Noncontact mapping of the left ventricle: insights from validation with transmural contact mapping

It is not clear whether the noncontact electrograms obtained using the EnSite system in the left ventricle resemble most closely endocardial, intramural, or epicardial contact electrograms or a summation of transmural electrograms. This study compared unipolar virtual electrograms from the EnSite system with unipolar contact electrograms from transmural plunge needle electrodes using a 256-channel mapping system. The study also evaluated the effects of differing activation sites (endocardial, intramural, or epicardial). A grid of 50-60 plunge needles was positioned in the left ventricles of eight male sheep. Each needle had four electrodes to record from the endocardium, two intramural sites, and the epicardium. Correlations between contact and noncontact electrograms were calculated on 32,242 electrograms. Noncontact electrograms correlated equally well in morphology and accuracy of timing with endocardial (0.88 +/- 0.15), intramural (0.87 +/- 0.15), epicardial (0.88 +/- 0.15), and transmural summation contact electrograms (0.89 +/- 0.14) during sinus rhythm, endocardial pacing, and epicardial pacing. There was a nonlinear relationship between noncontact electrogram accuracy as measured by correlation with the contact electrogram and distance from the multielectrode array (MEA): beyond 40 mm accuracy decreased rapidly. The accuracy of noncontact electrograms also decreased with increasing distance from the equator of the MEA. Virtual electrograms from noncontact mapping of normal left ventricles probably represent a summation of transmural activation. Noncontact mapping has similar accuracy with either endocardial or epicardial sites of origin of electrical activity provided the MEA is within 40 mm of the recording site.     

Distinct Activation Patterns of Idioventricular Rhythms and Sympathetically-Induced Ventricular Tachycardias in Dogs with Atrioventricular Block

To investigate mechanisms of ventricular impulse formation in response to sympathetic stimulation in the healthy canine heart in situ, we compared the patterns of ventricular activation during the idioventricular rhythms arising after complete atrioventricular (AV) block and ventricular tachycardias induced by RSG or LSG stimulation. Isochronal maps were generated by computer from 116-127 unipolar electrograms recorded from the entire ventricular epicardium in 15 open chest, anesthetized dogs. In eight of these, bipolar electrograms were recorded with plunge electrodes from 11 selected endocardial sites located below epicardial breakthrough areas. Intracardiac recordings from the His-Purkinje system were made with electrode catheters. After electrograms were recorded during sinus rhythm, complete AV block was induced by injecting formaldehyde into the AV node and idioventricular rhythms occurred spontaneously at a rate of 37 +/- 12 beats/min (mean +/- SD, n = 25). During idioventricular rhythms, endocardial activation preceded the earliest epicardial breakthrough, which occurred in either the right anterior paraseptal region, antero-apical left ventricle, or postero-apical left ventricle. These sites were consistent with a focal origin in the subendocardial His-Purkinje system. Total epicardial activation times lasted for 47 +/- 13 msec (n = 40). Idioventricular rhythms were suppressed by overdrive pacing (intermittent trains of ten beats with decremental cycle length from 500 to 200 msec) or by intravenous calcium infusion (to plasma levels of 10.1-15.2 mM). Right or left stellate ganglion stimulation increased idioventricular rhythm rates (to 52 +/- 13 beats/min, n = 28) and also induced, in all preparations, ventricular tachycardias that had significantly faster rates (189 +/- 55 beats/min, n = 27, P less than 0.005). Ventricular fibrillation was induced after brief runs of ventricular tachycardia in five of the preparations. During ventricular tachycardias, epicardial activation occurred on the right ventricular outflow tract or the postero-lateral wall of the left ventricle, and preceded endocardial activation in 50% of cases. Total epicardial activation times (103 +/- 29 beats/min) were significantly longer than during idioventricular rhythms (P less than 0.005). Ventricular tachycardias displayed overdrive excitation at critical pacing cycle lengths (360-280 msec) and were not suppressed by calcium infusion. Thus, differential mechanisms of impulse formation with distinct localizations can be elicited from healthy ventricular myocardium.     

Origin of acetyl strophanthidin-induced ventricular arrhythmias.

