Complex structure of electrophysiological gradients emerging during long-duration ventricular fibrillation in the canine heart.
Complex structure of electrophysiological gradients emerging during long-duration ventricular fibrillation in the canine heart.
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犬心脏长时间心室颤动期间出现的电生理梯度的复杂结构。
DOI：
10.1152/ajpheart.00419.2010
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Zaitsev,AlexeyV
中科院分区：
文献类型：
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作者：
Venable,PaulW;Taylor,TysonG;Shibayama,Junko;Warren,Mark;Zaitsev,AlexeyV
全心缺血心脏中的长时间室颤(LDVF)是心脏骤停的常见情况。LDVF期间的电异质性可能会影响除颤和复苏的结果。以前在大型哺乳动物心脏上的研究已经调查了浦肯野纤维和心内膜(Endo)和心外膜(Epi)之间的电生理梯度的作用。对于LDVF中右、左室之间以及各腔内的压差，我们所知的要少得多。在开胸犬LDVF模型上，用针刺电极研究了室颤激活率(VFR)在右室、左室交界处及右室、左室、间隔交界处的跨壁分布。我们还利用光学标测技术分析了LDVF时VFR、动作电位时程和舒张期间期在RV和LV的Epi分布。跨室壁VFR梯度在右室和左室均可形成，且心内膜VFR较快。同时，EpiVFR梯度较大，RV-Sep交界处VFR最快，RV居中，LV最慢。光学标测显示VFR在LV和RV内的离散度逐渐增加，在LDVF后4-8min出现马赛克完全不兴奋的区域。跨室壁、腔间和腔内VFR的不均质性程度相似。在LDVF的所有时间点上，在两个心腔内，VFR的倒数与DI高度相关，而与apd无关。我们的结论是，犬心脏LDVF期间复杂的VFR梯度不能仅用浦肯野纤维的分布来解释，而且与LDVF继发的电抑制的区域差异有关。
Long-duration ventricular fibrillation (LDVF) in the globally ischemic heart is a common setting of cardiac arrest. Electrical heterogeneities during LDVF may affect outcomes of defibrillation and resuscitation. Previous studies in large mammalian hearts have investigated the role of Purkinje fibers and electrophysiological gradients between the endocardium (Endo) and epicardium (Epi). Much less is known about gradients between the right ventricle (RV) and left ventricle (LV) and within each chamber during LDVF. We studied the transmural distribution of the VF activation rate (VFR) in the RV and LV and at the junction of RV, LV, and septum (Sep) during LDVF using plunge needle electrodes in opened-chest dogs. We also used optical mapping to analyze the Epi distribution of VFR, action potential duration (APD), and diastolic interval (DI) during LDVF in the RV and LV of isolated hearts. Transmural VFR gradients developed in both the RV and LV, with a faster VFR in Endo. Concurrently, large VFR gradients developed in Epi, with the fastest VFR in the RV-Sep junction, intermediate in the RV, and slowest in the LV. Optical mapping revealed a progressively increasing VFR dispersion within both the LV and RV, with a mosaic presence of fully inexcitable areas after 4–8 min of LDVF. The transmural, interchamber, and intrachamber VFR heterogeneities were of similar magnitude. In both chambers, the inverse of VFR was highly correlated with DI, but not APD, at all time points of LDVF. We conclude that the complex VFR gradients during LDVF in the canine heart cannot be explained solely by the distribution of Purkinje fibers and are related to regional differences in the electrical depression secondary to LDVF.