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1.
Clin Case Rep ; 12(8): e8965, 2024 Aug.
Article in English | MEDLINE | ID: mdl-39091619

ABSTRACT

Trans-coronary ethanol ablation for ventricular tachycardia originating from the ventricular septum is effective, but there are cases with no septal perforator from left anterior descending artery. CT and angiography can reveal the optimal vessel.

2.
Pacing Clin Electrophysiol ; 45(10): 1194-1206, 2022 10.
Article in English | MEDLINE | ID: mdl-35989415

ABSTRACT

INTRODUCTION: Pulmonary vein (PV) isolation (PVI) including the left atrial posterior wall (LAPW) (Box-PVI) is proposed as an additional strategy for non-paroxysmal atrial fibrillation (NPAF), however, the efficacy remains controversial. The more reliable and durable the Box-PVI we can create, the better the rhythm outcomes might be than with a conventional PVI alone. This study focused on the potential exit conduction of the box lesion and investigated whether the conventional Box-PVI would be sufficient. METHODS AND RESULTS: We enrolled 350 consecutive patients with NPAF that underwent a conventional encircling Box-PVI and examined whether latent exit conduction and dormant "exit" conduction independently remained on the LAPW and in the PVs using high frequency stimulation (HFS) and an adenosine triphosphate (ATP) injection. All electrograms inside the box lesion were eliminated in all cases, however, HFS inside the box propagated outward in 23 cases (6.6%) without any exit conduction by conventional burst stimulation, and 24 cases (6.9%) exhibited only dormant "exit" conduction of the LAPW. Additional ablation where positive HFSs were observed created a complete bidirectional Box-PVI in 43 (41.3%) of the cases without a first pass Box-PVI. The recurrence rates depended on the groups classified according to the HFS response. CONCLUSION: HFS delivered with an ATP injection on the LAPW and in the PVs following a Box-PVI could not only elucidate true exit block but also identified possible incomplete lesions or connections outside the ablation line, whose elimination could achieve a complete Box-PVI leading to a better rhythm outcome.


Subject(s)
Atrial Fibrillation , Catheter Ablation , Pulmonary Veins , Humans , Atrial Fibrillation/surgery , Treatment Outcome , Catheter Ablation/methods , Pulmonary Veins/surgery , Adenosine , Adenosine Triphosphate , Recurrence
3.
Cell Rep ; 18(10): 2401-2414, 2017 03 07.
Article in English | MEDLINE | ID: mdl-28273455

ABSTRACT

Hematopoietic stem cell and multipotent progenitor (MPP) commitment can be tuned in response to an infection so that their differentiation is biased toward myeloid cells. Here, we find that Bach2, which inhibits myeloid differentiation in common lymphoid progenitors, represses a cohort of myeloid genes and activates those linked to lymphoid function. Bach2 repressed both Cebpb and its target Csf1r, encoding C/EBPß and macrophage colony-stimulating factor receptor (M-CSFr), respectively, whereas C/EBPß repressed Bach2 and activated Csf1r. Bach2 and C/EBPß further bound to overlapping regulatory regions at their myeloid target genes, suggesting the presence of a gene regulatory network (GRN) with mutual repression between these factors and a feedforward loop leading to myeloid gene regulation. Lipopolysaccharide reduced the expression of Bach2, resulting in enhanced myeloid differentiation. The Bach2-C/EBPß GRN pathway thus tunes MPP commitment to myeloid and lymphoid lineages both under normal conditions and after infection.


Subject(s)
Basic-Leucine Zipper Transcription Factors/metabolism , CCAAT-Enhancer-Binding Proteins/metabolism , Gene Regulatory Networks , Hematopoietic Stem Cells/metabolism , Multipotent Stem Cells/metabolism , Animals , Binding Sites , Cell Differentiation/genetics , Down-Regulation/genetics , Enhancer Elements, Genetic/genetics , Hematopoietic Stem Cells/cytology , Lymphoid Progenitor Cells/cytology , Lymphoid Progenitor Cells/metabolism , Mice, Inbred C57BL , Multipotent Stem Cells/cytology , Myeloid Progenitor Cells/cytology , Myeloid Progenitor Cells/metabolism , Protein Binding
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