To examine the origin of digitalis-induced ventricular tachycardia (VT), acetyl strophanthidin (AS) (25 mug/min) was perfused into a limited zone of myocardium in intact anesthetized dogs through a catheter placed fluoroscopically in the left anterior descending artery without ischemia. A second catheter in the great cardiac vein sampled venous effluent from this region. His and left bundle branch depolarizations were recorded and bipolar intramural electrograms from endocardial and epicardial sites within the anterior descending region were obtained. No conduction alterations preceded arrhythmia. Cardiac venous K+ rose from 3.3 +/- to 4.4 +/- 0.2 meq/liter (P less than 0.001), indicating egress from the perfused zone. 10 animals (Group 1) were sacrificed 2 min after onset of VT while 11 (Group 2) continued until fibrillation (4-14 min). All showed normal (endocardial leads to epicardial) transmural depolarization during sinus rhythm, but 10/21 demonstrated reversal, usually late during VT, including 8/11 in Group 2. Epicardial activation preceded fascicular activation and QRS. Recordings from the border and circumflex regions in 10 additional dogs (Group 3) demonstrated activation reversal only in the border zone. Myocardial K+ was reduced (mean 63 +/- 1 mueq/g) and Na+ increased (mean 41 +/- 2 mueq/g) in the perfused zone (nonperfused circumflex area K+ 72 +/- 1, Na+ 33 +/- 1 mueq/g, P less than 0.001 for both); changes were similar in inner and outer ventricular wall. In related experiments, subepicardial injections of AS induced activation reversal within the immediate area, similar to recordings during coronary infusion. Reversed transmural activation with early epicardial depolarization suggest VT arises within myocardium; electrolyte gradients between adjacent regions may be causative.     

Experimental Myocardial Cryoinjury: Local Electromechanical Changes, Arrhythmogenicity, and Methods for Determining Depth of Injury

To characterize the electromechanical effects of acute and 2-week-old cryoinjury, programmed stimuiation and epicardial M-mode echo mapping (7.5 mHz) were performed prior to, at 15 minutes and 35 ± 2 days after cryoinjury in 10 dogs. Epicardial and intramural bipolar and unipoiar electrograms were recorded in five of the dogs. Cryoinjury was produced with a 5 mm in diameter flat cryoprobe at -60°C applied to the left ventricular epicardium for 10 minutes at each of six contiguous sites. Cryoinjury, acutely and at 2 weeks, was characterized by a loss of normal intramural systolic thickening and a decrease in echo density. The maximum depth of cryoinjury determined by echo ranged from .55 to .85 cm acutely, and .50 to .80 cm chronically and it correlated acutely and chronically (r = .80; r = .85) with pathologically documented depth of cryoinjury at 2 weeks. Acutely, the presence of either an abnormal intramural unipolar or bipolar electrogram also defined the depth of cryoinjury within .16 cm. In contrast, epicardiai electrograms were not useful for judging depth of cryoinjury. A QS complex on the epicardial unipolar electrogram was recorded over the cryoinjury acutely and at 2 weeks in four of five dogs despite preserved subendocardial systolic wall thickening and normal histology extending 40 to 65% of the wall thickness. Epicardiai bipolar eiectrograms uniformly showed a marked decrease in amplitude and siope of the intrinsic deflection, a small hut insignificant increase in width and no multicomponent activity. Ventricular fibrillation was reproducibly initiated with three ventricular extrastimuli in five of 10 dogs at 2 weeks. No ventricular tachycardia was initiated. Thus, cryoinjury produces characteristic echogram and electrogram changes that are immediate and persistent. The distinct echo signature as well as the presence of abnormal intramural electrograms can be used to judge the depth of cryoinjury. Cryoinjury does not potentiate the inducibility of ventricular tachycardia. The significance of the inducibility of ventricular fibrillation cannot be determined. Our cryoinjury model can be used to characterize electrograms which represent recordings of myocardial depolarization through an interface of cellular necrosis and early fibrosis.     

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 A V 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.     

