Hamabe Akira, Okuyama Yuji, Miyauchi Yasushi, Zhou Shengmei, Pak Hui-Nam, Karagueuzian Hrayr S, Fishbein Michael C, Chen Peng-Sheng
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif 90048, USA.
Circulation. 2003 Mar 25;107(11):1550-5. doi: 10.1161/01.cir.0000056765.97013.5e.
The roles of complex muscle sleeve geometry and fiber orientation in the pulmonary veins (PVs) in wave-front propagation are poorly understood.
We mapped the left superior PV (LSPV, n=7) and left inferior PV (LIPV, n=4) of dogs with 420 bipolar electrodes (1-mm resolution) and performed detailed histological examination. In the anterior LSPV-left atrial (LA) junction, myocardial muscle fibers were oriented perpendicular to PV blood flow. A wedge filled with connective tissues led to a complete muscle separation or an abrupt increase in muscle thickness between the PV and LA (0.42+/-0.12 versus 2.0+/-0.31 mm, P<0.01). Distal LSPV pacing resulted in conduction block at the anterior PV-LA junction, with double potentials. In contrast, the posterior LSPV-LA junction showed gradual muscle thickening and a fiber orientation parallel to the blood flow. The maximum PV muscle thickness in the anterior PV-LA junction is thinner than that in the posterior junction (0.83+/-0.15 versus 1.3+/-0.38 mm, P<0.01). Distal LIPV pacing showed multiple PV-LA breakthroughs, with segmental conduction block in the anterior PV-LA junction. The conduction block corresponded to segmental PV-LA muscle disconnection. Complex fiber orientations in the PV muscle sleeves away from the PV-LA junction were responsible for intra-PV conduction delay or block during rapid PV pacing.
We conclude that segmental muscle disconnection and differential muscle narrowing at PV-LA junctions and complex fiber orientations within the PV provide robust anatomical bases for conduction disturbance at the PV-LA junction and complex intra-PV conduction patterns.
肺静脉(PVs)中复杂的肌袖几何结构和纤维方向在波前传播中的作用尚不清楚。
我们用420个双极电极(分辨率为1毫米)绘制了犬的左上肺静脉(LSPV,n = 7)和左下肺静脉(LIPV,n = 4),并进行了详细的组织学检查。在前部LSPV-左心房(LA)交界处,心肌纤维垂直于PV血流方向排列。一个充满结缔组织的楔形结构导致PV和LA之间的肌肉完全分离或肌肉厚度突然增加(0.42±0.12对2.0±0.31毫米,P<0.01)。LSPV远端起搏导致前部PV-LA交界处传导阻滞,并出现双电位。相比之下,后部LSPV-LA交界处显示肌肉逐渐增厚,纤维方向与血流平行。前部PV-LA交界处的最大PV肌肉厚度比后部交界处薄(0.83±0.15对1.3±0.38毫米,P<0.01)。LIPV远端起搏显示多个PV-LA突破点,前部PV-LA交界处有节段性传导阻滞。传导阻滞与节段性PV-LA肌肉分离相对应。远离PV-LA交界处的PV肌袖中的复杂纤维方向是快速PV起搏期间PV内传导延迟或阻滞的原因。
我们得出结论,PV-LA交界处的节段性肌肉分离和不同程度的肌肉变窄以及PV内的复杂纤维方向为PV-LA交界处的传导障碍和复杂的PV内传导模式提供了有力的解剖学基础。