Helge Grendahl

Pacemaker follow-up with prolonged intervals in the stable period 1 to 5 years postimplant.

This pilot study focuses on pacemaker follow‐up in the technically stable period 1–5 years after a pacemaker implantation. Two hundred and thirty selected patients with single chamber pacemakers (215 WI, 15 AAI) had their follow‐up intervals prolonged to 2–4 years in this period. Sixty‐six patients fulfilled the study period uneventfully and 21 are still pending. Sixty‐nine patients had unscheduled visits to the pacemaker clinic. Of these, 7 were reoperated (1 for exit block, 4 had pocket erosions, and 2 were upgraded to DDD). Nine were reprogrammed (1 for sensing failure, 1 had the pulse duration increased, and in 7 the pacing rate was changed). Seventy‐four patients died. In 63, the cause of death is known not to be pacemaker related. Six died suddenly, and in five cases, the cause of death is unknown. This study indicates that frequent follow‐up visits may be omitted in this period in selected patients with single chamber pacemakers. A prerequisite is that the patients are registered at a pacemaker clinic and have easy access to the physician whenever they suspect pacemaker related problems.

The Effect of Propranolol and Verapamil On Atrial and Atrioventricular Refractory Periods in Man

The atrial effective (ERP) and relative (RRP) refractory periods were examined at high atrial pacing rates in 12 patients before and after intravenous injection of propranolol, and in 5 patients before and after injection of verapamil, using the technique of paired pacing. Seven of the patients had A-V block grade II-III and 10 patients had sinus rhythm. The range of atrial ERP in all patients was found to be 200 to 270 msec. and the range of atrial RRP was 230 to 330 msec. The atrial ERP and RRP were longer at a pacing rate of 160 per minute than at a pacing rate of 240 per minute. The conduction delay between the second impulse and the atrial depolarization was found to be due to increased interval between the stimulus and the start of the depolarization wave. The atrial ERP increased after injection of propranolol in 8 of 12 patients, decreased in 3 patients and was unchanged in one patient. The atrial RRP increased in 7 patients, decreased in one patient and was unchanged in 4 patients. In all patients the changes were of moderate degree. The conduction delay between the stimulating impulse and the atrial response was shorter after propranolol in 7 patients, longer in one patient and unchanged in 4 patients. The ERP of the atrioventricular conducting tissue was 220 to more than 380 millisec. After injection of propranolol it increased in all of 3 patients in whom it could be measured. After injection of verapamil no significant effects on the atrial ERP and RRP were found. ERP of the atrioventricular conducting tissue was lengthened in 4 of 5 patients, and the degree of A-V block during rapid atrial pacing increased after injection of verapamil. It is suggested that the effect of propranolol on atrial arrhythmias is due to its effect on ectopic pacemaker activity rather than any effect on the refractory period of the atrium. The effects of verapamil on the atrioventricular conducting tissue may explain some of the antiarrhythmic effects of this drug.

Long-Term Pacing in VVI-Modes Elicit Similar Sympathetic Drive

Ventricular inhibited (VVI] pacing in patients with atrioventricular (AV) hlock may increase sympathetic nervous tone compared to the hemodynamically superior AV synchronous mode even if symptoms of cardiac decompensation are lacking. Thus, short-term VVI pacing induces a higher release of norepinephrine into coronary sinus blood than does atrial pacing.^ However, this difference may subside due to adaptation during long-term pacing. A general increase in the adrenergic drive should be reflected in systemic catecholamine concentrations. We examined seven symptom-free patients, aged 32-74 years, treated with dual chamber pacemakers for high degree AV block: Cordis Sequicor 233 (Cordis Corp., Miami, FL, USA) in four and Intermedics 483-01 (Intermedics, Inc., Freeport, TX, USA) in three patients. Holter monitoring during VVI pacing demonstrated continuous pacing with the atria in stable sinus rhythm in all patients. In random succession the pacemakers were programmed either to VVI 70 ppm or to optimal DDD program. Each period lasted 7-21 days, and the patient was not informed of the pacing mode used. At the end of each period the patient was examined at 8 A.M. after at overnight fast and an abstension from drugs, coffee, tea, and tobacco. A plastic cannula was inserted into a forearm artery under local anaesthesia without epinephrine. After supine rest for 30 minutes in a quiet and dimly lit room, 5 mL of aterial blood was collected for catechoiamine assay. The patient was then exercised on a tricycle ergometer, and blood sampling was repeated at maximal work. The blood samples were immediately placed on ice with a preservative and centrifuged. The plaisma was stored at —70° until analysis. Plasma epinephrine and norepinephrine concentrations were measured by the method of Peuler and Johnson^ as previously reported.^ The resting plasma norepinephrine concentrations in VVI and DDD were 253 ± 28 pg/mL (mean ± SEM) and 226 ± 54 pg/mL, respectively, increasing during exercise to 2,962 ± 768 pg/mL and 2,848 ± 768 pg/mL. The corresponding plasma epinephrine concentrations were 60 ± 10 pg/mL and 58 ±C 10 pg/mL at rest and 353 ± 74 pg/mL and 338 ± 62 pg/mL during exercise.* None of the differences between VVI and DDD was statistically significant. Atrial rates were identical in both pacing modes, and Holter monitoring revealed that during the last 24 hours before blood sampling all patients had close to 100% paced rhythm. Thus, the preset study cannot demonstrate any difference between VVI and DDD long-term pacing with respect to arterial catecholamine concentrations. Arterial catecholamine concentrations reflect the total sympathetic stimulation, whereas, venous samples are influenced by organ secretion or extraction of catecholamines. Thus, during VVI and DDD pacing, any difference in myocardial catecholamine release or uptake, if present, was not large enough to appear in systemic circulation.

Escape Rhythm in Complete A‐V Block. The Recovery Phase after Overdrive Suppression from Artificial Ventricular Pacing

The recovery phase after overdrive suppression from artificial ventricular pacing. In 60 patients with third degree A‐V block, recovery of escape rhythm from overdrive suppression after ventricular pacing has been studied. Implanted unipolar VVI pacemakers were inhibited by chest wall stimuli. A total of 165 rhythmograms were studied. In 37, the rate was irregular, in the other 128 the escape rate increased gradually, following an exponential curve until stabilization after 3 minutes. In 29 of these rhythmograms, a possible exit block of the first escape impulse was observed. In 99 rhythmograms without exit block, escape rhythm recovery time was on an average 1.45 times basal escape RR intervals. Overdrive suppression was most marked in patients with a slow escape rhythm.