Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia

Intraoperative pace-mapping has been proposed as a method of identifying the origin of ventricular tachycardia; however, both epicardial activation and electrocardiographic configuration have limitations in localizing the origin of ventricular tachycardia. Because most ventricular tachycardias associated with ischemic heart disease appear to arise near the endocardium, this study evaluated the ability of bipolar catheter endocardial pacing at or near the endocardial site of origin of spontaneous ventricular tachycardia to mimic the QRS configuration of the spontaneous tachycardia. Twelve patients were studied who had ventricular tachycardia whose origin was determined with catheter endocardial mapping. Three patients had ventricular tachycardia with two distinct configurations. The electrocardiogram of ventricular tachycardia was compared with the electrocardiogram produced by pacing at the site of origin (10 patients) and at multiple (two to nine) additional sites in 8 patients. It was observed that (1) pacing at the known site of origin of ventricular tachycardia produced an electrocardiogram and activation sequence similar to those produced by the ventricular tachycardia; (2) pacing at sites in close proximity to the site of origin of ventricular tachycardia produced either a similar or a grossly different electrocardiographic pattern from that during ventricular tachycardia.It is concluded that catheter endocardial pace-mapping (1) is a corroborative method of identifying the origin of ventricular tachycardia; (2) may be useful in patients with noninducible ventricular tachycardia or rapid ventricular tachycardia who cannot undergo catheter or intraoperative mapping; and (3) is neither easier, more accurate nor quicker than direct localization by mapping during ventricular tachycardia.     

Electrocardiographic localization of the site of origin of ventricular tachycardia in patients with prior myocardial infarction

The utility of the 12 lead electrocardiogram (ECG) in identifying the site of origin of sustained ventricular tachycardia in patients with previous myocardial infarction was studied. A new mapping grid, based on biplanar fluoroscopic imaging of the heart, was utilized for the definition of left ventricular endocardial sites. On the basis of QRS configurations resulting from left ventricular endocardial pacing at disparate sites in 22 patients (Group I), ECG features that were specific for particular sites were identified and used to construct an algorithm. Apical and basal sites were differentiated by the QRS configuration in leads V4 and aVR, anterior and inferior sites by that in leads II, III and V6 and septal and lateral sites were differentiated using leads I, aVL and V1. The algorithm was used to predict the site of earliest endocardial activation during 44 episodes of sustained ventricular tachycardia in a second group of 42 patients (Group II) in a blinded fashion. Anterior sites were correctly predicted in 83% of cases, inferior sites in 84%, septal sites in 90% and lateral sites in 82% of cases. Apical and basal sites were each correctly predicted in 70% of cases, whereas intermediate sites were less well predicted (29 to 55%) on the basis of QRS configuration. Precise localization of the site of origin of ventricular tachycardia (in all three planes) was achieved in 17 cases (39%), and in 16 cases (36%) the site of origin was immediately adjacent to the predicted site. Prediction of the site of origin of ventricular tachycardia from the 12 lead ECG may serve as a useful, time-saving adjunct to, but not a substitute for, activation sequence mapping during ventricular tachycardia.     

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.     

Patterns of interectopic activation recorded during pleomorphic ventricular tachycardia after myocardial infarction in the dog

Sustained ventricular tachycardia, consisting of a regular rhythm with 100 or more consecutive ectopic beats, was studied in 14 dogs anesthetized with sodium pentobarbital 4 days after occlusion of the left anterior descending coronary artery. Electrocardiograms were recorded as well as composite (epicardial) and electrode catheter (endocardial) electrograms from the area of infarction. Sustained ventricular tachycardia was induced by atrial or ventricular pacing, or both (180 to 360/min) in 3 of 21 untreated dogs and 11 of 19 dogs treated with methylprednisolone (30 mg/kg body weight, intravenously) given at the time of coronary occlusion. Sustained ventricular tachycardia with two or more QRS configurations occurred in nine dogs, and seven dogs showed both right and left bundle branch block patterns. Ventricular tachycardia was associated with continuous electrical activation in composite epicardial electrograms that bridged interectopic intervals and showed regular patterns of electrical activation that were reproducible with each cardiac cycle. Interectopic activation patterns were distinctive for each QRS pattern. In some instances portions of activation patterns for two different configurations were similar; however, the electrographic configuration immediately before the onset of the QRS complex always differed. During ventricular tachycardia, spontaneous alterations in QRS configuration were observed in two dogs and were induced by atrial or ventricular pacing in five dogs. In all cases changes in QRS configuration during sustained ventricular tachycardia were preceded by changes in diastolic activation patterns.The results suggest that sustained ventricular tachycardia is frequently associated with stable reentrant pathways through areas of critically slow conduction. In this experimental preparation, specific, orderly and reproducible patterns were seen more often than chaotic “localized fibrillation.” Different QRS configurations after changes in interectopic patterns of continuous electrical activation are consonant with changes in specific reentrant pathways through the region of slow conduction.     

