58 research outputs found

    Electrocardiographic analysis for his bundle pacing at implantation and follow-up

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    His bundle pacing (HBP) is steadily gaining interest for providing physiological cardiac stimulation. Careful analysis of the electrocardiogram (ECG) is crucial to confirm capture of conduction tissue, which is a prerequisite for successful HBP at implantation and follow-up. However, interpretation of the ECG with HBP can be challenging. This review provides the reader with practical guidance on how to best use and troubleshoot the 12-lead ECG for HBP in daily clinical practice

    Permanent His Bundle Pacing: Electrophysiological and Echocardiographic Observations From Long-Term Follow-Up

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    Background Permanent His bundle pacing (HBP) is a physiological alternative to right ventricular pacing. It is not known whether HBP can cause His-Purkinje conduction (HPC) disease. The aim of our study is to assess His bundle capture and its effect on left ventricular (LV) function in long-term follow-up and to determine HPC at the time of pulse generator change (GC) in patients with chronic HBP. Methods HB electrograms were recorded from the pacing lead at implant and GC. HBP QRS duration (QRSd), His-ventricular (HV) intervals, and HB pacing thresholds at GC were compared with implant measurements. HPC was assessed by pacing at cycle lengths of 700 ms, 600 ms, and 500 ms at GC. LV internal diameters, ejection fraction (EF), and valve dysfunction at baseline were compared with echocardiography during follow-up. Results GC was performed in 20 patients (men 13; age 74 ± 14 years) with HBP at 70 ± 24 months postimplant. HV intervals remained unchanged from initial implant (44 ± 4 ms vs 45 ± 4 ms). During HBP at 700 ms, 600 ms, and 500 ms (n = 17), consistent 1:1 HPC was present. HBP QRSd remained unchanged during follow-up (117 ± 20 ms vs 118 ± 23 ms). HBP threshold at implant and GC was 1.9 ± 1.1 V and 2.5 ± 1.2 V @ 0.5 ms. Despite high pacing burden (77 ± 13%), there was no significant change in LVEF (50 ± 14% at implant) during follow-up (55 ± 6%, P = 0.06). Conclusions HBP does not appear to cause new HPC abnormalities and is associated with stable HBP QRSd during long-term follow-up. Despite high pacing burden, HBP did not result in deterioration of left ventricular systolic function or cause new valve dysfunction

    How to Implant His Bundle and Left Bundle Pacing Leads: Tips and Pearls

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    Cardiac pacing is the treatment of choice for the management of patients with bradycardia. Although right ventricular apical pacing is the standard therapy, it is associated with an increased risk of pacing-induced cardiomyopathy and heart failure. Physiological pacing using His bundle pacing and left bundle branch pacing has recently evolved as the preferred alternative pacing option. Both His bundle pacing and left bundle branch pacing have also demonstrated significant efficacy in correcting left bundle branch block and achieving cardiac resynchronisation therapy. In this article, we review the implantation tools and techniques to perform conduction system pacing

    Novel bradycardia pacing strategies

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    Contains fulltext : 229186.pdf (Publisher’s version ) (Closed access)The adverse effects of ventricular dyssynchrony induced by right ventricular (RV) pacing has led to alternative pacing strategies, such as biventricular, His bundle (HBP), LV septal (LVSP) and left bundle branch pacing (LBBP). Given the overlap, LVSP and LBBP are also collectively referred to as left bundle branch area pacing (LBBAP). Although among these alternative pacing sites HBP is theoretically the ideal strategy as it maintains a physiological ventricular activation, its application requires more skills and is associated with the most complications. LBBAP, where the ventricular pacing lead is advanced through the interventricular septum to its left side, creates ventricular activation that is only slightly more dyssynchronous. Preliminary studies have shown that LBBAP is feasible, safe and encounters less limitations than HBP. Further studies are needed to differentiate between LVSP and LBBP with regard to acute functional and long-term clinical outcome

    A randomized comparison of HBP versus RVP: Effect on left ventricular function and biomarkers of collagen metabolism

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    Background: Right ventricular pacing (RVP) can result in pacing-induced cardiomyopathy (PICM). It is unknown whether specific biomarkers reflect differences between His bundle pacing (HBP) and RVP and predict a decrease in left ventricular function during RVP. Aims: To compare the effect of HBP and RVP on the LV ejection fraction (LVEF) and to study how they affect serum markers of collagen metabolism. Methods: Ninety-two high-risk PICM patients were randomized to HBP or RVP. Their clinical characteristics, echocardiography, and serum levels of TGF-β1, MMP-9, ST2-IL, TIMP-1, and Gal-3 were studied before and six months after pacemaker implantation. Results: Fifty-three patients were randomized to HBP and 39 patients to RVP. HBP failed in 10 patients, which crossed over to the RVP group. Patients with RVP had significantly lower LVEF compared to HBP after six months of pacing (−5% and −4% in as-treated and intention-to-treat analysis, respectively). Levels of TGF-β1 after 6 months were lower in HBP than RVP (mean difference −6 ng/ml; P = 0.009) and preimplant Gal-3 and ST2-IL levels were higher in RVP patients with a decline in the LVEF ≥ 5% compared to those with a decline of < 5% (mean difference 3 ng/ml and 8 ng/ml; P = 0.02 for both). Conclusion: In high-risk PICM patients, HBP was superior to RVP in providing more physiological ventricular function, as reflected by higher LVEF and lower levels of TGF-β1. Among RVP patients, LVEF declined more in those with higher baseline Gal-3 and ST2-IL levels than those with lower levels
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