Early Afterdepolarizations and Arrhythmogenesis

El‐Sherif, Nabil; Craelius, William; Boutjdir, Mohamed; Gough, William B.

doi:10.1111/j.1540-8167.1990.tb01057.x

Cited by 79 publications

(49 citation statements)

References 67 publications

(57 reference statements)

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“…We measured the early QT intervals to the first peak of T waves. The rationale of our decision rests on the hypothesis that the second component of the T wave may be the manifestation of after-depolarizations [19,20] . Merri et al …”

Section: Discussionmentioning

confidence: 99%

Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome

Swan

Toivonen

Viitasalo

1998

European Heart Journal

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Objectives To improve the diagnostic criteria of the congenital long QT syndrome in borderline cases we examined rate adaptation of ventricular repolarization phases during exercise and subsequent recovery in children with the long QT syndrome and controls.Methods Nineteen children with definite long QT syndrome and 19 healthy controls underwent exercise testing. QT intervals were measured to the apex (early QT), to the end (total QT) and from apex to the end of the T wave (late QT) at heart rates from 90 by steps of 10 to 150 beats . min 1 . ResultsIn 11/19 long QT syndrome patients (61%) and 2/19 controls (12%) the total QT lengthened during the recovery phase compared with exercise (P=0·005) at the lowest comparable heart rate. No difference was found between the groups during exercise. The sensitivity of rate adaptation of repolarization intervals was analysed by calculating linear regression slopes relating the QT intervals to the heart rates. During recovery, slopes relating the total QT to heart rate were steeper in long QT syndrome patients than those in controls ( 2·50 0·82 vs 1·79 0·47, P=0·003). Total QT/heart rate slopes differed between exercise and recovery phases in the long QT syndrome group only ( 1·77 0·71 vs 2·50 0·82, P=0·009). In long QT syndrome patients, the difference in total QT/heart rate slopes was mainly because the late QT/heart rate slopes indicating inhomogeneity of repolarization were steeper during recovery ( 1·27 0·74) than during exercise ( 0·46 0·29, P<0·0001). ConclusionsAfter exercise in long QT syndrome children the QT interval lengthens abnormally and inhomogeneity of repolarization increases. Evaluation of the QT interval, and especially its late portion after exercise, may help in establishing the diagnosis of long QT syndrome.

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Section: Discussionmentioning

confidence: 99%

Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome

Swan

Toivonen

Viitasalo

1998

European Heart Journal

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“…4 The increased susceptibility to arrhythmias in chronic AVB has been related to an inhomogeneous prolongation of the monophasic ventricular action potential (in the left ventricle more than the right ventricle), leading to enhanced regional dispersion of repolarization. 4 Furthermore, class III-dependent early afterdepolarizations (EADs) are prominent, which may explain the more frequent observation of ventricular ectopic beats 5,6 in chronic-AVB dogs. 4 Structural adaptations accompany the altered hemodynamic load in the heart with AVB.…”

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confidence: 99%

Cellular Basis of Biventricular Hypertrophy and Arrhythmogenesis in Dogs With Chronic Complete Atrioventricular Block and Acquired Torsade de Pointes

et al. 1998

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Background-In the dog with chronic complete atrioventricular block (AVB), torsade de pointes arrhythmias (TdP) can be induced reproducibly by class III antiarrhythmic agents. In vivo studies reveal important electrophysiological alterations of the heart at 5 weeks of AVB, resulting in increased proarrhythmia. Autopsy studies indicate the presence of biventricular hypertrophy. In this study, the cellular basis of proarrhythmia and hypertrophy in chronic AVB was investigated. Methods and Results-From chronic-AVB dogs with increased heart weights and TdP, left midmyocardial and right ventricular myocytes were isolated by enzymatic dispersion. These myocytes were significantly larger than sinus rhythm (SR) controls. In chronic AVB, the action potential spike-and-dome configuration was preserved. However, the action potential duration (APD) at 95% and 50% of repolarization of the left midmyocardium was significantly larger in chronic AVB than in SR, with little change in the right ventricle, causing enhanced interventricular dispersion of repolarization at slow pacing rates. Treatment with the class III agent almokalant increased the APD to a much larger extent in chronic-AVB than in SR myocytes and resulted in a higher incidence of early afterdepolarizations (EADs). EADs had their takeoff potential between Ϫ35 and 0 mV. There was no evidence that spontaneous sarcoplasmic reticulum Ca 2ϩ release underlies these EADs. Conclusions-In

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“…Because of its relatively longer repolarization process, it is readily understandable that Purkinje cells are a initiating source of polymorphic VTs 4) as is suggested in the study using anthopleurin-A. 17) On the other hand, according to a series of experimental studies, M cells between epicardial and endocardial layers have a peculiar electrophysiologic properties characterized by remarkable prolongation of action potential in response to a slower pacing rate and in response to some pharmacological interventions.…”

Section: Cesium-induced Polymorphic Vtmentioning

confidence: 99%

“…Clinical and experimental studies unanimously support the view that triggered activity due to early afterdepolarization (EAD) is responsible for the occurrence of this arrhythmia. 3,4) Three hundred or more mutations have been reported in several types of long QT genes. 5) Electrocardiographically, dynamic oscillation of preceding RR intervals offers an electrophysiologic condition that favors the induction of TdP in 80% of events.…”

Section: Introductionmentioning

confidence: 99%

Focal and Reentrant Mechanisms of Torsades de Pointes: EAD, Reentry, or Chimera?

Murakawa

2011

J Arrhythmia

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Torsades de pointes (TdP) is characterized not only by its electrocardiographic morphology but also by a tendency to spontaneously terminate. Although clinical and experimental studies suggested that TdP is triggered exclusively by early afterdepolarization, the reentrant mechanism seems to play a certain role in its maintenance. In this article, I review the studies that investigated the origin and activation sequences of the twisting QRS complexes of TdP, and discuss whether it is fortunate or unfortunate for us if TdP has something to do with reentry. (J Arrhythmia 2011; 27: 28-37)

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Early Afterdepolarizations and Arrhythmogenesis

Cited by 79 publications

References 67 publications

Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome

Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome

Cellular Basis of Biventricular Hypertrophy and Arrhythmogenesis in Dogs With Chronic Complete Atrioventricular Block and Acquired Torsade de Pointes

Focal and Reentrant Mechanisms of Torsades de Pointes: EAD, Reentry, or Chimera?

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