D Wu

Electrophysiological studies in patients with chronic recurrent ventricular tachycardia.

SUMMARY Seventeen consecutive patients with chronic recurrent ventricular tachycardia (VT) were studied in an attempt to delineate the reproducibility and mechanism of this arrhythmia. Six patients had nonsustained and 11 had sustained VT. The following electrophysiological techniques were utilized in an attempt to reproduce VT: 1) rapid atrial and ventricular pacing (17 pts); 2) atrial extrastimulus technique (17 pts); 3) ventricular extrastimulus technique (17 pts); 4) V1V2V3 stimulation technique (5 pts); 5) ventricular pacing from two or more sites (5 pts). Ventricular tachycardia was induced in six of 11 (54%) patients with sustained VT. However, in four there was only a single induction and only in the remaining two patients could VT be repetitively induced. In the latter two patients ventricular tachycardia was induced with both atrial and ventricular stimulation. Ventricular tachycardia could not be induced in any patient with nonsustained VT, although three had spontaneous episodes of ventricular tachycardia during study. In conclusion, in the present series of patients with chronic recurrent VT, this rhythm could not be reproducibly induced in the majority of patients in the cardiac catheterization laboratory utilizing catheter stimulation techniques.

Effects of cycle length on atrial vulnerability.

The effect of cycle length on atrial vulnerability was studied in 14 patients manifesting reproducible repetitive atrial firing during atrial extra-stimulus (A2) testing. Repetitive atrial firing was defined as the occurrence of two or more premature atrial responses with return cycle (A2-A2) of 250 msec or less and subsequent mean cycle length of 300 msec or less, following A2. The zone of repetitive atrial firing could be defined in terms of its longest and shortest A,-A2 coupling intervals. Each patient was tested at a long cycle length (CL1) (mean 884 msec) and a short cycle length (CL2) (mean 557 msec). CL1 was sinus rhythm, and CL2, an atrial paced rhythm. Repetitive atrial firing occurred in two patients at CL, and in all patients at CL2. Of the former two patients (group 2), the zone of repetitive atrial firing was markedly widened in one at CL2 due to a shortening of atrial functional refractory period (FRP) at CL2. In the other, zone of repetitive atrial firing could not be totally defined due to induction of sustained atrial flutter preventing definition of atrial FRP. The occurrence of repetitive atrial firing at only CL2 in 12 patients (group 1) reflected: 1) a shortening of atrial FRP from 294 ± 11 msec at CL, to 242 ± 10 msec at CL2 (mean ± SEM; P < 0.01), allowing delivery of A2 at shorter coupling intervals (9); 2) the new occurrence of repetitive atrial firing at A,-A2 coupling intervals achievable at both cycle lengths (1); or 3) both effects (2).In conclusion, decrease of cycle length potentiated atrial vulnerability. This demonstration implies that atrial pacing could potentiate occurrence of paroxysmal atrial fibrillation or flutter.

Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia.

Electrophysiological studies in five patients with documented (4) or suspected (1) paroxysmal supraventricular tachycardia (PSVT), suggested sinus or atrial re-entrance (SR or AR). Two of the patients had preexcitation, three had evidence of atrial enlargement, and all had organic heart disease. The following observations supported a diagnosis of SR and AR: 1) induction of sustained PSVT with atrial extrastimulus technique allowing definition of an echo zone; 2) induction of sustained PSVT during constant rapid atrial pacing at a rate less than that producing A-V nodal Wenckebach periods, or producing normalization of QRS complex in patients with pre-excitation; 3) P waves preceding each QRS during PSVT with an A-H interval appropriate for the rate of the PSVT; 4) antegrade P wave morphology during PSVT, and normal high to low sequence of right atrial activation (SR), or P wave morphology and atrial activation sequence different from sinus (AR); 5) lack of correlation of PSVT induction with critical A-H interval. The rates of induced sustained PSVT ranged from 114 to 143 beats/min, and were similar to those observed during spontaneous episodes of PSVT in the four patients. PSVT could be terminated with critically timed extra-stimuli or carotid massage. In conclusion, SR and AR appear to be mechanisms of spontaneous PSVT in man. Rates of SR and AR PSVT tend to be relatively slow.

An unusual variety of atrioventricular nodal re-entry due to retrograde dual atrioventricular nodal pathways.

Three patients with paroxysmal supraventricular tachycardia (PSVT) had discontinuous ventriculo-atrial conduction curves (V,-V2, A,-A2), suggesting dual A-V nodal pathways. Ventricular echoes occurred simultaneously with sudden increase of V-A interval. These echoes were characterized by retrograde P waves occurring in front of QRS, suggesting utilization of a slow pathway for retrograde conduction and a fast pathway for antegrade conduction. In case one, atropine improved retrograde slow pathway and antegrade fast pathway conduction and made A-V nodal re-entry sustained, resulting in PSVT (with retrograde P in front of the QRS). In cases 2 and 3, atropine markedly shortened retrograde fast pathway refractory period and slightly improved antegrade slow pathway conduction. The discontinuous V1-V2, A,-A2 curves and echoes were no longer demonstrable. However, with improvement of retrograde fast pathway and antegrade slow pathway conduction, A-V nodal re-entrant echoes and PSVT were observed, utilizing the slow pathway for antegrade conduction and the fast pathway for retrograde conduction (P simultaneous with QRS).

Electrophysiological studies with multiple drugs in patients with atrioventricular re-entrant tachycardias utilizing an extranodal pathway.