Transmural Mapping of Myocardial Refractoriness and Endocardial Dispersion of Repolarization in an Ovine Model of Chronic Myocardial Infarction

Background: Myocardial refractoriness and repolarization is an important electrophysiological property that, when altered, increases the risk of arrhythmogenesis. These electrophysiological changes associated with chronic myocardial infarction (MI) have not been studied in detail. We assessed the influence of left ventricular (LV) scarring on local refractoriness, repolarization, and electrogram characteristics. Methods: MI was induced in five sheep by percutaneous left anterior descending artery occlusion for 3 hours. Mapping was performed at 19 ± 6 weeks post‐MI. A total of 20 quadripolar transmural needles were deployed at thoracotomy in the LV within and surrounding scar. Bipolar pacing was performed from each needle to assess the effective refractory period (ERP) of the subendocardium and subepicardium. The activation (AT) and repolarization (RT) times, and modified activation recovery interval (ARI_m) were determined from endocardial unipolar electrograms recorded in sinus rhythm simultaneously from all needles. Scarring was quantified histologically and compared with electrophysiological characteristics. Results: Increased scarring corresponded with increased ERP (P < 0.01), decreased subendocardial electrogram amplitude (P < 0.001), and slope (P < 0.001). ERP did not differ between endocardium and epicardium (P > 0.05). The ARI_m and RT were prolonged during early myocardial activation (P < 0.001). After adjusting for AT, the RT and ARI_m were prolonged in areas of scarring (P < 0.001). After adjusting for electrogram amplitude, the ARI_m was prolonged in dense scar (P < 0.05). Conclusions: We confirmed histologically that scarring contributes to prolongation of repolarization, increased refractoriness, and reductions in conduction and voltage post‐MI. Prolongation of repolarization may be further augmented when local activation is earliest or electrogram voltage is decreased within scar.     

Antiarrhythmic and antifibrillatory actions of the beta adrenergic receptor antagonist, dl-sotalol

The antiarrhythmic and antifibrillatory actions of the beta adrenergic receptor antagonist, dl-sotalol, were examined in the canine heart subjected to myocardial ischemic injury. Programmed electrical stimulation of the heart was done 4 to 7 days after a 2-hr occlusion followed by reperfusion of the left anterior descending coronary artery. The resulting dysrhythmias consisted of nonsustained ventricular tachycardia (n = 1), sustained ventricular tachycardia (n = 5) or polymorphous ventricular tachycardia degenerating to ventricular fibrillation (n = 3). After dl-sotalol (8 mg/kg), programmed stimulation failed to produce ventricular arrhythmias in five animals with only nonsustained ventricular tachycardia observed in the other animals. Epicardial activation delays produced in ischemically injured myocardium by premature ventricular stimuli were not altered by treatment with sotalol. However, the increase in ventricular refractoriness (156 +/- 5 msec predrug vs. 191 +/- 7 msec post 8 mg/kg of sotalol, P less than .01) prevented the introduction of premature ventricular stimuli at coupling intervals previously producing ventricular tachyarrhythmias despite the presence of continuous diastolic electrical activity recorded with epicardial composite electrodes over the region of chronic myocardial injury. In a conscious canine model which spontaneously develops ventricular fibrillation, dl-sotalol (2 mg/kg, n = 7; 8 mg/kg, n = 13) decreased the incidence of ventricular fibrillation and increased survival at 24 hr (13 of 20, 65% vs. control, 1 of 15, 7%; P less than .001). Composite electrograms recorded from the anterior and posteriorlateral surfaces of the heart demonstrated the rapid development of activation delays on the posteriorlateral surface with the appearance of ischemic ST segment changes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Orthogonal Electrode Catheter Array for Mapping of Endocardial Focal Site of Ventricular Activation