Twelve-lead ECG features to identify ventricular tachycardia arising from the epicardial right ventricle.

BACKGROUND: Usefulness of 12-lead ECG for predicting an epicardial origin for ventricular tachycardia (VT) arising from the right ventricle (RV) has not been assessed. An epicardial approach is sometimes warranted to eliminate RV VT. OBJECTIVES: The purpose of this study was investigate the hypothesis that specific ECG features identify an epicardial origin for RV VT. METHODS: To mimic an endocardial or epicardial origin, we paced representative sites in 13 patients undergoing RV endocardial/epicardial mapping (134/180 pace map sites). RESULTS: QRS duration from epicardial vs endocardial sites was not different (183 +/- 27 ms vs 185 +/- 28 ms, P = .3). Reported cut-off values for identifying epicardial left ventricular origin, pseudo-delta wave (> or =34 ms), intrinsicoid deflection time (> or =85 ms), and RS complex (> or =121 ms) did not apply to the RV. A Q wave in lead II, III, or aVF was more likely noted from inferior epicardial vs endocardial sites (53/73 vs 16/43, P <.01). A Q wave in lead I was more frequently present from epicardial vs endocardial anterior RV sites (30/82 vs 5/52, P <.001). QS in lead V(2) was noted from anatomically matched epicardial anterior RV sites (22/33 vs 13/33, P <.05). In the RV outflow tract, no ECG feature distinguishing epicardial/endocardial origin reached statistical significance. CONCLUSION: A Q wave or QS in leads that best reflect local activation suggest an epicardial origin for RV depolarization and may help in identifying a probable epicardial site of origin for RV VT. QRS duration and reported criteria for epicardial origin of VT in the left ventricle do not identify a probable epicardial origin in the RV.     

Site-specific twelve-lead ECG features to identify an epicardial origin for left ventricular tachycardia in the absence of myocardial infarction.

BACKGROUND: Identification of an epicardial origin for left ventricular tachycardia (LV-VT) based on electrocardiogram (ECG) criteria facilitates the approach to catheter ablation. Reported criteria, although helpful, may not apply uniformly to all LV regions. OBJECTIVE: We hypothesized that unique region-specific ECG patterns identify epicardial LV-VTs in patients without myocardial infarction. METHODS: The QRS morphologies during pace mapping from 402 epicardial and 234 comparable endocardial sites and 19 epicardial VTs were analyzed in 15 patients with respect to morphology and duration of all and components of the QRS. RESULTS: Basal superior (N = 244) and apical superior (N = 141) pace mapping sites showed Q wave in lead I more commonly from epicardial vs corresponding endocardial sites (90% vs 16%, 88% vs 26% respectively; P <.001). The absence of Q wave in leads II-III-aVF identified epicardial basal superior sites, P = .002. Basal inferior (N = 140) and apical inferior (N = 76) epicardial sites showed Q wave in leads II-III-aVF (81% vs 37%, 92% vs 33%, P <.001). These morphologic criteria identified 16 of 19 VTs. The QRS duration was longer from the epicardium, 213 +/- 45 ms vs 191 +/- 41 ms, P <.001, although significant overlap existed. Reported criteria (pseudodelta wave > or =34 ms, intrinsicoid deflection time > or =85 ms, and shortest RS complex > or =121 ms) were region specific in their ability to identify epicardial origin, with some criteria not having value in specific regions and sensitivity/specificity varying from 14% to 99% and 20% to 94%. CONCLUSION: ECG features distinguishing epicardial LV-VT are site specific, including the presence or absence of a Q wave in leads that reflect local ventricular activation.     

Epicardial activation patterns of torsade de pointes in canine hearts with quinidine-induced long QT interval but without myocardial infarction

We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained polymorphic ventricular tachycardia and six episodes of monomorphic ventricular tachycardia were induced. Of 22 episodes of nonsustained polymorphic ventricular tachycardia, 12 episodes showed typical torsion of the spikes of the QRS complex around the isoelectric line (torsade de pointes). Isochronal maps were made from 38 simultaneously recorded bipolar electrograms and showed that each change in QRS morphology was associated with a change in the earliest epicardial activation site and/or a change of epicardial activation sequence. During episodes of torsade de pointes, the earliest epicardial activation site migrated gradually from one site to another site. The transitional QRS complexes had their earliest epicardial activation sites between the new and old site of the earliest epicardial activation. The changes in the earliest epicardial activation site during polymorphic ventricular tachycardia without torsade de pointes pattern was not as great as that noted during torsade de pointes. This study suggests that in a noninfarcted canine model torsade de pointes is produced by alteration in the earliest site of activation rather than by competition from two or more competing foci.     

