Measurement of ventricular electrogram amplitude during intraoperative induction of ventricular tachyarrhythmias.

Adequate sensing of ventricular tachycardia (VT) and ventricular fibrillation (VF) is necessary for proper functioning of an implantable cardioverter defibrillator (ICD). Several ICDs currently undergoing investigation have programmable fixed gain sensitivity for tachycardia detection. If intracardiac electrogram amplitude decreases below the programmed sensitivity during VT or VF, detection of a ventricular arrhythmia may be delayed or missed. The mean amplitude of intracardiac electrograms (ICEGM) recorded with bipolar epicardial or transvenous sensing leads was measured in 63 patients during induced VT and VF recorded in the operating room at the time of ICD implantation. The mean amplitude of the ICEGM during 41 episodes of VF in 15 patients decreased from 14.9 +/- 0.9 mV during sinus rhythm to 8.8 +/- 0.7 mV at 1 second, 9.7 +/- 0.7 mV at 5 seconds, and 9.4 +/- 0.7 mV at 10 seconds (p < 0.0001 vs sinus rhythm ICEGM) with endocardial leads. The mean amplitude of the ICEGM recorded during 173 episodes of VF in 43 patients with epicardial leads decreased from 10.4 +/- 0.3 mV in sinus rhythm to 7.8 +/- 0.3 mV at 1 second, 8.3 +/- 0.3 mV at 5 seconds and 8 mV at 10 seconds (p <0.0001 vs sinus rhythm ICEGM). The mean amplitude of epicardial and transvenous ICEGMs recorded during 34 episodes of monomorphic VT decreased from 18.5 +/- 1.8 mV (epicardial) and 14.4 +/- 2.0 mV (transvenous) during sinus rhythm (p = 0.15, epicardial vs transvenous) to 16.0 +/- 1.7 mV (epicardial) and 13.7 +/- 1.9 mV (transvenous) at 10 seconds (< 10% of baseline amplitude).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Shock-induced epicardial and endocardial virtual electrodes leading to ventricular fibrillation via reentry, graded responses, and transmural activation

INTRODUCTION: The mechanism of ventricular fibrillation (VF) induction by T wave shocks has been attributed to reentry, propagated graded responses (PGR), and triggered activity. The limitation of recording transmembrane potential (V(m)) from only a single surface has hampered efforts to elucidate the relative role of these phenomena and their relationship to shock-induced virtual electrodes. METHODS AND RESULTS:V(m) patterns from epicardial and endocardial surfaces of isolated sheep right ventricles were recorded with two CCD cameras for monophasic (M) and biphasic (B) shocks delivered at various coupling intervals (CI) from a unipolar mesh electrode on the epicardium. VF was induced via (1) the formation of reentry following make or break excitation; (2) propagated graded responses during apparent isoelectric window; and (3) breakthrough activation patterns coincident with endocardial-to-epicardial gradients in V(m). M shocks depolarized both surfaces at long CIs and polarized epicardial and endocardial surfaces oppositely at short CIs. At intermediate CIs, postshock V(m) patterns could lead to reentry on one surface or endocardial-to-epicardial gradients resulting in breakthrough. B induced VF less than M for short and intermediate CIs due to more homogeneous end-shock V(m) patterns. However, at long CIs these homogeneous patterns resulted in more VF induction because B left the tissue closer to the V(m) threshold for propagation. CONCLUSION: Postshock activity occurred either immediately via epicardial or endocardial reentry, or after a delay caused by transmural propagation or propagated graded responses. These findings could explain the isoelectric window and focal activation patterns observed on the epicardium following VF induction shocks.     