Precise location of the endocardial site of origin of ventricular tachycardia may facilitate surgical and catheter ablation of this arrhythmia. The endocardial catheter mapping technique can locate the site of ventricular tachycardia within 4–8 cm² of the earliest site recorded by the catheter. This report describes an orthogonal electrode catheter array (OECA) for mapping and radiofrequency ablation (RFA) of endocardial focal site of origin of a plunge electrode paced model of ventricular activation in dogs. The OECA is an 8 F five pole catheter with four peripheral electrodes and one central electrode (total surface area 0.8 cm²). In eight mongrel dogs, mapping was performed by arbitrarily dividing the left ventricle (LV) into four segments. Each segment was mapped with OECA to find the earliest segment. Bipolar and unipolar electrograms were obtained. The plunge electrode (not visible on fluoroscopy) site was identified by the earliest wave front arrival times of -30 msec or earlier at two or more electrodes (unipolar electrograms) with reference to the earliest recorded surface ECG (I, AVF, and V₁). Validation of the proximity of the five electrodes of the OECA to the plunge electrode was performed by digital radiography and RFA. Pathological examination was performed to document the proximity of the OECA to the plunge electrode and also for the width, depth, and microscopic changes of the ablation. To find the segment with the earliest LV activation a total of 10 ± 3 (mean ± SD) positions were mapped. Mean arrival times at the two earlier electrodes were - 39 ± 4 msec and -35 ± 3 msec. Digital radiography showed the plunge electrode to be within the area covered by all five electrodes in all eight dogs. The plunge electrode was within 1 cm² area of the region of RFA in all eight dogs. The width and depth of ablation were 5 ± 3.5 and 7 ± 3.5 mm, respectively. Microscopic changes revealed coagulative necrosis, hemorrhage, and inflammatory changes in all RFAs. In conclusion, the OECA can map the endocardial focal site of origin of paced ventricular activation within 1 cm² area in a canine model. RFA from the OECA can cause discrete ablations representing all five electrodes or cross-shaped ablation connecting central electrode to all four peripheral electrodes. This catheter holds promise for extending surgical and clinical catheter ablation procedures.     

Sinus Rhythm Mapping in a Canine Model of Ventricular Tachycardia

The relationship between electrograms recorded during sinus rhythm and the activation sequence during ventricular tachycardia induced by programmed stimulation was investigated in a canine model of myocardial infarction. Thirteen dogs were studied 3 days (n = 10) or 14 days (n = 3) after coronary occlusion. Sixty-three unipolar electrograms were simultaneously recorded with a sock electrode array connected to a digital recording system, and analyzed by computer. Bipolar electrograms were recorded sequentially from the same sites with an analog recorder. Categories of unipolar electrograms were defined with reference to the QRS complex during sinus rhythm as follows: Class A included electrograms with an intrinsic deflection inscribed within the QRS complex, class B included those which did not exhibit any intrinsic rs deflection, and class C included those with an intrinsic deflection inscribed later than QRS. The epicardial distribution of each class of electrograms was significantly different between the preparations with, and those without inducible tachycardia (72% versus 63% of electrograms being in class A, 20% versus 35% in class B, and 8% versus 2% in class C; p less than 0.005). When tachycardia was inducible, class C epicardial electrograms were located in an area extending across the region of infarction, which corresponded to the common reentrant pathway of figure-of-eight patterns mapped during tachycardia. When ventricular tachycardia was not inducible, class B electrograms were recorded all over this region. The morphology of bipolar electrograms had no predictive value in identifying the common reentrant pathway. These results support the view that the inducibility of reentrant tachycardia is dependent upon critically located delayed activity detected during sinus rhythm by unipolar recordings.     

Origin of electrical activation within the right atrial and left ventricular walls: differentiation by electrogram characteristics using the noncontact mapping system

Clinical data using the noncontact mapping system (Ensite 3000) suggest that characteristics of the reconstructed unipolar electrograms may predict the origin of electrical activation within the atrial and ventricular walls (endocardial vs myocardial vs epicardial origin). Experimental data are lacking. In ten open-chest pigs (mean body weight 62 kg) cardiac pacing was performed at a cycle length of 600 ms with a pulse width of 2 ms and twice diastolic threshold from the endo-, the myo-, and the epicardium, respectively. Pacing was undertaken at three right atrial and three left ventricular sites, and cardiac activation was recorded with the Ensite system. Reconstructed unipolar electrograms at the location of earliest endocardial activation assessed by color coded isopotential maps were analyzed systematically for differences in morphology. The positive predictive value of atrial electrograms exhibiting an initial R wave during pacing for a subendocardial origin (i.e., myocardial or epicardial) was 0.96. The negative predictive value was 0.48. Electrograms generated during myocardial pacing exhibited increased maximal negative voltage and maximal dV/dt (-3 +/- 1.8 mV, -798 +/- 860 mV/ms, respectively) than the electrograms obtained during endocardial (-2 +/- 1 mV, -377 +/- 251 mV/ms, respectively) and epicardial pacing (-2.1 +/- 0.7 mV, -440 +/- 401 mV/ms, respectively, P<0.01 for both parameters). During pacing at the left ventricular wall, occurrence of an initial R wave did not differ significantly between electrograms reconstructed during endocardial and subendocardial pacing. All other characteristics of the unipolar ventricular electrograms analyzed, except latency, did not differ significantly when compared to stimulation depth. Morphological characteristics of unipolar electrograms generated by the noncontact mapping system during pacing of the atrium allowed for discrimination of an endocardial versus a subendocardial origin of activation. At the ventricular level, characteristics of unipolar electrograms did not predict the origin of cardiac activation in this experimental setting.     

