Tai C T, Chen S A, Chiang C E, Lee S H, Ueng K C, Wen Z C, Huang J L, Chen Y J, Yu W C, Feng A N, Chiou C W, Chang M S
Department of Medicine, National Yang-Ming University, School of Medicine, Veterans General Hospital-Taipei and Kaoshiung, Taiwan, ROC.
Circulation. 1997 Oct 21;96(8):2601-11. doi: 10.1161/01.cir.96.8.2601.
Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown.
Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length.
The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.
既往对典型心房扑动患者的电生理研究提示，缓慢传导区可能位于右房下部峡部，该峡部为由下腔静脉口、欧氏瓣/嵴、冠状窦口和三尖瓣环构成的路径。该解剖峡部在心房起搏时的传导特性及对阵发性心律失常药物的反应尚不清楚。
对44例患者进行了研究，其中20例阵发性室上性心动过速患者（第1组）和24例临床记录的阵发性典型心房扑动患者（第2组）。将一根20极环状电极导管置于三尖瓣环周围。从右房下部和冠状窦口进行递增起搏，以测量在基线状态下以及静脉输注普鲁卡因胺或索他洛尔后沿峡部和侧壁的传导时间和速度。在两组中，递增起搏时峡部的传导速度在输注抗心律失常药物前后均显著低于侧壁。此外，峡部逐渐出现的传导延迟伴单向阻滞与典型心房扑动的起始有关。与第1组相比，第2组峡部的传导速度较低且右房不应期较短。普鲁卡因胺显著降低了传导速度，但索他洛尔未改变传导速度。相比之下，索他洛尔显著延长了心房不应期，延长程度高于普鲁卡因胺。输注普鲁卡因胺后，峡部传导时间的增加占扑动周期长度增加的52±19%，12例患者中有5例（42%）典型扑动自发终止。输注索他洛尔后，12例患者中仅6例（50%）诱发了典型扑动，扑动周期长度无显著延长。
具有频率依赖性缓慢传导特性的右房下部峡部对典型人类心房扑动的起始至关重要。它可能是未来抗心律失常药物潜在的药理学靶点。
