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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

M-cell action potential duration in response to slowing of the stimulation rate. Transmembrane recordings were obtained from epicardial (Epi), endocardial (Endo) portions of the canine right and left ventricles at cycle lengths of 300, 1,000, 2,000 and 5,000 ms. Modified and reprinted with permission from Lippincott Williams & Wilkins [9].
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Figure 1: M-cell action potential duration in response to slowing of the stimulation rate. Transmembrane recordings were obtained from epicardial (Epi), endocardial (Endo) portions of the canine right and left ventricles at cycle lengths of 300, 1,000, 2,000 and 5,000 ms. Modified and reprinted with permission from Lippincott Williams & Wilkins [9].

Mentions: The concept of electrical heterogeneity in the myocardium arose from a seminal study in 1991, in which Sicouri and Antzelevitch described a subpopulation myocardial cells with distinct electrophysiological properties, known as M cells [9]. Amongst its characteristics, the M cell generates an action potential which prolongs to a greater degree than that of the epicardium and endocardium when the heart rate slows [9,10]. (Figure 1) Electrical heterogeneity has been demonstrated in various animal species and in the human myocardium [11].


Is cardiac resynchronisation therapy proarrhythmic?

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

M-cell action potential duration in response to slowing of the stimulation rate. Transmembrane recordings were obtained from epicardial (Epi), endocardial (Endo) portions of the canine right and left ventricles at cycle lengths of 300, 1,000, 2,000 and 5,000 ms. Modified and reprinted with permission from Lippincott Williams & Wilkins [9].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: M-cell action potential duration in response to slowing of the stimulation rate. Transmembrane recordings were obtained from epicardial (Epi), endocardial (Endo) portions of the canine right and left ventricles at cycle lengths of 300, 1,000, 2,000 and 5,000 ms. Modified and reprinted with permission from Lippincott Williams & Wilkins [9].
Mentions: The concept of electrical heterogeneity in the myocardium arose from a seminal study in 1991, in which Sicouri and Antzelevitch described a subpopulation myocardial cells with distinct electrophysiological properties, known as M cells [9]. Amongst its characteristics, the M cell generates an action potential which prolongs to a greater degree than that of the epicardium and endocardium when the heart rate slows [9,10]. (Figure 1) Electrical heterogeneity has been demonstrated in various animal species and in the human myocardium [11].

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