Mechanism of decrease in the atrial potential after implantation of a single-lead VDD pacemaker: atrial histological changes after implantation of a VDD pacemaker lead in dogs.
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.
Higashi
Yukei
Y
Cardiovascular Division, Showa University Fujigaoka Hospital, 1-30 Fujigaoka Aoba-ku, Yokohama, Japan 227-8501. y.higashi@showa-university-fujigaoka.gr.jp
Sato
Tokutada
T
Shimojima
Hisa
H
Takeyama
Youichi
Y
Goto
Ko
K
Mitsuya
Toshiaki
T
Sagawa
Fumiaki
F
Ishikawa
Ryokichi
R
Ishikawa
Yumi
Y
D000818:Animals; D016275:Atrial Function / Q000502:physiology*; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004285:Dogs; D004567:Electrodes, Implanted; D006325:Heart Atria / Q000473:pathology; D006329:Heart Conduction System / Q000502:physiology; D010138:Pacemaker, Artificial