Impact of Preexisting Left Bundle Branch Block in Transcatheter Aortic Valve Replacement Recipients

BACKGROUND The impact of preexisting left bundle branch block (LBBB) in transcatheter aortic valve replacement (TAVR) recipients is unknown. The aim of this study was to determine the impact of preexisting LBBB on clinical outcomes after TAVR. METHODS AND RESULTS This multicenter study evaluated 3404 TAVR candidates according to the presence or absence of LBBB on baseline ECG. TAVR complications and causes of death were defined according to Valve Academic Research Consortium-2 definitions. Follow-up outpatient visits or telephone interviews were conducted at 30 days, 12 months, and yearly thereafter. Echocardiography examinations were performed at baseline, at hospital discharge, and at 1-year follow-up. Preexisting LBBB was present in 398 patients (11.7%) and was associated with an increased risk of permanent pacemaker implantation (PPI; 21.1% versus 14.8%; adjusted odds ratio, 1.51; 95% CI, 1.12-2.04) but not death (7.3% versus 5.5%; adjusted odds ratio, 1.33; 95% CI, 0.84-2.12) at 30 days. At a mean follow-up of 22±21 months, there were no differences between patients with and without preexisting LBBB in overall mortality (adjusted hazard ratio, 0.94; 95% CI, 0.75-1.18) and cardiovascular mortality (adjusted hazard ratio, 0.90; 95% CI, 0.68-1.21). In a subanalysis of 2421 patients without PPI at 30 days and with complete follow-up about the PPI, preexisting LBBB was not associated with an increased risk of PPI or sudden cardiac death. Patients with preexisting LBBB had a lower left ventricular ejection fraction (LVEF) at baseline and at 1-year follow-up ( P <0.001 for both), but those with low LVEF exhibited a similar increase in LVEF over time after TAVR compared with patients with no preexisting LBBB ( P=0.327). CONCLUSIONS Preexisting LBBB significantly increased the risk of early (but not late) PPI after TAVR, without any significant effect on overall mortality or cardiovascular mortality. Preexisting LBBB was associated with lower LVEF pre-TAVR but did not prevent an increase in LVEF post-TAVR similar to patients without LBBB

TCT-657 Post-Procedural And Follow-Up Management In Patients Undergoing Transcatheter Aortic Valve Implantation: Results From The Written (WoRldwIde TAVI ExpieNce) Survey

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TCT-695 Clinical Impact and Evolution Of Mitral Regurgitation Following Transcatheter Aortic Valve Replacement: A Meta-Analysis

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TCT-637 Transcatheter Aortic Valve Implantation in Patients with Small Aortic Annuli Using the Edwards SAPIEN XT 20mm Balloon-Expanding Heart Valve: Early Clinical Results from A Multi-Center Registry

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AT 1} receptor blockade prevents the decrease in conduit artery flow-mediated dilatation during NOS inhibition in humans

International audienceWhether AT1 receptor blockade can prevent the decrease in conduit artery flow-mediated dilatation during NO-synthase inhibition by endothelial alternative pathways has not previously been explored in humans. In 12 healthy subjects, we measured radial artery diameter (echotracking) and flow (Doppler) during flow-mediated dilatation induced by sustained reactive hyperemia in control period and following NO-synthase inhibition (L-NMMA: 1.5 mg.min -1}.L -1}), after single oral administration of telmisartan (80 mg) or placebo, during a double-blind, randomized, cross-over study. In 6 volunteers, we also assessed the roles of prostacyclin and endothelium-derived hyperpolarizing factor during radial flow-mediated dilatation after AT 1} receptor blockade by oral administration of aspirin (500 mg) alone and associated with L-NMMA and by the addition of the cytochrome epoxygenases inhibitor fluconazole (0.37 mg.min -1}.L -1}). Telmisartan did not affect radial artery flow-mediated dilatation in control period (placebo: 10.9±0.6% vs. telmisartan: 9.9±0.7%) but prevented its decrease after L-NMMA (placebo: 9.3±0.8% vs. telmisartan: 12.6±1.2%, P<0.05) with no modification in baseline parameters, hyperemia and radial artery endothelium-independent dilatation to sodium nitroprusside. Moreover, in telmisartan-treated subjects, the radial flow-mediated dilatation, compared with control (9.0±1.0%), was not modified by aspirin alone (9.4±0.7%) or associated with L-NMMA (9.5±0.5%) but in fact was reduced by the combination of aspirin, L-NMMA and fluconazole (7.5±0.6%, P<0.05). These results demonstrate that AT 1} receptor blockade prevents the decrease in conduit artery flow-mediated dilatation during NO-synthase inhibition in humans suggesting the development of an endothelial compensatory mechanism. This mechanism seems to be independent of prostacyclin and could possibly be related to an endothelium-derived hyperpolarizing factor release