Antidromic tachycardia utilizing decremental, latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia

Objectives. We studied two patients with latent, decremental atrioventricular (AV) fibers in whom pre-excitation could be demonstrated only during wide complex tachycardia. Background. The presence of decremental AV fibers participating in antidromic AV reentrant tachycardia is usually suspected by the presence of pre-excitation either in sinus rhythm or during atrial pacing. Methods. Two patients were referred for evaluation and treatment of wide complex tachycardia whose configuration suggested ventricular tachycardia that could be terminated with adenosine infusion. They underwent standard electrophysiologic studies. Results. Baseline AH and HV intervals were normal. No pre-excitation was noted with atrial overdrive at multiple sites or during atrial extrastimulation. Retrograde conduction was present with a sequence compatible with AV node conduction. Sustained wide complex tachycardia was induced with ventricular overdrive pacing. Late atrial premature depolarizations during tachycardia pre-excited the subsequent ventricular activation. Earlier atrial premature depolarizations delayed the subsequent ventricular activation. In one patient, early atrial premature depolarizations terminated the tachycardia without activating the ventricle. In the other patient, spontaneous tachycardia termination was accompanied by ventriculoatrial block. The earliest ventricular activation was at the annulus in the posteroseptal region in one patient and at the left posterior region in the other. Atrioventricular node reentry and atrial tachycardia with by-stander AV fibers were also excluded. These findings establish the diagnosis of antidromic AV reentrant tachycardia utilizing a slow, decrementally conducting AV pathway. Conclusions. This is the first report describing the presence of latent, decremental accessory AV pathways in which conduction was manifest only during antidromic AV reentrant tachycardia. To differentiate these wide complex tachycardias from adenosine-sensitive ventricular tachycardia, we recommend that atrial premature depolarizations be applied during tachycardia to rule out the presence of a latent, decremental AV fiber even in patients who do not otherwise have pre-excitation with atrial pacing techniques

Effect of Increased Drive-train Stimulus Intensity on Dispersion of Ventricular Refractoriness

Background Most studies evaluating the effects of high-intensity drive-train (S 1 ) stimulation on the measurement of the ventricular effective refractory period (VERP) demonstrated a shortening of the VERP. Because this effect may be due to the local release of catecholamines, VERP shortening would be expected to occur only near the site of stimulation. Local shortening in the VERP should then result in an increased dispersion of refractoriness during high-intensity drive-train stimulation. Thus, this study evaluated the spatial distribution of the VERP shortening resulting from high-intensity S 1 stimulation and its effect on dispersion of refractoriness. Methods and Results Three groups of patients were studied. In group 1, 10 subjects without structural heart disease had VERP determinations performed at the right ventricular apex (RVA) and outflow tract (RVOT) while the S 1 site was changed to evaluate the effects of low-intensity S 1 stimulation on the measured VERP. In group 2, the effect of high-intensity S 1 stimulation on the VERP was studied 0, 7, 14, and 21 mm away from the S 1 site to measure the spatial distribution of VERP shortening and the effect on dispersion of refractoriness; 10 additional subjects without structural heart disease made up group 2. Because increased dispersion of refractoriness may be deleterious in certain clinical situations, the effect of high-intensity S 1 stimulation was studied in group 3, which comprised 10 subjects with chronically implanted transvenous defibrillators; noninvasive measurements of the VERP through the chronic lead were made while the S 1 stimulus intensity was varied from low to high intensity. All VERP determinations were performed during continuous pacing by use of an incremental method and a low stimulus intensity for the extrastimulus. In group 1, the RVA VERPs were 218±9 and 214±10 ms when the S 1 site was the RVA and RVOT, respectively ( P =NS). The RVOT VERPs were also unchanged when the S 1 site was changed from the RVOT to the RVA. In group 2, high-intensity S 1 changed the VERP from 224±8 (at twice the threshold) to 203±10 ms ( P <.01), 220±11 to 209±12 ms ( P <.01), 222±12 to 221±12 ms, and 220±11 to 221±11 ms at 0, 7, 14, and 21 mm away from the S 1 site, respectively. High-intensity S 1 stimulation led to an increase in the dispersion of refractoriness from 13±4 to 22±9 ms ( P =.006). In group 3, high-intensity S 1 stimulation shortened the VERP from 309±23 to 285±30 ms ( P =.0003). Conclusions Low-intensity S 1 stimulation has no significant effect on the VERP. High-intensity S 1 stimulation shortens the refractory period maximally at the site of stimulation; the VERP shortening dissipates between 7 and 14 mm away from the site of S 1 stimulation, resulting in an increased dispersion of refractoriness. The local VERP shortening with high-intensity stimulation is noted in patients with chronically implanted defibrillator leads, which may have implications for the mechanism of proarrhythmia during high-intensity stimulation

