Method for simultaneous epicardial and endocardial mapping of in vivo canine heart: application to atrial conduction properties and arrhythmia mechanisms.

INTRODUCTION: It has been suggested that the three-dimensional structure of the atria may be crucial in arrhythmogenesis; however, previous in vivo atrial activation mapping studies have been limited to either endocardial or epicardial approaches. METHODS AND RESULTS: To investigate the role of endocardial and epicardial structures and their interaction in atrial conduction and arrhythmias, we used five epicardial plaques and two intra-atrial balloon arrays to record a total of 368 unipolar electrograms from the entire epicardial and endocardial surface of both atria. During regular 1:1 pacing from the right atrial appendage, right atrial endocardial activation spread considerably faster than epicardial (total activation time 45+/-12 msec vs 60+/-19 msec, respectively [mean +/- SD]; P < 0.05), pointing to preferential conduction over structures like the crista terminalis and pectinate muscles. No such differences were noted in the left atrium. Transseptal spread occurred via discrete anterior and posterior pathways, causing separate breakthroughs in anterior and posterior atrial regions, respectively. Dissociation between septal pathways played a role in reentry during vagal atrial fibrillation. In 2 of 4 dogs with atrial fibrillation associated with congestive heart failure, single macroreentrant circuits involving endocardial and epicardial components were revealed during the arrhythmia. CONCLUSION: We conclude that activation mapping using simultaneous recording from both epicardial and endocardial surfaces provides potentially important insights into the mechanisms of atrial conduction and arrhythmogenesis.

Effect of vasoactive intestinal peptide on pacemaker location and heart rate in the dog atrium.

Vasoactive intestinal polypeptide (VIP) was either injected intravenously (300 pmol.kg-1) or perfused (1 nmol in 1 min) into the sinus node artery (SNA) in anesthetized dogs to study its effect on subsidiary atrial pacemakers. Isochronal maps were obtained from 128 unipolar electrograms recorded on the epicardial surface of both atria in nine animals. When VIP was perfused into the SNA or injected intravenously, heart rate increased by 29 +/- 16% and 12 +/- 12%, and blood pressure decreased by 16 +/- 15 mmHg (1 mmHg = 133.3 Pa) and 24 +/- 18 mmHg, respectively. No significant change in heart rate (3 +/- 6% decrease) accompanied a similar decrease in blood pressure after an intravenous sodium nitroprusside perfusion. The perfusion of VIP into the SNA as well as the intravenous injection of VIP induced a shift of the pacemaker site to the region of Bachmann's bundle in a third of the preparations, while the pacemaker remained in the sinus node area in two thirds. A perfusion of isoproterenol into the SNA produced a similar heart rate increase (32 +/- 14%, NS vs. VIP), and shifted the pacemaker site rostrally within the sinus node in three of five preparations, or to the region of Bachmann's bundle in two of five preparations. The response to VIP in the location of the pacemaker was significantly different from the response to isoproterenol. Repeated perfusions of VIP into the SNA after 10-, 25-, 40-, and 60-min intervals produced 2 +/- 13% (p < 0.005 vs. the effect of first VIP administration), 14 +/- 12% (p < 0.05), 10 +/- 12% (p < 0.05) and 30 +/- 13% (NS) heart rate increases, respectively, thereby demonstrating a tachyphylactic effect. In conclusion, VIP seems to exert its positive chronotropic effect directly (probably via specific VIP receptors), although the phenomenon of tachyphylaxis may suggest an indirect sympathomimetic mechanisms.

Can L-arginine improve myocardial protection during cardioplegic arrest? Results of a phase I pilot study.

