Optical Mapping Laboratory, Arrhythmia Unit, Cardiovascular Institute, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), CP 28040, Madrid, Spain.
Cardiovasc Res. 2013 Aug 1;99(3):576-85. doi: 10.1093/cvr/cvt093. Epub 2013 Apr 23.
The mechanisms underlying ventricular fibrillation (VF) are still disputed. Recent studies have highlighted the role of KATP-channels. We hypothesized that, under certain conditions, VF can be driven by stable and epicardially detectable rotors in large hearts. To test our hypothesis, we used a swine model of accelerated VF by opening KATP-channels with cromakalim.
Optical mapping, spectral analysis, and phase singularity tracking were performed in eight perfused swine hearts during VF. Pseudo-bipolar electrograms were computed. KATP-channel opening almost doubled the maximum dominant frequency (14.3 ± 2.2 vs. 26.5 ± 2.8 Hz, P < 0.001) and increased the maximum regularity index (0.82 ± 0.05 vs. 0.94 ± 0.04, P < 0.001), the density of rotors (2.0 ± 1.4 vs. 16.0 ± 7.0 rotors/cm²×s, P < 0.001), and their maximum lifespans (medians: 368 vs. ≥3410 ms, P < 0.001). Persistent rotors (≥1 movie = 3410 ms) were found in all hearts after cromakalim (mostly coinciding with the fastest and highest organized areas), but they were not epicardially visible at baseline VF. A 'beat phenomenon' ruled by inter-domain frequency gradients was observed in all hearts after cromakalim. Acceleration of VF did not reveal any significant regional preponderance. Complex fractionated electrograms were not found in areas near persistent rotors.
Upon KATP-channel opening, VF consisted of rapid and highly organized domains mainly due to stationary rotors, surrounded by poorly organized areas. A 'beat phenomenon' due to the quasi-periodic onset of drifting rotors was observed. These findings demonstrate the feasibility of a VF driven by stable rotors in hearts whose size is similar to the human heart. Our model also showed that complex fractionation does not seem to localize stationary rotors.
心室颤动（VF）的机制仍存在争议。最近的研究强调了 KATP 通道的作用。我们假设，在某些情况下，VF 可以由大心脏中稳定且可在心脏外膜检测到的转子驱动。为了验证我们的假设，我们使用 cromakalim 打开 KATP 通道来加速猪的 VF 模型。
在 8 个灌注猪心脏的 VF 期间进行了光学映射、频谱分析和相奇点跟踪。计算了伪双极电图。KATP 通道的开放几乎使最大主导频率增加了一倍（14.3 ± 2.2 对 26.5 ± 2.8 Hz，P < 0.001），并增加了最大规则指数（0.82 ± 0.05 对 0.94 ± 0.04，P < 0.001）、转子密度（2.0 ± 1.4 对 16.0 ± 7.0 转子/cm²×s，P < 0.001）和它们的最大寿命（中位数：368 对≥3410 ms，P < 0.001）。在用 cromakalim 后，所有心脏中都发现了持续的转子（≥1 个电影= 3410 ms）（主要与最快和最高组织区域重合），但在基线 VF 时它们在心脏外膜上不可见。在用 cromakalim 后，所有心脏中都观察到一种由域间频率梯度控制的“跳动现象”。VF 的加速并没有显示出任何明显的区域性优势。在持续转子附近的区域未发现复杂的碎裂电图。
在 KATP 通道开放后，VF 主要由快速和高度组织的区域组成，主要是由于稳定的转子，周围是组织不良的区域。观察到由于漂移转子准周期性发作引起的“跳动现象”。这些发现证明了在类似于人心大小的心脏中，稳定的转子驱动 VF 的可行性。我们的模型还表明，复杂的碎裂似乎不能定位稳定的转子。