Ventricular fibrillation during no-flow global ischemia in isolated rabbit hearts

Introduction: The dominant frequency (DF) during ventricular fibrillation (VF) in Langendorff-perfused guinea pig hearts is higher in left ventricle (LV) than in right ventricle (RV). However, the onset of VF invariably leads to global ischemia. Whether or not a high DF source exists in LV during global ischemia is unknown.
Methods and Results: By using a two-camera optical mapping system, epicardial activation patterns of VF were studied in 12 isolated rabbit hearts during baseline, no-flow global ischemia, and reperfusion. Simultaneous endocardial electrode recording was performed in 4 of the 12 hearts. Optical mapping showed type 1 VF at baseline, with multiple wandering and short-lived wavelets. After the onset of global ischemia, VF showed progressively increased spatiotemporal periodicity. The majority (65%) of VF recorded after 7 minutes of global ischemia showed type 2 VF, containing a single epicardial site with stable (≥3.85 seconds in duration) repetitive activities. Among the 33 sites with these activities, 24 were located near the interventricular septum, and 27 showed an epicardial breakthrough pattern with centrifugal propagation and wavebreaks distant from the focal site. After 10 minutes of global ischemia, the DF was lower on LV epicardium (5.0 ± 1.4 Hz) than on RV epicardium (8.6 ± 2.5 Hz, P < 0.001). However, there was no DF gradient between RV and LV endocardium (9.7 ± 1.0 vs 9.6 ± 0.9 Hz).
Conclusions: VF during prolonged global ischemia is consistent with type 2 VF with a single subepicardial source of rapid activation, mostly near the interventricular septum. The DF in LV is not higher than in RV.     

Role of Epicardial Mapping in Catheter Ablation of Postmyocardial Infarction Ventricular Tachycardia

The role of epicardial mapping for radiofrequency (RF) catheter ablation of postmyocardial infarction monomorphic ventricular tachycardia (VT) is still under investigation. We present two septuagenarian patients with a history of myocardial infarction, poor left ventricular function, and drug-refractory monomorphic VT who were treated with RF catheter ablation. The first patient had a history of myocardial infarction, left ventricular aneurysm, and mitral valve replacement complicated by recurrent drug refractory VT and congestive heart failure. The second patient had ischemic cardiomyopathy and VT and was implanted with a cardioverter defibrillator and subsequently suffered repeated episodes of VT refractory to multiple antiarrhythmic drugs. In both patients, coronary sinus mapping was performed with a multipolar catheter as endocardial mapping did not reveal satisfactory sites for ablation. Epicardial catheter mapping provided stable electrograms and identification of areas of slow conduction during VT. RF lesions guided by epicardial mapping resulted in successful ablation of VT and no recurrence at long-term follow-up. This report emphasizes the potential usefulness of coronary sinus mapping as an adjuvant to endocardial mapping to guide VT ablation.     

Role of the posterior papillary muscle and purkinje potentials in the mechanism of ventricular fibrillation in open chest dogs and Swine: effects of catheter ablation

BACKGROUND: Papillary muscle (PM) ablation may terminate ventricular fibrillation (VF) in rabbit hearts. Whether or not PM ablation prevents ventricular fibrillation (VF) induction in large animals is unknown. METHODS: We performed noncontact endocardial mapping and/or high-density epicardial mapping during VF in 12 dogs and 16 swine and tested the effects of posterior PM (PPM) ablation on VF inducibility. RESULTS: During VF in progressive global ischemia (3 swine and 2 dogs), the highest dominant frequency (DF) was near PPM. The majority of the reentrant wavefronts during a propranolol infusion (swine) were anchored to the PPM. Purkinje potentials onset were recorded on the PPM both during sinus rhythm and during VF. Radiofrequency (RF) ablation of the endocardium on the PPM with a linear extension of the ablation line from the PPM to the mitral valve annulus and then the left ventricular apex in 7 dogs reduced the VF inducibility from 100% at baseline to 22% after ablation (P < 0.0001). RF applications to the anterolateral wall of dogs (n = 3) did not prevent VF induction. The application of RF energy near the PPM frequently initiated VF in swine (n = 7), preventing subsequent testing of VF inducibility. CONCLUSION: In dogs and swine, the highest DF and majority of reentrant wavefronts during VF with acute global ischemia or during a propranolol infusion were located on the PPM. RF ablation targeted at the PPM reduced the inducibility of VF in normal dogs. However, the same ablation provoked incessant VF in swine, preventing subsequent testing of VF inducibility.     