BACKGROUND: L-arginine appears to improve myocardial protection during cardioplegic arrest in animal models. METHODS: To study the clinical effect and safety of L-arginine in humans, a phase I pilot study was performed with 50 patients who underwent coronary artery bypass grafting. We randomly assigned half to a treatment group, which received 1 g of L-arginine administered during the first 30 minutes of cardioplegic arrest induced by either warm or cold blood cardioplegia, and half to a control group, which did not receive L-arginine supplementation. RESULTS: Age, sex, and preoperative clinical status were similar in both groups. Seventeen patients of each group were administered intermittent warm antegrade blood cardioplegia, whereas the solution needed to be cooled to obtain complete standstill of the remaining eight hearts in each group. An internal thoracic artery graft to the left anterior descending coronary artery was performed in all patients. There was no death and no myocardial infarction in the treatment group, but there were one death and two infarctions in the control group. The amount of serial release of troponin I during the first 72 hours after the operation was similar between the L-arginine group and the control group (p > 0.05). Peak serum troponin levels averaged 4.9 +/- 1.0 microg/L in the arginine group and 3.9 +/- 1.0 microg/L in the control group (p > 0.05). A multivariate analysis of variance showed no effect of L-arginine (p > 0.05) but a significant effect of the temperature of the cardioplegic solution on the release of troponin I (p < 0.05). Serum troponin I levels averaged 2.2 +/- 0.4 microg/L, 4.5 +/- 0.4 microg/L, and 6.9 +/- 0.4 microg/L in the patients with cold cardioplegia and 1.4 +/- 0.3 microg/L, 2.4 +/- 0.3 microg/L, and 3.3 +/- 0.3 microg/L in the patients with warm cardioplegia 1, 2, and 6 hours, respectively, postoperatively. CONCLUSIONS: The administration of 1 g of L-arginine during the first 30 minutes of blood cardioplegic arrest did not result in a decrease in the postoperative release of cardiac enzyme; however, cold cardioplegic arrest significantly increased the release of cardiac troponin I postoperatively. There was no significant side effect related to the addition of L-arginine to the cardioplegic solution.

Mapping of septal ventricular tachycardia: clinical and experimental correlations.

In patients with chronic myocardial infarction, ventricular tachycardia originating in the interventricular septum may account for a significant number of arrhythmia recurrences after direct ablative operations. We used total computer-assisted cardiac mapping (epicardial sock, left and right ventricular endocardial balloon electrode arrays) to assess whether tachycardia originating in deep or right-sided layers of the interventricular septum is associated with a specific pattern of epicardial activation sequence. We performed these studies during operations in 18 patients and during experiments in 12 dogs in which a septal myocardial infarction was produced by ligating the anterior septal coronary artery. Intraseptal needle electrodes were plunged into the septum of all animal preparations to generate pace-mapping data and to obtain intraseptal recordings (six preparations) during reentrant ventricular tachycardia induced by programmed stimulation. In addition, pace-mapping data of infarcted canine heart preparations were compared with those of nine healthy heart preparations. In the clinical study, 31 ventricular tachycardias with a septal site of origin were analyzed. Twenty tachycardias displayed an epicardial breakthrough in the area of the interventricular groove, whereas 11 had an epicardial breakthrough in the right ventricular free wall. Biventricular endocardial mapping revealed that left septal endocardial activation preceded right septal activation in the former and that right septal activation occurred earlier in the latter. In the experimental study, 14 ventricular tachycardias (cycle length 146 +/- 34 msec) were induced by programmed stimulation in 11 infarcted heart preparations. Eight tachycardias displaying an epicardial breakthrough on the right ventricle were found to originate in the right ventricular septal subendocardial layers, whereas six tachycardias in which the epicardial breakthrough occurred on the anterior interventricular groove originated in the left ventricular septal subendocardial layers. The epicardial breakthrough preceded the left ventricular endocardial breakthrough in six tachycardias (85.7%) originating in intermediate or right ventricular septal layers, but in only one of five tachycardias originating in the left ventricular septal layers. In the pace-mapping study, the epicardial breakthrough shifted progressively from the right ventricular free wall toward the interventricular groove area in response to pacing from the right, intermediate, and left ventricular thirds of the basal septum. This relationship was similar for infarcted and noninfarcted hearts, although transseptal conduction time was prolonged in infarcted hearts (45 +/- 10 msec vs 33 +/- 7 msec, p < 0.01). Therefore the information integrated from the localization of the epicardial breakthrough and the relative timing between the epicardial and the left ventricular endocardial breakthroughs can be used to estimate the depth of the site of origin of septal ventricular tachycardias. This study confirms that a three-dimensional view of the substratum of ventricular tachycardia can be derived from simultaneous epicardial and left ventricular endocardial mapping and can provide a superior basis for therapeutic interventions.

Surgical treatment of ventricular tachycardia. Indications and results.

