Misier A R, Opthof T, van Hemel N M, Vermeulen J T, de Bakker J M, Defauw J J, van Capelle F J, Janse M J
Academic Medical Center, University of Amsterdam, Department of Clinical and Experimental Cardiology, The Netherlands.
Circulation. 1995 May 15;91(10):2566-72. doi: 10.1161/01.cir.91.10.2566.
Postinfarction ventricular tachycardias (VTs) may degenerate into ventricular fibrillation (VF), but this does not happen in all patients. The underlying mechanism is not exactly known, but dispersion of refractory periods is considered a major factor in both induction and persistence of reentrant arrhythmias in general. Hypertrophied, noninfarcted myocardium has altered electrophysiological characteristics. We hypothesized that noninfarcted ventricular tissue may provide the heterogeneities that cause the transition from VT into VF. Local fibrillation intervals, ie, the average interval between local activations during VF, have previously been shown to correlate well with local refractoriness in human and canine atrium and in porcine and canine ventricle and may therefore be used as an index of local refractoriness. This technique permits simultaneous assessment of refractoriness at multiple sites.
We measured local fibrillation intervals at 32 to 64 sites in the noninfarcted part of the left ventricle in patients undergoing antiarrhythmic surgery for symptomatic, drug-refractory, postinfarction ventricular tachyarrhythmias. The grid of electrodes (interelectrode distance, 7 mm) was attached to the epicardium of the left ventricle remote from the infarcted tissue. Group 1 consisted of 7 patients with hemodynamically tolerable sustained VT (VT group). Group 2 consisted of 7 patients with cardiac arrest and documented VF (VF group). With the patients on cardiopulmonary bypass, VF was induced by multiple premature stimulation. The VF interval was not significantly different in the two study groups (VT group, 136 +/- 5.5 ms; VF group, 129 +/- 3.4 ms, mean +/- SEM). However, spatial dispersion of the VF intervals (remote from the infarcted area) expressed as the coefficient of variation of VF intervals (SD x 100/mean VF interval in each heart) was significantly larger in the VF group. It was 3.63 +/- 0.56 in the VF group and 1.55 +/- 0.40 in the VT group (mean +/- SEM; P < .01). Differences between the shortest and longest VF intervals in one and the same heart and the largest difference between two adjacent sites were also larger in the VF group (P < .02 and P < .05, respectively).
This study shows larger dispersion in VF intervals and therefore suggests larger dispersion of refractory periods in parts of the myocardium remote from the infarction in patients with postinfarction VF than in patients with postinfarction VT.
心肌梗死后室性心动过速（VT）可能恶化为心室颤动（VF），但并非所有患者都会如此。其潜在机制尚不完全清楚，但一般认为不应期离散是折返性心律失常诱发和持续的主要因素。肥厚的非梗死心肌具有改变的电生理特性。我们推测非梗死心室组织可能提供导致从VT转变为VF的异质性。局部颤动间期，即VF期间局部激动之间的平均间期，先前已被证明在人和犬的心房以及猪和犬的心室中与局部不应期密切相关，因此可作为局部不应期的指标。该技术允许同时评估多个部位的不应期。
我们在因有症状的、药物难治性心肌梗死后室性快速心律失常而接受抗心律失常手术的患者的左心室非梗死部分的32至64个部位测量了局部颤动间期。电极网格（电极间距7 mm）附着于远离梗死组织的左心室心外膜。第1组由7例血流动力学可耐受的持续性VT患者组成（VT组）。第2组由7例心脏骤停且记录到VF的患者组成（VF组）。在患者进行体外循环时，通过多次早搏刺激诱发VF。两个研究组的VF间期无显著差异（VT组，136±5.5 ms；VF组，129±3.4 ms，平均值±标准误）。然而，以VF间期变异系数（标准差×100/每个心脏的平均VF间期）表示的VF间期（远离梗死区域）的空间离散在VF组中显著更大。VF组为3.63±0.56，VT组为1.55±0.40（平均值±标准误；P<.01）。同一心脏中最短和最长VF间期之间的差异以及两个相邻部位之间的最大差异在VF组中也更大（分别为P<.02和P<.05）。
本研究显示VF间期离散更大，因此提示心肌梗死后VF患者梗死灶外心肌部分的不应期离散比心肌梗死后VT患者更大。