Perioperative Mapping of Parahisian Accessory Pathways

VERBEET, T.W., ET AL.: Perioperative Mapping of Parahisian Accessory Pathways. In 1989, two patients were operated for deep septal "parahisian" pathways in our institution. Three different mapping techniques were used. (1) Epicardial activation mapping with a belt of 21 bipolar electrodes positioned around the heart. This belt was positioned either on the atrial or on the ventricular side of the atrio-ventricular annulus in order to localize both the atrial and the ventricular insertion of the bypass tract. (2) Right intra-atrial activation mapping on the normothermic beating heart with a bipolar hand-held probe. (3) Right intra-atrial cryomapping at 0°C. The "parahisian" pathways are remote from the epicardium and the pattern of epicardial activation is different from that of the free-wall pathways. Case 1: The electrophysiological study showed a concealed anteroseptal bypass tract. The peroperative atrial epicardial mapping during orthodromic tachycardia (OT) showed simultaneous activation of the posteroseptal area and of the basis of the right appendage. Right intra-atrial mapping during OT showed an anteroseptal "parahisian" pathway. Case 2: The ECG and electrophysiological study showed a right posterior pathway. The first site of epicardial ventricular activation during atrial stimulation was the right posterior area, 30 ms after the onset of the delta wave. The first site of epicardial atrial activation during OT was the posteroseptal area. The right intra-atrial mapping showed a posteroseptal "parahisian" bypass tract. This localization was confirmed with cryomapping. Conclusions: Some patterns of epicardial mapping may suggest the presence of a deep septal "parahisian" bypass tract: retrograde atrial activation at different sites (mimicking activation among multiple pathways); delay between the delta wave and the first epicardial electrogram. Right intra-atrial activation and cryomapping are useful to confirm the diagnosis.     

Experimental Measures of Ventricular Activation and Synchrony

Background: A widened QRS complex as a primary indication for cardiac resynchronization therapy (CRT) for heart failure patients has been reported to be an inconsistent indicator for dyssynchronous ventricular activation. The purpose of this study was to conduct a detailed experimental investigation of total ventricular activation time (TVAT), determine how to measure it accurately, and compare it to the commonly used measure of QRS width. In addition, we investigated a measure of electrical synchrony and determined its relationship to the duration of ventricular activation. Methods: Unipolar electrograms (EGs) were recorded from the myocardial volume using plunge needle electrodes, from the epicardial surface using “sock” electrode arrays, and from the surface of an electrolytic torso‐shaped tank. EGs were analyzed to determine a root mean square (RMS)‐based measure of ventricular activation and electrical ventricular synchrony. Results: The RMS‐based technique provided an accurate means of measuring TVAT from unipolar EGs recorded from the heart, the entire tank surface, or the precordial leads. In normal canine hearts, a quantification of ventricular electrical synchrony (VES) for normal ventricular activation showed that the ventricles activate, on average, within 3 ms of each other with the left typically activating first. Conclusion: Conclusions from this study are: (1) ventricular activation was reflected accurately by the RMS width obtained from direct cardiac measurements and from precordial leads on the tank surface and (2) VES was not strongly correlated with TVAT.     