Possible intramural site of reentrant circuit in ventricular tachycardia of nonischemic cause. Pre and intraoperative mapping studies.

A patient with a drug-refractory sustained ventricular tachycardia (VT) of nonischemic cause was mapped for the site of VT origin. The intraoperative mapping showed the earliest site of activation of VT on the epicardial surface at which the initial deflection of the local electrogram preceded the onset of the QRS complex of VT by 45 msec. The endocardial mapping could not indicate the site at which the electrogram was found prior to the onset of the QRS complex of VT. However, at the earliest site of the endocardial mapping, VT was entrained without change in the configuration of the QRS complex. After cessation of the rapid pacing, VT resumed at the intrinsic rate and the first post-paced return cycle was identical to each paced cycle length. The interval from the stimulus to the orthodromically captured local electrogram at the pacing site was identical to the cycle length of VT. Catheter ablation from the endocardial side and a cryoablative procedure from the epicardial side failed to eradicate the VT. These findings suggest an intramural site of VT origin and reentrant circuit of which the exit and the entrance face the epicardial and the endocardial surfaces, respectively.     

Mechanisms Underlying Different Surface ECG Morphologies of Recurrent Monomorphic Ventricular Tachycardia and Their Modification by Procainamide

ECG Pleomorphism of Ventricular Tachycardia. Introduction: Distinct surface ECG morphologies (ECGMs), from one episode to the next, of recurrent monomorphic ventricular tachycardia (VT) in the same patient complicate endocardial catheter mapping and the success of ablative therapy. This study investigates the incidence and mechanisms of multiple ECGMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI). Methods and Results: Computerized ECG analysis and simultaneous endocardial and epicardial activation mapping with a 64 bipolar electrode array were used to analyze the relation between site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI. Pairwise comparisons of all VTs induced in the same animal were done in drug-free state (47 VTs) and after intravenous procainamide (25 VTs). In drug-free state, VT pairs with similar surface ECGMs manifested endocardial hreak-through sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001). Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001). Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocardial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with similar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS). Conclusions: In the same heart, similar surface ECGMs of recurrent VT are highly predictive of closely spaced endocardial BSs in drug-free state, hut not after procainamide administration. Nearly half of the VTs with different surface ECGMs still originate from closely spaced endocardial BSs but commonly manifest a change in the endocardial activation spread from this site. Thus, assumptions about different mechanisms and sites of VT origin based on dilTerent surface ECGMs should be made with caution.     

Termination of ventricular tachycardia with epicardial laser photocoagulation: a clinical comparison with patients undergoing successful endocardial photocoagulation alone

Electrical activation-guided laser photocoagulation was used intraoperatively to terminate ventricular tachycardia in patients with ischemic heart disease. During ventricular tachycardia, laser irradiation was delivered to mapped sites with local diastolic activation. In 30 long-term survivors, 85 ventricular tachycardia configurations were terminated by ablation; 72 (84.7%) were terminated by endocardial photocoagulation. Thirteen (15.3%) required epicardial photocoagulation; however, these 13 ventricular tachycardias occurred in 10 (33%) of the 30 patients. An aneurysm was present in 70% of patients with successful endocardial photocoagulation, but in only 10% of patients requiring epicardial photocoagulation for at least one ventricular tachycardia configuration; 90% of all patients requiring epicardial laser photocoagulation had no aneurysm and had either a right or a left circumflex coronary artery-related infarction. In this group, epicardial activation data were similar to those described for ventricular tachycardia with an "endocardial" origin and included 1) delayed potentials during sinus rhythm, 2) presystolic or pandiastolic activation sequences during ventricular tachycardia, and 3) regions of block near the presumed region of reentry during ventricular tachycardia. This study suggests that the critical anatomic substrates supporting reentry in postinfarction ventricular tachycardia may occur at intramural or epicardial sites, particularly in patients with right or circumflex coronary artery-related infarction and no aneurysm.     

