Kalman Ausubel’s research while affiliated with Albert Einstein College of Medicine and other places

Pacemaker-mediated tachycardias are a well-recognized complication of atrial synchronized dual chamber pacing systems.1 They result from the sensing of retrograde P waves or ectopic atrial activity by the atrial sensing circuit with consequent triggering of ventricular pacing. Most pacemaker-mediated tachycardias are initiated by ventricular ectopic beats with retrograde atrial activation. Other initiating mechanisms have been reported2,3 including tracking of a sinus P wave.4 When these arrhythmias are sustained by consistent retrograde atrial activity following each paced ventricular beat which then triggers the following beat, they have been termed "endless loop tachycardias."5 This category of pacemaker-mediated tachycardia persists until either sensing of retrograde P waves ceases or ventriculoatrial conduction terminates. Endless loop tachycardias are generally maintained at the programmed upper rate limit of the pacemaker.2,6 We recently saw a patient with an endless loop tachycardia that had persisted for several days and was ended by magnet application. The tachycardia persisted despite an algorithm in the generator that stops atrial tracking after 15 responses at the upper rate limit. Because the pacemaker was normal, it was postulated that the tachycardia rate was below the upper rate limit. In such a tachycardia, the sum of the retrograde ventriculoatrial conduction time and the atrioventricular (AV) interval is greater than the cycle length of the programmed upper rate limit. We detail the interrelations between the ventriculoatrial conduction time and AV interval in several patients who manifested endless loop tachycardias below the programmed upper rate limit.

DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 +/- 18 ms during sinus rhythm to 122 +/- 30 ms during right atrial pacing (p less than 0.001). In 16 patients with P wave duration less than 110 ms interatrial conduction prolonged from 85 +/- 10 ms during sinus rhythm to 111 +/- 9 ms during right atrial pacing (p less than 0.01) compared to 114 +/- 20 ms prolonging to 111 +/- 19 ms (p less than 0.01) in 9 patients with P wave duration greater than 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60-160 beats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p less than 0.001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.

An endless loop tachycardia starts when the atrial sensory amplifier of a dual chamber pacemaker identifies an early atrial signal originating from a ventricular or atrial premature depolarization or from myopotential noise. The tachycardia will continue as long as ventriculoatrial conduction is sustained. By selecting the appropriate atrial sensitivity setting, postventricular atrial refractory period, or upper rate limit, it is possible to eliminate sustained endless loop tachycardia. Electrophysiological data obtained at the time of dual chamber pacemaker implantation can assist the physician when selecting these settings. This report summarizes our intraoperative data on ventriculoatrial conduction obtained from 432 consecutive patients. One hundred sixty-two patients had evidence of ventriculoatrial conduction including 14% of patients with antegrade complete heart block and 32% with 2:1 AVB. The majority of patients with preserved antegrade conduction had sustained retrograde conduction. During incremental ventricular pacing, ventriculoatrial conduction prolonged in the majority of patients, and with faster ventricular pacing rates, ventriculoatrial block developed. Ventriculoatrial block developed in half of the patients at a ventricular pacing rate exceeding 120 bpm. Analysis of these data suggests that by selecting an upper rate limit of 140 bpm, a postventricular atrial refractory period of 300 msec, and an atrioventricular interval of 125 msec, approximately 90% of patients will not have sustained endless loop tachycardia.

Pacemaker-mediated endless loop tachycardia is usually caused by a P wave displaced from the physiologic position preceding a QRS complex to a time of atrial channel sensitivity after the QRS. Five cases are described of endless loop tachycardia starting after a normally-timed P wave, either spontaneous and preceding a ventricular stimulus or a P wave produced by an atrial channel stimulus followed by a ventricular stimulus and QRS complex. In each instance, the atrial refractory interval (ARI) was shorter than the retrograde conduction time. In four of the cases, prolongation of the atrial refractory interval after the ventricular event ended the tachycardias. In the fifth, in which the pulse generator could not be so programmed, the ventricular inhibited mode was required.

The pacemaker syndrome is an iatrogenic disorder that can result from hemodynamic sequelae of ventricular pacing. Symptoms range from fatigability to syncope and occur during the time the ventricles are being stimulated by the pulse generator. Postulated mechanisms include loss of atrioventricular synchrony, vasodepressor reflexes, and retrograde atrial activation. Prevention is attempted by selection of the appropriate pacing mode for the individual patient. Remission results from restoration of atrioventricular synchrony.

Although atrial synchronous and rate-responsive ventricular pacing have been compared, the importance of maintaining synchronized atrial systole in addition to rate responsiveness has been incompletely defined. That is, the effects of these two pacing modes on cardiac volumes and contractility have not been studied. Accordingly, 16 patients with normal ventricular function were studied while in the upright position and at rest with gated radionuclide ventriculography during both atrial synchronous and ventricular pacing. Twelve of these patients were also studied during low-level upright exercise (300 kilopond-meters). Rest and exercise ventricular pacing heart rates were matched to those recorded with synchronous pacing. Ventricular volumes were determined with a counts-based method. The ejection fraction and peak systolic pressure/end-systolic volumes or contractility between the two pacing modes. However, during exercise to identical heart rates, blood pressures, and workloads, although stroke volume was the same during exercise with atrial synchronous and ventricular pacing (78 +/- 13 vs 75 +/- 12 ml), end-diastolic and end-systolic volumes were lower with ventricular pacing than with atrial synchronous pacing (end-diastolic volume 101 +/- 13 vs 113 +/- 16 ml, p less than .001; end-systolic volume 26 +/- 4 vs 35 +/- 7 ml, p less than .001). Stroke volume during ventricular paced exercise was maintained at atrial synchronous pacing levels by means of increased contractility (ejection fraction of 74 +/- 4% during ventricular pacing vs 69 +/- 5% during atrial synchronous pacing, p = .002; peak systolic pressure/end-systolic volume ratio of 6.51 +/- 1 during ventricular pacing vs 4.85 +/- 1 during atrial synchronous pacing, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

The pacemaker syndrome is a complex of clinical signs and symptoms related to the adverse hemodynamic and electrophysiologic consequences of ventricular pacing in the absence of other causes. Neurologic symptoms or those suggesting low cardiac output or congestive heart failure, temporally related to the onset of ventricular pacing, are indicative of the pacemaker syndrome. The evolution of a clinically recognized syndrome, an analysis of possible mechanisms and clinical manifestations, and diagnostic approaches and their implications for management are discussed.

Revue de cet ensemble de troubles lies a des effets hemodynamiques et electrophysiologiques de la stimulation ventriculaire. Indices de diagnostic: troubles neurologiques, signes de baisse du debit cardiaque ou d'insuffisance cardiaque lies dans le temps a la pose du stimulateur. Evolution d'un cas cliniquement reconnu, discussion des mecanismes et des methodes de diagnostic