Chu Chih-Sheng, Lee Kun-Tai, Cheng Kai-Hong, Lin Tsung-Hsien, Lee Min-Yi, Voon Wen-Chol, Lai Wen-Ter, Chu Chih-Sheng, Lee Kun-Tai, Cheng Kai-Hong, Lin Tsung-Hsien, Lee Min-Yi, Voon Wen-Chol, Sheu Sheng-Hsiung, Lai Wen-Ter
Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital and Department of Cardiology, Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Kaohsiung J Med Sci. 2007 Dec;23(12):599-610. doi: 10.1016/S1607-551X(08)70058-5.
Atrial electrical remodeling (ER) after spontaneous or pacing-induced atrial fibrillation has been previously described in humans. We investigated atrial ER induced by a 5-minute period of rapid atrial pacing and the pharmacologic effects of verapamil and procainamide on this atrial ER phenomenon. The atrial effective refractory periods (ERPs) at drive cycle lengths of 400 (ERP 400 ) and 600 (ERP 600 ) ms, at five representative atrial sites (high right atrium [HRA]; proximal, middle and distal coronary sinus; interatrial septum), were determined in 20 patients at baseline and immediately after cessation of a 5-minute period of rapid pacing from the HRA at a rate of 150 bpm. The degrees of atrial ERP 400 and ERP 600 shortening after pacing were calculated as acute atrial ER. The same protocol was repeated in another 15 patients after intravenous administration of verapamil (0.15 mg/kg) and in another 15 patients after intravenous administration of procainamide (15 mg/kg). The results demonstrated that, in the control state acute atrial ER can be significantly demonstrated at each atrial representative site ( p < 0.001). The mean ERP 400 and ERP 600 shortenings were 9 +/- 4% and 8 +/- 4%, respectively. After procainamide infusion, but not after verapamil, baseline ERP 400 and ERP 600 values were significantly prolonged at the five representative atrial sites ( p < 0.01). Acute atrial ER could still be demonstrated at each atrial site after procainamide or verapamil infusion ( p < 0.001). In conclusion, acute atrial ER can be demonstrated after only a 5-minute period of rapid atrial pacing in humans. Intravenous verapamil or procainamide does not abolish this ER process.
自发性或起搏诱导的心房颤动后的心房电重构(ER)此前已在人类中有所描述。我们研究了5分钟快速心房起搏诱导的心房ER以及维拉帕米和普鲁卡因胺对此心房ER现象的药理作用。在20例患者的基线状态以及从右心房高位(HRA)以150次/分钟的速率进行5分钟快速起搏停止后,测定五个代表性心房部位(右心房高位[HRA];冠状窦近端、中端和远端;房间隔)在驱动周期长度为400(ERP 400 )和600(ERP 600 )毫秒时的心房有效不应期(ERP)。起搏后心房ERP 400 和ERP 600 的缩短程度计算为急性心房ER。在另外15例患者静脉注射维拉帕米(0.15 mg/kg)后以及另外15例患者静脉注射普鲁卡因胺(15 mg/kg)后重复相同方案。结果表明,在对照状态下,每个心房代表性部位均可显著显示急性心房ER(p < 0.001)。平均ERP 400 和ERP 600 缩短分别为9 +/- 4%和8 +/- 4%。输注普鲁卡因胺后,但维拉帕米输注后未出现这种情况,五个代表性心房部位的基线ERP 400 和ERP 600 值显著延长(p < 0.01)。输注普鲁卡因胺或维拉帕米后,每个心房部位仍可显示急性心房ER(p < 0.001)。总之,在人类中仅5分钟快速心房起搏后即可显示急性心房ER。静脉注射维拉帕米或普鲁卡因胺并不能消除这种ER过程。