Contrast echocardiography for cardiac radio-frequency ablation.

The authors presented a first application of 2-D contrast-enhanced ICE in localizing RF ablation lesions and, more importantly, accurately and reproducibly quantifying their extent and depth within the myocardium in the intact beating heart. Furthermore, the study extended this application and presented, for the first time, a novel method based on contrast-enhanced 3-D ICE to describe details of contiguous linear lesions.

Functional and clinical characterization of a mutation in KCNJ2 associated with Andersen-Tawil syndrome.

BACKGROUND: Andersen-Tawil syndrome (ATS) is a rare inherited disorder, characterised by periodic paralysis, cardiac dysarrhythmias, and dysmorphic features, and is caused by mutations in the gene KCNJ2, which encodes the inward rectifier potassium channel, Kir2.1. This study sought to analyse KCNJ2 in patients with familial ATS and to determine the functional characteristics of the mutated gene. METHODS AND RESULTS: We screened a family with inherited ATS for the mutation in KCNJ2, using direct DNA sequencing. A missense mutation (T75R) of Kir2.1, located in the highly conserved cytoplasmic N-terminal domain, was identified in three affected members of this family. Using the Xenopus oocyte expression system and whole cell voltage clamp analyses, we found that the T75R mutant was non-functional and possessed a strong dominant negative effect when co-expressed with the same amount of wild type Kir2.1. Transgenic (Tg) mice expressing the mutated form of Kir2.1 in the heart had prolonged QTc intervals compared with mice expressing the wild type protein. Ventricular tachyarrhythmias were observed in 5 of 14 T75R-Tg mice compared with 1 of 7 Wt-Tg and none of 6 non-transgenic littermates. In three of five T75R-Tg mice with ventricular tachycardia, their ECG disclosed bidirectional tachycardia as in our proband. CONCLUSIONS: The in vitro studies revealed that the T75R mutant of Kir2.1 had a strong dominant negative effect in the Xenopus oocyte expression system. It still preserved the ability to co-assemble and traffic to the cell membrane in mammalian cells. For in vivo studies, the T75R-Tg mice had bidirectional ventricular tachycardia after induction and longer QT intervals.

Global comparisons between contact and noncontact mapping techniques in the right atrium: role of cavitary probe size.

In the right atrium (RA) we globally investigated: (1) the properties of noncontact electrograms measured by multielectrode cavitary probes, (2) the features of endocardial electrograms computed from the noncontact probe electrograms, and (3) the impact of the probe size on both the noncontact and the computed electrograms. We deployed a custom catheter in the dog RA, which consisted of a cylindrical probe with 64 electrodes on its surface, for measuring noncontact cavitary electrograms, and a concentric endocardial basket carrying an additional array of 64 electrodes, for measuring contact endocardial electrograms (the "gold standard"). Both a 5-mm- and a 10-mm-diam probe (P5 and P10, respectively) were sequentially tested in the same RA of one dog. Unipolar electrograms from both the probe and the basket were simultaneously acquired during normal as well as during paced rhythms (n > or =24 protocols per probe). Boundary element method and numeric regularization were applied to compute endocardial electrograms at the basket electrode locations. We found that noncontact electrograms were attenuated and smoothed, and this effect was exaggerated with the small probe. Computed endocardial electrograms more accurately reconstructed important amplitude distribution and morphological features; peak-to-peak amplitude error, 35% for P5 and 34% for P10. Activation and spatial errors of computed endocardial electrograms were 8.8+/-6.8 ms and 5.1+/-6.1 mm for P5, respectively, and 6.0+/-5.5 ms and 3.2+/-4.4 mm for P10, respectively. In conclusion, global RA activation may be delineated directly from noncontact cavitary electrograms alone, but may be affected by volume attenuation, smoothing, and probe size. Accurate endocardial electrograms, however, can be successfully computed from noncontact electrograms acquired with small probes and be used to reconstruct both electrogram amplitude and detailed morphology.

Electrical conduits within the inferior atrial region exhibit preferential roles in interatrial activation.

