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      Comparison of hemodynamic effects of biventricular versus left ventricular only pacing in patients receiving cardiac resynchronization therapy: A before–after clinical trial

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          Abstract

          Background

          Biventricular (BiV) pacing is the most common mode of delivering cardiac resynchronization therapy (CRT). However, initial clinical studies have indicated that left ventricular (LV) pacing is not inferior to BiV pacing. This study was conducted to address whether LV only pacing can provide the same hemodynamic response as BiV pacing.

          Methods

          This before–after clinical trial was conducted at Ekbatan Hospital, from July 2012 to November 2014. Patients with a LV ejection fraction ≤35% and a QRS duration ≥0.12 s who had a standard indication for ventricular pacing were enrolled. The CRT devices of all patients had already been set for BiV pacing. Therefore, their CRT devices were set for LV only pacing for 3 months. The hemodynamic status of the patients was assessed by echocardiography before setting the CRT device to LV only pacing (as a control) and 3 months after (as an intervention).

          Results

          There was no statistically significant difference between the effect of BiV pacing and LV only pacing on the hemodynamic responses including LV ejection fraction, LV end diastolic and systolic volume, and velocity time integral of the aortic valve. Moreover, no significant difference was seen between men and women either.

          Conclusions

          LV only pacing is not inferior to BiV pacing, and the hemodynamic response was similar in the two groups. However, the LV mode has a number of advantages over the BiV mode. More evidence, based on large clinical trials, is needed to confirm our results.

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          Most cited references20

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          Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay.

          Ventricular pacing can improve hemodynamics in heart failure patients, but direct effects on left ventricular (LV) function from varying pacing site and atrioventricular (AV) delay remain unknown. We hypothesized that the magnitude and location of basal intraventricular conduction delay critically influences pacing responses and that single-site pacing in the delay-activated region yields similar or better responses to biventricular pacing. Aortic and LV pressures were measured in 18 heart failure patients (mean+/-SD: LV ejection fraction, 19+/-7%; LV end-diastolic pressure, 25+/-8 mm Hg; QRS duration, 157+/-36 ms). Data under normal sinus rhythm were compared with ventricular pacing (VDD) at varying sites and AV delays (randomized order). Right ventricular (RV) apical or midseptal pacing had negligible contractile/systolic effects. However, LV free-wall pacing raised dP/dtmax by 23.7+/-19.0% and pulse-pressure by 18.0+/-18.4% (P<0.01). Biventricular pacing yielded less change (+12.8+/-9.3% in dP/dtmax, P<0.05 versus LV). Pressure-volume analysis performed in 11 patients consistently revealed minimal changes with RV pacing but increased stroke work and lower end-systolic volumes with LV pacing. Optimal AV intervals averaged 125+/-49 ms, and within this range, AV delay had less influence on LV function than pacing site. Basal QRS duration positively correlated with %DeltadP/dtmax (P<0.005), but pacing efficacy was not associated with QRS narrowing. Conduction delay pattern generally predicted pacing sites with most effect. VDD pacing acutely enhances contractile function in heart failure patients with intraventricular conduction delay. Single-site pacing at the site of greatest delay achieves similar or greater benefits to biventricular pacing in such patients. These data clarify pacing-effect mechanisms and should help in candidate identification for future studies.
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            QRS duration and mortality in patients with congestive heart failure.

