and aggravates its fall in the ischaemic heart. Ventricular adrenoceptor activation counteracts the EFT fall related to tachycardia in the healthy heart, but not in the ischaemic heart. Therefore, the protection against ischaemic fibrillation due to beta-blockers would be essentially attributable to their action on the sinus nodes.

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Time course of electrical fibrillation threshold during brief periods of myocardial ischemia and the genesis of fibrillation: Role of calcium

Cited by 6 publications

References 10 publications

Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold

Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold

Ischaemia‐induced loss or reversal of the effects of the class I antiarrhythmic drugs on vulnerability to fibrillation

Cardiac β-adrenoceptor activation and ventricular fibrillation under normal and ischaemic conditions

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