Despite the excellent results achieved with the endocardial resection procedure in the management of patients with life-threatening ventricular tachycardia. Most surgical electrophysiology teams have experienced a decline in the number of direct operations performed for life-threatening ventricular tachycardia. This is probably due to the widespread use of thrombolytic therapy during the acute phase of infarct formation. But also to the advent of implantable cardioverter-defibrillators that are increasingly sophisticated, easy to use and effective. Their increased use over the past few years is related to the belief that direct operations for the eradication of ventricular tachycardia foci bear a high operative mortality rate. However, today the operative mortality is less than 5%, and long term survival is up to 85% at 5 years with an extremely low incidence of ventricular tachycardia recurrence and sudden death. We report the results obtained in our first 100 patients in whom ventricular tachycardia surgical ablation was guided by computerized mapping of both the endocardium and epicardium. A particular type of ventricular tachycardia activation pattern was found to be associated with a higher rate of electrical failure due to a deep septal substratum. Appropriate management of this condition may further decrease the rate of ventricular tachycardia reinducibility and long term return of ventricular tachycardia to a level yet unachieved by any other therapeutic modality. The results of catheter ablation are promising, but access to intramural substrates remains unresolved. In patients with sustained monomorphic ventricular tachycardia associated with a discrete akinetic area of the left ventricle, surgery offered as a last resort is less likely to produce favourable results and the decision of its use should therefore be taken early before unjustified drug trials go on.

Regional distribution of atrial electrical changes induced by stimulation of extracardiac and intracardiac neural elements.

UNLABELLED: Autonomic nerves and intrinsic cardiac neural elements are known to influence the electrophysiologic and dynamic properties of the heart. This study describes the regional distribution in the canine atria of electrophysiologic effects induced by stimulation of the right and left cervical vagosympathetic complexes, the right atrial ganglionated plexus, and the right and left stellate ganglia. Local atrial effects were determined from changes in QRST area of unipolar electrograms recorded from multiple sites with plaque electrodes sewn onto the atria in 16 anesthetized dogs. RESULTS: (1) Although being very consistent in any given preparation, atrial changes varied between animals when similar neural structures were stimulated. (2) Among the common features identified between preparations, consistent effects were induced by neural stimulation in the region of the sinus node, indicating that this atrial region is the most richly innervated. (3) All other regions of the atria could be affected by stimulation of either right-sided or left-sided efferent nerves. (4) Responses to right atrial ganglionated plexus stimulation after atropine administration indicated that the corresponding fat pad contains both sympathetic and parasympathetic neural elements. CONCLUSION: This study demonstrates that there is considerable overlapping of atrial innervation affecting all regions of the atria, as well as the sinus node region.

[Comparison of the infusion of acetylcholine into the artery of the sinoatrial node with the electric stimulation of cardiac parasympathetic nerves]. / Comparaison de l'infusion d'acétylcholine dans l'artère du noeud sinusal avec la stimulation électrique des nerfs cardiaques parasympathiques.

Atrial fibrillation occurring after open heart surgery largely depends on heterogeneous dispersion of refractoriness. To investigate the contribution of the autonomic nervous system in this phenomenon, we studied the regional distribution of neurally induced atrial electrophysiological events. Electrical stimulation of the right atrial fat pad, acetylcholine injection into the sinus node artery, and stimulation of the right and left vagosympathetic trunks were compared with respect to detailed atrial mapping. Unipolar electrograms were recorded from 127 atrial sites before and after neural stimulation or acetylcholine injection (10(-7) mol) in 8 anesthetized dogs. Regional changes in atrial repolarization were estimated by epicardial isointegral maps generated from computed values of the area under each electrogram and plotted on an atrial grid. The anatomical distribution of the sinus node artery was assessed by intra-arterial injection of microspheres. The effects of right and left vagal and right atrial fat pad stimulation extended contralaterally. Acetylcholine injected into the sinus node artery affected the lower left atrium whereas no microspheres could be found in this region upon microscopic examination. Therefore, this effect was possibly related to cholinergic activation of neuronal cell bodies located in the right atrial wall and projecting to the lower left atrium, supporting the hypothesis that local circuit neurons were involved in the activation of the intrinsic nervous system of the heart.

Computer interview for screening blood donors for risk of HIV transmission.

To test the ability of a computer-based interview to detect factors related to the risk of the human immunodeficiency virus (HIV) among potential blood donors, and to determine donor reactions to the use of the computer, we compared the rate of detection of HIV-related factors elicited by the computer interview with the rate elicited by standard American Red Cross procedures (written questionnaires and face-to-face interviews) for assessment of donor suitability. The study was performed at a Red Cross blood donor center and a hospital. A consecutive sample of 294 male and female blood donors 18 to 75 years of age participated in a randomized crossover trial in which the order of the two methods was reversed. Among 272 prospective donors who provided complete data, the computer identified 12 who reported either behavior associated with a risk of acquiring HIV or symptoms compatible with AIDS. None of these 12 was so identified by face-to-face interviews or written questionnaires. Only one used the confidential unit exclusion procedure to prevent use of his donated blood. Tests for antibody to HIV were negative in blood from all 272 subjects. The subjects enjoyed the computer interview and judged it to be more private than the standard method for donor assessment.