Endocardial and Epicardial Ablation Guided by Nonsurgical Transthoracic Epicardial Mapping to Treat Recurrent Ventricular Tachycardia

Nonsurgical Epicardial Ablation. Introduction : An epicardial site of origin of ventricular tachycardia (VT) may explain unsuccessful endocardial radiofrequency (RF) catheter ablation. A new technique to map the epicardial surface of the heart through pericardial puncture was presented recently and opened the possibility of using epicardial mapping to guide endocardial ablation or epicardial catheter ablation. We report the efficacy and safety of these two approaches to treat 10 consecutive patients with VT and Chagas' disease.
Methods and Results : Epicardial mapping was carried out with a regular steerable catheter introduced into the pericardial space. An epicardial circuit was found in 14 of 18 mapable VTs induced in 10 patients. Epicardial mapping was used to guide endocardial ablation in 4 patients and epicardial ablation in 6. The epicardial earliest activation site occurred 107 ± 60 msec earlier than the onset of the QRS complex. At the epicardial site used to guide endocardial ablation, earliest activation occurred 75 ± 55 msec before the QRS complex. Epicardial mid-diastolic potentials and/or continuous electrical activity were seen in 7 patients. After 4.8 ± 2.9 seconds of epicardial RF applications, VT was rendered noninducible. Hemopericardium requiring drainage occurred in 1 patient; 3 others developed pericardial friction without hemopericardium. Patients remain asymptomatic 5 to 9 months after the procedure. Interruption during endocardial pulses occurred after 20.2 ± 14 seconds (P = 0.004), hut VT was always reinducible and the patients experienced a poor outcome.
Conclusion : Epicardial mapping does not enhance the effectiveness of endocardial pulses of RF. Epicardial applications of RF energy can safely and effectively treat patients with VT and Chagas' disease.     

Successful radiofrequency catheter ablation of incessant ventricular tachycardia with a delta wave-like beginning of the QRS complex

Ventricular tachycardia with a delta wave-like beginning of the QRS complex is considered to be refractory to endocardial catheter ablation because it originates from the epicardial region. A 45-year-old woman had incessant ventricular tachycardia with a delta wave-like beginning of the QRS complex which was resistant to several antiarrhythmic drugs. The origin of the arrhythmia was at the mitral annulus on the antero-lateral left ventricular wall. The earliest endocardial activation preceded the QRS complex by 18 msec. After 7 sec of endocardial radiofrequency application ventricular tachycardia was terminated. During a 2 year follow-up ventricular tachycardia did not recur and only small numbers of premature ventricular contractions (< 100/day) were noted. VT with delta wave-like QRS morphology which originates from the basal region of the ventricle may be treated successfully with radiofrequency catheter ablation using an endocardial approach.     

Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation

BACKGROUND. Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry. METHODS AND RESULTS. This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface. CONCLUSIONS. This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.     

Successful radiofrequency ablation of adenosine-sensitive right ventricular outflow tract tachycardia

We report on a patient without evidence of structural heartdisease who presented with adenosine-sensitive sustained ventriculartachycardia with left bundle branch block and right axis QRSmorphology. Endocardial catheter mapping revealed the originof ventricular tachycardia to be located in the right ventricularoutflow tract, where the earliest endocardial activation duringventricular tachycardia was registered 30–40 ms priorto onset of QRS complex in the surface ECG. Pacemapping providedno additional information; we found a good match between 12lead surface ECGs registered during spontaneous episodes ofventricular tachycardia and those recorded during pacing ina relatively large area in the right ventricular outflow tract.The 10th application of radiofrequency current abolished ventriculartachycardia temporarily, but it recurred within 30 min. Afterthe 28th radiofrequency current delivery ventricular tachycardiawas permanently abolished.     

Epicardial Macro-Reentrant Ventricular Tachycardia Exhibiting an Endocardial Centrifugal Activation Pattern in a Case with Arrhythmogenic Right Ventricular Cardiomyopathy

A 55-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent catheter ablation of ventricular tachycardia (VT) with left bundle branch block and left superior axis QRS morphology with an early precordial transition. Endocardial mapping during the VT revealed a focal activation pattern from a small region of low voltage in the left ventricular (LV) septum. Despite earliest endocardial activation in the LV septum, epicardial mapping demonstrated a macro-reentrant circuit with successful catheter ablation at an inferior peritricuspid annular site. Activation from the reentrant circuit propagated through the scar area in the epicardial right ventricle to the remote endocardial LV breakout site.     

