Intraoperative electrical ablation of ventricular arrhythmias: a "closed heart" procedure.

Both intraoperative endocardial mapping and surgical ablation for ventricular arrhythmias have until now required a ventriculotomy. Such an incision may be associated with an increase in morbidity and mortality, especially when performed through friable myocardium. A "closed heart" technique of intraoperative endocardial mapping and ablation of ventricular arrhythmias was developed in which a balloon array of 112 electrodes was introduced into the left ventricular cavity by a transmitral approach. The array permitted safe delivery of repeated electrical discharges of up to 150 J at each electrode. In four patients with coronary artery disease and no ventricular aneurysm, this "closed heart" technique was used to map and treat seven distinct ventricular tachycardias. The time taken to map each tachycardia varied from 3 to 13 minutes. Between 100 and 150 J was then delivered at each of 10 to 42 electrode sites, and the ablation procedure took 7 to 16 minutes per patient to complete. One patient died 24 hours postoperatively from preexisting thrombocytopenic purpura. There was no significant deterioration in left ventricular function in the three survivors and all have remained arrhythmia free, without antiarrhythmic agents, for 4 to 11 months. This technique offers a new method of surgical treatment of ventricular tachycardia without ventriculotomy, and is particularly suited to patients without a discernible left ventricular aneurysm.

Activation sequence of ventricular tachycardia: endocardial and epicardial mapping studies in the human ventricle.

Thirty-five patients with ischemic heart disease and ventricular arrhythmias underwent intraoperative activation mapping at the time of coronary artery bypass surgery. During ventricular tachycardia, the sequence of activation in the intact ventricle was recorded simultaneously from 110 endocardial or 110 epicardial sites, or both. A balloon array of electrodes, inserted across the mitral valve, was used to obtain endocardial recordings in the left ventricle, and this appeared to facilitate the induction of ventricular tachycardia. Of 61 episodes of tachycardia, 16 (15 patients) were recorded with the epicardial sock and 45 (20 patients) with the additional use of the endocardial balloon. The sequence of activation during tachycardia was observed to conform to one of four configurations: monoregional spread was the most common activation sequence recorded on both the endocardium and epicardium, while biregional activation and figure eight sequences were recorded exclusively on the epicardium and endocardium, respectively. The fourth sequence was a circular spread of activation observed on both surfaces. Continuous activation throughout the tachycardia cycle length was an infrequent finding. Simultaneous recordings of endocardial and epicardial activation were obtained in 45% of episodes. The sequence of activation recorded on one surface was matched by a similar sequence on the remaining surface in less than half of these. The onset of endocardial activation preceded that of the epicardium in greater than 90% of tachycardia episodes, and the duration of left ventricular endocardial excitation often exceeded that recorded epicardially over both ventricles. The epicardium, however, did appear to be an important determinant of surface electrocardiographic configuration.

Endocardial photoablation by excimer laser.

A xenon-chlorine excimer laser was used to irradiate normal endocardium of fresh sheep and pig hearts as well as unfixed human endocardial scar. Forty pulses of 370 J and 35 ns each resulted in penetration of up to 12 mm in normal tissue and only 3.5 mm in scarred endocardium. Dosimetry indicated that the volume of vaporized scarred tissue was 1/10th that of normal endocardium (0.19 to 0.40 versus 1.35 to 3.22 mm3/J). Ultrastructurally, there was a sharp demarcation of only 10 mu between the region of injury and normal myocardium, with little evidence of heat injury. The high power and short duration of these lasers coupled with the lack of a boundary zone of injury suggest that excimers may be an ideal tool for arrhythmia ablation.

Endocardial mapping of ventricular tachycardia in the intact human ventricle: evidence for reentrant mechanisms.

