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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

Changes in QT interval, R-on-T ventricular extrasystoles and the development of torsade-de-pointes ventricular tachycardia in response to pacing at different sites. After switching from right ventricular endocardial pacing (RVEndoP) to left ventricular epicardial pacing (LVEpiP), the QT interval increased. Continued LVEpiP led to ventricular extrasystoles (B) and, eventually, to torsade-de-pointes ventricular tachycardia (C). Switching from RVEndoP to biventricular pacing (BiVP) led to an increase in the QT interval duration and to the emergence of R-on-T ventricular extrasystoles. Reproduced with permission from Lippincott Williams  & Wilkins [7].
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Figure 4: Changes in QT interval, R-on-T ventricular extrasystoles and the development of torsade-de-pointes ventricular tachycardia in response to pacing at different sites. After switching from right ventricular endocardial pacing (RVEndoP) to left ventricular epicardial pacing (LVEpiP), the QT interval increased. Continued LVEpiP led to ventricular extrasystoles (B) and, eventually, to torsade-de-pointes ventricular tachycardia (C). Switching from RVEndoP to biventricular pacing (BiVP) led to an increase in the QT interval duration and to the emergence of R-on-T ventricular extrasystoles. Reproduced with permission from Lippincott Williams & Wilkins [7].

Mentions: In humans, reversal of the normal sequence of activation has similarly been linked to arrhythmogenesis. Medina-Ravell et al [7] showed that, in one patient, switching from endocardial to epicardial left ventricular pacing, the QT interval increased from 485 to 580 ms, an effect which was associated with the development of torsade-de-pointes ventricular tachycardia. (Figure 4) Switching from right ventricular endocardial pacing to BiVP led to an increase in the T interval followed by R-on-T ventricular extrasystoles. Importantly, a substudy of 29 patients with heart failure showed that LV epicardial pacing and BiVP led to increases in QT, JT and transmural dispersion of depolarisation [7]. (Figure 5) These data suggest that a BiVP- or LV epicardial-dependent increase in the QT interval and transmural dispersion of repolarisation has the potential for increasing the risk for the development of ventricular arrhythmias.


Is cardiac resynchronisation therapy proarrhythmic?

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

Changes in QT interval, R-on-T ventricular extrasystoles and the development of torsade-de-pointes ventricular tachycardia in response to pacing at different sites. After switching from right ventricular endocardial pacing (RVEndoP) to left ventricular epicardial pacing (LVEpiP), the QT interval increased. Continued LVEpiP led to ventricular extrasystoles (B) and, eventually, to torsade-de-pointes ventricular tachycardia (C). Switching from RVEndoP to biventricular pacing (BiVP) led to an increase in the QT interval duration and to the emergence of R-on-T ventricular extrasystoles. 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 4: Changes in QT interval, R-on-T ventricular extrasystoles and the development of torsade-de-pointes ventricular tachycardia in response to pacing at different sites. After switching from right ventricular endocardial pacing (RVEndoP) to left ventricular epicardial pacing (LVEpiP), the QT interval increased. Continued LVEpiP led to ventricular extrasystoles (B) and, eventually, to torsade-de-pointes ventricular tachycardia (C). Switching from RVEndoP to biventricular pacing (BiVP) led to an increase in the QT interval duration and to the emergence of R-on-T ventricular extrasystoles. Reproduced with permission from Lippincott Williams & Wilkins [7].
Mentions: In humans, reversal of the normal sequence of activation has similarly been linked to arrhythmogenesis. Medina-Ravell et al [7] showed that, in one patient, switching from endocardial to epicardial left ventricular pacing, the QT interval increased from 485 to 580 ms, an effect which was associated with the development of torsade-de-pointes ventricular tachycardia. (Figure 4) Switching from right ventricular endocardial pacing to BiVP led to an increase in the T interval followed by R-on-T ventricular extrasystoles. Importantly, a substudy of 29 patients with heart failure showed that LV epicardial pacing and BiVP led to increases in QT, JT and transmural dispersion of depolarisation [7]. (Figure 5) These data suggest that a BiVP- or LV epicardial-dependent increase in the QT interval and transmural dispersion of repolarisation has the potential for increasing the risk for the development of ventricular arrhythmias.

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