Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands.
Circulation. 2010 Oct 26;122(17):1674-82. doi: 10.1161/CIRCULATIONAHA.109.910901. Epub 2010 Oct 11.
During persistent atrial fibrillation (AF), waves with a focal spread of activation are frequently observed. The origin of these waves and their relevance for the persistence of AF are unknown.
In 24 patients with longstanding persistent AF and structural heart disease, high-density mapping of the right and left atria was performed during cardiac surgery. In a reference group of 25 patients, AF was induced by rapid pacing. For data analysis, a mapping algorithm was developed that separated the fibrillatory process into its individual wavelets and identified waves with a focal origin. During persistent AF, the incidence of focal fibrillation waves in the right atrium was almost 4-fold higher than during acute AF (median, 0.46 versus 0.12 per cycle per 1 cm² (25th to 75th percentile, 0.40 to 0.77 and 0.01 to 0.27; P<0.0001). They were widely distributed over both atria and were recorded at 46 ± 18 of all electrodes. A large majority (90.5) occurred as single events. Repetitive focal activity (>3) happened in only 0.8. The coupling interval was not more than 11 ms shorter than the average AF cycle length (P=0.04), and they were not preceded by a long interval. Unipolar electrograms at the site of origin showed small but clear R waves. These data favor epicardial breakthrough rather than a cellular focal mechanism as the underlying mechanism. Often, conduction from a site of epicardial breakthrough was blocked in 1 or more directions. This generated separate multiple wave fronts propagating in different directions over the epicardium.
Focal fibrillation waves are due to epicardial breakthrough of waves propagating in deeper layers of the atrial wall. In patients with longstanding AF, the frequency of epicardial breakthroughs was 4 times higher than during acute AF. Because they provide a constant source of independent fibrillation waves originating over the entire epicardial surface, they offer an adequate explanation for the high persistence of AF in patients with structural heart disease.
在持续性心房颤动（AF）中，常观察到具有局灶性激活传播的波。这些波的起源及其与 AF 持续性的相关性尚不清楚。
在 24 例患有长期持续性 AF 和结构性心脏病的患者中，在心脏手术期间对右心房和左心房进行高密度标测。在 25 例对照患者中，通过快速起搏诱发 AF。为了数据分析，开发了一种映射算法，该算法将纤颤过程分离成其各个波，并识别具有局灶起源的波。在持续性 AF 中，右心房局灶性颤动波的发生率几乎是急性 AF 的 4 倍（中位数，每 1 cm² 每周期 0.46 比 0.12 个（25 至 75 百分位数，0.40 至 0.77 和 0.01 至 0.27；P<0.0001）。它们广泛分布于两个心房，在所有电极的 46±18 处记录到。绝大多数（90.5%）为单个事件。重复的局灶性活动（>3）仅发生 0.8。耦合间隔不比平均 AF 周期长度短 11 ms 以上（P=0.04），并且它们之前没有长间隔。起源部位的单极电图显示出小但清晰的 R 波。这些数据支持心外膜突破而不是细胞局灶机制作为潜在机制。起源部位的局灶性活动通常在 1 个或多个方向上被阻断。这在心脏外膜上产生了不同方向传播的多个独立的波阵面。
局灶性颤动波是由于在心房壁的深层传播的波的心外膜突破引起的。在长期 AF 患者中，心外膜突破的频率是急性 AF 的 4 倍。由于它们提供了源自整个心脏外膜表面的独立颤动波的恒定源，因此它们为结构性心脏病患者 AF 持续性高提供了充分的解释。