特发性室性心动过速的射频消融

目的:对经射频消融术证实的特发性室性心动过速的病例进行总结分析,探讨室性心动过速的发病状况、心电图特点、消融靶点的确定及消融结果。方法:对68 例特发性室性心动过速的起源部位和体表心电图进行分析,所有患者在诱发出室性心动过速后进行射频消融治疗,观察特发性室性心动过速的射频消融成功率和复发率以及它们和消融靶点的关系。结果:本组特发性室性心动过速患者中右室室性心动过速较左室室性心动过速多见。右室特发性室性心动过速心电图表现为左束支传导阻滞,左室特发性室性心动过速心电图则多表现为右束支传导阻滞。消融靶点的确定右室特发性室性心动过速主要采用起搏标测法,左室特发性室性心动过速主要采用激动顺序标测法。右室流出道室速组在起搏标测时起搏ECG和VT时ECG的12导联QRS波完全相同处消融成功率较高。结论:室性心动过速发作时的体表心电图可初步估计特发性室性心动过速的起源部位,射频消融术治疗特发性室性心动过速成功率高,并发症少。     

射频消融特发性室性心动过速的标测方法初探（附五例分析）

５例特发性室性心动过速（ＶＴ）经射频电流导管消融（ＲＦＣＡ）而获治愈。本文从成功的ＲＦＣＡ结果着重探讨特发性ＶＴ兴奋灶的标测方法。心内膜激动时间标测，以局部电图较体表导联ＱＲＳ波时间提前≥１０ｍｓ处定为心室最早激动点（ＥＶＡ），５例平均心室最早激动至ＱＲＳ波起始时间为１８±１１．７ｍｓ，在ＥＶＡ处放电消融仅１例成功。采用起搏标测法定位以略低于自发ＶＴ的频率沿ＥＶＡ上下左右逐点标测，寻找起搏电图至少１１个导联的ＱＲＳ波形态、振幅、极性与自发ＶＴ相同的标测点放电消融，４例均获成功。消融成功的局部电图较ＱＲＳ波平均提前２６±１２．８ｍｓ。结果提示联合应用心内膜激动时间标测和起搏标测并侧重于后者，可能是提高ＲＦＣＡ特发性ＶＴ成功率的一种有效方法。     

Epicardial ablation of ventricular tachycardia using a new high-density mapping system

We report the case of a 44-year-old woman who was referred for ablation of recurrent ventricular tachycardia (VT) in the setting of dilated cardiomyopathy secondary to myocarditis. The ECG displayed a right bundle branch block morphology and superior axis in the frontal plane, associated with a pseudo delta wave in the precordial leads that suggested an epicardial origin.Cardiac magnetic resonance performed prior to the procedure showed late gadolinium enhancement at the lateral wall of the left ventricle (LV) and excluded subendocardial fibrosis in either ventricle. This information was crucial and influenced the ablation strategy, identifying the target area as exclusively epicardial, thus avoiding unnecessary mapping of the endocardial surface of the LV.Epicardial activation mapping and ablation during VT were performed using the Orion® high-density catheter (Boston Scientific Inc.) and the Rhythmia® mapping system (Boston Scientific Inc.). Applications near the exit site immediately terminated the tachycardia, which was no longer inducible.One year after the procedure the patient was still in sinus rhythm with no episodes of VT or non-sustained VT recorded by continuous monitoring via an implanted cardioverter-defibrillator.     

特发性室性心动过速的射频消融

目的对经射频消融术证实的特发性室性心动过速的病例进行总结分析,探讨室性心动过速的发病状况、心电图特点、消融靶点的确定及消融结果。方法对32例特发性室性心动过速的起源部位和体表心电图进行分析,所有患者在诱发出室性心动过速后进行射频消融治疗,观察特发性室性心动过速的射频消融成功率和复发率,以及它们和消融靶点的关系。结果右室特发性室性心动过速心电图表现为左束支传导阻滞,左室特发性室性心动过速心电图则多表现为右束支传导阻滞。消融靶点的确定右室特发性室性心动过速主要采用起搏标测法,左室特发性室性心动过速主要采用激动顺序标测法。右室流出道室速组在起搏标测起搏ECG和VT时ECG的12导联QRS波完全相同处消融成功率较高。结论室性心动过速发作时的体表心电图可初步估计特发性室性心动过速的起源部位,射频消融术治疗特发性室性心动过速成功率高、并发症少。     

Signal Averaging of the Surface QRS Complex: Practical Applications

Signal-Averaged ECG. Signal averaging of the surface QRS complex has been used in recent years to detect electrical signals of small amplitude not otherwise evident on the surface ECG. The technique enables detection of low-amplitude signals in the terminal portion of the QRS complex and the ST segment. These low-amplitude signals termed late potentials (LPs) have been correlated with the presence of fragmented electrical activity recorded from endocardial and epicardial sites due to inhomogeneous propagation of conduction in scarred myocardium. Recent studies have supported the value of the signal-averaged ECG for risk stratification postmyocardial infarction, in the management of patients with syncope and patients with sustained ventricular tachycardia (VT), and survivors of cardiac arrest.