Differences between conduction properties of interatrial conduits and their roles in initiation and maintenance of supraventricular arrhythmias remain unclear. Our objective was to determine details of interatrial activation in inferior atrial region and to correlate intra-atrial and interatrial activation patterns with the site of origin of atrial ectopic activation. In 9 dogs, basket-catheters carrying 64 electrodes were deployed into both the right atrium (RA) and left atrium (LA). A 10-electrode catheter was inserted into the coronary sinus (CS). Activation patterns of the RA, LA, and CS were compared during pacing in the CS, in RA inferoparaseptum posterior to Eustachian ridge-tendon of Todaro (TT), and in inferior RA near the CS ostium (anterior to TT). We found that pacing in proximal and middle CS resulted in a RA breakthrough invariably at the CS ostium, consistent with conduction through a CS-RA connection. Meanwhile, LA breakthrough emerged in inferoposterior region (inferior to mitral annulus), suggesting conduction through a CS-LA connection. While pacing in distal CS, LA breakthrough shifted to middle posterolateral wall. Whereas, the RA was activated by the LA directly through the septum. During pacing in RA inferoparaseptum posterior to TT, the LA was activated directly through the septum at 22 +/- 4 ms. Whereas, during pacing anterior to TT, the LA was activated through both the CS and the septum while earliest activation was delayed by 38 +/- 5 ms. In conclusion, both the interatrial septum and CS musculature form electrical conduits in inferior atrial region in canine. Differences in activation properties between the conduits in inferior interatrial region result in selective interatrial activation patterns during ectopic activation.

Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler.

OBJECTIVES: Our goal was to identify the hemodynamic determinants of the mitral annulus (MA) diastolic velocities by tissue Doppler. BACKGROUND: The MA diastolic velocities are promising indexes of left ventricular (LV) diastolic function. However, their hemodynamic determinants have not yet been evaluated. METHODS: Ten adult mongrel dogs underwent left atrial (LA) and LV pressure measurements by Millar catheters while tissue Doppler was applied to record the MA diastolic velocities at the septal and lateral comers. Conventional transmitral flow was also obtained. Left atrial and LV pressures were modified utilizing fluid administration and caval occlusion, whereas dobutamine and esmolol were used to change LV and LA relaxation. Left ventricular filling pressures were altered during different lusitropic states to evaluate for the possible interaction of preload and LV relaxation on the early diastolic velocity (Ea). RESULTS: In the majority of dogs, a positive significant relation was observed between Ea and the transmitral pressure gradient (r = 0.57, p = 0.04). The Ea had strong correlations with tau (r = -0.83, p < 0.001), LV -dP/dt (r = 0.8, p < 0.001) and minimal LV pressure (r = -0.76, p < 0.01). However, there was no relation between Ea and the transmitral pressure gradient in experimental stages where tau >50 ms. Furthermore, the late diastolic velocity at both corners of the MA had significant positive relations with LA dP/dt (r = 0.67, p < 0.01) and LA relaxation (r = 0.73, p < 0.01) but an inverse correlation with LV end-diastolic pressure (r = -0.53, p = 0.01). CONCLUSIONS: Left ventricular relaxation, minimal pressure and preload determine Ea while late diastolic velocity determinants include LA dP/dt, LA relaxation and LV end-diastolic pressure.

Activation effects of single-site and dual-site right atrial pacing in canine.

Medical therapy for managing atrial fibrillation remains less than satisfactory. Electrical therapy such as right atrial (RA) pacing was shown to reduce rate of recurrence of atrial fibrillation, while evidently dual-site pacing was more effective than single-site pacing. However, similarities and/or differences in the electrophysiological consequences of single-site and dual-site RA pacing are unclear. Our objective was to simultaneously map RA and left atrial (LA) activation patterns and compare intra-atrial and interatrial activation properties during single-site and dual-site RA pacing in the normal canine heart. Basket-shaped catheters carrying 64 electrodes were deployed under the guidance of fluoroscopy and echocardiography into both the RA and LA of 7 dogs. Basket unipolar electrograms were simultaneously recorded while pacing at high lateral RA (HRA) alone, at inferior RA septum (RAS) alone, and at both sites simultaneously. We found that pacing at HRA alone resulted in the longest interatrial conduction time (47+/-6 ms). Pacing at RAS alone significantly shortened interatrial conduction time (29+/-5 ms) and completely activated both the RA and LA simultaneously (70+/-6 ms and 69+/-8 ms, respectively). Dual-site pacing at HRA and RAS significantly abbreviated RA complete activation time (52+/-7 ms), but did not alter interatrial conduction time or LA activation pattern compared to pacing at RAS alone. In conclusion, single-site pacing at RAS shortened interatrial conduction time compared to HRA and completely activated both atria simultaneously in canines with normal atria. In addition to shortening interatrial conduction time, dual-site pacing at HRA and RAS abbreviated RA complete activation time.