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.     

Mechanism of arrhythmogenicity of the short-long cardiac sequence that precedes ventricular tachyarrhythmias in the long QT syndrome

OBJECTIVES: The purpose of this study was to investigate the electrophysiologic mechanism(s) that underlie the transition of one or more short-long (S-L) cardiac sequences to ventricular tachyarrhythmias (VTs) in the long QT syndrome. BACKGROUND: One or more S-L cardiac cycles, usually the result of a ventricular bigeminal rhythm, frequently precedes the onset of VT in patients with either normal or prolonged QT interval. Electrophysiologic mechanisms that underlie this relationship have not been fully explained. METHODS: We investigated electrophysiologic changes associated with the transition of a S-L cardiac sequence to VT in the canine anthopleurin-A model, a surrogate of LQT3. Experiments were performed on 12 mongrel puppies after administration of anthopleurin-A. Correlation of tridimensional activation and repolarization patterns was obtained from up to 384 electrograms. Activation-recovery intervals were measured from unipolar electrograms and were considered to represent local repolarization. RESULTS: We analyzed 24 different episodes of a S-L sequence that preceded VT obtained from 12 experiments. The VT followed one S-L sequence (five episodes), two to five S-L sequences (12 episodes) and more than five S-L sequences (seven episodes). The single premature ventricular beats coupled to the basic beats were consistently due to a subendocardial focal activity (SFA). There were two basic mechanisms for the development of VT after one or more S-L sequences: 1) in 10 examples of a S-L sequence due to a stable unifocal bigeminal rhythm, the occurrence of a second SFA, which arose consistently from a different site, infringed on the pattern of dispersion of repolarization (DR) of the first SFA to initiate reentrant excitation; 2) in the remaining 14 episodes of a S-L sequence, a slight lengthening (50 to 150 ms) in one or more preceding cycle lengths (CLs) resulted in alterations of the spatial pattern of DR at key sites to promote reentry. The lengthening of the preceding CL produced differentially a greater degree of prolongation of repolarization at midmyocardial and endocardial sites compared with epicardial sites with consequent increase of DR. The increased DR at key adjacent sites resulted in the development of de novo zones of functional conduction block and/or slowed conduction to create the necessary prerequisites for successful reentry. CONCLUSIONS: The occurrence of VT after one or more S-L cardiac sequences was due to well defined electrophysiologic changes with predictable consequences that promoted reentrant excitation.     

Endocardial excitation and conduction during reperfusion arrhythmias

In order to clarify the role of Purkinje fibers in the occurrence of reperfusion arrhythmias, endocardial mapping was performed on perfused canine hearts by attaching 42 close bipolar electrodes to the endocardial surface of the left ventricular septum. Reperfusion with oxygenated Krebs-Ringer solution following 30 min of coronary occulusion induced ventricular tachycardia (VT) in 14 out of 23 preparations. These VT degenerated into ventricular fibrillation (VF) within 1 min after the reperfusion in all but 3 cases. Endocardial mapping revealed that the excitations during VT were always initiated by the Purkinje activities and that myocardial excitations were expanded in a centrifugal manner through Purkinje-muscle junctional area. Furthermore, this excitation pattern was preserved, in the early phase of VT, even though the propagation pattern was distorted. VF was always induced by reperfusion following 30 min of ischemic condition, that is, coronary perfusion with a hyperkalemic (K = 10 mM), acidic (pH = 6.8) and hypoxic (PO2 = 20-40 mmHg) solution (4/4 cases). Elimination of hyperkalemia from the ischemic condition markedly prevented occurrence of VF (1/6 cases) during reperfusion but it did not affect occurrence of VT (4/6 cases); this implies that hyperkalemia causes the onset of VF but has less effect on the occurrence of VT. It has been separately confirmed by micro-electrode experiment, using the dissected papillary muscle of the canine right ventricle, that abnormal impulse formation during re-oxygenation was triggered in Purkinje fibers around Purkinje-muscle junction.     

