Higashi Yukei, Sato Tokutada, Shimojima Hisa, Takeyama Youichi, Goto Ko, Mitsuya Toshiaki, Sagawa Fumiaki, Ishikawa Ryokichi, Ishikawa Yumi
Cardiovascular Division, Showa University Fujigaoka Hospital, 1-30 Fujigaoka Aoba-ku, Yokohama, Japan 227-8501.
Pacing Clin Electrophysiol. 2003 Mar;26(3):685-91. doi: 10.1046/j.1460-9592.2003.00118.x.
The single-lead VDD pacemaker system (VDDPS) enables atrial synchronous ventricular pacing with only one lead in patients with an atrioventricular block. There are some cases in which the atrial potential decreases after implantation of a VDDPS, making physiological pacing difficult. The mechanism of this decrease has not been elucidated yet. To elucidate the possible relationship between the decrease of the atrial potential after implantation of a VDDPS and histopathological changes of the atrium. We implanted a VDDPS from the jugular vein under anesthesia in 10 adult dogs. The tip of the pacing lead was fixed in the right ventricular apex of the heart under fluoroscopic guidance. Then, the lead was ligated and fixed to the jugular vein at a point where a favorable atrial potential was obtained. The end of the lead was passed from the neck to the back subcutaneously; then pulled outside and fixed there to measure the atrial potential. The atrial potential was measured using a pacing system analyzer under anesthesia on days 3 (n = 9) and 7 (n = 8), as well as on weeks 2 (n = 6), 3 (n = 4), and 4 (n = 3), after the implantation. The heart was removed from the dogs on day 3 (n = 2), day 7 (n = 2), week 2 (n = 2), and week 4 (n = 4) to examine the atrial histological findings. The atrial potential was 2.7 +/- 0.7 mV at the time of the implantation, 1.7 +/- 1.1 mV (P < 0.05) on day 3, and 1.7 +/- 0.7 mV on week 4 after the implantation. Macroscopically, the pacemaker lead was covered with thrombus, and adhered to the atrial wall in 80% of animals. Microscopically, the endocardium was hypertrophic due to fibrous tissue; besides RBC extravasation, inflammatory cells infiltration and degeneration of myocardial cells, were observed under the endocardium. Inflammatory changes developed in the atrial wall after implantation of the VDDPS, and this seemed to be one of the mechanisms for the decrease of the atrial potential of the VDDPS.
单导联VDD起搏器系统（VDDPS）能够在房室传导阻滞患者中仅通过一根导联实现心房同步心室起搏。在某些情况下，植入VDDPS后心房电位会降低，导致生理性起搏困难。这种降低的机制尚未阐明。为了阐明VDDPS植入后心房电位降低与心房组织病理学变化之间的可能关系。我们在10只成年犬麻醉状态下经颈静脉植入VDDPS。起搏导线尖端在荧光透视引导下固定于心脏右心室心尖部。然后，在获得良好心房电位的部位将导线结扎并固定于颈静脉。导线末端经皮下从颈部穿至背部；然后拉出并固定在那里以测量心房电位。在植入后的第3天（n = 9）、第7天（n = 8）以及第2周（n = 6）、第3周（n = 4）和第4周（n = 3），在麻醉状态下使用起搏系统分析仪测量心房电位。在植入后的第3天（n = 2）、第7天（n = 2）、第2周（n = 2）和第4周（n = 4），从犬体内取出心脏以检查心房组织学结果。植入时心房电位为2.7±0.7 mV，植入后第3天为1.7±1.1 mV（P < 0.05），第4周为1.7±0.7 mV。宏观上，起搏器导线被血栓覆盖，80%的动物中导线与心房壁粘连。微观上，心内膜因纤维组织而肥厚；除了红细胞外渗，在心内膜下还观察到炎性细胞浸润和心肌细胞变性。VDDPS植入后心房壁出现炎性改变，这似乎是VDDPS心房电位降低的机制之一。
