Klos Matthew, Calvo David, Yamazaki Masatoshi, Zlochiver Sharon, Mironov Sergey, Cabrera José-Angel, Sanchez-Quintana Damian, Jalife José, Berenfeld Omer, Kalifa Jérôme
SUNY Upstate Medical University (M.K.), Syracuse, NY, USA.
Circ Arrhythm Electrophysiol. 2008 Aug;1(3):175-83. doi: 10.1161/CIRCEP.107.760447.
The posterior left atrium (PLA) and pulmonary veins (PVs) have been shown to be critical for atrial fibrillation (AF) initiation. However, the detailed mechanisms of reentry and AF initiation by PV impulses are poorly understood. We hypothesized that PV impulses trigger reentry and AF by undergoing wavebreaks as a result of sink-to-source mismatch at specific PV-PLA transitions along the septopulmonary bundle, where there are changes in thickness and fiber direction.
In 7 Langendorff-perfused sheep hearts AF was initiated by a burst of 6 pulses (CL 80 to 150ms) delivered to the left inferior or right superior PV ostium 100 to 150 ms after the sinus impulse in the presence of 0.5 micromol/L acetylcholine. The exposed septal-PLA endocardial area was mapped with high spatio-temporal resolution (DI-4-ANEPPS, 1000-fr/s) during AF initiation. Isochronal maps for each paced beat preceding AF onset were constructed to localize areas of conduction delay and block. Phase movies allowed the determination of the wavebreak sites at the onset of AF. Thereafter, the PLA myocardial wall thickness was quantified by echocardiography, and the fiber direction in the optical field of view was determined after peeling off the endocardium. Finally, isochrone, phase and conduction velocity maps were superimposed on the corresponding anatomic pictures for each of the 28 episodes of AF initiation. The longest delays of the paced PV impulses, as well as the first wavebreak, occurred at those boundaries along the septopulmonary bundle that showed sharp changes in fiber direction and the largest and most abrupt increase in myocardial thickness.
Waves propagating from the PVs into the PLA originating from a simulated PV tachycardia triggered reentry and vagally mediated AF by breaking at boundaries along the septopulmonary bundle where abrupt changes in thickness and fiber direction resulted in sink-to-source mismatch and low safety for propagation.
左心房后壁(PLA)和肺静脉(PVs)已被证明对房颤(AF)的起始至关重要。然而,PV冲动引发折返和房颤的详细机制尚不清楚。我们推测,PV冲动通过在沿间隔肺静脉束特定PV-PLA过渡处因汇-源不匹配而经历波裂来触发折返和房颤,在此处厚度和纤维方向会发生变化。
在7个Langendorff灌注的绵羊心脏中,在存在0.5微摩尔/升乙酰胆碱的情况下,在窦性冲动后100至150毫秒向左下或右上PV口输送一串6个脉冲(CL 80至150毫秒)来引发房颤。在房颤起始期间,以高时空分辨率(DI-4-ANEPPS,1000帧/秒)绘制暴露的间隔-PLA心内膜区域。构建房颤发作前每个起搏搏动的等时图以定位传导延迟和阻滞区域。相位电影可确定房颤发作时的波裂部位。此后,通过超声心动图量化PLA心肌壁厚度,并在剥离心内膜后确定视野中的纤维方向。最后,将28次房颤起始发作中每次发作的等时、相位和传导速度图叠加在相应的解剖图片上。起搏PV冲动的最长延迟以及第一个波裂发生在沿间隔肺静脉束的那些边界处,这些边界处纤维方向有急剧变化,心肌厚度有最大且最突然的增加。
从PVs传播到起源于模拟PV心动过速的PLA中的波,通过在沿间隔肺静脉束的边界处破裂而触发折返和迷走神经介导的房颤,在此处厚度和纤维方向的突然变化导致汇-源不匹配和低传播安全性。