Epicardial ablation as a bailout in electrical storm?

Electrical storm (ES) is one of the most challenging clinical scenarios facing electrophysiologists, and in certain settings emergency ablation should be performed. The majority of ES occurs in patients with structural heart disease, predominantly coronary heart disease and nonischemic heart disease like right ventricular arrhythmogenic dysplasia and previous myocarditis as well as other cardiomyopathies. Implantable cardioverter-defibrillators (ICDs) are the first-line therapy in patients with ventricular tachycardia (VT) and structural heart disease. Recurrent VT episodes or ES are major problems in patients who receive an ICD after a spontaneous sustained VT. In addition, in patients with an ICD implanted for primary prevention of sudden cardiac death, 20?% will experience at least one VT episode within 3–5 years after ICD implantation. Catheter ablation has a high success rate in the acute setting in eliminating clinical VT. However, several factors make enodocardial catheter ablation of VT more difficult especially in advanced ischemic heart disease with heart failure and aneurysm. Frequently in nonischemic cardiomyopathies (NICM) there tends to be an epicardial and intramyocardial substrate where the critical VT zone can occasionally be epicardial or intramural in location. In some patients, an epicardial approach should be warranted first together with an endocardial approach or after failure of enodocardial ablation. Currently, the success rates of endocardial ablation in the acute setting are acceptable, but in the long term they are still not well defined. The purpose of this article is to highlight the importance of epicardial ablation as an alternative approach in controlling ES and to confirm the need for highly qualified centers to manage such challenging cases.     

Ventricular tachycardia originating from the posteroseptal process of the left ventricle with inferior wall healed myocardial infarction.

Ventricular tachycardia (VT) substrates may form in preferential locations and similar electrocardiographic patterns may be observed when ventricular activation starts from a particular site. We examined the role of the posterior inferior process of the left ventricle in the mechanism of VT occurring after inferior wall myocardial infarction. We reviewed isochronal maps of 40 VTs obtained at surgery in 13 patients, with a 128-electrode system using epicardial sock and endocardial balloon electrode arrays. Based on the epicardial to left endocardial relation we observed 7 tachycardias in 7 patients with onset of activation over the crux of the heart. This activation mimicked excitation through a posteroseptal accessory pathway. Endocardial activation maps showed breakthroughs occurring 6 to 40 ms later and did not give evidence in favor of macroreentry. In all but 1 VT, left-axis deviation was present (-30 to -75 degrees) with a positive concordance from leads V2 to V6 (QRS wave patterns were variable in V1). These tachycardias, which were clinical in 3 of 7 cases, were interpreted as arising from the posterior inferior process of the left ventricle and successfully ablated by left septal and epicardial cryolesions. In another patient, this concept was further validated by percutaneous radiofrequency ablation of a tachycardia with the previously described morphology. In conclusion, VT may originate from the posteroseptal process of the left ventricle with inferior wall healed myocardial infarction. Because these tachycardias can be successfully eliminated, their characteristic morphologies may provide clinical markers for the identification of patient candidates to surgical or nonsurgical ablative therapy.     

