Structural barrier increases QT-peak dispersion in swine left ventricle in vivo.

Structural barrier increases QT-peak dispersion in swine left ventricle in vivo.
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结构屏障增加了猪体内左心室的 QT 峰值离散度。

DOI:
10.1109/iembs.2006.260609
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发表时间:
2006
期刊:
Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
影响因子:
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通讯作者:
Christini,DavidJ
Christini,DavidJ
中科院分区:
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文献类型:
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作者:
Lu,Sheng;Gong,Yunfan;Iwai,Sei;Stein,KennethM;Lerman,BruceB;Christini,DavidJ

文献摘要

相似文献

QT离散度(QTd)被认为代表了室性复极的局部不均匀,可作为室性心律失常易感性和心脏性猝死(SCD)风险的预后指标。在这项研究中,我们使用活体猪模型来研究引入左心室(LV)自由壁结构屏障(SB)前后QT峰离散度的变化。基线起搏和消融后起搏被送至:(I)心外膜左室底,(Ii)心外膜左室尖,(Iii)右室心内膜。以胸内电极为参照物,测量了四个单极心电图。在两个电极对的中间通过冷冻消融产生一个Sb(~4×1×1 cm(长、宽、深))。QTd被计算为来自跨越SB区域的两个电极的每个搏动的QT峰间隔之间的差值。加入SB后,6只动物的QTd均显著增加(p<0.05)。这些结果可能反映了由于SB干扰电紧张性耦合而引起的解剖复极不均一性的加剧。考虑到复极离散度和折返开始之间的联系,这些发现与结构性心脏病心律失常风险的增加是一致的。
QT dispersion (QTD) is thought to represent the regional nonuniformity of ventricular repolarization and can serve as a prognostic marker for vulnerability to ventricular arrhythmias and risk for sudden cardiac death (SCD). In this study, we used an in vivo swine model to investigate the change of QT-peak dispersion before and after the introduction of a left-ventricular (LV) free-wall structural barrier (SB). Baseline and post-ablation pacing were delivered to: (i) the epicardial LV base, (ii) the epicardial LV apex, and (iii) the right ventricular (RV) endocardium. Four unipolar electrograms were measured from LV free wall epicardial sites referenced to an intrathorax electrode. An SB (~4 × 1 × 1 cm (length, width, depth)) was created by cryoablation in the middle of the two electrode pairs. QTD was computed as the difference between QT-peak intervals for each beat from two electrodes across the SB region from one another. A significant increase of QTD occurred (p<0.05) after the introduction of the SB in all six animals. These results may reflect the accentuation of anatomical repolarization heterogeneity due to SB disruption of electrotonic coupling. Given the link between dispersion of repolarization and initiation of reentry, these findings are consistent with the increased arrhythmia risk of structural heart disease.