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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

Kaplan-Meier survival curves according to change in QT dispersion (QTD) from baseline to 48 days following biventricular pacemaker implantation. Reproduced with permission from Elsevier [29].
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Figure 7: Kaplan-Meier survival curves according to change in QT dispersion (QTD) from baseline to 48 days following biventricular pacemaker implantation. Reproduced with permission from Elsevier [29].

Mentions: We sought to determine whether QT interval duration and QT dispersion prior to and following implantation predict major arrhythmic events (MAE) following CRT [29]. In a study of 75 patients, 11 patients suffered a MAE over a follow-up of 807 days. Disappointingly, neither the QT interval or QT dispersion prior to implantation predicted MAE. Following CRT, however, a differential effect of CRT on QT dispersion was observed, with 47% of patients exhibiting an increase in QT dispersion above baseline, and 53% showing a decrease. (Figure 6). Major arrhythmic events occurred in 29% of patients exhibiting an increase in QT dispersion and in 3% of those exhibiting a decrease (p=0.0017). In multiple regression analyses, change in QT dispersion from baseline strongly predicted MAE, independently of changes in QTc, QRS duration, left ventricular ejection fraction and end-diastolic volume (p<0.001). Differences in survival curves were observed when patients were dichotomised according to whether QT dispersion increased or decreased in relation to baseline values (p<0.0001). (Figure 7) These findings raise the possibility that CRT has differential effects on the arrhythmogenic substrate, antiarrhythmic in some and arrhythmogenic in others. Similar differential effects on the arrhythomogenic substrate have been observed with other treatments, such as class I antiarrhythmic agents [30].


Is cardiac resynchronisation therapy proarrhythmic?

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

Kaplan-Meier survival curves according to change in QT dispersion (QTD) from baseline to 48 days following biventricular pacemaker implantation. Reproduced with permission from Elsevier [29].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 7: Kaplan-Meier survival curves according to change in QT dispersion (QTD) from baseline to 48 days following biventricular pacemaker implantation. Reproduced with permission from Elsevier [29].
Mentions: We sought to determine whether QT interval duration and QT dispersion prior to and following implantation predict major arrhythmic events (MAE) following CRT [29]. In a study of 75 patients, 11 patients suffered a MAE over a follow-up of 807 days. Disappointingly, neither the QT interval or QT dispersion prior to implantation predicted MAE. Following CRT, however, a differential effect of CRT on QT dispersion was observed, with 47% of patients exhibiting an increase in QT dispersion above baseline, and 53% showing a decrease. (Figure 6). Major arrhythmic events occurred in 29% of patients exhibiting an increase in QT dispersion and in 3% of those exhibiting a decrease (p=0.0017). In multiple regression analyses, change in QT dispersion from baseline strongly predicted MAE, independently of changes in QTc, QRS duration, left ventricular ejection fraction and end-diastolic volume (p<0.001). Differences in survival curves were observed when patients were dichotomised according to whether QT dispersion increased or decreased in relation to baseline values (p<0.0001). (Figure 7) These findings raise the possibility that CRT has differential effects on the arrhythmogenic substrate, antiarrhythmic in some and arrhythmogenic in others. Similar differential effects on the arrhythomogenic substrate have been observed with other treatments, such as class I antiarrhythmic agents [30].

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