Incidence of nonsustained and sustained ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) is a frequent phenomenon in some patients with heart disease, but its association with sustained ventricular tachycardias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) is still not clear. The aim of this study was to determine whether NSVT incidence was associated with sustained VT/VF in patients with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Retrospective data analysis was conducted in 923 ICD patients with a mean follow-up of 4 months. NSVT and sustained VT/VF were defined as device-detected tachycardias. The incidence rates of NSVT and sustained VT/VF as well as ICD therapies were determined as episodes per patient. The NSVT index was defined as the product of NSVT episodes/day times the mean number of beats per episode, i.e., total beats/day. The NSVT index peak was defined as the highest value on or prior to the day with sustained VT/VF episodes. Patients (n = 393) with NSVT experienced a higher incidence of sustained VT/VF (17.2 +/- 63.0 episodes/patient) and ICD therapies (15.2 +/- 61.4 episodes/patient) than patients (n = 530) without NSVT (sustained VT/VF: 0.5 +/- 6.6 and therapies: 0.5 +/- 5.6; P < 0.0001). Approximately 74% of NSVT index peaks occurred on the same day or <3 days prior to sustained VT/VF episodes. The index was higher for peaks < or =3 days prior to the day with sustained VT/VF (94.3 +/- 140.1 total beats/day) than for peaks >3 days prior to the day with sustained VT/VF (32.7 +/- 55.9 total beats/day; P < 0.0001). CONCLUSION: ICD patients with NSVT represent a population more likely to experience sustained VT/VF episodes with a temporal association between an NSVT surge and sustained VT/VF occurrence.     

Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: the importance of low-voltage scars

OBJECTIVES: The purpose of this study was to evaluate the occurrence, locations, and relationship of ventricular tachycardia (VT) to low-voltage areas in dilated cardiomyopathy (DCM). BACKGROUND: The substrate causing monomorphic VT after infarction is characterized by regions of low-voltage (<1.5 mV) scar on electroanatomic maps. The substrate causing VT associated with DCM is less well defined. METHODS: A total of 28 patients were studied with endocardial (26 patients) and epicardial (8 patients) electroanatomic mapping. The VT circuits were defined by entrainment or pace mapping. RESULTS: Ventricular tachycardia was due to focal VT in 5, bundle-branch re-entry in 2, and myocardial re-entry in 22 patients (both focal and re-entry VTs in 1 patient). All patients with myocardial re-entry had endocardial (20 of 20 patients) and/or epicardial (7 of 7 patients mapped) scar. Most (63%) endocardial scars were adjacent to a valve annulus. Of the 19 VT circuit isthmuses identified, 12 were associated with an endocardial scar and 7 with an epicardial scar. All myocardial re-entrant VTs were abolished in 12 of 22 patients, and inducible VT was modified in 4 patients. During follow-up of 334 +/- 280 days, 54% of patients with myocardial re-entry were free of VT despite frequent episodes before ablation. CONCLUSIONS: The VTs in DCM are most commonly the result of myocardial re-entry associated with scar. Scars are often adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicardium than on the endocardium. The use of epicardial mapping and radiofrequency is likely to improve success.     

Obstacle-induced transition from ventricular fibrillation to tachycardia in isolated swine right ventricles: insights into the transition dynamics and implications for the critical mass

OBJECTIVES: The study was done to test the hypothesis that an artificial anatomical obstacle prevents the maintenance of ventricular fibrillation (VF) by stabilizing reentrant wavefronts (RWF) and increases the critical mass (CM) of myocardium required to sustain VF. BACKGROUND: Artificial obstacles can anchor RWF in simulated models of VF. Whether an artificial obstacle affects multiple-wavelet VF in real tissue is unclear. METHODS: The endocardial surfaces of seven isolated, perfused swine right ventricles were mapped using a plaque of 477 bipolar electrodes with 1.6-mm resolution. An 8-mm hole was punched in the tissue. The CM was reached by tissue mass reductions, at which VF converted to periodic activity (ventricular tachycardia, VT). RESULTS: After the creation of the obstacle, the VF cycle length increased from 71.6+/-18.4 ms to 87.5+/-13.0 ms (p<0.05). The obstacle, together with the papillary muscle, facilitated the transition from VF to VT by serving as attachment sites for the RWF. When one RWF attaches to the obstacle and another attaches to the papillary muscle, it may result in stable VT with figure-eight patterns. The CM for VF in the presence of an 8-mm hole (28.7+/-3.8 g) was higher than in the control group (swine right ventricles without holes, 24.0+/-3.4 g, p<0.05). CONCLUSIONS: An artificial anatomical obstacle induces slowing and regularization of VF, impairs the persistence of VF as judged by an increase of the CM, and can convert VF to VT by serving as an attachment site to reentrant excitation.     