Atrial and accessory pathway activation direction in patients with orthodromic supraventricular tachycardia: Insights from vector mapping

Objectives. The purpose of this study was to utilize vector mapping to investigate atrial and accessory pathway activation direction during orthodromic supraventricular tachycardia. Background. Although advances have been made in the electrophysiologic evaluation and management of accessory pathways, our understanding of accessory pathway anatomy and physiology remains incomplete. Vector mapping has been validated as a method of studying local myocardial activation. Methods. In 28 patients with a left-sided or posteroseptal accessory atrioventricular (AV) pathway referred for ablation, atrial and accessory AV pathway activation direction was determined during ventricular pacing or orthodromic supraventricular tachycardia, or both, by summing three orthogonally oriented bipolar electrograms recorded from the coronary sinus to create three-dimensional vector loops. Atrial and accessory AV pathway activation direction was determined in all patients from the maximal amplitude vectors of the vector loops. Because of beat to beat variability in the directions of the vector loops, data from 8 of 28 patients could not be analyzed. Results. At 81 of 83 sites, atrial activation direction along the long axis of the coronary sinus corresponded with the direction suggested by activation time mapping. Activation direction along the anteroposterior and inferosuperior axes was variable, potentially due to variations in the level of the atrial insertion of the accessory AV pathway and in the depth or angling of pathway fibers in the AV fat pad. In eight patients, at least one recording was obtained at the site of an accessory AV pathway potential. Accessory AV pathway activation proceeded superiorly and to the right in seven of eight patients; in one patient with a posteroseptal pathway, accessory AV pathway activation proceeded superiorly and to the left. Conclusions. 1) Vector mapping is a useful technique for localizing accessory AV pathways; 2) left-sided accessory AV pathways angle from left to right as they traverse the AV groove; and 3) variable activation directions of the atrial myocardium adjacent to the coronary sinus suggest that accessory AV pathway insertion into the atrium differs from patient to patient

Electrical Activation During Ventricular Fibrillation in the Subacute and Chronic Phases of Healing Canine Myocardial Infarction

Background Little information is available regarding the effects of myocardial infarction on the characteristics of ventricular fibrillation (VF). Epicardial activation during VF can be characterized by the cycle length and by the characteristics of activation wave fronts. Methods and Results VF was induced by programmed stimulation in 6 dogs with subacute healing (1 week) myocardial infarction (MI), 5 dogs with chronic (8 week) healing MI, and 6 dogs without MI. Using a plaque electrode array with a 2.5-mm interelectrode distance, 112 electrograms were recorded and 91 vector loops were created for each cycle of VF from either the anterior (infarcted) or lateral (noninfarcted) wall. Direction of maximum epicardial activation was determined at each site for the first 10 cycles of VF (early) and for 10 cycles after 5 seconds of VF (late). Wave front size was determined based on a similarity in epicardial activation directions within a given area and by a statistical analysis that determined the degree of spatial linking at varying distances over the recording plaque. VF cycle length was defined as the mean interval of 10 consecutive local activation times. Differences among groups and differences between the anterior and posterolateral walls were determined by ANOVA. The mean wave front area was significantly larger in the presence of subacute MI (97±4 mm 2 , early; 78±3 mm 2 , late) or chronic MI (94±5 mm 2 , early; 78±5 mm 2 , late) than in noninfarcted animals (73±5 mm 2 , early; 61±3 mm 2 , late). The degree of linking of epicardial activation directions was similar in the three groups at distances of 2.5 and 5.0 mm but was lower at a distance of 7.5 mm among animals without infarction, confirming a smaller wave front size and suggesting less organization of activation. VF cycle length was significantly longer in the presence of infarction (98±5 ms, normal control animals; 121±13 ms, subacute MI; 127±13 ms, chronic MI). VF cycle length was significantly longer over the anterior than the lateral wall in the presence of subacute MI (131±8 ms, anterior; 109±5 ms, lateral) or chronic MI (136±9 ms, anterior; 119±6 ms, lateral) but not in noninfarcted animals (99±5 ms, anterior; 97±5 ms, lateral). The prolongation of VF cycle length among animals with infarction was associated with slower estimated conduction velocities during VF. Conclusions During VF, in animals with subacute or chronic healing MI, (1) the size of activation wave fronts is larger, (2) the cycle length of VF is longer, (3) the conduction velocities are slower, and (4) the degree of organization is greater than in control animals. Thus, the characteristics of VF throughout the heart are altered by the presence of regional myocardial infarction. The implications of these findings for the initiation and maintenance of VF in the presence of different underlying myocardial substrates require further study