A balloon array of 112 electrodes was used to obtain simultaneous recordings of endocardial electrograms during intraoperative mapping studies of ventricular tachycardia. Introduction of the balloon through a left atriotomy and across the mitral valve allowed endocardial activation maps to be obtained in the intact left ventricle. Of 20 patients with coronary artery disease studied in this way, suggestive evidence of endocardial reentry was found in 6. Three separate reentrant mechanisms were observed. In two patients, a single broad wave front of continuous recirculating activation reminiscent of a vortex was initiated by the formation of a functional arc of block in response to premature stimuli. In five patients, premature stimuli again produced a functional arc of block, which was circumvented by two opposing wave fronts that united on the distal side. Retrograde penetration by a narrow isthmus of slow conduction through the block initiated the tachycardia, whose activation sequence was consistent with figure eight reentry. In one patient, premature stimuli produced a region of delayed potentials. Critical timing of these resulted in microreentry in an adjacent circumscribed site, which formed the site of origin of the ensuing tachycardia. The microreentrant signals were not detected by standard unipolar recordings, but were seen on simultaneously recorded high gain electrograms. In 14 patients, although mapping identified a site of origin, the activation patterns showed either radial spread or incomplete circles. Detection of reentrant mechanisms during intraoperative mapping required high density electrode arrays and refined high gain recordings. An intact ventricle may facilitate intraoperative initiation of tachycardia.

Endocardial mapping of ventricular tachycardia in the intact human heart. II. Evidence for multiuse reentry in a functional sheet of surviving myocardium.

OBJECTIVE: The purpose of this study was to obtain improved detection and characterization of reentrant circuits in the infarcted human ventricle. BACKGROUND: The return path of reentrant ventricular arrhythmias usually is not manifested in clinical mapping studies but is thought to be formed by isolated bundles of surviving myocytes whose presence is difficult to detect by standard recording techniques. METHODS: We obtained simultaneous unipolar and high gain bipolar recordings using a left ventricular endocardial balloon array in 10 patients with chronic ischemic heart disease undergoing intraoperative mapping of ventricular tachycardia. RESULTS: Three patients demonstrated seven separate ventricular tachycardias that utilized a return tract that was manifested on up to 20% of all left ventricular electrode sites. The recordings suggested an extensive sheet of surviving myocardial fibers with multiple entry and exit points allowing for different reentrant paths at different times all in the same heart. In one patient, five different ventricular tachycardias could be induced, four of which utilized such a sheet. Two of these tachycardias had the same exit point (site of origin) but two different entry points with a long and short return path resulting in long and short tachycardia cycle lengths. The same sheet sustained another tachycardia with one entry and two exit points resulting in two separate "sites of origin" on the endocardium. Such sheets also were seen to insert into the left bundle system. In one patient portions of the sheet could be detected epicardially. CONCLUSION: The existence of such a structure of surviving myocardium with functional pleomorphism may account for unexplained changes in tachycardia cycle length, epicardial entrainment and spontaneous morphologic changes during ventricular tachycardia.

On-line epicardial mapping of intraoperative ventricular arrhythmias: initial clinical experience.

An on-line automatic mapping system was developed for beat by beat display of epicardial activation during ventricular tachycardia induced at the time of cardiac surgery. A sock array of 110 button electrodes was used to record and display local activation on a video monitor at 8.3 ms intervals. On instant replay in slow motion, epicardial pacing sites were accurately localized to the nearest electrode. Local unipolar electrograms were also recorded, first from the sock array, then from an array of 16 transmural needle electrodes. The epicardial display was verified by retrospective manually derived maps using the recorded epicardial electrograms. In four patients with coronary artery disease and recurrent inducible ventricular tachycardia, earliest epicardial activation was located on slow motion replay within 1 minute. Subendocardial sites of early activation were located within 10 minutes by replay of electrograms from the needle array before ventriculotomy. Transmural and endocardial resection of these sites prevented inducibility of the tachycardia on postoperative electrophysiologic study in three of the four patients. There has been no clinical recurrence of ventricular tachycardia after 3 to 14 months of follow-up despite cessation of antiarrhythmic therapy in three of the patients. This technique has unique advantages over existing mapping methods. It provides beat by beat display of activation sequences so that clinical tachycardias that are short in duration or pleomorphic in configuration now become amenable to mapping. In addition, it markedly shortens total time on cardiopulmonary bypass.

