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Is cardiac resynchronisation therapy proarrhythmic?

Leyva F, Foley PW - Indian Pacing Electrophysiol J (2008)

Bottom Line: Animal and human studies have shown that reversal of normal sequence of myocardial activation during epicardial pacing, as applied during CRT, increases the transmural dispersion of repolarisation (TDR), a substrate for ventricular arrhythmias.Cohort studies in humans suggest that CRT has a differential effect on the arrhythmogenic substrate, antiarrhythmic in some and proarrhythmic in others.This review the focuses on the possibility that CRT may, under certain circumstances, promote arrhythmogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Birmingham, Good Hope Hospital, West Midlands, England. francisco.leyva@eartofengland.nhs.uk

ABSTRACT
It is well established that cardiac resynchronisation therapy (CRT) using biventricular pacing prolongs survival by its effects on pump failure. The rate of sudden cardiac death in patients undergoing CRT, however, remains high. Animal and human studies have shown that reversal of normal sequence of myocardial activation during epicardial pacing, as applied during CRT, increases the transmural dispersion of repolarisation (TDR), a substrate for ventricular arrhythmias. Cohort studies in humans suggest that CRT has a differential effect on the arrhythmogenic substrate, antiarrhythmic in some and proarrhythmic in others. This review the focuses on the possibility that CRT may, under certain circumstances, promote arrhythmogenesis.

No MeSH data available.


Related in: MedlinePlus

Effects of endocardial pacing (Endo-P) and epicardial pacing (Epi-P) on: (A) QT interval duration and (B) TDR in arterially perfused rabbit left ventricular preparations with and without the administration of dofetilide. Note that epicardial Epi-P led to a more pronounced prolongation in TDR than the QT interval duration. Reproduced with permission from Lippincott Williams & Wilkins [7].
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Figure 3: Effects of endocardial pacing (Endo-P) and epicardial pacing (Epi-P) on: (A) QT interval duration and (B) TDR in arterially perfused rabbit left ventricular preparations with and without the administration of dofetilide. Note that epicardial Epi-P led to a more pronounced prolongation in TDR than the QT interval duration. Reproduced with permission from Lippincott Williams & Wilkins [7].

Mentions: In experiments using isolated arterially perfused rabbit LV wedge preparations, Medina-Ravell et al [7] have recently shown that switching from endocardial to epicardial pacing produces an increase in QT interval and transmural dispersion of repolarisation, without associated increases in ventricular transmembrane action potential durations. Administration of dofetilide, an agent which increases the action potential duration, led to a prolongation of the QT interval and TDR, an effect which was more pronounced with epicardial pacing. (Figure 3) In a further experiment, epicardial pacing was shown to facilitate transmural propagation of early repolarisations, the emergence of R-on-T extrasystoles and torsade-de-pointes ventricular tachycardia.


Is cardiac resynchronisation therapy proarrhythmic?

Leyva F, Foley PW - Indian Pacing Electrophysiol J (2008)

Effects of endocardial pacing (Endo-P) and epicardial pacing (Epi-P) on: (A) QT interval duration and (B) TDR in arterially perfused rabbit left ventricular preparations with and without the administration of dofetilide. Note that epicardial Epi-P led to a more pronounced prolongation in TDR than the QT interval duration. Reproduced with permission from Lippincott Williams & Wilkins [7].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2572030&req=5

Figure 3: Effects of endocardial pacing (Endo-P) and epicardial pacing (Epi-P) on: (A) QT interval duration and (B) TDR in arterially perfused rabbit left ventricular preparations with and without the administration of dofetilide. Note that epicardial Epi-P led to a more pronounced prolongation in TDR than the QT interval duration. Reproduced with permission from Lippincott Williams & Wilkins [7].
Mentions: In experiments using isolated arterially perfused rabbit LV wedge preparations, Medina-Ravell et al [7] have recently shown that switching from endocardial to epicardial pacing produces an increase in QT interval and transmural dispersion of repolarisation, without associated increases in ventricular transmembrane action potential durations. Administration of dofetilide, an agent which increases the action potential duration, led to a prolongation of the QT interval and TDR, an effect which was more pronounced with epicardial pacing. (Figure 3) In a further experiment, epicardial pacing was shown to facilitate transmural propagation of early repolarisations, the emergence of R-on-T extrasystoles and torsade-de-pointes ventricular tachycardia.

Bottom Line: Animal and human studies have shown that reversal of normal sequence of myocardial activation during epicardial pacing, as applied during CRT, increases the transmural dispersion of repolarisation (TDR), a substrate for ventricular arrhythmias.Cohort studies in humans suggest that CRT has a differential effect on the arrhythmogenic substrate, antiarrhythmic in some and proarrhythmic in others.This review the focuses on the possibility that CRT may, under certain circumstances, promote arrhythmogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Birmingham, Good Hope Hospital, West Midlands, England. francisco.leyva@eartofengland.nhs.uk

ABSTRACT
It is well established that cardiac resynchronisation therapy (CRT) using biventricular pacing prolongs survival by its effects on pump failure. The rate of sudden cardiac death in patients undergoing CRT, however, remains high. Animal and human studies have shown that reversal of normal sequence of myocardial activation during epicardial pacing, as applied during CRT, increases the transmural dispersion of repolarisation (TDR), a substrate for ventricular arrhythmias. Cohort studies in humans suggest that CRT has a differential effect on the arrhythmogenic substrate, antiarrhythmic in some and proarrhythmic in others. This review the focuses on the possibility that CRT may, under certain circumstances, promote arrhythmogenesis.

No MeSH data available.


Related in: MedlinePlus