Analysis of the Initiation of Fibrillation by Electrographic Studies

Moe, Gordon K.; Harris, Andrew; Wiggers, Carl J.

doi:10.1152/ajplegacy.1941.134.3.473

Cited by 108 publications

(29 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In both patients, acceleration of VT occurred before Vfib. These findings are consistent with the mechanism of Vfib described by Moe et al 32 No patients had Vfib in the DP group. This is thought to be attributable to the fact that, by preventing VT from developing immediately after reperfusion, dipyridamole may prevent the acceleration and degeneration of VT into Vfib.…”

Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiassupporting

confidence: 93%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

View full text Add to dashboard Cite

Background-Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. Methods and Results-First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (nϭ23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (nϭ38; PϽ0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (nϭ7) or sustained VT (nϭ2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. Conclusions-These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusioninduced AIVR and VT. (Circulation. 2000;101:624-630.)

show abstract

Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiassupporting

confidence: 93%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

View full text Add to dashboard Cite

show abstract

“…A year later, Wégria et al (58) demonstrated that the vulnerable phase was of longer duration in premature ventricular complexes than in normal beats. Also, Moe et al (59) carried out detailed electrographic studies of the mechanism of reentry initiation by shocks applied during the vulnerable phase. Their results indicated that repetitive impulses induced by the shock were accompanied by a progressive decrease in refractory period combined with an increase in conduction time.…”

Section: Electrical Induction Of Vf and The Vulnerable Domainmentioning

confidence: 99%

Ventricular Fibrillation: Mechanisms of Initiation and Maintenance

Jalife

2000

Annu. Rev. Physiol.

332

220

View full text Add to dashboard Cite

Ventricular fibrillation (VF) is the major immediate cause of sudden cardiac death. Traditionally, VF has been defined as turbulent cardiac electrical activity, which implies a large amount of irregularity in the electrical waves that underlie ventricular excitation. During VF, the heart rate is too high (> 550 excitations/minute) to allow adequate pumping of blood. In the electrocardiogram (ECG), ventricular complexes that are ever-changing in frequency, contour, and amplitude characterize VF. This article reviews prevailing theories for the initiation and maintenance of VF, as well as its spatio-temporal organization. Particular attention is given to recent experiments and computer simulations suggesting that VF may be explained in terms of highly periodic three-dimensional rotors that activate the ventricles at exceedingly high frequency. Such rotors may show at least two different behaviors: (a) At one extreme, they may drift throughout the heart at high speeds producing beat-to-beat changes in the activation sequence. (b) At the other extreme, rotors may be relatively stationary, activating the ventricles at such high frequencies that the wave fronts emanating from them breakup at varying distances, resulting in complex spatio-temporal patterns of fibrillatory conduction. In either case, the recorded ECG patterns are indistinguishable from VF. The data discussed have paved the way for a better understanding of the mechanisms of VF in the normal, as well as the diseased, human heart.

show abstract

“…The reason for the focus on the effect of shocks given to paced activations rather than fibrillatory activity rests with the strong link between cardiac vulnerability and defibrillation. A large body of research has demonstrated that an electric shock can induce ventricular arrhythmias if it is given during the 'vulnerable window' within the normal cardiac cycle (King, 1934;Moe et al, 1941;Wiggers, 1930). Furthermore, shocks that result in induction of arrhythmia are bound by a minimum and a maximum strength, the lower limit of vulnerability (LLV) and ULV (Fabiato et al, 1967).…”

Section: State-of-the-art 3d Models Of Defibrillationmentioning

confidence: 99%

“…However, numerous mapping studies, mostly electrical Chattipakorn et al, 2000a,b;Chen et al, 1986a,b;Shibata et al, 1988a;Usui et al, 1996;Zhou et al, 1993) but also some optical (Chattipakorn et al, 2001(Chattipakorn et al, , 2004Wang et al, 2001), predominantly of large hearts (dog and pig) have demonstrated that following failed defibrillation shocks or shocks applied during the vulnerable period, reentrant patterns are not always immediately observed. Although local activations were detected following strong shocks, these activations did not become global and quickly died (Chattipakorn et al, 1998;Idriss et al, 1999;Moe et al, 1941;Shibata et al, 1988b); the activations were followed by an electrically quiescent period termed the 'isoelectric window.' The duration of the isoelectric window was short for weak shocks but increased with the increase in shock strength extending for well over 50 ms (Chattipakorn et al, 2000a(Chattipakorn et al, ,b, 2001(Chattipakorn et al, , 2004Chen et al, 1986a,b;Shibata et al, 1988a;Usui et al, 1996;Wang et al, 2001;Zhou et al, 1993).…”

Section: Mechanisms For the Isoelectric Window Following Near-ulv Shocksmentioning

confidence: 99%

“…The duration of the isoelectric window was short for weak shocks but increased with the increase in shock strength extending for well over 50 ms (Chattipakorn et al, 2000a(Chattipakorn et al, ,b, 2001(Chattipakorn et al, , 2004Chen et al, 1986a,b;Shibata et al, 1988a;Usui et al, 1996;Wang et al, 2001;Zhou et al, 1993). Timing of shock delivery also influenced isoelectric window duration: it was found to be near zero at late coupling intervals, that is, near diastole, and to increase linearly as coupling interval decreased (Moe et al, 1941;Shibata et al, 1988b). Following the isolectric window pause, an activation appeared on the epicardium.…”

Section: Mechanisms For the Isoelectric Window Following Near-ulv Shocksmentioning

confidence: 99%

See 1 more Smart Citation