R. A. J. Spurrell

Detection of pathological tachycardia by analysis of electrogram morphology.

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.

Implantable automatic scanning pacemaker for termination of supraventricular tachycardia

Thirteen patients suffering from reentrant supraventricular tachycardia have undergone implantation of a scanning extrastimulus pacemaker. This pacemaker is fully implanted and automatic, and it requires no external control device to activate or control it. The pacemaker is activated when tachycardia occurs. After four cycles an extrastimulus is induced with a preset coupling time from a sensed intracardiac potential, and every four cycles thereafter a further extrastimulus occurs, but on each occasion there is a decrement in coupling cycle by 6 ms until 90 ms of the cardiac cycle has been scanned by extrastimuli. When necessary, two extrastimuli can be introduced with a fixed but preset coupling time between them. Every four beats two extrastimuli are induced but the coupling time between the spontaneous cardiac potential and the first stimulus is decreased by 6 ms until 90 ms of the cardiac cycle has been scanned. The coupling time between the two stimuli is fixed throughout the scan. When termination of tachycardia occurs the successful timing variables are retained in the pacemaker memory so that at the onset of the next episode of tachycardia these settings are used first. Pacemaker pulse width, sensitivity, tachycardia trigger rate, coupling intervals for both stimuli and the use of single or double extrastimuli are all programmable transcutaneously. Three patients required single, and seven patients double ventricular premature stimuli; three patients required double atrial premature stimuli for termination of tachycardia. Despite frequent attacks of tachycardia before implantation, only two patients had a sustained attack of tachycardia after pacemaker implantation.

Electrophysiological effects of sotalol--just another beta blocker?

The electrophysiological effects of intravenous sotalol hydrochloride (0.4 mg/kg) were assessed in 24 patients, including 13 with the Wolff-Parkinson-White syndrome, undergoing routine electrophysiological study. Fifteen to 30 minutes after sotalol administration there was a significant increase in sinus cycle length and in sinus node recovery time. There was a small increase in the AH interval, but the HV interval was unchanged. The QT and JT intervals, measured during sinus rhythm, were both increased. The atrial, ventricular, and atrioventricular nodal effective refractory periods were all prolonged, as was the atrioventricular nodal functional refractory period. In 13 patients with ventricular pre-excitation there was an increase of the accessory pathway anterograde and retrograde effective refractory periods. In 12 of these 13 sotalol was given during atrioventricular re-entrant tachycardia, resulting in termination in five. Tachycardia cycle length increased in all patients, with the major effect being in the atrioventricular direction. Though some of the effects seen in these patients are consistent with the beta adrenergic antagonist properties of sotalol, the effect on atrial, ventricular, and accessory pathway effective refractory periods and on ventricular repolarisation is not typical of that observed with other beta blockers but may be the result of lengthening of the action potential duration. These findings suggest that sotalol may be a more versatile antiarrhythmic agent than other beta receptor antagonists.

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias.

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QTc interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.

The Ventricular Paced QT Interval—The Effects of Rate and Exercise

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 < 0.001), but when correct ed for heart rate the QTc‐ lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT in terval 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 < 0.001). These results show first that Bazetts formula is unsuitable for correction of QT interval changes 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 resuits 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. (PACE, Vol. 5, May‐June, 1982)

Sinoatrial function after cardiac transplantation

The function of both the denervated donor and innervated recipient sinus nodes of 14 asymptomatic cardiac transplant recipients was assessed. Tests of sinoatrial function were performed in 14 donor and 10 recipient atria. The mean spontaneous cycle length of the recipient atria was significantly longer than that of the donor atria (944 +/- 246 versus 663 +/- 158 ms, p less than 0.01). Donor sinus node recovery time was prolonged in four patients (greater than 2,500 ms in two) and recipient recovery time was prolonged in six patients. In those patients with normal sinus node function tests, the recovery time of the recipient sinus node was longer than that of the donor sinus node (1,170 +/- 207 versus 864 +/- 175 ms, p less than 0.02). The pattern of response of recovery times to increasing pacing rate was predictable and organized in the donor but chaotic in the recipient, and the longest sinus node recovery time occurred at the shortest pacing cycle length used in 12 of the 14 donor atria but in only 1 of the 10 recipient atria (p less than 0.001). Secondary pauses occurred in none of the normal donor atria and in all of the abnormal donor atria (p less than 0.001); however, they occurred in both normal and abnormal recipient atria. The recipient and donor atria were paced alone and synchronously in the same patients. Synchronous pacing had no effect on the recovery times of the donor sinus node but significantly lengthened those of the recipient (sinus node recovery time: 1,266 +/- 218 to 1,547 +/- 332 ms, p less than 0.02; corrected recovery time: 322 +/- 102 to 686 +/- 188 ms, p less than 0.01). In the donor atria, abnormal recovery time was invariably associated with abnormal sinoatrial conduction time. There was a strong correlation between sinoatrial conduction time measured by the methods of Strauss and Narula and their coworkers in the donor atria (r = 0.98, p less than 0.001) but not in the recipient atria (r = 0.72). In the absence of autonomic influences, tests of sinus node function of the donor atria produce predictable and consistent results and, therefore, may be more clinically reliable than in intact human subjects. There is a high incidence of recipient sinus node dysfunction in asymptomatic long-term survivors of cardiac transplantation.

Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.

Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.

The response of regular re-entrant supraventricular tachycardia to right heart stimulation.

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re‐entrant “supravenlricular” tachycardias. LStandard eleclrophysio‐logical 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. fntranodal 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 utrial 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 Jess successful than a single atrial exlrastimulus 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.

Electrophysiological abnormalities in the transplanted human heart.

Fourteen relatively long term survivors of cardiac transplantation underwent systematic electrophysiological evaluation and ambulatory electrocardiographic monitoring. Six patients had prolonged conduction intervals during sinus rhythm. Sinus node function could be assessed in all donor atria and in 10 recipient atria. Sinus node recovery times were prolonged in four of the donor atria and in six recipient atria. In the donor atria abnormalities of sinus node automaticity were invariably associated with abnormalities of sinoatrial conduction. Four patients showed functional duality of atrioventricular nodal conduction during programmed extrastimulation, but no patient developed re-entrant arrhythmia. During ambulatory electrocardiographic monitoring no pronounced tachyarrhythmias were recorded. Three patients showed abnormalities of sinus node impulse formation. All three patients had abnormal sinus node recovery times during their electrophysiological study. Long term survivors of cardiac transplantation have a high incidence of electrophysiological abnormalities. Abnormalities of donor sinus node function are probably of clinical significance. The clinical significance of abnormalities detected within the atrioventricular conduction system of the denervated heart remains to be elucidated.