Within-subject electrocardiographic differences at equal heart rates: role of the autonomic nervous system

Frederiks, J.; Swenne, Cees A.; Kors, Jan A.; Herpen, Gerard van; Maan, Arie C.; Levert, J.V.; Schalij, Martin J.; Bruschke, Albert V.G.

doi:10.1007/s004240000487

Cited by 31 publications

(28 citation statements)

References 38 publications

(47 reference statements)

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“…Although the clinical applicability of these concepts remains to be fully validated, significant progress toward validation of the T peak-T end interval as an index of TDR has been achieved. Recent studies suggest that the T peak-T end interval may be a useful index of transmural dispersion and thus may be prognostic of arrhythmic risk under a variety of conditions (13)(14)(15)(16)(17)(18)(19)(20). Direct evidence in support of T peak-T end as a valuable index to predict TdP in patients with long QT syndrome was provided by Yamaguchi et al (21).…”

Section: Role Of Electrical Heterogeneity In the Inscription Of The Tmentioning

confidence: 96%

Potential Proarrhythmic Effects of Biventricular Pacing

Fish

Brugada

Antzelevitch

2005

Journal of the American College of Cardiology

127

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Resynchronization therapy involving right ventricular endocardial and left ventricular epicardial pacing improves cardiac output, quality of life, and New York Heart Association functional class in patients with congestive heart failure. Although a great deal of attention has been directed at showing the mechanical benefits and in fine-tuning the biventricular pacing configuration and protocol, little attention has been focused on the consequences of reversing the direction of activation of the left ventricular wall. Recent basic science and clinical studies have shown a proarrhythmic effect of reversing the direction of activation of the left ventricular wall. Reversal of the normal activation sequence prolongs the QT interval and increases the existing transmural dispersion of repolarization, creating the substrate and trigger for re-entrant arrhythmias under long QT conditions. A number of case reports of R-on-T extrasystoles and ventricular tachyarrhythmia induction as a result of biventricular pacing support this observation, and raise concern that biventricular pacing may be proarrhythmic in select cases, particularly when associated with a prolonged QT interval. Our focus in this review is on current understanding of transmural heterogeneity of repolarization that exists across the left ventricular wall, how this dispersion of repolarization is amplified as a consequence of reversal of the normal activation sequence, and how these basic experimental findings may apply to patients receiving cardiac resynchronization therapy.

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Section: Role Of Electrical Heterogeneity In the Inscription Of The Tmentioning

confidence: 96%

Potential Proarrhythmic Effects of Biventricular Pacing

Fish

Brugada

Antzelevitch

2005

Journal of the American College of Cardiology

127

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“…The T peak -T end interval is unlikely to provide an absolute measure of transmural dispersion in vivo, as elegantly demonstrated by Xia and co-workers (151). However, changes in this parameter are thought to be capable of reflecting changes in spatial dispersion of repolarization, particularly TDR, and, thus, may be prognostic of arrhythmic risk under a variety of conditions (57,102,125,126,144,150). Takenaka et al (125) recently demonstrated exercise-induced accentuation of the T peak -T end interval in LQT1, but not LQT2, patients.…”

Section: Long Qt Syndromementioning

confidence: 99%

Role of spatial dispersion of repolarization in inherited and acquired sudden cardiac death syndromes

Antzelevitch

2007

American Journal of Physiology-Heart and Circulatory Physiology

228

175

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Antzelevitch C. Role of spatial dispersion of repolarization in inherited and acquired sudden cardiac death syndromes. Am J Physiol Heart Circ Physiol 293: H2024-H2038, 2007. First published June 22, 2007; doi:10.1152/ajpheart.00355.2007.-This review examines the role of spatial electrical heterogeneity within the ventricular myocardium on the function of the heart in health and disease. The cellular basis for transmural dispersion of repolarization (TDR) is reviewed, and the hypothesis that amplification of spatial dispersion of repolarization underlies the development of life-threatening ventricular arrhythmias associated with inherited ion channelopathies is evaluated. The role of TDR in long QT, short QT, and Brugada syndromes, as well as catecholaminergic polymorphic ventricular tachycardia (VT), is critically examined. In long QT syndrome, amplification of TDR is often secondary to preferential prolongation of the action potential duration (APD) of M cells; in Brugada syndrome, however, it is thought to be due to selective abbreviation of the APD of the right ventricular epicardium. Preferential abbreviation of APD of the endocardium or epicardium appears to be responsible for the amplification of TDR in short QT syndrome. In catecholaminergic polymorphic VT, reversal of the direction of activation of the ventricular wall is responsible for the increase in TDR. In conclusion, long QT, short QT, Brugada, and catecholaminergic polymorphic VT syndromes are pathologies with very different phenotypes and etiologies, but they share a common final pathway in causing sudden cardiac death. Among Wiggers' many seminal contributions to physiology and medicine was his elucidation of the mechanisms responsible for ventricular fibrillation (VF). He described approaches to the prevention and treatment of conditions associated with VF (149). I am pleased to have the opportunity to present some of the work we have done to further his important contributions to our field.My principal focus will be on the heterogeneity within the ventricular myocardium with respect to electrical activity: how this heterogeneity contributes to spatial dispersion of repolarization and the degree to which amplification of this spatial dispersion contributes to the development of life-threatening ventricular arrhythmias associated with inherited ion channelopathies (Table 1), such as long QT, short QT, and Brugada syndromes, as well as catecholaminergic polymorphic ventricular tachycardia (CPVT). Preferential prolongation of the action potential duration (APD) of M cells is responsible for amplification of transmural dispersion of repolarization (TDR) in most cases of long QT syndrome, whereas preferential abbreviation of the APD of the right ventricular (RV) epicardium is believed to responsible for amplification of spatial dispersion of repolarization in Brugada syndrome. Recent reports suggest that preferential abbreviation of APD of the endocardium or epicardium is responsible for amplification of TDR in different forms of short QT syndrome....

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“…4 On the contrary, if the QT/RR hysteresis is ignored, QTc correction can be polluted by substantial errors if data are taken from episodes during which the heart rate is changing, with potentially disputable conclusions. 26 At the same time, although QT/RR hysteresis correction reduces QTc variability and thus improves the power of studies of drug-induced QTc changes, 4 QT/RR hysteresis correction is not crucial (in the sense that it could lead to false positive or false negative conclusions) if QT readings are obtained only from episodes preceded by stable heart rates. In the studies of drug effects, this is unachievable only with very fast acting pharmaceuticals.…”

Section: Discussionmentioning

confidence: 99%