C Wyndham

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.

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

SUMMARYTwenty-one of 496 (4%) patients with chronic bifascicular block, studied and followed prospectively, had block distal to the His bundle (BDH) induced by atrial pacing during initial electrophysiologic studies. In six, BDH was noted during pacing-induced atrioventricular (AV) nodal Wenckebach periods (at paced rates of 150–190 beats/min), with BDH in the short HH cycles after the AV nodal blocked P (long cycle). The AH interval was normal in all six patients and HV was normal in four. None of the six patients has developed AV block during a mean follow-up of 5.33 ± 0.48 years.In 15 patients, pacing-induced BDH was noted during intact AV nodal conduction (paced rate of 80–200 beats/min). The AH interval was prolonged in one, and HV was prolonged in 10 of the 15 patients. During a mean follow-up of 3.4 ± 0.59 years, seven of these patients developed AV block, one had treadmill-provoked AV block, and two died suddenly (major morbid event in 10 of 15 patients).In conclusion, BDH induced by atrial pacing is an infrequent finding in patients with bifascicular block, and can be a functional as well as a pathologic response. The latter is associated with a high risk of major morbid events (AV block and sudden death).

Successful surgical excision of focal paroxysmal atrial tachycardia. Observations in vivo and in vitro.

A 41-year-old man had chronic, recurrent, drug-resistant paroxysmal right atrial tachycardia. Electrophysiologic studies revealed features suggesting atrial reentrance, including induction and termination of tachycardia with rapid atrial pacing and atrial extrastimuli. Endocardial catheter mapping localized the origin of tachycardia to the right atrial appendage. Intraoperative epicardial mapping refined the localization to the posterolateral rim of the appendage. The appendage was excised and the tachycardia was permanently cured. Microelectrode studies on the excised tissue revealed an inducible rhythm localized to a small area of the atrial endocardium, characterized by rapid pacing induction, rhythmicity generated from a suprathreshold afterdepolarization, low maximum diastolic potential, low overshoot potential and a smooth transition from phase 4 to phase 0, suggesting triggered automaticity. This is the first observation in man of probable triggerable atrial automaticity, which may be a direct counterpart of the clinical arrhythmia. The successful surgical outcome indicates that a focal atrial tachycardia can be excised in selected patients.

Natural history of chronic second-degree atrioventricular nodal block.

This report details our experience with documented chronic second-degree atrioventricular (AV) nodal block (proximal to His [H]) in 56 patients. Forty-six men (82%) and 10 women (18%), ages 18–87 years, were studied. Nineteen of the patients (34%) had no organic heart disease (including seven trained athletes) and 37 (66%) had organic heart disease. ECGs in all patients demonstrated episodes of type I seconddegree block; five patients also had periods of 2:1 block. Prospective follow-up of patients with no organic heart disease (157–2280 days, mean 1395 636 days) revealed one patient with clear indication for permanent pacing because of bradyarrhythmic symptoms (permanently placed on day 220 of follow-up). Two patients died nonsuddenly.In patients with organic heart disease (prospective follow-up of 60–2950 days, mean 1347 ± 825 days), pacemakers were implanted in 10 patients, primarily for treatment of congestive heart failure in eight and syncope in two. Sixteen patients died three suddenly, seven with congestive heart failure, two of an acute myocardial infarction and four of causes unrelated to cardiac disease.In summary, chronic second-degree AV nodal block has a relatively benign course in patients without organic heart disease. In patients with organic heart disease, prognosis is poor and related to the severity of underlying heart disease.

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.

Incidence and site of atrioventricular block in patients with chronic bifascicular block.

Four hundred fifty-two patients with chronic bifascicular block and initially intact atrioventricular (AV) conduction were detected, studied, and prospectively followed between January 1970 and March 1978. There were 360 males and 92 females, ages 18--93 years (mean +/- SD, 62 +/- 15 years). Follow-up ranged from 29-2804 days (mean 1066 +/- 97 days). AV block (2 degrees or 3 degrees) developed in 29 patients, nine with apparent cause and spontaneously in 20. Cumulative annual incidence of all heart block for 1--5 years was, respectively, 4%, 5.9%, 8.7%, 10.1% and 11.3%, and for spontaneous block was 2%, 3.1%, 5.2%, 6.7%, and 7.1%. Sites of spontaneous block were probably or definitely AV nodal in ten, His bundle in one, and trifascicular in nine. Cumulative incidence of AV block in surviving bifascicular block patients is 11% at 5 years, with 7% reflecting spontaneous block. The probable or definite site of AV block varies and is trifascicular in less than half of the patients. The small incidence of trifascicular block probably explains the difficulty in predicting this complication with electrophysiological studies.

