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Pacemaker recognition of pathological tachycardia relies on heart rate analysis. This can lead to misdiagnosis when sinus tachycardia exceeds the preset tachycardia response trigger rate. We have explored a method for automatic tachycardia diagnosis by analysis of bipolar endocardial electrogram morphology. Electrograms were recorded from 11 patients (pts) during sinus rhythm and during a total of 20 abnormal rhythms: retrograde atrial depolarization from ventricular pacing in six patients; atrioventricular reentry tachycardia in five patients with intermittent left bundle branch block in one of those; AV nodal reentry tachycardia in five patients and ventricular tachycardia in three patients. Posture and respiration were varied during all rhythms except ventricular tachycardia. The electrograms were then digitized and converted to a form in which the amplitudes were proportional to the rates of change of the original electrogram (equivalent to a first time derivative); the derived signal was then analyzed by a new gradient pattern detection (GPD) program. Analysis of the processed atrial signals by GPD resulted in automatic recognition of abnormal rhythms from sinus rhythm in all cases except for one patient's retrograde atrial depolarization. At the ventricular level, GPD successfully distinguished all abnormal rhythms from sinus rhythm including recognition of left bundle branch block and varying degrees of preexcitation. Respiratory and postural variation did not affect the recognition process. We conclude that electrogram GPD has successfully and automatically detected a variety of arrhythmias which can be treated by implantable pulse generators and may, therefore, be a useful adjunct to heart rate analysis in future generations of such antitachycardia pacemakers.

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.

Five patients aged between 27 and 48 years were referred for investigation of recurrent paroxysmal tachycardias. Electrophysiological studies revealed concealed ventriculoatrial accessory pathways in two patients, possible atrionodal pathways in two patients and dual intranodal pathways in one patient. During electrophysiological study, particular attention was paid to methods of terminating tachycardia by pacing techniques including single or double atrial and ventricular extrastimuli, atrial or ventricular underdrive, atrial overdrive pacing, and in two patients, rapid ventricular pacing. 'Autodecremental' atrial pacing was employed in all five patients and autodecremental ventricular pacing in two patients. This system is controlled by a microprocessor interfaced with a stimulator. When tachycardia of a cycle length less than 375 ms is sensed the system initiates pacing sequences. The initial stimulus is introduced at an interval less than the tachycardia cycle determined by a preset decremental value D. Each subsequent pacing interval is reduced by the value of D resulting in a gradual acceleration of pacing. The total duration of pacing is limited by the value of the pacing period (P). The final pacing rate is determined by P but cannot exceed 275 bpm (cycle length of 218 ms). Both P and D are operator programmable variables. Tachycardias of a cycle length less than 218 ms do not activate the pacemaker. The postpacing sensing deadtime of the system is set at 50 ms. In three patients, double atrial extrastimuli or atrial overdrive initiated atrial flutter or fibrillation. Autodecremental atrial pacing was successful in converting tachycardia to sinus rhythm in all five patients without initiation of other tachyarrhythmias. Autodecremental ventricular pacing was successful in one of the two patients in which it was used. This new modality of pacing has several theoretical advantages over conventional methods: the decremental mode may avoid stimulation in the vulnerable period and minimizes the risk of initiating other tachyarrhythmias; gradual acceleration of pacing over a short period results in stimulation at different phases of the tachycardia cycle length; and the operator variables D and P provide a flexible system which may be adjusted to suit a particular patient and tachycardia. The development of a fully implantable programmable system is made attractive by the simplicity and adaptability of this technique.

Atrial premature beats (APBs) which encounter sufficient AV delay may initiate junctional reentry tachycardia (JRT). This form of initiation may be prevented by rendering part of the reentry circuit refractory by artificial stimulation following an APB which would otherwise initiate JRT. Two such approaches have been suggested: preexcitation pacing, that is, ventricular stimulation with a short AV delay triggered by atrial depolarization; and preemptive pacing, which consists of early atrial stimulation coupled to the initiating APB. We compared these approaches and describe them as follows. Ten patients with JRT (six with atrioventricular reentry and four with AV nodal reentry) were studied. Against a background of regular atrial drive, the range of coupling intervals over which a stimulated APB initiated JRT (tachycardia initiation window) was determined (control). The tachycardia initiation window was also measured when a second atrial stimulus followed the initiating APB 20 ms after atrial recovery (preemptive pacing) or when a ventricular stimulus closely followed the initiating APB with an AV delay of 65 ms (preexcitation pacing). The tachycardia initiation window in response to an isolated APB was also assessed following regular AV pacing with a short (65 ms) AV delay (preconditioning pacing) and the effect of preexcitation pacing following the initiating APB was also assessed after a similar drive (combined preconditioning and preexcitation pacing). All protocols were performed at two basic drive cycle lengths. The results are arranged for the slow and fast drives, respectively, and were as follows: control initiating windows--49.5, 28.5 ms; preemptive pacing initiation windows--151, 38 ms; preexcitation pacing initiation windows--26, 23.5 ms; preconditioning pacing initiation windows--45.5, 35 ms; combined preconditioning and preexcitation pacing initiation windows--10.0, 2.5 ms. Whereas preemptive pacing tended to widen the tachycardia initiation windows (a proarrhythmic effect) the combination of preconditioning and preexcitation pacing considerably reduced the possibility of JRT initiation by an atrial premature beat.

Both antiarrhythmic drugs and bursts of rapid ventricular pacing provide alternatives to DC cardioversion for the treatment of paroxysmal ventricular tachycardia. This report considers the individual and combined success of burst ventricular pacing and intravenous disopyramide phosphate in the tretment of 11 examples of paroxysmal ventricular tachycardia. Rapid ventricular pacing, at a rate of up to 50 beats/min faster than the tachycardia rate terminated 7 of the tachycardias. Intravenous disopyramide resulted in increased tachycardiac cycle length (342 +/- 34 ms-385 +/- 56 ms), increased QRS complex width (147 +/- 42 ms-180 +/- 41 ms) and termination of 8 the tachycardias. The remaining 3 tachycardias could be terminated by bursts of ventricular pacing following the infusion of disopyramide. Of these, 2 could not be terminated prior to disopyramide. The use of both techniques allowed the extinction of all 11 tachycardias and prevented the need to proceed to DC conversion.

Changes in the QT and QTc intervals in 19 patients were studied at a ventricular paced rate difference of 50 beats/min. In all patients the measured QT interval shortened as the pacing rate was increased, from a mean value of 441 ms to 380 ms (p less than 0.001), but when corrected for heart rate the QTc lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT interval was measured at rest and immediately following exercise sufficient to increase the atrial rate by approximately 50 beats/min at identical ventricular paced rates. In all patients exercise-induced QT interval shortening from a mean value of 433 ms to 399 ms (p less than 0.001). These results show first that Bazett's formula is unsuitable for correction of QT interval induced by ventricular pacing, and second that heart rate and changes in sympathetic tone independently influence the duration of the QT interval. It is suggested that these results are relevant to the design of physiological pacemakers in which the duration of the QT interval influences the discharge frequency of the pacemaker and to the consideration of ventricular pacing for the treatment of abnormal repolarization syndromes.

An automatic, fully implantable scanning pacemaker was developed and has been used for tachycardia termination in man. Since January 1982, 22 patients have had this pacemaker implanted at St. Bartholomew's Hospital and over 125 devices have been used throughout the world. Clinical results have been encouraging, especially with the second-generation device.