Spatial regularization of the electrocardiographic inverse problem and its application to endocardial mapping.

Numeric regularization methods for solving the inverse problem of electrocardiography in realistic volume conductor models have been mostly limited to uniform regularization in the spatial domain. A method of spatial regularization (SR) was developed and tested in canine, where each spatial spectral component of the volume conductor model was considered separately, and a SR operator was selected based on explicit a posteriori criterion at each time instant through the heartbeat. The inverse problem was solved in the left ventricle by reconstructing endocardial surface electrograms based on cavitary electrograms measured with the use of a noncontact, multielectrode probe. The results were validated based on electrograms measured in situ at the same endocardial locations using an integrated, multielectrode basket-catheter. A probe-endocardium three-dimensional model was determined from multiplane fluoroscopic images. The boundary element method was applied to solve the boundary value problem and derive the relationship between endocardial and probe potentials. Endocardial electrograms were reconstructed during both normal and paced rhythms using SR as well as standard, uniform, zeroth-order Tikhonov (ZOT) regularization. Compared to endocardial electrograms measured by the basket, electrograms reconstructed using SR [relative error (RE) = 0.32, correlation coefficient (CC) = 0.97, activation error = 3.3 ms] were superior to electrograms reconstructed using ZOT regularization (RE = 0.59, CC = 0.79, activation error = 4.9 ms). Therefore, regularization based on spatial spectral components of the model improves the solution of the inverse problem of electrocardiography compared to uniform regularization.

Simultaneous multisite mapping of the right and the left atrial septum in the canine intact beating heart.

BACKGROUND: The spread of activation between the right atrium (RA) and left atrium (LA), particularly along the right and left aspects of the interatrial septum, is not clear. METHODS AND RESULTS: Basket-shaped catheters carrying 64 electrodes were deployed into both the RA and LA of 10 dogs. Position and orientation of the baskets were determined by fluoroscopy and echocardiography. Basket unipolar electrograms were simultaneously recorded in each dog during sinus rhythm, right ventricular pacing, and pacing of the right septum through the basket in the superior and inferior regions. Isochrone maps depicting all aspects of the atria, including the septum, were compared. During sinus rhythm and superior right septal pacing, wave fronts propagated predominantly from superior to inferior regions on both the right and left septum. However, activation of the left septum was delayed compared with the right septum. During right ventricular pacing and inferior right septal pacing, activation of the septum was discordant; 1 wave front propagated rapidly on the right septum from inferior to superior regions, whereas 2 opposing wave fronts originated on the left septum in both the superior and inferior regions. The left septum was activated predominantly by the superior wave front. Activation of the left septum was completed in a significantly shorter time during pacing of the right septum in the inferior region compared with the superior region. CONCLUSIONS: In dogs, activation of the right and left aspects of the interatrial septum is discordant. Electrical connections are present between the RA and LA in regions superior as well as inferior to the septum.

Electrophysiological imaging of the right atrium using a noncontact multielectrode cavitary probe: study of normal and abnormal rhythms.

Cavitary electrograms previously were measured from multiple directions simultaneously in the canine left ventricle with the use of noncontact multielectrode probes. The objective of the present study was to measure cavitary electrograms in the canine right atrium (RA) and describe the corresponding global activation sequences during normal and abnormal atrial rhythms. A 64-electrode custom probe was inserted into the RA of six dogs. Probe position and orientation were guided by fluoroscopy. Probe unipolar electrograms were acquired simultaneously during sinus rhythm, RA pacing, and ventricular pacing. Vagally mediated atrial fibrillation (AF) was induced in four dogs. Probe electrograms were acquired during AF induced at baseline and after intravenous infusion of ibutilide (0.075 mg/kg followed by 0.075 mg/kg infusion over 10 minutes). Isochrone maps were derived from noncontact probe electrograms and were displayed on a beat-by-beat basis during normal and paced rhythms. During AF, maps were displayed for 10 consecutive 100-ms windows. Isochrone maps of normal and paced beats revealed regions of early activation that were consistent with sites of wavefront initiation. During AF, multiple varying activation wavefronts were observed. At baseline, AF cycle length was 110 +/- 15 ms and the number of wavefronts was 1.72 +/- 0.25 per 100-ms window. After ibutilide, AF cycle increased to 182 +/- 36 ms (P = 0.018) and the number of wavefronts decreased to 0.82 +/- 0.14 per 100-ms window (P = 0.009). In conclusion, global electrophysiological imaging with a noncontact multielectrode probe delineates RA anatomy. Furthermore, images of AF activation depict multiple wandering wavefronts. Ibutilide reduces the number of these wavefronts and organizes AF.

