Electrical activation during ventricular fibrillation in the subacute and chronic phases of healing canine myocardial infarction.
Electrical activation during ventricular fibrillation in the subacute and chronic phases of healing canine myocardial infarction.
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犬心肌梗塞愈合的亚急性和慢性阶段心室颤动期间的电激活。
DOI：
10.1161/01.cir.92.3.535
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发表时间：
1995
期刊：
影响因子：
37.8
通讯作者：
Kadish,AH
中科院分区：
文献类型：
--
作者：
Damle,RS;Robinson,NS;Ye,DZ;Roth,SI;Greene,R;Goldberger,JJ;Kadish,AH
背景关于心肌梗死对室颤(VF)特征的影响的信息很少。室颤时心外膜电活动的周期长度和激活波峰的特征。方法和结果6只亚急性愈合(1周)心肌梗死犬、5只慢性(8周)愈合心肌梗死犬和6只无心肌梗死犬用程序刺激诱发室颤。使用电极间距为2.5 mm的斑块电极阵列，记录112个心电记录，并从前壁(梗死区)或侧壁区(非梗死区)为每个VF周期创建91个向量环。在室颤的前10个周期(早期)和5秒后的10个周期(晚期)，在每个部位确定心外膜最大激活方向。波前大小是根据给定区域内心外膜激活方向的相似性以及通过统计分析确定记录斑块上不同距离的空间连接程度来确定的。VF周期长度定义为连续10次局部激活时间的平均间隔。组间差异和前、后外侧壁之间的差异用方差分析确定。亚急性心肌梗死组(97±4mm2，早期；78±3mm2，晚期)或慢性心肌梗死组(94±5mm2，早期；78±5mm2，晚期)的平均波前面积明显大于非梗死组(73±5mm2，早期；61±3mm2，晚期)。心外膜激活方向在距离2.5 mm和5.0 mm处三组相似，但在非梗死组间在7.5 mm处较低，证实了较小的波前大小和较少的激活组织。心肌梗死时室颤周期明显延长(98±5ms，正常对照组；121±13ms，亚急性心肌梗死；127±13ms，慢性心肌梗死)。亚急性心肌梗死组(131±8ms，前壁；109±5ms，外侧壁)或慢性心肌梗死组(136±9ms，前壁；119±6ms，外侧壁)VF周期长度明显长于侧壁，而非梗死组(99±5ms，前壁；97±5ms，侧壁)无明显变化。梗死组VF周期延长与VF时传导速度估计值减慢有关。结论在VF过程中，亚急性期和慢性愈合性MI动物，(1)激活波前较大，(2)VF周长较长，(3)传导速度较慢，(4)组织化程度较大。因此，局部心肌梗死的存在改变了整个心脏的室颤特征。这些发现对存在不同心肌基质时室颤的启动和维持的影响需要进一步的研究。
BackgroundLittle information is available regarding the effects of myocardial infarction on the characteristics of ventricular fibrillation (VF). Epicardial activation during VF can be characterized by the cycle length and by the characteristics of activation wave fronts.Methods and ResultsVF was induced by programmed stimulation in 6 dogs with subacute healing (1 week) myocardial infarction (MI), 5 dogs with chronic (8 week) healing MI, and 6 dogs without MI. Using a plaque electrode array with a 2.5-mm interelectrode distance, 112 electrograms were recorded and 91 vector loops were created for each cycle of VF from either the anterior (infarcted) or lateral (noninfarcted) wall. Direction of maximum epicardial activation was determined at each site for the first 10 cycles of VF (early) and for 10 cycles after 5 seconds of VF (late). Wave front size was determined based on a similarity in epicardial activation directions within a given area and by a statistical analysis that determined the degree of spatial linking at varying distances over the recording plaque. VF cycle length was defined as the mean interval of 10 consecutive local activation times. Differences among groups and differences between the anterior and posterolateral walls were determined by ANOVA. The mean wave front area was significantly larger in the presence of subacute MI (97±4 mm2, early; 78±3 mm2, late) or chronic MI (94±5 mm2, early; 78±5 mm2, late) than in noninfarcted animals (73±5 mm2, early; 61±3 mm2, late). The degree of linking of epicardial activation directions was similar in the three groups at distances of 2.5 and 5.0 mm but was lower at a distance of 7.5 mm among animals without infarction, confirming a smaller wave front size and suggesting less organization of activation. VF cycle length was significantly longer in the presence of infarction (98±5 ms, normal control animals; 121±13 ms, subacute MI; 127±13 ms, chronic MI). VF cycle length was significantly longer over the anterior than the lateral wall in the presence of subacute MI (131±8 ms, anterior; 109±5 ms, lateral) or chronic MI (136±9 ms, anterior; 119±6 ms, lateral) but not in noninfarcted animals (99±5 ms, anterior; 97±5 ms, lateral). The prolongation of VF cycle length among animals with infarction was associated with slower estimated conduction velocities during VF.ConclusionsDuring VF, in animals with subacute or chronic healing MI, (1) the size of activation wave fronts is larger, (2) the cycle length of VF is longer, (3) the conduction velocities are slower, and (4) the degree of organization is greater than in control animals. Thus, the characteristics of VF throughout the heart are altered by the presence of regional myocardial infarction. The implications of these findings for the initiation and maintenance of VF in the presence of different underlying myocardial substrates require further study.
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心肌激活的计算机化向量图
DOI：
--
发表时间：
1990
期刊：
[1990] Proceedings Computers in Cardiology
影响因子：
--
作者：
N. Kanaan;J. Jenkins;R. Levy;A. Kadish
通讯作者：
A. Kadish
狗重复心肌缺血期间的跨膜电位变化和心室颤动。
影响因子：
--
作者：
D. Russell;J. Smith;M. Oliver
通讯作者：
M. Oliver
影响因子：
20.1
作者：
PERTSOV, AM;DAVIDENKO, JM;JALIFE, J
通讯作者：
JALIFE, J
影响因子：
20.1
作者：
T. Sano;H. Tsuchihashi;T. Shimamoto
通讯作者：
T. Shimamoto
心肌传导阻滞的识别：犬心外膜的体外观察。
影响因子：
10.8
作者：
Kadish,A;Spear,J
通讯作者：
Spear,J