A seventy years-old male, teacher, was admitted to Kansai Medical School Hospital because of the recurrent Stokes-Adams' attacks on April 28,1971. On admission, his Ecg showed 1° AV block (PR interval=0.44 sec) and on chest XP cardiac silhouette was normal in size and shape (CTR=49%). He was on predonisone 15 mg/day for chronic uveitis of the left eye. During the attacks, Ecg revealed complete AV block with idioventricular rhythm or 2: 1 AV block. On May 21,1971, a permanent cardiac pacing system was implanted by thoracotomy. Medtronic R-inhibited demand type pulse generator, Chardak® Model 5880 and a connector lead with bipolar myocardial electrodes Model 6914 were used. The electrodes were indwelled on the free wall of the left ventricle. The lead was led through the right side of the anterior mediastinum to the left upper abdominal wall, in which the generator was implanted. The cardiac pacing functioned well until March 18,1973, twenty-three months after the implant, when the pulse generator was electively exchanged with that of Model 5942. During those 2 years, aortic regurgitation was developed. Chest XP revealed cardiac enlargement (CTR=59%), and the pulse pressure became widened.
Seven months after the exchange, as the patient recognized arrhythmia and a decrease in pulse rate, he was admitted to monitor Ecg. His rhythm and pulse rate, however, did not revealed any abnormalities at all. Under a suspicion of pulse generator malfunction, the generator was removed to exchange with the same model on October 15,1973. On the following day, an abnormal pacing rhythm manifested itself on the monitor Ecg. The basic pacing interval was 0.84 sec, and all the QRS complexes were artificially induced. When the paced QRS complexes incidentally fell on slightly after P wave (PR interval=0.18 -0.28 sec) the following pacing intervals prolonged to 1.24 sec, as if the pulse generator were inhibited by sensing T wave. Chest XP was examined in details and one of the implanted myocardial electrodes was found to bend at 3mm from its tip. It was supposed that the electrodes was broken but electrically still competent and when atrial and ventricular contractions were incidentally synchronized, the ventricular contraction became so forceful to cause a break-away of the electrode for a moment, which was sensed by the generator as an inhibitory stimulus for resetting its demand mechanism. Thereupon, the broken electrode was disconnected from the generator and the unipolar myocardial pacing system was introduced. During this procedure, the patient experienced an episode of Stokes-Adams' attack. Two days later, then, frequent ventricular premature beats appeared on the monitor Ecg. Chest XP again obtained showed pneumo-hydrothorax of the right side. The Stokes-Adams' convulsion during the procedure was thought to cause suction of the air along through the pacing lead from the open wound to the right lung, this in turn aggravating heart failure to develop ventricular premature beats. The pneumo-hydrothorax and premature beats disappeared completely 3 days later. Thereafter, the cardiac pacing was going on well without any trouble or complication. On September 8,1975, the pulse generator was again electively removed to exchange with Xytronl Model 5951. At the present time, the broken fragment of the electrode parts from the reminder by a few milimeters.
