首页> 外文期刊>Journal of cardiovascular electrophysiology >Increased extracellular collagen matrix in myocardial sleeves of pulmonary veins: an additional mechanism facilitating repetitive rapid activities in chronic pacing-induced sustained atrial fibrillation.
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Increased extracellular collagen matrix in myocardial sleeves of pulmonary veins: an additional mechanism facilitating repetitive rapid activities in chronic pacing-induced sustained atrial fibrillation.

机译:肺静脉心肌套中细胞外胶原基质的增加:在慢性起搏引起的持续性心房纤颤中促进重复性快速活动的另一种机制。

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Increased ECM in canine PVs. INTRODUCTION: Cell uncoupling due to fibrosis or increased extracellular collagen matrix (ECM) affects the formation of ectopic focal activity. Whether or not the increase of ECM also exists in the pulmonary veins (PVs) with rapid atrial pacing is unknown. We sought to test the hypothesis that in chronic atrial pacing dogs with sustained atrial fibrillation (AF), the amount of ECM was increased in both atria and the PVs. METHODS AND RESULTS: We induced sustained AF in dogs by rapid atrial pacing. Computerized mapping techniques were used to map both atria and the PVs. We also used histological assessment to quantify the amount of ECM. After 118+/-24 days of rapid atrial pacing, sustained AF was induced in 7 dogs. Repetitive rapid activities (RRAs) either continuously or intermittently arose from the PVs during sustained AF. Histological study shows that there was no fibrosis in both atrial free walls and the PVs. However, the amount of ECM was increased in these regions. The mean ECM surface area fraction at each region in the dogs with sustained AF was all significantly higher compared to the corresponding region in normal dogs. Similarly, the heterogeneity of the ECM surface area fraction at each region in the dogs with sustained AF was also all significantly higher compared to normal dogs. CONCLUSIONS: In chronic atrial pacing-induced sustained AF, structural remodeling (i.e., inhomogeneous increase of ECM) also involves the PVs. Reduced coupling of the myocytes in the PV due to histological changes may provide an additional mechanism facilitating RRAs.
机译:犬PV中ECM增加。简介:由于纤维化或细胞外胶原基质(ECM)增加而引起的细胞解偶联会影响异位灶性活动的形成。心房起搏迅速在肺静脉(PV)中是否也存在ECM的增加。我们试图检验这一假设,即在患有持续性心房纤颤(AF)的慢性心房起搏犬中,心房和PV中ECM的量均增加。方法和结果:我们通过快速心房起搏诱导了狗的持续性房颤。使用计算机制图技术绘制心房和PV。我们还使用组织学评估来量化ECM的数量。快速心房起搏118 +/- 24天后,在7只狗中诱发了持续性房颤。在持续性房颤期间,PV连续或间歇地出现重复性快速活动(RRA)。组织学研究表明,在心房游离壁和PVs中均没有纤维化。但是,这些区域的ECM数量增加了。与正常狗的相应区域相比,持续性房颤的狗在每个区域的平均ECM表面积分数均显着更高。同样,持续性房颤犬的每个区域的ECM表面积分数的异质性也都比正常犬高得多。结论:在慢性心房起搏引起的持续性房颤中,结构重塑(即ECM的不均匀增加)也涉及PV。由于组织学改变,PV中心肌细胞的偶联减少可能会提供促进RRA的其他机制。

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