Endocardial mapping of ventricular tachycardia in the intact human ventricle. III. Evidence of multiuse reentry with spontaneous and induced block in portions of reentrant path complex.

OBJECTIVES: This study was conducted to characterize the functional nature of the reentrant tract responsible for ventricular tachycardia due to ischemic heart disease. BACKGROUND: A zone of slow conduction forming the return path is though to form a critical component of the reentrant mechanism in ventricular tachycardia. Despite its importance, detailed knowledge of the return path is rare in clinical studies. METHODS: Multielectrode arrays were used intraoperatively to obtain unipolar and high gain bipolar recordings of left ventricular endocardium in patients undergoing map-directed surgical ablation of ventricular tachycardia. A total of 224 local electrograms were analyzed for each tachycardia. RESULTS: Of 10 consecutive patients undergoing intraoperative cardiac mapping, detailed recording of the return tracts of eight ventricular tachycardias were obtained in three patients. The recordings demonstrated that return tracts can be complex and extensive, with multiple paths of entry and exit. Potential and actual alternate paths were observed. Spontaneous and induced block occurred within portions of the complex. Intermittent block in one of two paths of entry resulted in intermittent cycle length changes of the tachycardia without a change in configuration. Block in one exit path resulted in a shift to alternative exit paths, with dramatic changes in ventricular activation and tachycardia configuration. Termination of the tachycardia could result from block close to the entrant or exit portion of the return tract. Different tachycardias were seen to share common portions of a return tract. CONCLUSIONS: These observations enlarge and extend our knowledge of the functional repertoire of complex reentrant tracts that occur in infarct-related ventricular tachycardia. The use of common portions of a reentrant tract by several tachycardias is confirmed. Utilization of alternate pathways can account for changes in configuration and cycle length. Spontaneous and induced block can occur at points of entry and exit in a reentrant tract and may identify optimal targets for ablation attempts. Further advances will require greater emphasis on diastolic activation mapping.

Mechanisms of spontaneous shift of surface electrocardiographic configuration during ventricular tachycardia.

OBJECTIVES: The aim of this study was to examine, with multichannel direct cardiac mapping techniques, the mechanisms of spontaneous shift of the QRS configuration in the surface electrocardiogram during episodes of ventricular tachycardia. BACKGROUND: Ventricular tachycardias demonstrating a spontaneous shift in their surface electrocardiographic (ECG) features are occasionally encountered. It is not known whether such changes in configuration are primarily due to a significant change in the tachycardia site of origin or represent alterations in patterns of endocardial and epicardial activation. Knowledge of these features would be helpful, particularly when ablative therapy is considered for the arrhythmias. METHODS: During map-directed cardiac surgery, episodes of ventricular tachycardia were mapped from 224 epicardial and endocardial sites. Episodes of pleomorphic tachycardia were identified and isochronal maps of endocardial and epicardial activation were constructed from representative beats before and after the change in configuration. RESULTS: From 52 consecutive patients who underwent detailed intraoperative mapping, 9 patients with pleomorphic ventricular tachycardia were identified in whom 14 episodes of spontaneous shift occurred. An analysis of the epicardial activation patterns revealed that the sites of earliest epicardial breakthrough showed significant alteration at the time of QRS shift in all occurrences. In 10 of these shift episodes, however, the sites of tachycardia origin, located on the endocardial surface, remained closely adjacent (< 2 cm apart). Although these sites of origin remained relatively constant, significant alterations in the patterns of endocardial activation were seen in most episodes. These included changes in the direction of propagation of the wave front of activation and shifts between monoregional and figure eight patterns of activation. CONCLUSIONS: In most episodes of pleomorphic ventricular tachycardia, the arrhythmia site of origin remains relatively constant. However, patterns of epicardial activation do undergo significant change and appear to be the major determinant of the QRS configuration on the surface ECG.