Comparison of Epicardial and Endocardial Programmed Stimulation in Patients at Risk for Ventricular Arrhythmias After Cardiac Surgery

Programmed ventricular stimulation was performed on 36 patients after recent cardiac surgery using implanted right ventricular epicardial temporary wires and with catheters positioned percutaneously at two right ventricular endocardial sites. Patients were followed for a mean of 18.5 months (range 3 to 36 months). Epicardial wires were nonfunctional in 10 patients (28%) due to excessively high pacing thresholds. Overall, 22 patients (61%) had inducible sustained ventricular tachycardia; epicardial wires were functional in 15 (68%) of these patients. Six patients without inducible ventricular tachycardia with epicardial stimulation were inducible using endocardial stimulation. Of the 24 patients in whom epicardial and endocardial ventricular stimulation could be performed, concordant results were obtained in only 17 (71%), despite similar epicardial and endocardial ventricular effective and functional refractory periods. A total of 14 arrhythmic events occurred during the follow-up period. Of the 22 patients with an inducible sustained ventricular tachycardia, 12 (64%) had subsequent arrhythmic events. Only 2 of the 14 noninducible patients had follow-up arrhythmic events, one of which was caused by medication proarrhythmia. Endocardial ventricular stimulation had a superior sensitivity (83% versus 30%, P < 0.0001) and an improved negative predictive value (86% versus 61%, P < 0.05) compared with epicardial ventricular stimulation. These results indicate that noninducibility using epicardial programmed ventricular stimulation does not reliably portend a low risk for recurrent ventricular tachyarrhythmias. Epicardial programmed stimulation, used alone, may be inadequate for postoperative electrophysiological evaluation of patients at risk for ventricular arrhythmias.     

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64 +/- 22 ms after unsuccessful defibrillation and 339 +/- 292 ms after successful defibrillation (P less than 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated. Thus, after both successful and unsuccessful defibrillation with epicardial shocks of greater than or equal to 1 J, an isoelectric window occurs during which no activation fronts are present; the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; unsuccessful shocks transiently synchronize activation before fibrillation regenerates; activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of greater than or equal to 1 J halt all activation fronts after which VF regenerates.     

The Sock Electrode Array: A Tool for Determining Global Epicardial Activation during Unstable Arrhythmias

The conventional technique for mapping the sequence of epicardial activation uses a hand-held electrode moved over the heart to record from a number of epicardial sites one at a time, and requires 5–15 minutes to record from 50 or more sites distributed over the entire ventricular epicardium. This method is inadequate for arrhythmias that are transient or vary from beat to beat. To overcome these limitations the "sock electrode array," a contour-fitting sock containing 26 or 52 electrodes, has been developed. The nylon mesh sock is pulled over the heart and permits simultaneous recording of potentials from electrodes distributed over the entire ventricular epicardium. The electro-grams are recorded and converted to digital form for computer generation of isochronous maps. Maps of the epicardial activation sequence derived from the sock electrode were compared to those obtained by the hand-held electrode in six normal dogs during sinus rhythm and ventricular pacing. The sequence of local activation times acquired by both methods showed similar areas of early and late activation and comparable isochronous maps. The hand-held electrode technique required 10–15 minutes for data acquisition and another 15–30 minutes for analysis. The sock electrode array allowed electrograms from 26 epicardial electrodes to be recorded simultaneously during one cardiac cycle and computer generated isochronous maps could be displayed within 10 minutes. This method allows rapid recording and analysis of epicardial electrical phenomena and should meet the time constraints imposed during the intraoperative study of ventricular tachyarrhythmias in patients.     

Improved Spatial Resolution for Cardiac Mapping Using Current Source Density-Based Electrode Arrays

The time of the minimum slope (i.e., the fastest negative deflection) in monopolar (MP) electrograms from normal hearts compares closely with time of phase 0 of the action potential in cells underlying the electrode, but poor rejection of far-field activity may limit the utility ofMP electrode technology in dense arrays used for the study of ventricular tachycardia and fibrillation. The purpose of this study is to evaluate more myopic discrete bipolar (BP) and nondirectional, two-dimensional current source density (CSD) based arrays for rejection of far-field potentials and precision of activation time determination. Simultaneous recordings of the CSD, MP, and multiple BP electrograms were performed on normal dog epicardium. The time of the minimum slope in MP electrograms was compared to activation times in CSD and BP derivations using: (1) peak; (2) steepest slope; (3) zero crossing of the steepest sloping segment in either direction; and (4) waveform morphology. In vivo, CSD amplitude was reduced significantly more than MP and BP amplitudes by insertion of inert media between the heart and the electrodes. The time of the steepest slope in CSD electrograms designated activation times closest to the time of the minimum slope in MP electrograms (0.9 ± 1.3 msec). We conclude that CSD provides a nondirectional electrode system that accurately defines the time of local activation and possesses better spatial specificity than MP electrode systems and BP electrode systems having the same interelectrode distances.     