Clinical and electrophysiologic predictors of ventricular tachyarrhythmia recurrence in patients with implantable cardioverter defibrillators

INTRODUCTION: Not all patients experience recurrent sustained ventricular tachyarrhythmias after placement of an implantable cardioverter defibrillator (ICD). We evaluated the clinical and electrophysiologic predictors of ventricular tachycardia (VT) and ventricular fibrillation (VF) recurrence following ICD implantation. METHODS AND RESULTS: Consecutive patients (n = 133) underwent 4 +/- 3 serial electrophysiologic studies (EPS) over 50 +/- 26 months following ICD implantation. Sustained VT/VF could always be induced during follow-up EPS in 49 patients; sustained VT/VF was sometimes induced during follow-up EPS in 47 patients; and sustained VT/VF could never be induced during follow-up EPS in 37 patients. Spontaneous VT/VF requiring ICD therapy occurred in 107 patients during follow-up. Patients with sustained VT/VF that was always inducible or sometimes inducible during follow-up experienced more frequent episodes of VT/VF following ICD implant (20.5, 95% CI 12.7-33.0; and 17.8, 95% CI 11.3-28.1 episodes/patient respectively; vs 3.0, 95% CI 2.0-4.6 episodes/patient for patients with VT/VF never induced, P < 0.001). Inducibility of sustained VT/VF post-ICD implant (P < 0.001) and sustained VT as the presenting arrhythmia (P = 0.02) were independent predictors of spontaneous VT/VF recurrence. CONCLUSION: Reproducibly inducible VT/VF following ICD implantation predicts a high probability of VT/VF recurrence and identifies a cohort of patients who experience frequent episodes of VT/VF over time. Persistent noninducibility of sustained VT/VF identifies a group of patients who experience no or very few episodes of VT/VF recurrence.     

Localization of breakthrough site of canine monomorphic ventricular tachycardia by pacemapping. A vectorial approach

BACKGROUND. The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction. METHODS AND RESULTS. Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm. CONCLUSIONS. In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.     

69例植入型心律转复除颤器治疗患者的随访

目的 对全国50家医院69例植入型心律转复除颤器（implantable cardioverter defibrilla-tor,ICD)的患者通过较长期随访获得的实际经验,以期促进和提高我国ICD的应用水平。方法 资料来自全国50家医院的门诊随访、电话询问或厂家随访,通过常规心电图、动态心电图及ICD程控分析仪调出的资料,对串屠 情况及ICD工作情况进行分析,结果 平均随访2.3年中有30例患者接受成功的ICD治理,占全组患者43.5%,总共发作快速心律失常276次,其中VT236次占85.5%,VF40次占14.5%,VT由ATP终止135次,占57.2%,由CV终止101次,占42.8%,VF经DF（除颤）40次,全部一次成功,2例VT加速转成VF,2例无休止发作VT,电击成功,但瞬间又转为VT,2例服胺碘酮后VT频率减慢（140-100次/min),69例中有6例死亡,其中半数因心力衰竭加重所致,结论 ICD的治疗效果肯定,需加强随访及时修改参数,更准确地识别和治疗快速室性心律失常,同时需注意药物的辅助治疗,积极改善心功能,还应加强对患者的心理教育。     

Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 +/- 3 days following experimental myocardial infarction were placed on total cardiopulmonary bypass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43-62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.     

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.