Sustained ventricular tachycardia in adult patients late after repair of tetralogy of Fallot.

OBJECTIVES: We sought to determine the features associated with sustained monoform ventricular tachycardia (VT) in adult patients late after repair of tetralogy of Fallot (TOF) and to review their management. BACKGROUND: Patients with repair of TOF are at risk for sudden death. Risk factors for ventricular arrhythmia have been identified from patients with ventricular ectopic beats because of the low prevalence of sustained VT. METHODS: From a retrospective chart review of patients assessed between January 1990 and December 1994, 18 adult patients with VT were identified and compared with 192 with repaired TOF free of sustained arrhythmia. RESULTS: There was no significant difference in age at repair, age at follow-up or operative history. Patients with VT had frequent ventricular ectopic beats (6 of 9 vs. 21 of 101), low cardiac index ([mean +/- SD] 2.4 +/- 0.4 vs. 3.0 +/- 0.8) and more structural abnormalities of the right ventricle (outflow tract aneurysms and pulmonary or tricuspid regurgitation) than control patients. Electrophysiologic map-guided operation was performed in 10 of 14 patients who required reoperation. VT has reoccurred in three of these patients. Four patients did not undergo operation (three received amiodarone; one underwent defibrillator implantation). Two patients with VT also had severe heart failure and died. CONCLUSIONS: Most patients with VT late after repair of TOF have outflow tract aneurysms or pulmonary regurgitation, or both. These patients have a greater frequency of ventricular ectopic beats than arrhythmia-free patients after repair of TOF. A combined approach of correcting significant structural abnormalities (pulmonary valve replacement or right ventricular aneurysmectomy, or both) with intraoperative electrophysiologic-guided ablation may reduce the potential risk of deterioration in ventricular function and enable arrhythmia management to be optimized.

Ventricular tachycardia after surgical repair of tetralogy of Fallot: results of intraoperative mapping studies.

OBJECTIVES: Four patients with previous repair of tetralogy of Fallot and ventricular tachycardia underwent map-guided surgery to ablate the arrhythmias. BACKGROUND: Although patients with repaired tetralogy of Fallot are at increased risk of sudden death due to ventricular tachycardia, little is known of the origin and mechanism of this arrhythmia. METHODS: A customized right ventricular balloon with 112 electrodes was used to record endocardial activation and, where possible, simultaneous epicardial recordings were obtained with a sock electrode array. Three patients had an aneurysm of the right ventricular outflow tract and one had a septal aneurysm. All had moderate to severe pulmonary valve insufficiency. Preoperative electrophysiologic study demonstrated inducible rapid (cycle length 180 to 300 ms) hemodynamically unstable monoform ventricular tachycardias. RESULTS: Intraoperatively, five different tachycardias (two in one patient) were induced and mapped. The sites of earliest activation were located in the subendocardium of the right ventricular outflow tract in all, but they varied widely among the septum, free wall and parietal band and could not be identified by visible scar. All were due to a macroreentrant circuit initiated by a critical delay in activation beyond a functional arc of block. Two patients treated by cryoablation while the heart was beating and perfused at normal temperature had inducible ventricular tachycardia postoperatively. In the two subsequent patients, the application of cryoablation under anoxic cardiac arrest resulted in noninducibility of arrhythmia. CONCLUSIONS: Ventricular tachycardia in tetralogy of Fallot in these four patients was caused by macroreentry in the right ventricular outflow tract. Surgical success depends on detailed mapping and cryoablation under anoxic cardiac arrest. In patients at risk of sudden death, map-directed surgery may offer distinct advantages over either implantable devices or drug therapy.

Use of telemetry functions in the assessment of implanted antitachycardia device efficacy.