Three-dimensional electrophysiological imaging of the intact canine left ventricle using a noncontact multielectrode cavitary probe: study of sinus, paced, and spontaneous premature beats.

BACKGROUND: The feasibility of measuring cavitary electrograms using a noncontact probe and reconstructing endocardial surface electrograms and activation sequences during paced beats was previously demonstrated in the isolated canine left ventricle (LV). The objective of the present study was to develop and test a high-resolution, three-dimensional, endocardial electrophysiological imaging technique that simultaneously reconstructs endocardial surface electrograms and their corresponding activation sequences during normal and abnormal beats with the use of cavitary electrograms measured with a noncontact multielectrode probe in the intact canine LV. METHODS AND RESULTS: A 128-electrode probe was inserted into the intact canine LV. Probe unipolar electrograms were simultaneously acquired during sinus, artificially paced, and spontaneous premature beats. Representative endocardial electrograms were measured directly using eight needle electrodes (the "gold standard"). A probe-cavity realistic, three-dimensional geometric model was constructed using two-dimensional epicardial echocardiography. Boundary element methods and numeric regularization were used to compute electrograms at 194 sites on the endocardium. In eight pacing protocols, computed endocardial electrograms correlated well with directly measured electrograms (r=.88). Corresponding activation times were also in agreement with those determined from measured endocardial electrograms (activation error, 4.7 ms). The earliest region of activation was invariably in the vicinity of the pacing needle (spatial error, 9.2 mm). Subsequently, the site of origin of ischemia-induced spontaneous ventricular premature beats and the ensuing sequence of depolarization was identified. CONCLUSIONS: Noncontact mapping provides realistic, three-dimensional electrophysiological images of the endocardium, on a beat-by-beat basis, that localize the sites of origin of premature beats and reconstruct their activation sequences.

Noncontact endocardial mapping: reconstruction of electrograms and isochrones from intracavitary probe potentials.

INTRODUCTION: Mapping endocardial activation and repolarization processes is critical to the study of arrhythmias and selection of therapeutic procedures. Previously, we developed methodology for reconstructing endocardial potentials from potentials measured with a noncontact, intracavitary probe. This study further develops and evaluates the ability of the approach to provide detailed information on the spatiotemporal characteristics of the activation process. Specifically, we reconstructed endocardial electrograms and isochrones throughout the activation process over the entire endocardium during a single beat. METHODS AND RESULTS: Cavity potentials were measured with a 65-electrode probe placed inside an isolated canine left ventricle. Endocardial potentials were measured simultaneously using 52 electrodes. Potentials were acquired during subendocardial pacing from different locations. Computed electrograms at various sites closely resemble the measured electrograms (correlation coefficient > 0.9 at 60% of the electrodes). Computed isochrones locate subendocardial pacing sites with 10-mm accuracy. Two pacing sites, 17 mm apart, were resolved. Critical regions, such as areas of isochrone crowding, were accurately reconstructed. CONCLUSIONS: Results indicate the applicability of the approach to mapping the cardiac excitation process on a beat-by-beat basis without occluding the ventricle. The ability of locating electrical events (e.g., single or multiple initiation sites) is demonstrated. Importantly, the method is shown to be capable of reconstructing electrograms over the entire endocardium and determining nonuniformities of activation spread (e.g., areas of slow conduction). These capabilities are important to clinical application in the electrophysiology laboratory and experimental studies of arrhythmias in the intact animal.

