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Differential Effects of Ventricular Pacing Sites of Contraction Synchrony and Global Cardiac Performance.

ABSTRACT: BACKGROUND: Quantification of left ventricular (LV) dyssynchrony allows for objective measures of resynchronization therapy (CRT) effectiveness. We tested the hypothesis that site of LV pacing, fusion beats and baseline contractility alter contraction synchrony as quantified by regional and global measures of LV performance. METHODS AND RESULTS: In 8 open-chested pentobarbital-anesthetized canine preparations we compared the effects of right atrial (RA), RA-high right ventricular (RV) free wall, as a model of left bundle branch block contraction pattern, RA-LV apex (LVa), RA-LV free wall (LVfw), and RA-RV-apical LV (CRTa) and RA-RV-free wall LV (CRTfw), as CRT. LV pressure-volume loops recorded using high-fidelity pressure and conductance catheters and echocardiographic angle-corrected color-coded strain imaging of mid-LV short axis views analyzed radial strain from six segments. To control for contractile state esmolol-induced beta blockage was studied, and in 5 dogs to control for RA and ventricular pacing fusion beat artifacts, repeat studies were done following AV node ablation. RA-RV pacing reduced stroke work (SW) (57±18 to 33±13* mmHg·mL,*p<0.05 vs RA pacing), decreased LV end-diastolic volume and induced marked radial dyssynchrony (maximal time difference between peak segmental strain) from 31±15 to 234±60* ms. Changes in radial dyssynchrony correlated significantly with changes in SW (r=-0.53, p<0.01). Dyssynchrony improved with both CRTa and CRTfw (69*±31 and 98*±63 ms, respectively) while SW only improved with CRTa (62±22* and 37±13 mmHg·mL, respectively * p<0.05 vs RV pacing). CRTa also tended to increased LV end-diastolic volume over RA-RV. Esmolol slowed HR from 118±10 to 108±10 beats/min* and tended to decrease contractility (end-systolic elastance (Ees) from 12.1±7.9 to 8.9±3.9 mmHg/ml, p=0.167) but did not alter the degree of RV-pacing induced dyssynchrony. AV ablation had no effect on the observed apical and free wall contraction differences seen during baseline conditions. CONCLUSION: Although both CRTa and CRTfw reduced contraction dyssynchrony, CRTa tended to improve global LV performance more by increasing end-diastolic volume. Thus, CRT may improve global LV performance differently, depending on the LV pacing site.

SUBMITTER: Alhammouri M

PROVIDER: S-EPMC3178394 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature

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Differential Effects of Ventricular Pacing Sites of Contraction Synchrony and Global Cardiac Performance.

Alhammouri Mohammed M Kim Hyung Kook HK Mokhtar Yasser Y Cannesson Maxime M Tanabe Masaki M Gorcsan John J Schwartzman David D Pinsky Michael R MR

Critical care and shock 20090501 2

BACKGROUND: Quantification of left ventricular (LV) dyssynchrony allows for objective measures of resynchronization therapy (CRT) effectiveness. We tested the hypothesis that site of LV pacing, fusion beats and baseline contractility alter contraction synchrony as quantified by regional and global measures of LV performance. METHODS AND RESULTS: In 8 open-chested pentobarbital-anesthetized canine preparations we compared the effects of right atrial (RA), RA-high right ventricular (RV) free wall ...[more]

PMID: 21949483

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Project description:A five-state model of myofilament contraction was integrated into a well-established rabbit ventricular myocyte model of ion channels, Ca(2+) transporters and kinase signaling to analyze the relative contribution of different phosphorylation targets to the overall mechanical response driven by ?-adrenergic stimulation (?-AS). ?-AS effect on sarcoplasmic reticulum Ca(2+) handling, Ca(2+), K(+) and Cl(-) currents, and Na(+)/K(+)-ATPase properties was included based on experimental data. The inotropic effect on the myofilaments was represented as reduced myofilament Ca(2+) sensitivity (XBCa) and titin stiffness, and increased cross-bridge (XB) cycling rate (XBcy). Assuming independent roles of XBCa and XBcy, the model reproduced experimental ?-AS responses on action potentials and Ca(2+) transient amplitude and kinetics. It also replicated the behavior of force-Ca(2+), release-restretch, length-step, stiffness-frequency and force-velocity relationships, and increased force and shortening in isometric and isotonic twitch contractions. The ?-AS effect was then switched off from individual targets to analyze their relative impact on contractility. Preventing ?-AS effects on L-type Ca(2+) channels or phospholamban limited Ca(2+) transients and contractile responses in parallel, while blocking phospholemman and K(+) channel (IKs) effects enhanced Ca(2+) and inotropy. Removal of ?-AS effects from XBCa enhanced contractile force while decreasing peak Ca(2+) (due to greater Ca(2+) buffering), but had less effect on shortening. Conversely, preventing ?-AS effects on XBcy preserved Ca(2+) transient effects, but blunted inotropy (both isometric force and especially shortening). Removal of titin effects had little impact on contraction. Finally, exclusion of ?-AS from XBCa and XBcy while preserving effects on other targets resulted in preserved peak isometric force response (with slower kinetics) but nearly abolished enhanced shortening. ?-AS effects on XBCa and XBcy have greater impact on isometric and isotonic contraction, respectively.

Project description:Background The hemodynamic effects of cardiac resynchronization therapy in patients with left ventricular assist devices (LVADs) are uncharacterized. We aimed to quantify the hemodynamic effects of different ventricular pacing configurations in patients with LVADs, focusing on short-term changes in load-independent right ventricular (RV) contractility. Methods and Results Patients with LVADs underwent right heart catheterization during spontaneous respiration without sedation and with pressures recorded at end expiration. Right heart catheterization was performed at different pacemaker configurations (biventricular pacing, left ventricular pacing, RV pacing, and unpaced conduction) in a randomly generated sequence with >3 minutes between configuration change and hemodynamic assessment. The right heart catheterization operator was blinded to the sequence. RV maximal change in pressure over time normalized to instantaneous pressure was calculated from digitized hemodynamic waveforms, consistent with a previously validated protocol. Fifteen patients with LVADs who were in sinus rhythm were included. Load-independent RV contractility, as assessed by RV maximal change in pressure over time normalized to instantaneous pressure, was higher in biventricular pacing compared with unpaced conduction (15.7±7.6 versus 11.0±4.0 s-1; P=0.003). Thermodilution cardiac output was higher in biventricular pacing compared with unpaced conduction (4.48±0.7 versus 4.38±0.8 L/min; P=0.05). There were no significant differences in heart rate, ventricular filling pressures, or atrioventricular valvular regurgitation across all pacing configurations. Conclusions Biventricular pacing acutely improves load-independent RV contractility in patients with LVADs. Even in these patients with mechanical left ventricular unloading via LVAD who were relative pacing nonresponders (required LVAD support despite cardiac resynchronization therapy), biventricular pacing was acutely beneficial to RV contractility.

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Dataset Information

Differential Effects of Ventricular Pacing Sites of Contraction Synchrony and Global Cardiac Performance.

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Differential Effects of Ventricular Pacing Sites of Contraction Synchrony and Global Cardiac Performance.

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