Eleven patients with recurrent paroxysmal tachycardia (PSVT) underwent electrophysiological studies. In each patient, initial study revealed re-entrant PSVT with antegrade conduction via the normal pathway and retrograde conduction via an extranodal pathway (Kent bundle). A temporary electrode catheter was left at the conclusion of initial study and PSVT induction was performed on subsequent days before and after the following intravenous drugs: ouabain 0.01 mg/kg (OU), propranolol 0.1 mg/kg (PRO), ouabain + propranolol (OU + PRO) and procainamide 750 mg (PA). In all patients, control studies prior to drug administration revealed the ability to induce sustained PSVT. In five patients, OU, PRO, or OU + PRO prevented induction of sustained PSVT by increasing atrioventricular (A-V) nodal refractoriness. In four of the patients, (including one of the above), PA prevented induction of sustained PSVT: in one, by increasing His-Purkinje refractoriness, and in three by increasing refractoriness in the Kent bundle. Oral drug therapy based upon the above studies (8 pts) prevented recurrent sustained PSVT for a mean follow-up period of 9 ± 5 months. In the remaining three patients, all drugs failed to prevent induction of sustained PSVT. These patients were either treated with radiofrequency pacemakers or surgery. In conclusion, drug responses in patients with recurrent PSVT utilizing a Kent bundle are variable. Antiarrhythmic drugs may interfere with circus movements at the A-V node, His-Purkinje system, or Kent bundle. Chronic oral drug therapy based upon responses to electrophysiological studies with multiple drugs prevents recurrent sustained PSVT over a short-term followup period.

The determinants of atrioventricular nodal re-entrance with premature atrial stimulation in patients with dual A-V nodal pathways.

In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (A.), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no A. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 ± 32 msec (mean ± SEM; 10 pts). In contrast, all 21 patients with A, had intact V-A conduction with mean VABCL of 382 ± 21 msec (14 pts) (P < 0.05). Repetitive re-entrance occurred only when A. conducted to the ventricles. Seven patients had only single A0. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 ± 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 ± 18 msec (8 pts) (P < 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block.Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other. PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 + 25 to 336 ± 17 (p>0.05).Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.

The significance of second degree atrioventricular block and bundle branch block. Observations regarding site and type of block

His bundle (H) electrograms were recorded in 15 patients with second degree atrioventricular (A-V) block and bundle branch block and these patients were prospectively followed. Site of block was proximal to H in four (BPH), distal to H in nine (BDH), and undetermined in two (studied during 1:1 conduction). Surface electrocardiographic features were retrospectively examined to determine the value of these recordings in predicting the site of block. Patients with type I block, with or without type II or 2:1 block, had BPH. Patients with type II block, 2:1 block, or type II combined with 2:1 block had BDH. Heart failure was more common in those with BPH (three of four patients as compared to three of nine patients with BDH). Syncope developed more commonly in patients with BDH (six of nine patients) as compared to those with BPH (one of four patients). Permanent pacing was indicated in three of four patients with BPH, nine of nine patients with BDH, and one of two patients with block at undetermined site because of syncope or heart failure. Five of nine patients with BDH required pacemakers within ten days of initial admission.Most patients with second degree A-V block and bundle branch block will need permanent pacing. In patients with 2° BDH, pacemakers are indicated whether or not symptoms are present because of high risk of syncope and potential risk of sudden death. In asymptomatic patients with 2° BPH, careful observation is indicated.

Prospective observations in patients with chronic bundle branch block and marked H-V prolongation.

Eighteen of 388 patients with chronic bundle branch block, studied electrophysiologically and followed prospectively, had H-V intervals of 80 msec or greater. Five patients were functional class 1, five class II, seven class III, and one class IV. Follow-up ranged from 103 to 1919 days (mean 711 ± 118). Three patients needed permanent pacing for the following indications: sino-atrial block, sinus bradycardia post-cardiac surgery, and 2° block distal to the His bundle. Six patients died, three suddenly, and three nonsudden. The five initially asymptomatic patients are alive and without pacemakers (mean follow-up 732 ± 139 days).Although marked H-V prolongation was associated with high morbidity and mortality in this small series, this was only in patients with symptomatic heart disease. Asymptomatic patients (five patients) had a benign clinical course. Prophylactic pacing would probably not modify clinical course in the former group, and is probably not indicated in the latter group. Longer follow-up will be needed for definitive prognosticatio.

Demonstration of dual atrioventricular nodal pathways utilizing a ventricular extrastimulus in patients with atrioventricular nodal re-entrant paroxysmal supraventricular tachycardia.

In patients with atrioventricular (A-V) nodal re-entrant paroxysmal supraventricular tachycardia (PSVT), atrial extrastimulus technique frequently reveals discontinuous A1-A2, H1-H2 curves suggestive of dual A-V nodal pathways. To further test the hypothesis that these curves in fact reflect dual A-V nodal pathways, a ventricular extrastimulus (Vs) was coupled either to A2 at a fixed A1-A2 interval which reliably produced an A-V nodal re-entrant atrial echo (E) with a constant A2-E interval in two patients, or to QRS complex (V) during sustained PSVT with a constant E-E interval in one patient. Three response zones were defined: at longer A2-Vs or V-Vs coupling intervals, Vs manifested no effect on the timing of E (Zone 1). At closer A2-Vs or V-Vs coupling interval, Vs conducted to the atrium, shortening the apparent A2-E or E-E interval (Zone 2). At shortest A2-Vs or V-Vs coupling interval, Vs was blocked retrogradely, and no E was induced (Zone 3). The ability of Vs to preempt control of the atria (Zone 2 response) strongly suggests the presence of dual A-V nodal pathways in these PSVT patients. If only a single pathway were present, Vs would of necessity collide with the antegrade impulse and could not reach the atria. The Zone 3 response occurs because of retrograde refractoriness of the fast pathway. Failure of the echo during Zone 3 probably reflects concealed conduction to the fast pathway, or possibly interference in the slow pathway.