Spontaneous Termination of Reentry Ventricular Tachycardia in the Late Myocardial Infarction Period: An Experimental Study in the Dog

Forty episodes of induced ventricular tachycardia in the late myocardial infarction period (4-6 days old) were analyzed in 12 dogs in an attempt to identify the possible mechanisms for the termination of reentry tachycardia. Multiple epicardial and endocardial composite electrograms were recorded in and around the central ischemic zone of the infarction. During tachycardia, the earliest site of activation was identified in the epicardial surface of the border or normal zone immediately adjacent to the ischemic zone in 36 of the 40 episodes, suggesting efferent epicardial spread from the site of the activity. In four instances, the efferent pathways were directed to the endocardial surface. Four distinct patterns of activation sequences were observed during spontaneous termination: (a) a shift of the efferent pathways from epicardial to endocardial site (19 instances); (b) a change of the efferent pathways within the endocardium (4 instances); (c) a shift of the earliest site of activation between the left and right ventricles (9 instances); and (d) no apparent change in the epicardial efferent pathways (4 instances). In four other instances, ventricular tachycardia deteriorated into ventricular fibrillation. In patterns (a) and (c), a shift of the efferent pathways resulted in a more rapid and homogeneous activation of the border and normal zone epicardium. These changes were associated with cessation of delayed or continuous activity in the ischemic zone epicardium, resulting in termination of tachycardia.     

Observations on the Epicardial Activation of the Normal Human Heart

Serial hand mapping techniques in man have identified 3 to 5 sites of epicardial breaktrough (EBT). However, transmural epicardial excitation from the widely distributed His/Purkinje system suggests a more complicated pattern may exist. Multielectrode arrays used with large mapping systems during surgery often present complicated and sometimes inconsistent activation patterns. The purpose of this work is to reconcile epicardial activation in the normal human heart with anatomical and endocardial/intramural physiological recordings using multichannel computer mapping requiring only a single beat, and rigorously defined and applied activation time detection algorithms. Eighteen subjects undergoing surgery for Wolff-Parkinson-White syndrome were recorded with a 119 site sock array during nonpreexcited sinus rhythm. None had evidence of coronary artery disease and all exhibited a normal 12-lead ECG except during periods of preexcitation or tachycardia. Each was recorded bipolarly and four also were recorded monopolarly. Recordings revealed 8.0 +/- 1.6 EBTs (range 5 to 12). Closely spaced, multiple EBTs often were observed and usually confirmed using different activation time detection algorithms. The earliest EBT always occurred over the anterior right ventricle at 14.3 +/- 6.5 msec (range -1 to 29 msec) after QRS onset. Subsequent EBTs could occur at any ventricular site with variable latencies. In contrast to previous reports describing epicardial spread of activation from a few foci, a mosaic of epicardial activation emerges. These data are consistent with endocardially initiated transmural activation of the epicardium suggested by the anatomy of the His/Purkinje system and intramural recordings.     

Effects of lidocaine on reperfusion arrhythmias and electrophysiological properties in an isolated ventricular muscle model of ischemia and reperfusion

Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricles with standard microelectrode techniques. An ECG was also recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to the endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with "normal" Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 14 of 20 hearts (70%). Arrhythmias were accompanied by prolongation of transmural conduction time and abbreviation of endocardial effective refractory period. With lidocaine, at 1, 5, 10 and 50 microM, reperfusion arrhythmias occurred in 53.3, 22.2, 20.8 and 14.3% of hearts, respectively. The decreased incidence of arrhythmias was statistically significant for 5 to 50 microM lidocaine (P less than .01). The antiarrhythmic effect did not correlate with changes in transmural conduction time, endocardial effective refractory period, or endocardial excitability. However, antiarrhythmic concentrations of lidocaine selectively depressed epicardial excitability and significantly increased endo- to epicardial conduction block during late ischemic and early reperfusion periods. Epicardial inexcitability extended to late diastole and conduction block was not restricted to premature beats. Thus, in transmural reentry in which the epicardium is an essential component of the circuit, lidocaine may interrupt the circuit by selectively rendering this component inexcitable.