Computer-based interview for screening blood donors for risk of HIV transmission.

OBJECTIVE: To test the ability of a computer-based interview to detect factors related to the risk of the human immunodeficiency virus (HIV) among potential blood donors and to determine donor reactions to the use of the interview. DESIGN: A comparison of the rate of detection of HIV-related factors elicited by a computer interview with that obtained by standard American Red Cross procedures for assessment of donor suitability, including a randomized crossover trial in which the order of the two methods was reversed. Information obtained by the computer was not available to influence the use of blood components for transfusion. SETTING: The computer interview was administered to donors at an American Red Cross blood donor center and at a mobile blood drive at a hospital. SUBJECTS: Consecutive sample of 294 male and female blood donors 18 to 75 years of age. MAIN OUTCOME MEASURES: Subjects' responses to the computer-based interview as well as responses to the standard Red Cross written questionnaires and face-to-face interviews were used for donor assessment. RESULTS: The interview took an average of 8 minutes to complete. From among 272 donors who provided complete data, the computer identified 12 donors who reported either behaviors associated with a risk of HIV acquisition or symptoms compatible with the acquired immunodeficiency syndrome; none of these donors had been so identified either by routine written questionnaires or by face-to-face interviews used to screen potential blood donors. Only one of the 12 identified donors used the confidential unit exclusion procedure to prevent use of his donated unit. The rate of elicitation of HIV-related factors by the computer interview was 12 (4.4%) of 272 (95% confidence interval [CI], 2.3% to 7.6%), compared with two (0.13%) of 1536 (95% confidence upper bound, 0.28%) using the standard Red Cross procedure (P less than .0001). Tests for antibodies to HIV were negative in blood samples from all of the 272 subjects studied. The subjects enjoyed the computer interview and judged it to be more private than the standard donor assessment method. They also predicted that donors would be more honest with the computer interview than with a human interviewer. CONCLUSIONS: Computer-based screening elicits more HIV-related factors in the health histories of blood donors than do the standard questionnaire and interviewing methods currently in use. Computer-based screening is also acceptable to blood donors.

Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction. Is the origin of the tachycardia always subendocardially localized?

BACKGROUND: Left ventricular endocardial reentry is the conventional concept underlying surgery for ventricular tachycardia (VT). We assessed the incidences of patterns showing complete reentry circuits at either the subendocardial or subepicardial level and of patterns in which left ventricular endocardial mapping could only in part account for a reentrant mechanism. METHODS AND RESULTS: We retrospectively analyzed epicardial and left ventricular endocardial isochronal maps of 47 VTs induced in 28 patients with chronic myocardial infarction (inferior, 14 patients; anteroseptal, 14 patients). Electrograms were recorded intraoperatively from 128 sites with epicardial sock and transatrial left ventricular endocardial balloon electrode arrays. Given the methodology used in this study, the mapping characteristics of the tachycardias suggested five types of activation patterns: 1) complete (90% or more of VT cycle length) subendocardial reentry circuits in seven VTs (15%) and seven patients (25%), 2) complete subepicardial reentry circuits in four VTs (9%) and four patients (14%), 3) incompletely mapped circuits with a left ventricular endocardial breakthrough preceding the epicardial breakthrough in 25 VTs (53%) and 21 patients (75%), 4) incompletely mapped circuits with a left ventricular epicardial breakthrough preceding the endocardial breakthrough in three VTs (6%) and three patients (11%), and 5) a right ventricular epicardial breakthrough preceding the left ventricular endocardial breakthrough in eight VTs (17%) and seven patients (25%). After surgery, one type 3 VT and three type 5 VTs were reinducible. Thus, left ventricular endocardial reentry substrates (types 1 and 3) accounted for 68% of VTs, but substrates involving subepicardial (types 2 and 4) and deep septal layers (type 5) accounted for 32% of VTs. CONCLUSIONS: In a substantial number of VTs, a substrate localization that is at variance with the conventional concept can be detected by simultaneous epicardial and endocardial mapping and may require modification of the surgical approach conventionally aimed at endocardial layers.