Twenty patients (aged 50 +/- 21 years and mean left ventricular ejection fraction 37 +/- 17%) with recurrent ventricular arrhythmias were treated with an investigational, implantable combined antitachycardia-pacing cardioverter defibrillator. The device's telemetry capabilities include both stored (1-second snapshots) and real-time display of endocardial and device-circuit signals. The device can store these before, during and after up to 50 tachycardia and antitachycardia pacing episodes. All stored events are indexed to a 24-hour internal clock. During 10.1 +/- 5.1 months of follow-up, the device was used in 11 of 20 patients. In the entire group, antitachycardia pacing was activated on 44 +/- 14 occasions per patient (total 874) and shock delivery occurred on 8 +/- 14 occasions per patient (total 156). Reconstruction by stored telemetry of all device-therapy episodes was possible. Twenty-six percent of all shocks delivered were not appropriate and were due to atrial arrhythmias in 2 patients and dysfunction of the sensing lead in 3. The absence of a relation between symptoms and appropriate shock delivery was documented in 1 patient. Antitachycardia pace acceleration occurred in 5.3% of cases; 7% of attempts at pacing were unsuccessful and needed shock therapy. It is concluded that the enhanced telemetry available in newer antitachycardia devices enables more accurate assessment of device use and enhances diagnosis of inappropriate therapy delivery.

A new intraoperative approach for endocardial mapping of ventricular tachycardia.

Results of operation for control of ventricular tachycardia have improved since endocardial mapping techniques have been developed that allow a directed approach to the problem. In some patients, a limitation of established techniques has been difficulty in initiating the arrhythmia after a ventriculotomy has been made to allow introduction of endocardial recording electrodes. This paper describes a transatrial approach for endocardial mapping with a balloon array of 112 electrodes, which has been used intraoperatively in 15 patients. Surgical success in this group has been compared to that obtained in a similar group of patients in whom standard techniques of intraoperative mapping were used. With our new balloon technique we have been able to easily induce and map multiple episodes of ventricular tachycardia in all cases. On the basis of detailed endocardial maps, the locations of earliest activation and possible reentry loops have been identified and ablated with either endocardial excision or application of the cryoprobe. When indicated, concomitant procedures including aneurysm resection (9/15) and bypass grafting (14/15) have been performed. Hospital mortality in this group was 20%. None of the deaths have been related to recurrent ventricular tachycardia or complications of the mapping technique. Postoperative electrophysiologic studies performed at 2 weeks have been normal in 11 of 12 or 92% of patients. To date (mean follow-up 12 +/- 6 months) there has been no clinical recurrence or evidence of ventricular tachycardia by Holter monitoring in these patients. We conclude that the transatrial balloon approach to endocardial mapping facilitates intraoperative induction of ventricular tachycardia, allows complete mapping during multiple runs of the arrhythmia without prolonging cardiopulmonary bypass time, and improves results of operation using standard ablation techniques.

Transatrial balloon technique for activation mapping during operations for recurrent ventricular tachycardia.

Results of operations for recurrent ventricular tachycardia have improved since methods of mapping that allow a directed approach to the problem have been developed. With standard operative techniques (ventriculotomy and introduction of a hand-held probe or multiple electrode array), it has not always been possible to obtain satisfactory endocardial activation maps during the tachycardia. We have recently developed a new transatrial balloon approach that has greatly facilitated intraoperative mapping. This paper describes our total experience with the new approach and draws attention to details of the cardiopulmonary bypass technique and the surgical approach needed for safe balloon insertion across the mitral valve. We describe how correlation between position of target electrodes on the balloon and the internal geometry of the heart is achieved and discuss the choice and application of appropriate ablation techniques. In our series of 37 consecutive patients, 35% had a grade IV ventricle (ejection fraction less than 20%), 32% had a previous posterior infarct, 51% did not have a resectable aneurysm, and 54% had been receiving amiodarone within 1 month of the operation. These factors have been associated with poor operative results in other series. With the transatrial balloon technique, we were able to induce and map ventricular tachycardia in 100% of patients (average 2.6 +/- 1.3 morphologies per patient). Using a variety of ablation techniques (endocardial excision, cryoablation, or balloon electric shock ablation), we have achieved surgical control of the arrhythmias in 84% of patients with an operative mortality rate of 14%. We recommend transatrial balloon mapping as the procedure of choice for intraoperative identification of arrhythmogenic foci in patients with recurrent ventricular tachycardia.

