The influence of myocardial substrate on ventricular fibrillation waveform: a swine model of acute and postmyocardial infarction.

The influence of myocardial substrate on ventricular fibrillation waveform: a swine model of acute and postmyocardial infarction.
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DOI:
10.1097/ccm.0b013e31817d798c
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发表时间:
2008-07
影响因子:
8.8
通讯作者:
Berg RA
Berg RA
中科院分区:
医学1区
文献类型:
--
作者:
Indik JH;Donnerstein RL;Hilwig RW;Zuercher M;Feigelman J;Kern KB;Berg MD;Berg RA

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在由心室颤动引起的心脏骤停中,心室颤动波形可能是其持续时间和预测休克成功可能性的线索。然而,心室颤动发生在不同的心肌基质,如缺血、心力衰竭和结构正常的心脏。我们假设心室颤动是由心肌梗死改变的,并且在急性期和心肌梗死后有所不同。进行了动物干预研究,并与对照组进行比较。这项研究在一所大学的动物实验室进行。研究对象包括37头猪。左中前降支闭塞引起心肌梗死。在对照组猪、急性心肌梗死猪和心肌梗死后猪2周恢复期后诱导心室颤动。在11头急性心肌梗死猪、10头心肌梗死后猪和16头对照组猪中记录了心室颤动。分析频率(平均值、中位数、优势值和带宽)和与振幅相关的内容(斜率、slope-amp[斜率除以振幅]和幅谱面积)。在急性心肌梗死(所有频率特征p < 0.001)和心肌梗死后猪(平均p = 0.015)中,5分钟心室颤动的频率都发生了改变。中位数为002,。002表示主导频率,< 0.001表示带宽)。在5分钟时,对照组的中位数频率最高,为10.9±。4赫兹;急性心肌梗死最低,8.4±。5赫兹;心肌梗死后中等,9.7±。5hz(与对照组相比,急性心肌梗死p < 0.001,心肌梗死后p = 0.002)。三组之间的斜率和振幅谱面积相似,在第2分钟后略有下降,而急性心肌梗死猪的斜率-amp在第5分钟仍有显著变化(p = 0.003)。心室颤动频率取决于心肌底物,并从心肌梗死的急性期到愈合期演变。然而,与振幅相关的测量在这些组中是相似的。目前尚不清楚依靠心室颤动波形而不考虑心肌底物如何影响除颤。
In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods. An animal intervention study was conducted with comparison to a control group. This study took place in a university animal laboratory. Study subjects included 37 swine. Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period. Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten post-myocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude–spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 ± .4 Hz; lowest in acute myocardial infarction, 8.4 ± .5 Hz; and intermediate in postmyocardial infarction, 9.7 ± .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude–spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003). Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.