Eectrophysiological observations in pateints with rate dependent bundle branch block.

Electrophysiological studies were conducted in 15 patients with tachycardic rate dependent bundle branch block (RDBBB): ten with left, and five with right. No bradycardic RDBBB was observed, despite occurrence of cycle lengths (CL) longer than 1200 msec in over half the patients studied. Onset of RDBBB was abrupt in 13 patients, and gradual in two. In three patients, the CL allowing reversion to normal conduction (once RDBBB was initiated) was 50, 55, and 190 msec longer, respectively, than the CL inducing RDBBB. Bundle brance refractory periods (RP) were measured with atrial extrastimulus technique in five patients. All RP (except one) were prolonged at all tested CL when compared to patients without conduction disease. The expected decrease in RP with shortening of CL did not occur in four of the five patients. The electrophysiological abnormality in patients with DBBB thus appeared to be an increase in refractoriness in the affected bundle branch, along with a loss of the normal decrease in refractoriness with decrease in CL. Similar findings might be demonstrable in patients with early bundle branch disease.

Significance of chronic bifascicular block without apparent organic heart disease.

Eighty-six of 452 patients (19%) with chronic bifascicular block were found to have no clinically apparent associated organic heart disease (OHD) and were defined as having primary conduction disease (PCD). Comparison of patients with PCD and OHD revealed a significantly lower incidence of the following clinical variables in the PCD patients (p less than 0.001): exertional angina, dyspnea, congestive heart failure, cardiomegaly, functional class I (all by study design), left bundle branch block and premature ventricular contractions. Both mean AH and HV intervals were significantly shorter in patients with PCD (p less than 0.01). The incidence of HV prolongation was 21% in PCD and 41% in OHD patients (p less than 0.001). All patients were prospectively followed for 21-2998 days with a mean +/- SEM of 1209 +/- 66 days for PCD and 1172 +/- 36 days for OHD. Atrioventricular (AV) block developed in three patients from the PCD group and 26 from the OHD group (NS), with spontaneous block occurring in one (1%) PCD patient and 19 (5%) OHD patients (p less than 0.05). Annual mortality due to sudden death as well as total cardiovascular mortality (including sudden death) for the 5-year follow-up was significantly lower in patients with PCD. Patients with PCD have significantly lower incidence of electrophysiologic abnormalities and subsequent spontaneous AV block as well as cardiovascular and sudden death mortality. The diagnosis of PCD based on clinical criteria probably underestimates the presence of underlying OHD, as suggested by a small but definite risk of cardiovascular mortality.

Participation of fast and slow A-V nodal pathways in tachycardias complicating the Wolff-Parkinson-White syndrome. Report of a case.

Electrophysiological studies in one patient with type B pre-excitation and dual A-V nodal pathway revealed several types of paroxysmal narrow QRS tachycardia (PSVT). One type of PSVT reflected antegrade fast A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retorgrade activation of right atrial appendage, P following QRS and cycle length of 290 to 350 msec. A second PSVT reflected antegrade slow A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retrograde activation of right atrial appendage, P following QRS, and cycle length of 440 msec. A third PSVT reflected A-V nodal re-entrance with antegrade slow pathway and retrograde fast pathway conduction. This PSVT was characterized by normal retrograde atrial activation sequences, P simultaneous with QRS, and cycle length of 320 msec. All PSVT inductions could be explained in terms of antegrade and retrograde properties of fast and slow A-V nodal and anomalous pathways.

Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the lown-ganong-levine syndrome☆

Sixty-five patients with dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia were studied. Of these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals in the 65 patients demonstrated continuous unimodal functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not significant). The cycle length of paroxysmal tachycardia did not differ between the 11 patients with a short P-R interval (370 +/- 20 ms) and the 54 patients without a short P-R interval (382 +/- 11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p less than 0.001). The cycle length of dual pathway A-V nodal reentrant paroxysmal tachycardia is a function of the slow pathway A-H interval and not the P-R or A-H interval during sinus rhythm. Identification of short P-R intervals in patients with A-V nodal reentrant paroxysmal tachycardia has little significance.