Reoperation in adults with repair of tetralogy of fallot: indications and outcomes.

OBJECTIVE: The purpose of this study is to review indications, surgical procedures, and outcomes in adults with repaired tetralogy of Fallot referred for reoperation. METHOD: Sixty consecutive adults (age >/= 18 years) who underwent reoperation between 1975 and 1997 after previous repair of tetralogy of Fallot were reviewed. Mean age at corrective repair was 13.3 +/- 9.6 years and at reoperation 33.3 +/- 9.6 years. Mean follow-up after reoperation is 5.0 +/- 4.9 years. RESULTS: Long-term complications of the right ventricular outflow tract (n = 45, 75%) were the most common indications for reoperation: severe pulmonary regurgitation (n = 23, 38%) and conduit failure (n = 13, 22%) were most frequent. Less common indications were ventricular septal patch leak (n = 6) and severe tricuspid regurgitation (n = 3). A history of sustained ventricular tachycardia was present in 20 patients (33%) and supraventricular tachycardia occurred in 9 patients (15%). A bioprosthetic valve to reconstruct the right ventricular outflow tract was used in 42 patients. Additional procedures (n = 115) to correct other residual lesions were required in 46 patients (77%). There was no perioperative mortality. Actuarial 10-year survival is 92% +/- 6%. At most recent follow-up, 93% of the patients are in New York Heart Association classification I or II. Sustained ventricular tachycardia occurred in 4 patients (7%) during follow-up. CONCLUSIONS: Long-term complications of the right ventricular outflow tract were the main reason for reoperation. Mid-term survival and functional improvement after reoperation are excellent.

Late results of operation for ventricular tachycardia.

We have analyzed results in 54 consecutive patients with recurrent ventricular tachycardia and coronary artery disease in whom we used an aggressive surgical approach involving map-directed ventricular tachycardia ablation, scar excision and left ventricular remodeling, and coronary artery bypass grafting, as well as staged mitral valve replacement when necessary. We have previously shown age greater than 65 years to be an independent predictor of mortality and have excluded such patients from this series. Average age was 56 +/- 7 years. All patients had a previous myocardial infarction; 24% of the infarctions (13/54) were posterior in location. Symptoms included syncope or presyncope in 83% of the patients (45/54), angina in 54% (29/54), and congestive heart failure in 52% (28/54). Extensive coronary artery disease was found in 78% (42/54), and 89% (48/54) had serious compromise of left ventricular function (ejection fraction < 0.40; average ejection fraction, 0.28 +/- 0.12). Only 63% (34/54) appeared to have a resectable left ventricular aneurysm on the preoperative angiogram. Ablation techniques included endocardial excision in 82% (44/54), with the addition of cryoablation in 60% (32/54), and balloon electric shock ablation in 22% (12/54); coronary artery bypass grafting was performed in 85% (46/54). There were four hospital deaths (7%). The surgical cure rate (no inducible VT at postoperative electrophysiologic study was 72% (39/54). During follow-up (mean, 50 +/- 31 months) there have been six late deaths (1 sudden death, 1 stroke, 4 congestive heart failures with or without mitral regurgitation). Four patients with progressive congestive heart failure and serious mitral regurgitation have undergone repeat operation for mitral valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Are patients receiving amiodarone at increased risk for cardiac operations?

