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肺静脉起搏与右心耳起搏后电重构的差异。

Difference between electrical remodelling after pulmonary veins and right atrium appendage pacing.

作者信息

Hafid Kebbati A, Xin Huang Cong, Xi Wang, Yan Zhao Qing, Bo Yang

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan 430060, People's Republic of China.

出版信息

Europace. 2007 Aug;9(8):608-12. doi: 10.1093/europace/eum108. Epub 2007 Jul 13.

Abstract

OBJECTIVE

Pulmonary veins (PVs) are important sources of paroxysmal atrial fibrillation (AF). Rapid atrial pacing changes atrial electrophysiology, and facilitates the induction and maintenance of AF. The purpose of our study was to evaluate the changes in atrial effective refractory period (AERP) proprieties and in ionic currents in PVs myocytes from dogs subjected to rapid atrial pacing in PVs and right atrial appendage (RAA) and to relate these changes to the ability to induce AF.

METHODS

Twelve mongrel dogs in normal sinus rhythm were paced from the superior left PVs or RAA at 500 bpm for 4 h. Electrophysiological studies were conducted to determine the changes in AERP, dispersion, and rhythm. Ionic currents were evaluated using patch clamp technique in single PVs myocytes in sham-operated dogs, and the results were compared with those from PVs and RAA pacing groups.

RESULTS

The presence of rapid atrial pacing was associated with a marked shortening in AERP in both PVs and RAA pacing group with a marked increase in AERP dispersion in PVs pacing. Both L-type calcium current (I(Ca,L)) and the transient outward current (I(to)) were reduced in both groups with an increased significance in PVs pacing group. The density of I(Ca,L) was decreased significantly from (-6.03 +/- 0.63) pA/pF in the control group to (-3.21 +/- 0.34) pA/pF in the PVs pacing group and (-4.75 +/- 0.41) pA/pF in the RAA pacing group (n = 6, P < 0.05), whereas the density of I(to) was decreased significantly from (8.45 +/- 0.71) pA/pF in the control group to (5.21 +/- 0.763) pA/pF in the PVs pacing group and (6.84 +/- 0.69) pA/pF in the RAA pacing group (n = 6, P < 0.05).

CONCLUSION

Our findings provide likely ionic mechanisms of shortened repolarization in induced atrial tachycardia with a decrease in I(Ca,L) and I(to) densities, which is the likely mechanism for a decrease in action potential duration rate adaptation in the canine rapid pacing model more pronounced in the PVs pacing group underlying the crucial role of PVs in initiating AF.

摘要

目的

肺静脉(PVs)是阵发性心房颤动(AF)的重要来源。快速心房起搏可改变心房电生理,并促进房颤的诱发和维持。我们研究的目的是评估在肺静脉和右心耳(RAA)接受快速心房起搏的犬类肺静脉心肌细胞的心房有效不应期(AERP)特性和离子电流的变化,并将这些变化与诱发房颤的能力相关联。

方法

12只处于正常窦性心律的杂种犬从左上肺静脉或右心耳以500次/分钟的频率起搏4小时。进行电生理研究以确定AERP、离散度和节律的变化。使用膜片钳技术在假手术犬的单个肺静脉心肌细胞中评估离子电流,并将结果与肺静脉和右心耳起搏组的结果进行比较。

结果

快速心房起搏的存在与肺静脉和右心耳起搏组的AERP明显缩短相关,且肺静脉起搏组的AERP离散度显著增加。两组的L型钙电流(I(Ca,L))和瞬时外向电流(I(to))均降低,肺静脉起搏组的变化更显著。I(Ca,L)密度从对照组的(-6.03±0.63)pA/pF显著降低至肺静脉起搏组的(-3.21±0.34)pA/pF和右心耳起搏组的(-4.75±0.41)pA/pF(n = 6,P < 0.05),而I(to)密度从对照组的(8.45±0.71)pA/pF显著降低至肺静脉起搏组的(5.21±0.763)pA/pF和右心耳起搏组的(6.84±0.69)pA/pF(n = 6,P < 0.05)。

结论

我们的研究结果提供了诱导性房性心动过速复极化缩短的可能离子机制,即I(Ca,L)和I(to)密度降低,这可能是犬快速起搏模型中动作电位时程速率适应性降低的机制,在肺静脉起搏组中更为明显,这突出了肺静脉在引发房颤中的关键作用。

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