Body surface isopotential mapping of the entire QRST complex in the Wolff-Parkinson-White syndrome. Correlation with the location of the accessory pathway.

Body surface potential maps were recorded during sinus rhythm and during atrial pacing at the time of electrophysiologic studies in 42 patients with Wolff-Parkinson-White syndrome. The locations of the accessory pathways were determined by epicardial mapping during surgery in 34 patients and by multicatheter endocavitary electrophysiologic studies in eight additional patients. During delta wave inscription, the shape and extension of areas of the negative and positive potentials on the thorax correlated better with the preexcitation site (69% of patients) than with the localization of the minimum potential alone (45.2% of patients). Typical potential distributions were present from the beginning of the delta wave and remained stationary during the first half of the QRS complex. During marked preexcitation, the superposition of atrial activity on the delta wave produced a mixed pattern in the earliest maps. However, these alterations of early delta thoracic potential distribution did not persist longer than 30 msec. The spread of the negative potentials during the last half of the QRS complex also characterized each localization: right-sided preexcitation reproduced the depolarization sequence of left bundle branch block, left-sided preexcitation reproduced that of right bundle branch block, and posterior pathways resembled left anterior fascicular block. Anterior left ventricular and more anterior left lateral ventricular preexcitations mimicked a right bundle branch block-left posterior fascicular block pattern. There was good correlation between the body surface potential map obtained during the ST segment and the site of the right-sided preexcitation. However, in left-sided preexcitations, ST patterns concordant with delta wave patterns were found less frequently than in right-sided preexcitations.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram.

Stable atrial flutter induced in both conscious and open chest states was studied in 30 mongrel dogs after production of sterile pericarditis. During the conscious state studies, induced atrial flutter (mean cycle length 128 +/- 15 ms) was always sustained greater than 15 min and was stable. Three types of flutter wave polarity were noted in electrocardiogram (ECG) lead II: positive in 16 dogs, negative in 3 and flat or slightly positive in 11. Sequential site atrial mapping during atrial flutter (mean cycle length 133 +/- 18 ms) in the open chest state showed either clockwise (18 dogs) or counterclockwise (12 dogs) circus movement in the right atrium. In 19 of 30 dogs, the circus movement clearly did not require any naturally existing anatomic obstacle; in 11, the orifice of the superior vena cava probably was also involved. Double potentials were recorded from the center of the reentrant circuit during atrial flutter, and fractionated electrograms were recorded from a pivot point of the reentrant wave front. A positive flutter wave in ECG lead II (12 dogs with counterclockwise circus movement) was associated with early activation of the Bachmann's bundle region compared with the posteroinferior left atrium and activation of the left atrium mainly in a superoinferior direction. A negative flutter was associated with the early activation of the posteroinferior left atrium compared with Bachmann's bundle and activation of a considerable portion of the left atrium in an inferosuperior direction. A flat or slightly positive flutter wave (14 of 18 with clockwise circus movement) was associated with activation of the left atrium almost simultaneously by two wave fronts coming from both these sites. In conclusion, atrial flutter in this dog model is due to circus movement in the right atrium, the center of which does not necessarily require an anatomic obstacle. Although atrial flutter is generated by circus movement in the right atrium, the flutter wave polarity in the ECG is determined primarily by the activation sequence of the left atrium.

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis.

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.

Surgical treatment of the Wolff-Parkinson-White syndrome. Endocardial versus epicardial approach.

From 1983 to 1988, 51 patients with the Wolff-Parkinson-White syndrome underwent surgical ablation of an accessory conduction pathway, 25 by the classic endocardial approach and 26 by the epicardial technique supplemented by cryosurgery. In the endocardial and epicardial groups, the accessory pathway was in the left free wall in 22 and 18 patients, respectively, posterior septal in two and seven, and in the right free wall in one patient in each group. There was no early or late death in the endocardial group, and postoperative complications developed in five patients (20%). Pathway ablation was completely successful in 22 patients (88%), preexcitation recurred in two patients (8%), and one had recurrence of supraventricular tachycardia (4%). One of the failures occurred with a posterior septal pathway (50%), and the two others with a left free-wall pathway (9%). With the epicardial technique, there were no early deaths and one late death caused by atherosclerotic coronary artery disease. Five patients (19%) had postoperative complications. The pathway was ablated successfully in 22 patients (85%), preexcitation recurred in three patients (12%), and supraventricular tachycardia remained inducible in another patient despite disappearance of the delta wave. Three of those failures occurred with anterior left free-wall pathways (16%), but only one patient had recurrent supraventricular tachycardia (4%) requiring immediate reoperation, which was successful. In conclusion, although epicardial or endocardial approaches produced similar results, our observations suggest that left free-wall accessory pathways located high anteriorly may be ablated in a more reproducible way with the endocardial technique, whereas the epicardial approach appears easier for posterior septal pathways. We therefore believe that any surgeon beginning such surgery should be aware of the possibilities and limitations of each of the two techniques.