Amiodarone therapy has been implicated as a risk factor for cardiothoracic surgical procedures. In patients undergoing map-guided surgical procedures for the treatment of ventricular tachycardia, we compared the perioperative course of those receiving long-term amiodarone therapy (n = 36) versus that in those not receiving the drug (n = 31). The two groups were similar with respect to age, sex, presenting symptoms, functional class, extent of coronary artery disease, presence of a ventricular aneurysm, technique of ventricular tachycardia ablation, cross-clamp or pump time, the number of vessels grafted, the operative fluid balance, and a need for intraaortic balloon pump or inotropic agent support. In 5 patients receiving amiodarone, epinephrine was required to maintain a normal systemic vascular resistance and adequate arterial pressure. Postoperatively, 6 patients (17%) on amiodarone therapy suffered acute respiratory failure. In spite of aggressive therapy, 3 of these patients died. Only 1 patient not receiving amiodarone died of a stroke. We conclude that amiodarone therapy in patients undergoing open heart operations is associated with an increased risk of severe pulmonary complications (p = 0.03 by Fisher's exact test). Amiodarone therapy should be withheld in patients with ventricular tachycardia until they have been assessed as candidates for possible surgical intervention.

Characteristics of local electrograms with diastolic potentials: identification of different components of return pathways in ventricular tachycardia.

BACKGROUND: Diastolic potentials are often sought as a possible site for catheter ablation in post-infarct ventricular tachycardia. However, delivery of energy at such sites is often unsuccessful. The purpose of this study was to determine the characteristics of local electrograms with diastolic potentials and to identify activation pattern which might indicate the critical portion of the return path of the ventricular tachycardia reentry circuit. METHODS: In 17 patients with post-myocardial infarction ventricular tachycardia, 30 ventricular tachycardias were mapped with an 112 bipolar endocardial balloon at the time of surgery. Diastolic mapping of the return tract in ventricular tachycardia was performed. Four activation patterns were observed (15 figure 8 patterns, 2 circular patterns, 2 biregional patterns and 11 monoregional patterns). Of 3,360 local electrograms, 207 (6.2%) demonstrated a diastolic potential in ventricular tachycardia. They were classified into following four categories, based on the appearance and timing of the systolic component. Type A-1 electrogram: systolic activation was of low amplitude (< 2 mV) and was prolonged (> or = 100 msec), but preceded the onset of the surface QRS in ventricular tachycardia. Type A-2 electrogram: systolic activation was of low amplitude, was prolonged, but followed the onset of the surface QRS. Type B electrogram: systolic electrogram was fractionated, but relatively normal amplitude (2.0-3.6 mV). Type C electrogram: systolic electrogram was almost normal. RESULTS: Of all electrograms with diastolic potentials, three type A-1 electrograms (1.4%) were located at the exit of the return pathway, 11 type A-1 electrograms (5.3%) were located at the pre-exit site. No type A-1 was found at an entrance/bystander area. 21 type A-2 electrograms (10.1%) were at the pre-exit and 83 type A-2 electrograms (40.2%) were located at the entrance/bystander area, but such electrograms were never found at the exit site. 71 type B electrograms (34.3%) and 18 type C electrograms (8.7%) were located at the entrance/bystander area. To distinguish the type A-2 electrograms at the pre-exit site from those at the entrance/bystander area, the diastolic potential to QRS interval was measured. This interval at the pre-exit was significantly shorter than that at the entrance/bystander area (-47.2 +/- 10.7 vs -96.3 +/- 31.3 msec, p = 0.0001). CONCLUSION: Type A-1 electrograms indicated the exit or pre-exit site of return pathway. Type A-2 electrograms with diastolic potential to QRS interval < -50 msec indicated the pre-exit site. However, the other types of local electrograms with diastolic potential did not indicate the critical portion of the ventricular tachycardia circuit. These observations may be helpful during catheter mapping and ablation of patients with post-infarct ventricular tachycardia. CONDENSED ABSTRACT: Diastolic potentials are often sought to direct catheter ablation in post-infarct ventricular tachycardia. We investigated the characteristics of local electrograms showing diastolic activity in an attempt to determine whether critical portions of the ventricular tachycardia circuit could be identified by a typical "signature." In 17 patients with a remote myocardial infarction, 30 ventricular tachycardias were mapped with 112 bipolar endocardial balloon at the time of surgery. Diastolic potentials in association with low amplitude (< 2 mV) and prolonged (> or = 100 msec) systolic electrograms preceding the onset of QRS were found at the exit site and pre-exit site of return pathway. A similar systolic electrogram occurring after QRS onset with a diastolic potential to QRS interval of < -50 msec was found at the pre-exit site. However, other local electrograms with diastolic activity were at sites remote from the exit or pre-exit of the return pathway. These observations may be helpful during catheter mapping and ablation in patients with ventricular tachycardia.

