Catheter ablation of clinical intraatrial reentrant tachycardias resulting from previous atrial surgery: localizing and transecting the critical isthmus.

OBJECTIVES: We sought to evaluate the efficacy of anatomically based radiofrequency catheter ablation for the treatment of intraatrial reentrant tachycardia in patients with previous atrial surgery. BACKGROUND: Intraatrial reentrant tachycardias, a common late complication of atrial surgery, are often refractory to standard medical management. Data from experimental animals and from humans indicate that anatomic barriers resulting from residual atrial scars provide a substrate for intraatrial reentry. We speculated that these tachycardias require a narrow isthmus of tissue between surgical scars and native nonconductive boundaries and that transection of this isthmus with radiofrequency ablation would therefore constitute an effective treatment. METHODS: Fourteen patients with a history of atrial surgery and clinical intraatrial reentrant tachycardia underwent electrophysiologic testing. From activation mapping, putative surgical scars and patches that served as boundaries of reentrant circuits were identified. Radiofrequency lesions were then placed to transect the narrowest isthmus of conducting tissue between a surgical scar and an anatomic barrier. Catheter ablation was attempted only for tachycardias consistent with the patient's clinical arrhythmias. RESULTS: Radiofrequency catheter ablation was attempted for 17 (55%) of 31 tachycardias identified; it successfully terminated tachycardias in 13 (93%) of 14 patients (95% confidence interval [CI] 79% to 99%). There were clinical recurrences in six patients (46%, 95% CI 19% to 73%), each of whom underwent a repeat ablation that was successful. Twelve (86%) of 14 patients (95% CI 67% to 99%) have remained free of intraatrial reentrant tachycardia for a mean of 7.5 +/- 5.3 months. CONCLUSIONS: Anatomically guided radiofrequency catheter ablation is an effective technique for definitive management of intraatrial reentrant tachycardia in patients with previous atrial surgery.

Unmasking of retrograde conduction by isoproterenol in a concealed accessory pathway.

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635-700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285-315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.

Pseudo-oversensing of the T wave by an implantable cardioverter defibrillator: a nonclinical problem.

Two patients are described who had pseudo-oversensing of T waves during follow-up testing of the Medtronic PCD. Each patient exhibited appropriate T wave sensing following closely coupled spontaneous QRS complexes to subthreshold stimuli without having T wave sensing following sensed or paced complexes. One patient also revealed T wave sensing following fusion beats. The occurrence of T wave sensing in these unique clinical situations was due to the auto-adjusting sensitivity threshold function used by the PCD. Recognition of this normal sensing function will prevent inappropriate reprogramming of the sensitivity or postpace refractory period, interventions that could potentially lead to ventricular tachyarrhythmia undersensing.

Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation.

BACKGROUND: Potential gradient field determination may be a helpful means of describing the effects of defibrillation shocks; however, potential gradient field requirements for defibrillation with different electrode configurations have not been established. METHODS AND RESULTS: To evaluate the field requirements for defibrillation, potential fields during defibrillation shocks and the following ventricular activations were recorded with 74 epicardial electrodes in 12 open-chest dogs with the use of a computerized mapping system. Shock electrodes (2.64 cm2) were attached to the lateral right atrium (R), lateral left ventricular base (L), and left ventricular apex (V). Four electrode configurations were tested: single shocks of 14-msec duration given to two single anode-single cathode configurations, R:V and L:V, and to one dual anode-single cathode configuration, (R+L):V; and sequential 7-msec shocks separated by 1 msec given to R:V and L:V (R:V----L:V). Defibrillation threshold (DFT) current was significantly lower for R:V----L:V than for the other configurations and markedly higher for L:V. Despite these differences, the minimum potential gradients measured at DFT were not significantly different (approximately 6-7 V/cm for each electrode configuration). Potential gradient fields generated by the electrode configurations were markedly uneven, with a 15-27-fold change from lowest to highest gradient, with the greatest decrease in gradient occurring near the shock electrodes. Although gradient fields varied with the electrode configuration, all configurations produced weak fields along the right ventricular base. Early sites of epicardial activation after all unsuccessful shocks occurred in areas in which the field was weak; 87% occurred at sites with gradients less than 15 V/cm. Ventricular tachycardia originating in high gradient areas near shock electrodes followed 11 of 67 successful shocks. CONCLUSIONS: These data suggest that 1) defibrillation fields created by small epicardial electrodes are very uneven; 2) achievement of a certain minimum potential gradient over both ventricles is necessary for ventricular defibrillation; 3) the difference in shock strengths required to achieve this minimum gradient over both ventricles may explain the differences in DFTs for various electrode configurations; and 4) high gradient areas in the uneven fields can induce ectopic activation after successful shocks.

Response of relatively refractory canine myocardium to monophasic and biphasic shocks.

