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全景光学标测显示,心室颤动起始时在一个一致的解剖部位出现波断裂。

Panoramic optical mapping shows wavebreak at a consistent anatomical site at the onset of ventricular fibrillation.

机构信息

Department of Biomedical Engineering, The University of Alabama at Birmingham, 1670 University Blvd., Volker Hall B140, Birmingham, AL 35294, USA.

出版信息

Cardiovasc Res. 2012 Feb 1;93(2):272-9. doi: 10.1093/cvr/cvr327. Epub 2011 Dec 5.

DOI:10.1093/cvr/cvr327
PMID:22144474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3258655/
Abstract

AIMS

The first seconds of ventricular fibrillation (VF) are well organized and can consist of just one to two rotating waves (rotors). New rotors are spawned when local propagation block causes wave fragmentation. We hypothesized that this process, which leads to fully developed VF, begins at a consistent anatomic site.

METHODS AND RESULTS

We initiated VF with a stimulus timed to the local T-wave in 10 isolated pig hearts. Hearts were stained with a voltage-sensitive dye and four video cameras recorded electrical propagation panoramically across the epicardium. In each VF episode, we identified the position of the first wavebreak event that produced new rotor(s) that persisted for at least one cycle. The first such wavebreak occurred along the anterior right ventricular insertion (ARVI) in 26 of 32 VF episodes. In these episodes, wavebreak sites were 6 ± 4 mm from the midline of the ARVI. In the remaining 6 episodes, wavebreak sites were 24 ± 5 mm from the midline on either the LV or RV. During rapid pacing, conduction speed was locally depressed at the ARVI when waves crossed parallel to the midline. Action potential duration (APD) was slightly longer (2.2 ± 2.1 ms) at the ARVI compared with other sites (P< 0.01). Temporal APD alternans were small and not unique to the break site, suggesting that dynamic APD properties were not the cause of wavebreak.

CONCLUSION

The ARVI is the dominant site for wavebreak at the onset of VF in normal myocardium. This may be due to the anatomic complexity of the region.

摘要

目的

心室颤动(VF)的最初几秒钟是有组织的,可能只由一个到两个旋转波(转子)组成。当局部传播阻滞导致波碎裂时,新的转子就会产生。我们假设,导致完全发展的 VF 的这个过程始于一个一致的解剖部位。

方法和结果

我们在 10 个分离的猪心中用一个与局部 T 波同步的刺激来引发 VF。心脏用电压敏感染料染色,四个摄像机全景记录心外膜的电传播。在每个 VF 发作中,我们确定了产生新转子(至少持续一个周期)的第一个波破裂事件的位置。在 32 个 VF 发作中的 26 个中,第一个这样的波破裂发生在前右心室插入(ARVI)处。在这些发作中,波破裂部位距离 ARVI 的中线 6±4mm。在其余的 6 个发作中,波破裂部位距离 LV 或 RV 的中线 24±5mm。在快速起搏期间,当波平行于中线传播时,ARVI 处的局部传导速度会降低。与其他部位相比,ARVI 处的动作电位时程(APD)稍长(2.2±2.1ms)(P<0.01)。APD 的时程交替很小,而且不是仅在破裂部位出现,这表明动态 APD 特性不是波破裂的原因。

结论

在正常心肌中,VF 发作时 ARVI 是波破裂的主要部位。这可能是由于该区域的解剖复杂性所致。

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