Zhouqing Huang

Background: Left bundle branch pacing (LBBP) is a novel pacing method and has been observed to have low and stable pacing thresholds in prior small short-term studies. The objective of this study was to evaluate the feasibility and safety of LBBP in a large consecutive diverse group of patients with long-term follow-up. Methods: This study prospectively enrolled 632 consecutive pacemaker patients with attempted LBBP from April 2017 to July 2019. Pacing parameters, complications, ECG, and echocardiographic measurements were assessed at implant and during follow-up of 1, 6, 12, and 24 months. Results: LBBP was successful in 618/632 (97.8%) patients according to strict criteria for LBB capture. Mean follow-up time was 18.6±6.7 months. Two hundred thirty-one patients had follow-up over 2 years. LBB capture threshold at implant was 0.65±0.27 mV at 0.5 ms and 0.69±0.24 mV at 0.5 ms at 2-year follow-up. A significant decrease in QRS duration was observed in patients with left bundle branch block (167.22±18.99 versus 124.02±24.15 ms, P <0.001). Postimplantation left ventricular ejection fraction improved in patients with QRS≥120 ms (48.82±17.78% versus 58.12±13.04%, P <0.001). The number of patients with moderate and severe tricuspid regurgitation decreased at 1 year. Permanent right bundle branch injury occurred in 55 (8.9%) patients. LBB capture threshold increased to >3 V or loss of bundle capture in 6 patients (1%), 2 patients of them had a loss of conduction system capture. Two patients required lead revision due to dislodgement. Conclusions: This large observational study suggests that LBBP is feasible with high success rates and low complication rates during long-term follow-up. Therefore, LBBP appears to be a reliable method for physiological pacing for patients with either a bradycardia or heart failure pacing indication.

1. Inflammation is central to the pathogenesis of acute coronary syndrome (ACS) and is associated with adverse clinical outcomes after percutaneous coronary intervention (PCI). Recent in vitro work has demonstrated the anti-inflammatory effect of berberine, a primary component of the traditional Chinese medicine 'umbellatine'. In the present study, we further tested whether berberine had any beneficial effects on ACS patients following PCI. 2.In all, 130 ACS patients undergoing PCI were recruited to the present study. Sixty-one patients were treated with berberine (300 mg, t.i.d., for 30 days) in addition to standard therapy, whereas the remaining patients received standard therapy alone. Circulating inflammatory markers were measured by ELISA, whereas serum lipid profiles were measured by routine chemical assays. 3.In the berberine-treated group, matrix metalloproteinase (MMP)-9, intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, C-reactive protein, interleukin-6 and monocyte chemoattractant protein-1 were significantly reduced relative to baseline values. Furthermore, the changes in MMP-9, ICAM-1 and VCAM-1 from baseline to after 1 month of treatment differed significantly between the two patient groups. There was a tendency for berberine to induce a slightly greater reduction in low-density lipoprotein cholesterol and triglycerides than standard therapy alone, without affecting high-density lipoprotein cholesterol, but the differences failed to reach statistical significance. No severe adverse effects of berberine were observed. 4.The results of the present study provide the first clinical evidence of the anti-inflammatory action of berberine in ACS patients following PCI. Berberine may become adjunct therapy to further improve clinical outcomes via its anti-inflammatory effect in ACS patients.

Atherosclerosis is a progressive disease leading to loss of vascular homeostasis and entails fibrosis, macrophage foam cell formation, and smooth muscle cell proliferation. Recent studies have reported that epidermal growth factor receptor (EGFR) is involved vascular pathophysiology and in the regulation of oxidative stress in macrophages. Although, oxidative stress and inflammation play a critical role in the development of atherosclerosis, the underlying mechanisms are complex and not completely understood. In the present study, we have elucidated the role of EGFR in high-fat diet-induced atherosclerosis in apolipoprotein E null mice. We show increased EGFR phosphorylation and activity in atherosclerotic lesion development. EGFR inhibition prevented oxidative stress, macrophage infiltration, induction of pro-inflammatory cytokines, and SMC proliferation within the lesions. We further show that EGFR is activated through toll-like receptor 4. Disruption of toll-like receptor 4 or the EGFR pathway led to reduced inflammatory activity and foam cell formation. These studies provide evidence that EGFR plays a key role on the pathogenesis of atherosclerosis, and suggests that EGFR may be a potential therapeutic target in the prevention of atherosclerosis development.