Spontaneous changes in ventricular tachycardia cycle length and their relation to earliest sites of epicardial activation in a canine model.

BACKGROUND: The purpose of this study was to examine the spontaneous changes in cycle length during episodes of sustained monomorphic (MVT) and polymorphic (PVT) ventricular tachycardias and to relate these changes with the earliest epicardial activation site of the beat. METHODS: Isochronal activation maps were obtained from 127 unipolar electrograms recorded from the surface of both ventricles with a sock electrode array in 24 open chest anesthetized dogs. After atrioventricular block, the left anterior descending coronary artery was occluded for 60 min under ventricular pacing (140/min), followed by reperfusion. In 7 dogs the left stellate ganglion was stimulated 5 min after reperfusion. RESULTS: In 7 MVTs (reperfusion) and 4 PVTs (sympathetic stimulation), cycle length changes showed an initial acceleration, reaching a minimum cycle length and then decelerating before termination. Isochronal maps showed radial spread from earliest activation, without conduction block. Cycle length (481 +/- 80 msec) in MVT had beat to beat variations of 15 +/- 17 msec corresponding to small shifts in sites of the earliest activation, clustered along the border of the ischemic myocardium. In PVTs the cycle length (352 +/- 90 msec, p < 0.01) had a variability of 62 +/- 23 msec, corresponding to wide changes in the sites of earliest activation in right and left ventricles. Linear regression analysis showed a strong and significant correlation between cycle length variability and the number of electrodes with the earliest activation (r = 0.77, p < 0.0001). CONCLUSION: In these models of monomorphic and polymorphic ventricular tachycardias, cycle length variability showed a significant correlation with the number of electrodes with the earliest activation. MVTs showed concentrated origins with regular cycle length, whereas PVTs showed dispersed origins with irregular cycle length. These results suggest that the earliest epicardial activation site of the beat could be a factor in determining the dynamics in the cycle length.

Cycle length dynamics at the onset of postinfarction ventricular tachycardias induced in canines: dependence on interval-dependent excitation properties of the reentrant substrate.

INTRODUCTION: Postinfarction monomorphic ventricular tachycardias induced by programmed stimulation may display initial cycle length (CL) variations before stabilizing. METHODS AND RESULTS: To show that tachycardia onset dynamics depend on rate-dependent electrical properties of the reentrant substrate, we extracted activation times and maximum negative slopes of local activation complexes (-dV/dt(max)) from 191 unipolar electrograms recorded in the anterior left ventricular wall of anesthetized, 3-day-old infarct canine preparations. Measurements were made of the responses to programmed stimulation, as well as in early and later beats of tachycardias, which displayed either a constant trend in CL (group A, n = 5 preparations) or one in which CL prolongation occurred according to an exponential course before stabilizing (group B, n = 9). Stimulation protocols inducing the tachycardias were more aggressive and their CL was significantly shorter (CL = 159 +/- 24 msec) in group A than in group B (stabilized CL = 206 +/- 34 msec). Reentrant activity occurred in subepicardial areas in which the absolute value of -dV/dt(max) (absolute value(-dV/dtmax)) was heterogeneously depressed (<2 mV/msec). Absolute value(-dV/dtmax) was reduced and activation delay increased in the successive responses to extrastimuli. Further reductions in absolute value(-dV/dtmax) (10% to 23%) were shown to occur between early and later beats in 5 of the 9 tachycardias in group B (no change in the 4 others), and they were associated with localized prolongation of conduction times in reentrant pathways. In contrast, absolute value(-dV/dtmax) improved in all group A tachycardias (7% to 25%). CONCLUSION: This study provides evidence that the onset dynamics of postinfarction ventricular tachycardias are determined by interval-dependent electrical changes occurring in the reentrant substrate.

Cycle length dynamics and spatial stability at the onset of postinfarction monomorphic ventricular tachycardias induced in patients and canine preparations.

