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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

Top: Effects of epicardial (Epi) versus endocardial (Endo) pacing on QT interval, Tpeak-end (Tp-Te) and TDR in homogenous myocardium and in heterogenous myocardium. Note that, when switching from endocardial to epicardial pacing, the QT interval, Tpeak-end (Tp-Te) and TDR are unchanged in homogenous myocardium but prolonged in heterogenous myocardium. Modified and reprinted with permission from Lippincott Williams & Wilkins [8].
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Figure 2: Top: Effects of epicardial (Epi) versus endocardial (Endo) pacing on QT interval, Tpeak-end (Tp-Te) and TDR in homogenous myocardium and in heterogenous myocardium. Note that, when switching from endocardial to epicardial pacing, the QT interval, Tpeak-end (Tp-Te) and TDR are unchanged in homogenous myocardium but prolonged in heterogenous myocardium. Modified and reprinted with permission from Lippincott Williams & Wilkins [8].

Mentions: The QT interval, the morphology of the T wave and the Tpeak-Tend interval are dependent on the activation sequence of the myocardium. In an elegant study using mathematical modelling, Fish et al [8] demonstrated the difference between transmural conduction in homogenous versus heterogenous myocardium. (Figure 2) In homogenous myocardium, reversing of the direction of stimulation leads to a change in the polarity of the QRS complex and the T wave, but not to changes in the duration of the action potential, the QT interval, TDR or the Tpeak-Tend interval. In heterogenous myocardium consisting of epicardium, endocardium and M cells, reversal of the transmural direction of activation does lead to a prolongation of TDR and the Tpeak-Tend interval, reflecting the fact that the epicardium depolarises and repolarises earlier and the M calls depolarise and repolarise later.


Is cardiac resynchronisation therapy proarrhythmic?

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

Top: Effects of epicardial (Epi) versus endocardial (Endo) pacing on QT interval, Tpeak-end (Tp-Te) and TDR in homogenous myocardium and in heterogenous myocardium. Note that, when switching from endocardial to epicardial pacing, the QT interval, Tpeak-end (Tp-Te) and TDR are unchanged in homogenous myocardium but prolonged in heterogenous myocardium. Modified and reprinted with permission from Lippincott Williams & Wilkins [8].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Top: Effects of epicardial (Epi) versus endocardial (Endo) pacing on QT interval, Tpeak-end (Tp-Te) and TDR in homogenous myocardium and in heterogenous myocardium. Note that, when switching from endocardial to epicardial pacing, the QT interval, Tpeak-end (Tp-Te) and TDR are unchanged in homogenous myocardium but prolonged in heterogenous myocardium. Modified and reprinted with permission from Lippincott Williams & Wilkins [8].
Mentions: The QT interval, the morphology of the T wave and the Tpeak-Tend interval are dependent on the activation sequence of the myocardium. In an elegant study using mathematical modelling, Fish et al [8] demonstrated the difference between transmural conduction in homogenous versus heterogenous myocardium. (Figure 2) In homogenous myocardium, reversing of the direction of stimulation leads to a change in the polarity of the QRS complex and the T wave, but not to changes in the duration of the action potential, the QT interval, TDR or the Tpeak-Tend interval. In heterogenous myocardium consisting of epicardium, endocardium and M cells, reversal of the transmural direction of activation does lead to a prolongation of TDR and the Tpeak-Tend interval, reflecting the fact that the epicardium depolarises and repolarises earlier and the M calls depolarise and repolarise later.

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