Pharmacologic enhancement of atrial electrical defibrillation efficacy: role of ibutilide.

The study was designed to identify the influence of ibutilide on activation during atrial fibrillation (AF) and determine its role in enhancing the efficacy of electrical conversion of AF. Vagally-mediated acute AF was induced in 12 anesthetized dogs. In 5 dogs, a cross-shaped epicardial patch containing 16 recording electrodes was placed on the right atrium. In 7 dogs, defibrillation patch electrodes overlying both atria were used to deliver biphasic shocks (50% tilt; 90 microF). Measurements were made at baseline and following ibutilide (0.075 mg/kg bolus followed by 0.075 mg/kg infusion over 10 minutes). Right atrial multisite electrogram recordings revealed significant prolongation in AF cycle length at all sites following ibutilide. In all dogs, AF cycle length increased with ibutilide from 90 +/- 23 to 130 +/- 49 ms (p < 0.005). Whereas, atrial defibrillation threshold decreased from 0.83 +/- 0.5 to 0.53 +/- 0.29 J (p = 0.020). In conclusion, ibutilide prolongs cycle length of canine vagally-mediated acute AF. Furthermore, ibutilide facilitates electrical conversion of AF by lowering energy requirement. Thus, controlled drug infusion in conjunction with electrical defibrillation may be useful for managing AF.

Role of proximal electrode position in transvenous ventricular defibrillation.

Transvenous defibrillation lead systems have been demonstrated to reduce operative morbidity and mortality associated with implantation of cardioverter-defibrillators. To determine the best position for the proximal electrode in transvenous systems, defibrillation thresholds were compared for three positions in a single-pathway, two-lead system. Two defibrillation lead electrodes were transvenously inserted into seven dogs. The distal electrode was positioned in the right ventricular apex. The proximal electrode was randomized to one of three positions: (1) the superior (cranial) vena cava (SVC) at the junction of the right atrium, (2) the left innominate vein at the junction of the SVC, or (3) the external jugular vein. Biphasic defibrillation thresholds for converting electrically induced ventricular fibrillation were determined for the three positions of the proximal electrode in each dog. The innominate vein position resulted in the lowest defibrillation threshold (555 +/- 123 V) as compared to the SVC (640 +/- 126 V; p = 0.0612) and the jugular vein (709 +/- 117 V; p = 0.0013). Lead impedance gradually increased with increasing distance between the two shocking electrodes: 58.4 +/- 11.4 omega for SVC, 76.2 +/- 13.8 omega for innominate vein, and 94.9 +/- 10.2 omega for jugular vein proximal lead electrode position (p < 0.05 for all pairwise comparisons). In two-electrode transvenous defibrillation lead systems, positioning the proximal electrode in the left innominate vein produced the lowest defibrillation threshold.

Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity.

OBJECTIVES: This study assessed the useful role of intracardiac mapping and radiofrequency catheter ablation in eliminating drug-refractory monomorphic ventricular ectopic beats in severely symptomatic patients. BACKGROUND: Ventricular ectopic activity is commonly encountered in clinical practice. Usually, it is not associated with life-threatening consequences in the absence of significant structural heart disease. However, frequent ventricular ectopic beats can be extremely symptomatic and even incapacitating in some patients. Currently, reassurance and pharmacologic therapy are the mainstays of treatment. There has been little information on the use of catheter ablation in such patients. METHODS: Ten patients with frequent and severely symptomatic monomorphic ventricular ectopic beats were selected from three tertiary care centers. The mean frequency +/- SD of ventricular ectopic activity was 1,065 +/- 631 beats/h (range 280 to 2,094) as documented by baseline 24-h ambulatory electrocardiographic (ECG) monitoring. No other spontaneous arrhythmias were documented. These patients had previously been unable to tolerate or had been unsuccessfully treated with a mean of 5 +/- 3 antiarrhythmic drugs. The site of origin of ventricular ectopic activity was accurately mapped by using earliest endocardial activation time during ectopic activity or pace mapping, or both. RESULTS: During electrophysiologic study, no patient had inducible ventricular tachycardia. The ectopic focus was located in the right ventricular outflow tract in nine patients and in the left ventricular posteroseptal region in one patient. Frequent ventricular ectopic beats were successfully eliminated by catheter-delivered radiofrequency energy in all 10 patients. The mean number of radiofrequency applications was 2.6 +/- 1.3 (range 1 to 5). No complications were encountered. During a mean follow-up period of 10 +/- 4 months, no patient had a recurrence of symptomatic ectopic activity, and 24-h ambulatory ECG monitoring showed that the frequency of ventricular ectopic activity was 0 beat/h in seven patients, 1 beat/h in two patients and 2 beats/h in one patient. CONCLUSIONS: Radiofrequency catheter ablation can be successfully used to eliminate monomorphic ventricular ectopic activity. It may therefore be a reasonable alternative for the treatment of severely symptomatic, drug-resistant monomorphic ventricular ectopic activity in patients without significant structural heart disease.

