2008
DOI: 10.1093/europace/eun019
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Right ventricular pacing is an independent predictor for ventricular tachycardia/ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter-defibrillator

Abstract: Cumulative RV pacing > 2% and EF < 40% are independent predictors for VT/VF occurrence and mortality and hospitalization for heart failure in predominantly secondary prophylactic ICD patients. Our data show that algorithms capable of reducing cumulative RV pacing should be used more frequently in clinical practice.

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Cited by 40 publications
(29 citation statements)
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“…28 The ventricular dyssynchrony associated with PVCs, particularly when the PVC burden is high, may contribute to LV dilation and impaired function in a fashion previously described for patients with left bundle branch block or chronic right ventricular pacing. [25][26][27][28][29] Right ventricular pacing is notably associated with dyssynchronous ventricular contraction, 39 changes in cardiac sympathetic activity, histopathology as well as ion channel expression and function 40 ; animal models have shown that right ventricular pacing induces asymmetrical myocardial hypertrophy, myofibrillar disarray, and increased catecholamine concentrations in the myocardium. [41][42][43] Although clinical studies describe LV dysfunction developing over reasonably long periods of time (Ͼ4 years in the series of Niwano et al 13 ), in canine models, LV dysfunction occurred within 4 to 12 weeks of induced ventricular ectopy.…”
Section: Mechanisms and Pathophysiologymentioning
confidence: 99%
“…28 The ventricular dyssynchrony associated with PVCs, particularly when the PVC burden is high, may contribute to LV dilation and impaired function in a fashion previously described for patients with left bundle branch block or chronic right ventricular pacing. [25][26][27][28][29] Right ventricular pacing is notably associated with dyssynchronous ventricular contraction, 39 changes in cardiac sympathetic activity, histopathology as well as ion channel expression and function 40 ; animal models have shown that right ventricular pacing induces asymmetrical myocardial hypertrophy, myofibrillar disarray, and increased catecholamine concentrations in the myocardium. [41][42][43] Although clinical studies describe LV dysfunction developing over reasonably long periods of time (Ͼ4 years in the series of Niwano et al 13 ), in canine models, LV dysfunction occurred within 4 to 12 weeks of induced ventricular ectopy.…”
Section: Mechanisms and Pathophysiologymentioning
confidence: 99%
“…In post-MI patients, RV apical pacing was associated with a worsening of LV function, suggesting at the same time that among MI survivors, the need for pacemaker may be a marker of worse outcome [50]. Cumulative RV pacing > 2% and EF < 40% are independent predictors of ventricular tachycardia/ /ventricular fibrillation occurrence, higher mortality rate and HF hospitalizations in patients after cardioverter-defibrillator implantation [51].…”
Section: Ewa Majos Et Al the Right Ventricle In Patients With Chronmentioning
confidence: 99%
“…24 The mechanism of heart failure development in chronic right ventricular pacing is not entirely known but may in part be due to an abnormal activation pattern of the ventricle. This hypothesis is supported by the fact that various forms of abnormal ventricular activation have been shown to adversely affect left ventricular systolic function including chronic right ventricular pacing, [25][26][27] left bundle branch block 28,29 and ventricular pre-excitation. 30,31 Given this, chronic atrial pacing is likely a more pure model of TIC, as it should result in fewer electromechanical changes in the ventricles beyond increased rate.…”
Section: Introductionmentioning
confidence: 99%