Josephson Clinical Cardiac Electrophysiology


■ Josephson’s Clinical Cardiac Electrophysiology

delayed afterdepolarizations and abnormal automaticity are the mechanisms. The automatic rhythms are difficult to treat pharmacologically and require large doses of antiarrhythmic agents, but on occasion must be ablated. We have encountered seven patients in the absence of digitalis, two of whom re quired ablation, in one of whom conduction was maintained. All of those due to triggered activity postsurgery disappeared after weeks on antiarrhythmic agents. Hamdan and cowork ers reported a series of 11 patients with junctional tachycardia ablation. In nine patients, ablation targeted the site of earliest atrial activation; one of nine had heart block (earliest atrial ac tivation was in the mid-septal region). In two other patients without V-A conduction, empiric lesions were given to either the posteroseptal or anteroseptal region. In all, ablation was successful in 10 of 11 patients and complicated by heart block requiring pacing in one. 39 In this series, there was no attempt to localize the site of origin within the “junction”; it is conceiv able that this strategy would be superior for arrhythmias origi nating from the A-V node, whereas a His bundle focus would be much more difficult to approach. FASCICULAR DEPOLARIZATIONS Automatic or triggered foci in the fascicles of the proximal spe cialized conduction system can give rise to premature impulses or escape rhythms similar to those resulting from such foci in the His bundle. 40 These rhythms may be manifested by wide QRS morphologies, or they may produce concealed conduc tion analogous to His bundle depolarizations (see Chapter 5). The diagnosis of fascicular rhythms relies on the ability to re cord His bundle deflections before or just within the ventricu lar electrogram. The recorded His bundle deflection results from retrograde His bundle depolarization, and its position relative to ventricular depolarization depends on the relative antegrade and retrograde conduction times from the site of impulse formation. If a His bundle spike appears before the QRS complex during a fascicular depolarization, by defini tion, it must have a shorter H-V interval than a sinus impulse ( Figure 6.18 ). If the His bundle is activated before ventricular activation, retrograde conduction of the impulse is faster than antegrade conduction. Most investigators have inferred that such a finding means that the origin of the impulse is closer to the His bundle than to the ventricles; however, their inference assumes that antegrade and retrograde conduction velocities are equal, an assumption that has not been validated in most cases. 41,42 It, therefore, only means that retrograde conduction to the His bundle occurs earlier than antegrade conduction to the ventricles. Retrograde His bundle deflections are seen in approxi mately 85% of patients during ventricular pacing when 5-mm interelectrode distances are used (see Chapter 1). Typically, the His deflection is recorded as a stimulus-to- retrograde His (S-H) interval that is typically 10 msec greater than the antegrade H-V interval. The use of para-Hisian pacing facilitates recording of a His bundle after the QRS. In my experience, ventricular stimulation from multiple sites
















in either ventricle has never resulted in an S-H interval less than the H-V interval (see Chapter 1). An unquantifiable amount of time is required to reach the His-Purkinje sys tem from the ventricular site of origin of a paced ventricular complex; the same would be true for spontaneous impulses arising from ventricular myocardial cells with abnormal automaticity or triggered activity. Thus, indirect evidence suggests that retrograde conduction to the His bundle is no faster than antegrade conduction. One, therefore, probably can safely assume that, in a normal heart, the impulse has a fascicular origin if the His bundle deflection occurs within 20 msec after the onset of ventricular activity. Certainly, the recording of a “retrograde” His potential before the QRS suggests an origin quite proximal in the fascicle. In general, fascicular rhythms or premature depolarizations that have short H-V intervals are narrower and show greater similarity to the sinus complex than do those with His bundle deflec tions inscribed just within the QRS complex ( Figures 6.19 and 6.20 ). Rhythms arising at the junction of the Purkinje fibers and ventricular myocardium will have a His inscribed within the QRS and will look more like a ventricular prema ture depolarization (VPD). In cases where there is proximal conduction delay or block in the left bundle branch, a retro grade His will be buried in the QRS or seen after the QRS due to retrograde conduction over the RBB ( Figure 6.21 ). Fas cicular rhythms from all three fascicles theoretically can be observed. An RBB origin produces a left bundle branch block morphology, whereas origins from the anterior and posterior divisions of the left bundle branch produce an RBB block. FIGURE 6.18 Premature fascicular depolarization with more rapid ret rograde than antegrade conduction. The sinus complex (first impulse) manifests a right bundle branch block pattern with right axis deviation The H-V of the sinus beats is 80 msec. A premature complex (second impulse) with a morphology very similar to that of sinus rhythm arises from the left anterior-superior fascicle. A retrograde His bundle deflec tion (H) appears 20 msec before local ventricular depolarization and at the onset of the surface QRS. Thus, retrograde conduction from the site of impulse formation through the fascicles to the His bundle was faster than antegrade conduction to ventricular myocardium. This phenomenon results in a pattern of ventricular activation similar to that during sinus rhythm. See text for further discussion. CS, coronary sinus; HBE, His bundle electrogram; HRA, high right atrium; T, time lines.

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