Reconstruction of endocardial potentials and activation sequences from intracavitary probe measurements. Localization of pacing sites and effects of myocardial structure.

BACKGROUND: Mapping of endocardial activation is an important procedure for diagnosing cardiac arrhythmias and locating the arrhythmogenic site before treatment. The objective of the present study was to develop and test a mathematical method to reconstruct the endocardial potentials and activation sequences (isochrones) from potential data measured with a noncontact, intracavitary multielectrode probe (the "inverse problem"). METHODS AND RESULTS: A boundary element based mathematical method, combined with a numeric regularization technique, was developed for computing the inverse solution. Endocardial potentials were computed from intracavitary potentials measured with a multielectrode probe placed in the cavity of an isolated, perfused canine left ventricle. Data were acquired during rhythms induced by electrical stimuli applied at different locations and varying depths within the myocardium. Endocardial potentials were measured using intramural needles to evaluate the accuracy of the inverse solutions by direct comparison. Inversely computed endocardial potentials, from measured probe potentials, reconstruct with good accuracy the major features (potential maxima and minima, regions of negative and positive potentials) compared with the measured endocardial potentials. During early activation, the computed endocardial potentials exhibit a potential minimum in close proximity to the pacing site, determining the location of the stimulus with good accuracy (within 10-mm error). Multiple stimuli, as close as 10 to 20 mm to each other, can be distinguished and localized to their sites of origin by the inverse reconstruction. Similar to the measured endocardial potentials, the spatial distribution of the computed endocardial potentials reflects the underlying cardiac fiber direction, and dynamic changes of the computed endocardial potentials reflect the rotation of fibers with intramural depth. Maps of isochrones show good correspondence between the isochrones determined from the computed endocardial potentials and those determined directly from the measured endocardial potentials. CONCLUSIONS: Compared with actual, measured endocardial potentials and activation sequences, endocardial potential patterns and activation sequences can be reconstructed on a beat-by-beat basis from cavitary potentials measured with a multielectrode, noncontact probe. The approach presented here is shown to reconstruct, with 10-mm accuracy and resolution of 10 to 20 mm, local events of cardiac excitation (eg, pacing sites). In addition, the reconstructed endocardial potentials correctly reflect the underlying fibrous structure of the myocardium. These results demonstrate the feasibility of the approach. In the experiments, the probe position and endocardial geometry were determined invasively. To be clinically applicable, the reconstruction method should be combined with a noninvasive method for determining the probe-cavity geometry in the catheterization laboratory. It could then be developed into a catheter-based technique for locating arrhythmogenic sites and for studying and diagnosing conduction abnormalities, reentrant activity, and the effects of drugs and other interventions on cardiac activation and arrhythmias.

Effects of internal defibrillation on an implanted pacing system with programmable polarity.

Management of multiple cardiac arrhythmias in some patients with both an implantable cardioverter defibrillator (ICD) and a pacemaker has demonstrated several advantages. In such circumstances, it is imperative that pacemaker function and its programmed parameters be preserved following a defibrillation shock. This article describes the effects encountered by a specific programmable polarity pacemaker (RelayR 294-03) when subjected to electrical defibrillation in a canine model. Three pacemakers were repeatedly tested in three separate dog experiments. Each pacemaker, with its leads implanted in the right atrium and the right ventricle, was subjected to a minimum total number of 24 high energy biphasic and monophasic shocks (600-700 V) delivered by a coexisting ICD system using three different defibrillating lead configurations. None of the pacemaker systems showed any failure in function; all pacemakers continued to function within preshock specification and conversion to unipolar pacing and/or backup mode was not observed in any of the tests. Intracardiac electrical potentials measured directly off the ICD and the pacemaker leads, during a defibrillation shock (mean 566.6 V; 23.7 J), showed that potentials measured in a bipolar configuration (tip-ring: mean 21.0 V in atrium, 12.0 V in ventricle) were significantly less than potentials measured in a unipolar configuration (tip-can: mean 387.9 V in atrium, 394.0 V in ventricle; ring-can: mean 405.6 V in atrium, 395.4 V in ventricle). Our compatibility tests demonstrate that use of this programmable-polarity pacemaker in concert with an ICD system appears to be safe. Testing similar to the present study should be conducted prior to complete clinical acceptance of combined ICD and pacemaker implantation.

