Department of Biomedical Engineering, Washington University, St. Louis, Missouri 63130, USA.
J Am Coll Cardiol. 2010 Oct 19;56(17):1386-94. doi: 10.1016/j.jacc.2010.03.098.
We sought to confirm our hypothesis that the human sinoatrial node (SAN) is functionally insulated from the surrounding atrial myocardium except for several exit pathways that electrically bridge the nodal tissue and atrial myocardium.
The site of origin and pattern of excitation within the human SAN has not been directly mapped.
The SAN was optically mapped in coronary-perfused preparations from nonfailing human hearts (n = 4, age 54 ± 15 years) using the dye Di-4-ANBDQBS and blebbistatin. The SAN 3-dimensional structure was reconstructed using histology.
Optical recordings from the SAN had diastolic depolarization and multiple upstroke components, which corresponded to the separate excitations of the SAN and atrial layers. Excitation originated in the middle of the SAN (66 ± 17 beats/min), and then spread slowly (1 to 18 cm/s) and anisotropically. After a 82 ± 17 ms conduction delay within the SAN, the atrial myocardium was excited via superior, middle, and/or inferior sinoatrial conduction pathways. Atrial excitation was initiated 9.4 ± 4.2 mm from the leading pacemaker site. The oval 14.3 ± 1.5 mm × 6.7 ± 1.6 mm × 1.0 ± 0.2 mm SAN structure was functionally insulated from the atrium by connective tissue, fat, and coronary arteries, except for these pathways.
These data demonstrated for the first time, to our knowledge, the location of the leading SAN pacemaker site, the pattern of excitation within the human SAN, and the conduction pathways into the right atrium. The existence of these pathways explains why, even during normal sinus rhythm, atrial breakthroughs could arise from a region parallel to the crista terminalis that is significantly larger (26.1 ± 7.9 mm) than the area of the anatomically defined SAN.
我们试图验证这样一个假设,即人类窦房结(SAN)除了几个电桥接结节点组织和心房心肌的出口途径外,在功能上与周围的心房心肌隔离开来。
人类 SAN 的起源部位和兴奋模式尚未直接绘制。
使用 Di-4-ANBDQBS 和 blebbistatin 对来自非衰竭人心冠状动脉灌注标本中的 SAN 进行光学映射(n=4,年龄 54±15 岁)。使用组织学重建 SAN 的 3 维结构。
来自 SAN 的光学记录具有舒张期去极化和多个上升成分,这与 SAN 和心房层的单独兴奋相对应。兴奋起源于 SAN 的中部(66±17 次/分),然后缓慢(1 至 18cm/s)和各向异性地传播。在 SAN 内经过 82±17ms 的传导延迟后,心房心肌通过上、中、下 SAN 传导途径兴奋。心房兴奋始于起搏主导部位前 9.4±4.2mm 处。椭圆形的 14.3±1.5mm×6.7±1.6mm×1.0±0.2mm 的 SAN 结构通过结缔组织、脂肪和冠状动脉与心房隔离开来,除了这些途径。
这些数据首次在我们所知的范围内证明了主导 SAN 起搏部位的位置、人类 SAN 内的兴奋模式以及进入右心房的传导途径。这些途径的存在解释了为什么即使在正常窦性节律期间,心房突破也可能源自与冠状窦末端平行的区域,该区域明显大于(26.1±7.9mm)解剖定义的 SAN 区域。