BACKGROUND: The aim of this study was to determine whether cycle length (CL) variations at the onset of monomorphic ventricular tachycardias follow distinctive patterns. METHODS AND RESULTS: We retrospectively analyzed 59 monomorphic ventricular tachycardias induced in 40 patients in whom intraoperative mapping was performed with 63 epicardial and 64 endocardial electrograms recorded simultaneously. Activation times and CL were determined at each electrode site over several beats (36+/-10 beats, mean+/-SD) starting with the first after programmed stimulation. In the majority of the tachycardias, CL variations were accounted for by fitting to an exponential function: CL=CLs+Ae-b/tau, where CLs is the stable CL, b is beat number, tau is the time constant (in beat number), and A is the magnitude of CL relaxation. A decelerating trend (with reference to rate) (negative A) accounted for 21 tachycardias, an accelerating trend in rate (positive A) accounted for 12 tachycardias, and 4 others displayed a double dynamic behavior, with an initial acceleration followed by a decelerating trend in rate. Among the ventricular tachycardias that were not fitted to exponential models, 12 showed a constant trend and 10 others showed irregular CL fluctuations. The monomorphic character of the tachycardias was established by principal-component analysis, which also indicated that CL dynamics associated with the accelerating and decelerating trends may be related to shortening and prolongation of activation times, respectively, occurring in equal proportion at all recording sites. In canine preparations in which reentry circuits could be mapped with high resolution, CL showed an accelerating trend in rate when circus movement of excitation occurred around a transmural scar in muscle generating unipolar electrograms with relatively high -dV/dtmax, and a decelerating trend in rate occurred when functional reentry occurred in muscle generating unipolar electrograms with depressed -dV/dtmax. CONCLUSIONS: Beat-to-beat CL variations may occur at the onset of sustained monomorphic ventricular tachycardia as a result of uniform acceleration or deceleration of activation times while the overall activation pattern remains constant. The associated initial trends in the rate of sustained monomorphic ventricular tachycardia follow typical patterns that might provide "signatures" corresponding to reentry substrates with distinctive functional properties.

Electrode polarity does not alter the initial ventricular activation sequence during pacing with extracardiac electrodes.

Ventricular epicardial mapping was performed in six closed-chest anesthetized dogs to investigate the cardiac electrical response to external pacing. A right thoracotomy was performed, complete AV block was produced by formaldehyde injected into the AV node and a sock electrode array, comprised of 127 unipolar electrodes, was placed over the ventricles. Isopotential and isochronal epicardial maps were generated by computer from the unipolar electrograms. Unipolar stimulation pulses were applied between pairs of different types of cutaneous (metal, carbon) and esophageal (metal) electrodes, and recordings were performed at maximum lung inflation. Isopotential maps recorded during the stimulation artifacts showed that the epicardial electrical field was little affected by the type of electrode but depended mostly on electrode position. A reproducible and relatively uniform apex-to-base potential gradient was regularly produced with anteroposterior and anteroesophageal electrode configurations. This uniform potential gradient induced ventricular activation sequences that showed interindividual differences. Thus, for each dog, the areas of initial activation observed on the isochronal maps during pacing tended to remain the same (i.e., apical, lateral, and anterior) despite changes in the stimulation protocol. Inverting the polarity of the electrodes did not appreciably change the site of origin of activation (81% remained the same) and activation never originated from the area showing the most negative potential during the stimulation artifact. In conclusion, since electrode polarity does not seem to alter the ventricular activation sequence during cardiac pacing with extracardiac electrodes, the standard nomenclature for cutaneous patches, which defines the negative electrode as the "active" electrode, may have to be revised.

Body surface potential distributions during idiopathic ventricular tachycardia.

BACKGROUND: The purpose of this report is to describe the body surface potential maps (BSPMs) during idiopathic ventricular tachycardia (VT) and to determine what differences exist between different idiopathic VT morphologies. METHODS AND RESULTS: We performed BSPMs during VT on 12 consecutive patients (3 women and 9 men; mean age, 42 +/- 13 years) presenting symptomatic idiopathic VT referred to our institution for electrophysiological study. Basal ECG, chest radiograph, and echocardiogram were normal in all patients. Clinical tachycardia showed left bundle branch block pattern (LBBB) in 9 patients, with sustained VT in 5 and nonsustained VT in 4, and right bundle branch block pattern (RBBB) in 3 with sustained VT. We found a unique pattern of BSPMs in each of the 9 patients during idiopathic LBBB VT configuration, whether sustained or nonsustained VT. This pattern appeared at the onset of the QRS and remained stable during the whole QRS complex. The area of minimal potential located in the upper anterior part of the torso was compatible with an origin of VT in the right ventricular outflow tract, as confirmed in 5 patients by successful radiofrequency ablation. We found an evolving pattern with two phases in each of the three RBBB VTs. The electrical axis during the initial part of the QRS could correspond to an endocardial-epicardial vector. The second phase, with a high voltage and area of minimal potential located in the inferior and anterior part of the torso, was compatible with a left ventricular apical origin that was confirmed by epicardial and endocardial mapping during cryosurgery in 1 patient. For all the VTs, the QRS isoarea maps showed the same pattern as the second phase of the QRS. CONCLUSIONS: Two different BSPM patterns were found. All LBBB VTs had the same stable pattern corresponding to an infundibular origin. All RBBB VTs had an evolving pattern that stabilized in the second part of the QRS complex corresponding to an apical origin.

Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle.

OBJECTIVE: Anisotropic conduction characteristics, which may be expressed as the ratio of conduction velocities in the longitudinal (Vlong) and transverse (Vtrans) fibre directions, have been shown to stabilise reentry and favour the induction of sustained, uniform ventricular tachycardia. The aim of this study was to investigate whether interventions affecting either excitability (lignocaine) or both excitability and cell coupling (hypercalcaemia) might produce differential effects on the Vlong/Vtrans ratio, and whether an intervention reducing this ratio might prevent the induction of sustained reentrant ventricular tachycardia. METHODS: The effects of hypercalcaemia [8.2(SD 3.8) mmol.litre-1] and lignocaine infusion [to 24.4(19) and 42.3(29) mumol.litre-1] on Vlong and Vtrans were determined from 127 electrograms recorded with a plaque electrode on the anterior left ventricular wall of healthy dogs or 3 d after occlusion of the left anterior descending coronary artery. Vlong and Vtrans were computed from isochronal maps displaying ellipsoid patterns with a long axis corresponding to longitudinal conduction and a short axis corresponding to transverse conduction, as determined during basic (S1) and premature (S2) stimulation from the centre of the plaque electrode. Infarcted heart preparations were subjected to programmed stimulation for induction of reentrant ventricular tachycardias. RESULTS: Hypercalcaemia reduced both Vlong and Vtrans (P < 0.05) but did not modify either the Vlong/Vtrans ratio or the induction and patterns of ventricular tachycardias. Lignocaine reduced Vlong and the Vlong/Vtrans ratio during premature stimulation (S2) of infarcted heart preparations (P < 0.05) and stabilised reentrant ventricular tachycardias in preparations in which only nonsustained, multiform ventricular tachycardias were induced under control conditions. CONCLUSIONS: Conduction velocities in the longitudinal and transverse directions can be differentially affected by selected pharmacological interventions, but the Vlong/Vtrans ratio is not a representative index of the facilitating influence of tissue anisotropy on reentry. Therefore, the role of anisotropy in this model of reentry is not confined to establishing disparity of a functional character between conduction velocities in the longitudinal and transverse directions.

Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction.

We measured the conduction characteristics at the epicardial surface of the left anterior ventricular wall in the in situ canine heart before and 3 to 5 days (n = 9 dogs) after permanent occlusion of the left anterior descending coronary artery (LAD). During ventricular stimulation generating wavefronts conducted along the longitudinal or the transverse fiber direction, 61 unipolar electrograms were recorded with a fine-meshed plaque electrode. Before occlusion, the fastest conduction velocity was consistently found in a direction perpendicular to the nearby LAD segment (longitudinal direction), and the slowest velocity in a direction parallel to the LAD segment (transverse fiber direction). In 3- to 5-day-old infarct preparations, a layer of subepicardial muscle with 1 to 3 mm thickness survived over necrotic tissue. The velocities and directions of fast and of slow conduction measured in ischemic subepicardial muscle were not significantly different from preocclusion values during stimulation at a basic rate, but excitability was found to be depressed in response to premature stimuli. Premature impulses initiated in nonischemic myocardium and conducted into ischemic tissue in the longitudinal or in the transverse directions induced sustained (greater than 100 beats) monomorphic tachycardias during which figure-eight activation patterns were mapped with sock-array electrodes. During these tachycardias, the direction of the common reentrant wavefront of the figure-eight pattern was preferentially oriented along the longitudinal fiber direction, independently of the direction of the initiating impulse. When polymorphic beats were induced, tachycardia terminated spontaneously within 20 beats, or changed to a monomorphic pattern, as described above. In conclusion, the anisotropic organization of surviving subepicardial muscle overlying an infarct provides a spatial constraint that determines a preferential direction of reentrant propagation and may contribute to sustaining monomorphic tachycardia.