Comparative accuracy of the vectorcardiogram and electrocardiogram in the localization of the accessory pathway in patients with Wolff-Parkinson-White syndrome: validation of a new vectorcardiographic algorithm by intraoperative epicardial mapping and electrophysiologic studies.

The scalar electrocardiograms (ECGs) and vectorcardiograms (VCGs) of 41 patients with Wolff-Parkinson-White (WPW) syndrome were used to compare the accuracy of these techniques in the identification of the site of preexcitation. The location of the accessory pathway (AP) was determined by endocavitary electrophysiologic studies in all patients and the location was confirmed during intraoperative epicardial mapping in 28 of them. The ECGs were classified according to Gallagher's criteria and with Milstein's algorithm, whereas the VCGs were classified according to a new two-step algorithm. The presence of multiple accessory pathways and coexisting myocardial infarctions were major limitations in both the VCG and ECG classification procedures. In patients with a single accessory pathway, three AP localizations (right free ventricular wall, posterior, or left free ventricular wall) were identified with the first step of the VCG algorithm, with an overall sensitivity (96.5%), specificity (90.7%), and positive predictive values (80%) that were greater than those obtained with the ECG Milstein algorithm (77.1%, 91.5%, and 75%, respectively). The second step of the VCG algorithm made it possible to identify an AP location in one of the following sites: anterior right, lateral right, posterior right, posterior left, lateral left, or anterior left ventricle. The overall sensitivity, specificity, and positive predictive values were greater for the second step of the VCG algorithm than for the ECG criteria proposed by Gallagher (43.6% versus 39.3%, 92.1% versus 87.4%, and 51.5% versus 33.3%, respectively). It was concluded that the VCG seems to be more specific and sensitive than the ECG in the identification of the preexcitation site and should be given preference in the initial evaluation of the WPW syndrome.

Surgical treatment of ventricular tachycardia. Regional cryoablation guided by computerized epicardial and endocardial mapping.

Extended cryoablation as a single method of myocardial ablation was used for surgical treatment of 33 patients with ventricular tachycardia associated with coronary artery disease. Surgery was guided by roving-probe mapping in 14 patients and by computerized epicardial and computerized, left ventricular, endocardial, multielectrode mapping in 19 patients. In the latter group, the anatomic correlation between sites of the earliest epicardial activation (EA-EPI) and those of the earliest endocardial activation (EA-ENDO) was found to be consistent in the apical region. In contrast, the EA-ENDO corresponding to the EA-EPI localized in the left anterolateral and posterobasal free-wall regions could be localized either in an underlying area or on the septum. All tachycardias with EA-EPI in anterior and posterior right ventricular regions had their corresponding EA-ENDOs in the interventricular septum. EA-ENDO preceded EA-EPI in 33 of 41 tachycardias studied. The converse was observed in the remaining eight tachycardias. Cryoablation was applied regionally in areas corresponding to EA-ENDO, along with standard aneurysmectomy and coronary artery bypass grafting when indicated. Among the entire group of 33 patients, there were two (6%) operative deaths. Ventricular tachycardias recurred spontaneously in two (6%) patients and remained inducible in four (13%), of whom one (3%) died suddenly. After hospital deaths were taken into account, actuarial survival was 74 +/- 9% (mean +/- SD) at 48 months after operation. Among the 10 patients who had an EA-EPI on the right ventricle and an EA-ENDO on the interventricular septum, deep septal involvement was suspected, and arrhythmic failure occurred in five patients; in contrast, complete surgical success was obtained in all nine patients who did not display this pattern during intraoperative investigation. We conclude that regional cryoablation alone in areas of the earliest left ventricular activation is highly effective for treatment of ventricular tachycardia, except in a subset of patients with specific markers of deep septal involvement, which can be detected by computerized epicardial and endocardial mapping.