BACKGROUND: Certain biphasic waveforms defibrillate at lower energies than monophasic waveforms, although the mechanism is unknown. METHODS AND RESULTS: The relative ability of monophasic and biphasic shocks to stimulate partially refractory myocardium was compared because defibrillation is thought to involve stimulating relatively refractory myocardial tissue. Shocks of 25-125 V were given during regularly paced rhythm in 11 open-chest dogs. Computerized recordings of shock potentials, and of activations before and after the shocks, were made at 117 epicardial sites. To quantify the shock field strength, the shock potential gradients were calculated at the electrode sites. Monophasic action potential (MAP) electrode recordings, obtained in five dogs, confirmed direct myocardial excitation by the shock, that is, activations beginning during the shock. Tissue was directly excited up to 4 cm from the shocking electrode, and the area directly excited increased as the shock was made stronger or given less prematurely. In six dogs, strength-interval curves for direct excitation were determined from plots of potential gradient versus refractoriness at each electrode site. The biphasic curves were located to the right of the monophasic curves by 8 +/- 4 msec, indicating a lesser ability to excite refractory myocardium. When the gradient at the directly excited border was at least 3.8 +/- 1 V/cm, conduction failed to propagate away from the directly excited zone after the shock, and MAP recordings made near the border showed a shock-induced graded response. This graded response, which prolonged repolarization, may have been responsible for the failure of conduction from the directly excited zone. Although better for defibrillating, the biphasic waveform was thus less effective than the monophasic one in exciting relatively refractory myocardium. CONCLUSIONS: These results indicated that waveform selection for defibrillation should not be guided solely by the ability of the waveform to stimulate tissue, as these two properties can be discordant.

Potential distribution in three-dimensional periodic myocardium--Part II: Application to extracellular stimulation.

Modeling potential distribution in the myocardium treated as a periodic structure implies that activation from high-current stimulation with extracellular electrodes is caused by the spatially oscillating components of the transmembrane potential. This hypothesis is tested by comparing the results of the model with experimental data. The conductivity, fiber orientation, the extent of the region, the location of the pacing site, and the stimulus strength determined from experiments are components of the model used to predict the distributions of potential, potential gradient, and the transmembrane potential throughout the region. Next, assuming that a specific value of the transmembrane potential is necessary and sufficient to activate fully repolarized myocardium, the model provides an analytical relation between large-scale field parameters, such as gradient and current density, and small-scale parameters, such as transmembrane potential. This relation is used to express the stimulation threshold in terms of gradient or current density components and to explain its dependence upon fiber orientation. The concept of stimulation threshold is generalized to three dimensions, and an excitability surface is constructed, which for cardiac muscle is approximately conical in shape. The numerical values of transmembrane potential and stimulation thresholds calculated using asymptotic analysis are in agreement with the results of animal experiments, confirming the validity of this approach to study the electrophysiology of periodic cardiac muscle.

Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium.

The hypothesis was tested that the field of a premature (S2) stimulus, interacting with relatively refractory tissue, can create unidirectional block and reentry in the absence of nonuniform dispersion of recovery. Simultaneous recordings from a small region of normal right ventricular (RV) myocardium were made from 117 to 120 transmural or epicardial electrodes in 14 dogs. S1 pacing from a row of electrodes on one side of the mapped area generated parallel activation isochrones followed by uniform parallel isorecovery lines. Cathodal S2 shocks of 25 to 250 V lasting 3 ms were delivered from a mesh electrode along one side of the mapped area to scan the recovery period, creating isogradient electric field lines perpendicular to the isorecovery lines. Circus reentry was created following S2 stimulation; initial conduction was distant from the S2 site and spread towards more refractory tissue. Reentry was clockwise for right S1 (near the septum) with top S2 (near the pulmonary valve) and for left S1 with bottom S2; and counterclockwise for right S1 with bottom S2 and left S1 with top S2. The center of the reentrant circuit for all S2 voltages and coupling intervals occurred at potential gradients of 5.1 +/- 0.6 V/cm (mean +/- standard deviation) and at preshock intervals 1 +/- 3 ms longer than refractory periods determined locally for a 2 mA stimulus. Thus, when S2 field strengths and tissue refractoriness are uniformally dispersed at an angle to each other, circus reentry occurs around a "critical point" where an S2 field of approximately 5 V/cm intersects tissue approximately at the end of its refractory period.

Transmural activations and stimulus potentials in three-dimensional anisotropic canine myocardium.

