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Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated.

Although the antiarrhythmic aspect of amiodarone has been extensively studied, its effects on His-Purkinje system conduction and refractoriness have not been systematically investigated in human beings. In 24 patients, anterograde His-Purkinje system conduction (HV intervals) and variables of His-Purkinje system refractoriness using the ventricular extrastimulus (V2) technique were analyzed before and after long-term therapy with amiodarone. The mean duration of amiodarone therapy at the time of repeat study was 16.2 ± 7.7 weeks (range 11 to 42). The anterograde His-Purkinje system conduction time (HV interval) measured 49.6 ± 9.5 ms (range 40 to 80) before and 60.6 ± 10.7 ms (range 45 to 90) after amiodarone (p < 0.005). During retrograde refractory period studies, the longest V2V2interval at which a retrograde His bundle potential (H2) emerged from the V2electrogram (relative refractory period of the His-Purkinje system) was consistently longer after amiodarone as compared with the control period (376.4 ± 46.6 versus 318.8 ± 33.1 ms, p < 0.005). Similarly, the shortest and longest His-Purkinje system conduction times (V2H2interval) at comparable V2V2intervals were uniformly and significantly prolonged after administration of the drug. Amiodarone also abolished macroreentry in the His-Purkinje system in six of the nine patients who showed such reentry during the control period. The effective refractory period of the ventricular myocardium was also increased from a mean of 227.1 ± 13.9 to 259.2 ± 20.2 ms (p < 0.005) in this series of patients.

A pacing model was designed that simulated “endless loop tachycardia,” a complication found in the new generation of DDD (atrioventricular [AV] universal) pacemakers. The functional characteristics of the train of ventricular impulses simulating endless loop tachycardia were studied during both AV sequential pacing and basic ventricular drive. AV sequential pacing, by causing a decrease in ventriculoatrial (VA) conduction time of the first beat of the endless loop tachycardia, was associated with a decrease in the cycle length at which VA block occurred in 9 of 12 patients. The site of block was the His-Purkinje system in 4 of these 12 patients and the AV node in the remaining 8. At a cycle length with 1:1 VA conduction, a steady state VA conduction time was achieved in 2 to 4 beats (VA conduction time accommodation). The pattern of such accommodation depended on the site (His-Purkinje system versus AV node) of the maximal conduction delay. The steady state VA conduction time itself was altered with AV sequential pacing in patients showing His-Purkinje system delay, but not in patients with AV nodal delay.

Candidates for the dual chamber “universal” (DDD) pacemaker are frequently tested for the presence of intact ventriculoatrial (VA) conduction to identify those at risk for developing endless loop tachycardia. However, recent reports have cited instances where clinical endless loop tachycardia has occurred even when no VA conduction could be demonstrated during ventricular pacing. A pacing protocol was designed to assess the effect of atrioventricular (AV) sequential pacing on VA conduction in 13 patients who showed no evidence of VA conduction during routine electrophysiologic testing. The absence of VA conduction was inferred by pacing the ventricle at several cycle lengths without obtaining a retrograde atrial capture. With the AV sequential method, which consisted of an AV sequential drive with a programmed AV interval of 100 to 160 ms, the presence or absence of VA conduction was tested utilizing a premature ventricular stimulus (V2) over a wide range of coupling intervals. During the AV sequential method, the V2effectively propagated to the atria in S of 13 patients with V2A2intervals ranging from 200 to 460 ms (mean 304 ± 97).

The effect of improved conduction in areas of delay was tested during macro-reentry within the His-Purkinje system, in an attempt to separate the role of conduction delay from that of prematurity of the extrastimulus as the key determinant of reentry. Using the right ventricular extrastimulus technique (S1S2method), both the critical His-Purkinje system delays and the zone of S1S2intervals causing His-Purkinje system reentry were determined. Then, using a previously described technique of atrioventricular (AV) sequential pacing during the basic drive, the potential site of His-Purkinje system conduction delay was (anterogradely) excited earlier (preexcitation), as compared with the control S1S2method. This produced a decrease in retrograde His-Purkinje system delay (S2H2), as compared with the same S1S2interval during the control method. Changing the degree of pre-excitation at each S1S2interval allowed for determination of the critical (or shortest) S2H2delay necessary for His-Purkinje system reentry at each coupling interval. Of importance was the observation that the critical delay was not specific for each case but varied with the prematurity of S2. For example, the critical S2H2delay required for reentry was actually less at shorter S1S2intervals as compared with longer S1S2intervals (from 206 ± 25 to 187 ± 20 ms, p < 0.01).

Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.

The electrophysiologic effects of intravenous verapamil (0.15 ml/kg) on retrograde atrioventricular (AV) nodal conduction were studied in 17 patients who had no evidence of supraventricular reentrant tachycardia, demonstrable dual AV nodal refractory period curves or accessory pathways. Using the His bundle electrogram, incremental ventricular pacing and the ventricular ex-trastimulus (V2) technique, the ventriculoatrial (VA), retrograde His-Purkinje system (V2H2) and AV nodal conduction (H2A2) times were measured before and after treatment with verapamil.