A model study of volume conductor effects on endocardial and intracavitary potentials.

An idealized mathematical model was developed to study the effects of variations in conductive and geometric parameters on measured endocardial and intracavitary potentials. The model consists of a spherical multielectrode probe located eccentrically within a system of concentric spheres that represent a blood cavity, myocardium, lung region, and surface muscle layer. Solutions were found for endocardial and intracavitary probe potentials produced by two different configurations of equivalent myocardial sources: 1) multiple activation wave fronts oriented radially, representing global fronts in the myocardium; and 2) pairs of equal and opposite dipoles on a line oriented tangentially to the endocardial surface, representing cardiac sources during early ectopic activation. It was found that the complexities of the cardiac source configurations are reflected in the endocardial potential but not in the associated probe potential, which exhibits a smoothed-out, low-amplitude distribution. In addition, probe potential depends on probe size and location within the cavity. Furthermore, endocardial and probe potentials are influenced by variations in the conductivity of different regions; an increase in blood conductivity results in a decrease in both endocardial and probe potential magnitudes produced by either type of cardiac sources, and an increase in myocardial conductivity results in an increase in both potential magnitudes, whereas an increase in lung conductivity results in an increase in the magnitude of the potential produced by radial sources but a small decrease in the magnitude of the potential produced by tangential sources. The effects of variations in skeletal muscle conductivity are negligible. The volume conductor effects of myocardial anisotropy (9:1 anisotropy ratio) are to attenuate both endocardial and probe potentials by as much as 60% and 71%, respectively, for radial sources and by 96% and 85%, respectively, for tangential sources. In conclusion, volume conductor influences should be considered in the interpretation of measured cavity potentials. Multiple myocardial events are resolved in endocardial potentials but not in potentials measured by an intracavitary multielectrode probe. This observation indicates that for the purpose of resolving cardiac activity, efforts should be directed at inverse reconstruction of endocardial potentials from potentials measured with an intracavitary probe.

Tachycardia control with cardiac pacemakers.

Techniques used to treat tachyarrhythmias with brief electrical impulses are described. The disease process is described, identifying the prevention of one of the three conditions required for reentry (which provides the mechanism for most electrically convertible rhythms) as the basis for therapy. The risk of inducing fibrillation is discussed. The four major pacing techniques used to treat tachycardia are described. The first technique involves using additional pacemaker pulses to establish the appropriate conditions permitting interruption of the tachycardia. The second technique, which permits adaptation to the variations in tachycardia characteristics, is scanning. Scanning changes the intervals on successive bursts in an interactive process, allowing a series of paced intervals to be tested. The third technique is usually called an adaptive or automatic technique. The final technique is ramp pacing, which allows extrastimuli to be introduced at progressively premature intervals within a burst of stimuli.

Tachycardia recognition algorithms for implantable systems.

The detection algorithm of current antitachycardia pacing systems incorporates derivatives of heart rate as the only objective parameter used for recognition. Present pacing systems use one or more rate-related parameters: (1) rate cutoff, (2) sudden onset, (3) rate stability, and (4) sustained high rate. Recently, the development of antitachycardia systems has focused on combining the four detection criteria to form multiple recognition algorithms. Nevertheless, inability to differentiate between supraventricular and ventricular tachycardias at compatible rates remains a limitation. Incorporating atrial sensing capability, in addition to ventricular sensing capability, an alternative strategy that potentially could enhance diagnostic accuracy, is discussed. The incorporation of time and frequency analysis, arterial pressure, and stroke volume are also examined.