Epicardial and endocardial pacing are widely used, yet little is known about the three-dimensional distribution of potentials generated by the pacing stimulus or the spread of activation from these pacing sites. In six open-chest dogs, simultaneous recordings were made from 120 transmural electrodes in 40 plunge electrodes within a 35 X 20 X 5-mm portion of the right ventricular outflow tract during epicardial and endocardial pacing at a strength of twice diastolic threshold and at 1 mA. The magnitude of extracellular potentials generated by the stimulus and the activation times were compared in regions proximal (less than 10-12 mm) and distal to the pacing site. Local fiber orientation was histologically determined at each recording electrode. For endocardial pacing, endocardial potentials were larger than epicardial potentials only in the proximal region (p less than 0.001); while in the distal region, epicardial potentials were larger (p less than 0.001), and endocardial activation occurred earlier than epicardial activation for both regions (p less than 0.001). For epicardial pacing, epicardial potentials were larger than endocardial potentials in both regions (p less than 0.001), and epicardial activation occurred earlier only in the proximal region (p less than 0.02), while endocardial activation occurred before epicardial activation in the distal region (p less than 0.01). In planes of recording electrodes parallel to the epicardium and endocardium, the initial isochrones were elliptical with the major axes of the ellipses along the mean fiber orientation between the pacing site and recording plane rather than along the local fiber orientation in the recording plane. Thus, the ellipses in each plane rotated with respect to each other so that in three dimensions the activation front was helicoid, yet the twist of the helix was less than that of the corresponding transmural rotation of fibers. For pacing from the right ventricular outflow tract, we conclude that beyond 10-12 mm from endocardial and epicardial pacing sites epicardial stimulus potentials in both cases are larger than endocardial potentials because of resistivity differences inside and outside the heart wall and activation in both cases is primarily endocardial to epicardial because of rapid endocardial conduction, and we conclude that the initial spread of activation is helicoid and determined by transmural fiber direction.

Extracellular field required for excitation in three-dimensional anisotropic canine myocardium.

It is not known how well potential gradient, current density, and energy correlate with excitation by extracellular stimulation in the in situ heart. Additionally, the influence of fiber orientation and stimulus polarity on the extracellular thresholds for stimulation expressed in terms of these factors has not been assessed. To answer these questions for myocardium in electrical diastole, extracellular excitation thresholds were determined from measurements of stimulus potentials and activation patterns recorded from 120 transmural electrodes in a 35 X 20 X 5-mm region of the right ventricular outflow tract in six open-chest dogs. Extracellular potential gradients, current densities, energies, and their components longitudinal and transverse to the local fiber orientation at each recording site were calculated from the stimulus potentials produced by 3-msec constant-current stimuli. The resulting values in regions directly excited by the stimulus field were compared with the values in regions not directly excited but activated by the spread of wavefronts conducting away from the directly excited region. Magnitudes of 3.66 mA/cm2 for current density, 9.7 microJ/cm3 for energy, and 804 mV/cm for potential gradient yielded minimum misclassifications of 8%, 13%, and 17%, respectively, of sites directly and not directly excited. A linear bivariate combination of the longitudinal (l) and transverse (t) components of the potential gradient yielded 7% misclassification (threshold ratio t/l of 2.88), and linear combination of corresponding current density components yielded 8% misclassification (threshold ratio t/l of 1.04). Anodal and cathodal thresholds were not significantly different (p = 0.39). Potential gradient, current density, and energy strength-duration curves were constructed for pulse durations (D) of 0.2-20 msec. The best fit hyperbolic curve for current density magnitude (Jm) was Jm = 3.97/D + 3.15, where Jm is in mA/cm2, and D is in msec. Thus, for stimulation during electrical diastole 1) both current density magnitude and longitudinal and transverse components of the potential gradient are closely correlated with excitation, 2) the extracellular potential gradient along cardiac cells has a lower threshold than across cells, while current density thresholds along and across cells are similar, 3) anodal and cathodal thresholds are approximately equal for stimuli greater than or equal to 5 mA, and 4) the extracellular potential gradient, current density, and energy excitation thresholds can be expressed by strength-duration equations.

Mechanism of ventricular vulnerability to single premature stimuli in open-chest dogs.

To determine the mechanism of ventricular vulnerability to electrical stimulation, we simultaneously recorded from 120 transmural electrodes in a 35 X 20 X 5-mm portion of right ventricular infundibulum in seven dogs. Baseline pacing (S1) was performed from outside the mapped region followed by single premature stimulation (S2) of increasing strength at the center of the mapped region. In five of six episodes of ventricular fibrillation and 26 of 30 episodes of repetitive responses, complete reentrant pathways were observed. Earliest activation following S2 was not at the site of S2 stimulation but was at a point between the S1 and S2 sites of stimulation. Activation spread away from the early site toward the opposite side of the mapped region around the sides of an arc of block near the S2 site to form a "figure-of-eight." The activation fronts coalesced to activate the region around the S2 site last and, if the difference in times between activation at the early site and near the S2 site was large, reentered the tissue toward the S1 site. Ventricular refractory periods were determined in four dogs following S1 pacing; the regions with the greatest nonuniformity in the dispersion of refractoriness were not the regions of unidirectional block after S2 stimulation. Thus, 1) ventricular fibrillation and repetitive responses induced electrically with S1 and S2 stimuli at different ventricular sites arise by figure-of-eight reentry, 2) this reentry is caused by the ability of S2 stimulation both to prolong refractoriness near the S2 site and to initiate a propagated response in the region between the S1 and S2 sites, and 3) a nonuniform dispersion of refractoriness is not crucial for the electrical induction of reentry leading to ventricular fibrillation or repetitive responses when S1 and S2 stimuli are given at different locations on the right ventricular outflow tract.