Markus Rottmann, A. Kleber, M. Barkagan, J. Sroubek, E. Leshem, Ayelet Shapira-Daniels, A. Buxton, E. Anter
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Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.\n\n\nRESULTS\nOf 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. 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Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.\\n\\n\\nRESULTS\\nOf 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. 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引用次数: 8
摘要
背景:在梗死相关性室性心动过速(VT)中,该电路通常对应于窦性心律(SR)期间激活减慢的位置。然而,SR期间的激活减慢与再入脆弱性之间的关系以及与VT电路组成的相关性尚不清楚。这项研究考察了SR期间的激活减慢和再入脆弱性之间的关系,并将这些区域与回路的组成部分联系起来。方法在猪梗死愈合模型中,比较SR和VT的心内膜激活速度的空间分布。使用激活和夹带映射将峡部定义为电路内显示舒张活动的区域,而将旁观者定义为电路外显示舒张活动的区域。结果15头猪中,9头猪可诱导VT(每头5.2±3.0),6头猪在2个传动系的4个左室和左室部位进行6次额外刺激后仍不能诱导VT。伴有VT的梗死在sr期间具有更大程度的激活减慢。诱导性和非诱导性梗死的最小心内膜激活速度切断≤0.1 m/s (P=0.015)。SR期间最大心内膜减慢的区域对应于室速峡(曲线下面积=0.84 95% CI, 0.78-0.90),而旁观者部位在SR期间表现出接近正常的激活。室速电路复杂,41.7%表现出不连续传播,伴有缓慢传导的壁内桥和延迟的准同步心内膜激活。结论静息期心肌激活减慢可能是区分易发生室性心动过速梗死和不易发生室性心动过速梗死的重要依据。静息期心肌激活减慢的部位与形成室性心动过速的部位相对应,而与旁观者部位不一致。
Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and Nonarrhythmogenic Scar.
BACKGROUND
In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit.
METHODS
In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.
RESULTS
Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT.
CONCLUSIONS
Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.