Sotalol in patients with implanted automatic defibrillators: effects on defibrillation and comparison with amiodarone.

OBJECTIVES: Although many patients receiving implanted cardioverter defibrillators receive concomitant antiarrhythmic therapy, the risks and benefits of different agents for such patients are not well understood. It was hypothesized that sotalol, a drug with beta-blocking and class II antiarrhythmic properties would be useful in these patients. DESIGN: Nonrandomized prospective cohort study of the effects of sotalol versus other antiarrhythmic therapy on defibrillation energy requirements. SETTING: Tertiary care referral centre. PATIENTS: Patients referred for management of life threatening ventricular arrhythmia in whom an implanted cardioverter defibrillator was indicated on standard clinical grounds. INTERVENTIONS: Intraoperative testing of defibrillation energy requirements, exercise testing, electrophysiological testing. MAIN RESULTS: Fifteen patients were treated with oral sotalol (173.3 +/- 59.8 mg/day). Sotalol blunted maximal heart rate during treadmill exercise (120.9 +/- 29.9 beats/min). Mean right ventricular effective refractory period increased from 251.7 +/- 21.7 to 276.7 +/- 25.7 ms (P = 0.05). All patients received one large (28 cm2) and one small (14 cm2) epicardial electrode patch. The lowest energy to defibrillate successfully from induced ventricular fibrillation (VF) was 5.9 +/- 3.7 J (median 4.1 J), with all patients defibrillated at 15 J or less. In a concurrent comparison group of 16 similar patients not treated with sotalol (13 on amiodarone and three on beta-blockers), with identical or larger patch size, and identical placement, the lowest successful energy to defibrillate from induced VF was significantly higher (16 +/- 8.8 J) (P < 0.05). Mean cycle length of VF from intracardiac recordings was 232 +/- 37 ms, and was significantly inversely correlated with lowest successful energy (r = 0.61, P < 0.05). CONCLUSIONS: Oral sotalol may be useful in conjunction with an automatic defibrillator; it is associated with low defibrillation energy requirements in humans, and may alter VF.

Antiarrhythmic potential of chloroquine: new use for an old drug.

Amiodarone and chlorpromazine are phospholipase inhibitors which produce cytoplasmic inclusion bodies and have important electrophysiologic properties. Chloroquine also inhibits phospholipase activity, resulting in similar inclusion bodies, but electrophysiologic information about this drug is lacking. In this study, the cellular electrophysiologic effects of two doses of chloroquine were examined in sheep Purkinje fibres and ventricular muscle cells. Both concentrations produced a significant reduction in maximum velocity of upstroke of the action potential and prolongation of the action potential duration and refractory period in Purkinje fibres. These effects were observed in the absence of significant changes in threshold of stimulation or action potential amplitude and were partially reversible following washout of the lower drug concentration. In addition to these experimental data, clinical evidence of antiarrhythmic action was determined by administering 500 mg chloroquine daily over nine weeks to six subjects with frequent asymptomatic ventricular premature complexes. In four patients there was a reduction in ventricular ectopy, which recurred when the drug was discontinued, while a fifth patient reverted to sinus rhythm from atrial fibrillation previously resistant to other antiarrhythmic medication. Thus, chloroquine has important electrophysiologic properties. The underlying mechanism of this action remains unproven at the present time.