            It has been suggested that prolongation of the QRS duration (>120 ms) is an independent risk factor for mortality in patients with cardiomyopathy. The purpose of this study was to examine the association between QRS duration and survival in patients with heart failure. We performed a retrospective analysis to examine the association between QRS prolongation (> or =120 ms) and mortality. The study population included 669 patients with heart failure. Two groups, on the basis of baseline QRS duration or =120 milliseconds, were identified. The groups were compared with respect to total mortality and sudden death. Subgroups were also stratified by right bundle branch block and left bundle branch block, ejection fraction (EF) or =30% to 40%, ischemic and nonischemic cardiomyopathy, amiodarone and placebo. Prolonged QRS was associated with a significant increase in mortality (49.3% vs 34.0%, P =.0001) and sudden death (24.8% vs 17.4%, P =.0004). Left bundle branch block was associated with worse survival (P =.006) but not sudden death. In patients with an EF <30%, QRS prolongation continued to be associated with a significant increase in mortality (51.6% vs 41.1%, P =.01) and sudden death (28.8% vs 21.1%, P =.02). In those with an EF of 30% to 40%, QRS prolongation was associated with a significant increase in mortality (42.7% vs 23.3%, P =.0036) but not in sudden death (13.3% vs 12.0%, P =.625). After adjustment for baseline variables, independent predictors of mortality were found to be prolongation of QRS (P =.0028, risk ratio 1.46) and depressed EF (P =.0001, risk ratio 0.965). Age, type of cardiomyopathy, and drug treatment group were not predictive of mortality. QRS prolongation is an independent predictor of both increased total mortality and sudden death in patients with heart failure.
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              Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block.

              Left ventricular or biventricular pacing/stimulation can acutely improve systolic function in patients with dilated cardiomyopathy (DCM) and intraventricular conduction delay by resynchronizing contraction. Most heart failure therapies directly enhancing systolic function do so while concomitantly increasing myocardial oxygen consumption (MVO(2)). We hypothesized that pacing/stimulation, in contrast, incurs systolic benefits without raising energy demand. Ten DCM patients with left bundle-branch block (ejection fraction 20+/-3%, QRS duration 179+/-3 ms, mean+/-SEM) underwent cardiac catheterization to measure ventricular and aortic pressure, coronary blood flow, arterial-coronary sinus oxygen difference (DeltaAVO(2)), and MVO(2). Data were measured under sinus rhythm or with left ventricular or biventricular pacing/stimulation at the same heart rate. These results were then contrasted to intravenous dobutamine (n=7) titrated to match systolic changes during LV pacing. Systolic function rose quickly and substantially from LV pacing (18+/-4% rise in arterial pulse pressure, which correlates with cardiac output, and 43+/-6% increase in dP/dt(max); both P<0.01). However, DeltaAVO(2) and MVO(2) declined -4+/-2% and -8+/-6.5%, respectively (both P<0.05). Similar results were obtained with biventricular activation. In contrast, dobutamine raised dP/dt(max) 37+/-6%, accompanied by a 22+/-11% rise in per-beat MVO(2) (P<0.05 versus pacing). Ventricular resynchronization by left ventricular or biventricular pacing/stimulation in DCM patients with left bundle-branch block acutely enhances systolic function while modestly lowering energy cost. This should prove valuable for treating DCM patients with basal dyssynchrony.
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                Author and article information

                Contributors
                Journal
                J Arrhythm
                J Arrhythm
                Journal of Arrhythmia
                Elsevier
                1880-4276
                1883-2148
                30 August 2016
                April 2017
                30 August 2016
                : 33
                : 2
                : 127-129
                Affiliations
                [a ]Department of Cardiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
                [b ]Clinical Research Development Unit of Farshcian Cardiology Hospital, Hamadan University of Medical Sciences, Hamadan, Iran
                [c ]Modeling of Noncommunicable Diseases Research Center, Department of Epidemiology & Biostatistics, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
                Author notes
                [* ]Correspondence to: Department of Cardiology, School of Medicine, Hamadan University of Medical Sciences, P.O. Box 65178-38678, Shahid Fahmideh Avenue, Hamadan, Iran. Fax: +98 81 3838 0548.Department of Cardiology, School of Medicine, Hamadan University of Medical SciencesP.O. Box 65178-38678, Shahid Fahmideh AvenueHamadanIran dr.bfaghfourian@ 123456gmail.com
                Article
                S1880-4276(16)30102-8
                10.1016/j.joa.2016.07.014
                5388040
                28416979
                2ca52a77-d8df-4da2-862f-4be7865fd21c
                © 2016 Japanese Heart Rhythm Society. Published by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 23 April 2016
                : 18 July 2016
                : 26 July 2016
                Categories
                Original Article

                biventricular pacing,cardiac resynchronization therapy,heart failure,left ventricular only pacing

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