Ramesh C. Dhingra

Demonstration of Dual A-V Nodal Pathways in Patients with Paroxysmal Supraventricular Tachycardia

Electrophysiological evidence suggestive of dual atrioventricular (A-V) nodal pathways is presented in two patients with normal P-R interval and reentrant paroxysmal supraventricular tachycardia (PSVT). His bundle recordings and atrial stimulation were used to obtain this electrophysiological evidence.Refractory periods were measured with the atrial extra-stimulus technique. Plotting of H1-H2 responses against A1-A2 coupling intervals revealed that as A1-A2 decreased, H1-H2 decreased appropriately. At a critical A1-A2, a sudden marked increase in H1-H2 occurred, suggesting failure of fast pathway, (defining the fast pathway effective refractory period ERP). Further shortening of A1-A2 defined a second H1-H2 curve. The longest A1-A2 with no H2 response was defined as the slow pathway ERP. Echo zones coincided with A1-A2 intervals equal to or less than the fast pathway ERP.These results provide the first electrophysiological demonstration of dual A-V nodal pathways in patients with normal P-R interval and PSVT, as manifest by dual A-V nodal conduction times and refractory periods. Antegrade failure of the fast pathway with subsequent availability for retrograde conduction could allow A-V nodal reentry. These findings provide a basis for reentrance in some patients with reentrant PSVT.

Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined in 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia. In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.

The Effects of Cycle Length on Cardiac Refractory Periods in Man

The effects of pacing-induced changes in cycle length on the refractory periods of the atrium, A-V node and His-Purkinje system were studied in 24 patients using the extra stimulus technique. Refractory period determinations were made at two or more cycle lengths in all patients. Slopes relating cycle length and refractory periods were calculated using the least squares method.Both the effective and functional refractory periods (ERP and FRP) of the atrium shortened with decreasing cycle lengths, with a mean slope of +0.155 and +0.129 respectively. A-V nodal ERP lengthened (mean slope, −0.177) while A-V nodal FRP shortened slightly (mean slope, +0.126). Bundle branch refractory periods as well as relative refractory periods of the His-Purkinje system also decreased, with mean slopes of +0.270 and +0.360, respectively. The ERP of the A-V node at any cycle length was related to the A-H at that cycle length (r = +0.646, P < 0.001).The responses of the human heart to changes in cycle length are generally similar to those previously described in the animal laboratory. Such information contributes to our understanding of electrocardiographic phenomena such as aberrant conduction.

Dual atrioventricular nodal pathways. A common electrophysiological response.

Evidence of dual atrioventricular nodal pathwats (a sudden jump in H1-H2 at critical A1-A2 coupling intervals) was shown in 41 out of 397 patients studied with atrial extrastimulus techniques. In 27 of these 41, dual pathways were demonstrable during sinus rhythm, or at a cycle length close to sinus rhythm (CL1). In the remaining 14, dual pathways were only demonstrated at a shorter cycle length (CL2). All patients with dual pathways at cycle length who were also tested at cycle length (11 patients) had dual pathways demonstrable at both cycle lengths. In these 11 patients both fast and slow pathway effective refractory periods increased with decrease in cycle length. Twenth-two of the patients (54%) had either an aetiological factor strongly associated with atrioventricular nodal dysfunction or one or more abnormalities suggesting depressed atrioventricular nodal function. Dvaluation of fast pathway properties suggested that this pathway was intranodal. Seventeen of the patients had previously documented paroxysmal supraventricular tachycardia (group 1). Eight patients had recurrent palpitation without documented paroxysmal supraventricular tachycardia (group 2), and 16 patients had neither palpitation nor paroxysmal supraventricular tachycardia (group 3). Echo zones were demonstrated in 15 patients (88%) in group 1, no patients in group 2, and 2 patients (13%) in group 3.

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.

Significance of the HV interval in 517 patients with chronic bifascicular block.

In January 1975, we reported results of a prospective follow-up study (mean 538 +/- 42 days) of 119 patients with chronic bifascicular block (BFB), and concluded that BFB patients with normal and prolonged HV (NHV and PHV) had a similar incidence of atrioventricular (AV) block and mortality. In this report, we update these findings in 517 patients with a follow-up of 21 days to 9.8 years (mean 3.4 +/- 0.2 years). Three hundred nineteen patients (61%) had NHV and 198 (39%) had PHV (greater than 55 msec). The NHV and PHV groups were similar in regard to age (NHV vs PHV, 61 +/- 1 vs 62 +/- 1 years) and sex (80% male, 20% female vs 82% male and 18% female). The following were more common (p less than 0.05) in patients with PHV (percent of patients with finding in NHV vs PHV groups): angina (18% vs 27%), congestive failure (27% vs 42%), cardiomegaly (48% vs 66%), New York Heart Association functional class II-IV (34% vs 56%), premature ventricular complexes (20% vs 29%), and organic heart disease (OHD) (75% vs...

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).

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.

The Effects of Propranolol on Induction of A-V Nodal Reentrant Paroxysmal Tachycardia

Twelve patients with paroxysmal supraventricular tachycardia (PSVT) were studied before and after administration of 0.1 mg/kg i.v. propranolol. Echo zones for inducing atrioventricular (A-V) nodal reentry were determined using His bundle recording and the atrial extrastimulus technique. After propranolol the echo zone was abolished in two patients, decreased in one, unchanged in five, increased in two. In two patients echo zones appeared only after propranolol. Nine patients had episodes of sustained PSVT prior to propranolol. Following propranolol PSVT persisted in only five. In these five patients propranolol slowed the rate of PSVT.The data were analyzed by plotting A1-A2 and H1-H2 interval curves. On the basis of these curves the patients were separated into those with “dual pathways’ and those with “reflection.’ The effects of propranolol on both conduction patterns are discussed.In summary, the actions of propranolol in PSVT patients were variable. Potentially beneficial effects included slowing of induced PSVT, loss of the ability to sustain PSVT, and decrease or total elimination of echo zones. Potentially deleterious effects included potentiation of the echo phenomenon with either increase or development of echo zones.