Ventricular Tachycardia Morphologies Research Articles

Catheter Ablation for Ventricular Tachycardia

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with heart disease.1 Implantable cardioverter-defibrillators (ICDs) terminate VT episodes, reducing the risk of sudden death. Recurrent VT develops in 40% to 60% of patients who receive an ICD after an episode of spontaneous sustained VT. A first episode of VT occurs in ≈20% of patients within 3 to 5 years after ICD implantation for primary prevention of sudden death in high-risk groups.2–4 ICD shocks reduce quality of life and are associated with an increased risk of death.2–4 Antiarrhythmic drug therapy with amiodarone or sotalol reduces VT episodes but with disappointing incidence of side effects and efficacy.2 Catheter ablation is useful for reducing VT episodes and can be life-saving when VT is incessant.1,5,6 Idiopathic VTs occur in patients without structural heart disease and rarely cause sudden death. Electrophysiological study with catheter ablation is often warranted to confirm the diagnosis, to provide further evidence for the absence of ventricular scar or other disease, and often to cure the arrhythmia. Ablation is also an option for symptomatic nonsustained VT and frequent ventricular ectopy in these patients.1 The appearance of the VT on ECG often suggests its likely cause and associated heart disease (Figure 1). Monomorphic VT has the same QRS complex from beat to beat, indicating repetitive ventricular activation from a structural substrate or focus that can be targeted for ablation. Most are due to reentry through regions of ventricular scar.7 Figure 1. ECG types of VT and most common causes are shown with characteristic ECG features of selected VTs. LBBB indicates left bundle-branch block; LVOT, LV outflow tract; RBBB, right bundle-branch block; L, left; and R, right. Polymorphic VTs have a changing ventricular activation sequence that can be due to …

Epicardial Conduction Properties and Electrocardiographic Characteristics of Premature Ventricular Complexes or Ventricular Tachycardias That Originate at the Aortic Cusp

Background and Objectives: Premature ventricular contraction (PVC) or ventricular tachycardia (VT) that originates from the aortic cusp (AC) has a similar left bundle branch block (LBBB) pattern with a inferior axis as those LBBB patterns originating from the right ventricular outflow tract, but the electrocardiogram (ECG) characteristics are distinct. We sought to characterize the ECG morphology of PVCs or VTs from the AC and to assess whether these foci exit out to the surrounding epicardium by preferential conduction, resulting in an ECG with epicardial foci. Subjects and Methods: The study subjects were ten patients (M:F=6:4, 40.9±11.6 years old) with VTs or PVCs that originated from the AC and they underwent radiofrequency catheter ablation (RFCA). We performed simultaneous activation mapping at the AC, the anterior interventricular vein (AIV) and the anterior mitral annulus (AMA). The conduction velocities (CV) between the successful ablation site to the epicardium in the AIV, and the endocardial earliest activation (EA) site at the AMA were calculated by triangular algebra at right anterior oblique (RAO) 35° and left anterior oblique (LAO) 35°, respectively. Results: Successful ablation sites were above the left coronary cusp (LCC) in 7 patients, above and beneath the right coronary cusp (RCC) in 1 patient each, respectively, and beneath the LCC in 1 patient. The QRS width was 149.2±19.9 ms, the maximal depolarization time (MDT) was 88.9±14.9 ms and the ratio of the MDT to the QRS was 59.5±5.7%. The PVC from the LCC had rS or S waves in lead I and R or RS waves in V1, whereas those from the RCC had R waves in lead I and an rS wave in V1. The CV between the successful ablation site at the AC to the epicardial EA site (1.7 ±0.8 m/s) was faster than that to the endocardial EA site (0.8±0.4 m/s, p<0.05). Conclusion: Most of the PVC/VTs from the AC originated from the above LCC and they displayed a faster CV to the epicardial side of the AIV than that to the endocardial side of the AMA. This suggests the existence of preferential conduction from the AC to the left ventricle (LV) epicardium. (Korean Circ J 2007;37:616-622)

P4-113: Two ventricular tachycardias which showed the opposite axis shared the critical isthmus in a patient with double outlet right ventricle after Rastelli procedure

A 33-year-old male, s/p Rastelli procedure at the age of 9 y/o for double outlet right ventricle (DORV) was admitted to our hospital due to ventricular tachycardia (VT). The morphology of clinical VT was LBBB, superior axis (CL 410 ms). During the EP study, 2 types of VTs including the clinical VT were induced. VT2 had LBBB with inferior axis (CL 440 ms). Activation mapping was performed both in VT1 and VT2, early-diastolic potential during VT1 and mid-diastolic potential during VT2 were recorded at the same channel in LVOT.

Postextrastimulus delay of ventricular tachycardia return cycle: Indicator of a good ablation site

3 A 67-year-old man was referred for catheter ablation of ncessant ventricular tachycardia (VT). He had suffered a yocardial infarction 10 years earlier. VT had occurred 2 ears ago, prompting insertion of an implantable cardioerter-defibrillator (ICD). He began having palpitations folowed by shocks. ICD interrogation showed VT episodes cycle length (CL) 450 ms] terminated by a single shock ach after failed antitachycardia pacing attempts. Intraveous amiodarone was administered. Episodes became more requent and then became incessant but slower (CL 590 ms). T ablation was attempted after retrograde aortic access to he left ventricle. Based on the ECG morphology of VT, the nferobasal free wall was mapped. An electrogram in this egion showed early and late diastolic components (Abld, igure 1). Burst pacing at this site resulted in entrainment ith concealed fusion with a stimulus-to-QRS interval qual to the electrogram-to-QRS interval and a postpacing nterval equal to VT CL. Single extrastimuli were delivered rom this site to ascertain if termination would occur. At elatively long coupling intervals, resetting occurred with a timulated QRS identical to VT. At short coupling intervals, he extrastimulus (S) caused delay of the next VT complex again with identical QRS; asterisk in Figure 1). Intervals in he figure correspond to R-R intervals in the right ventriclar (RV) recording. Based on these findings, radiofre-

Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

Multiple morphologies, hemodynamic instability, or noninducibility may limit ventricular tachycardia (VT) ablation in patients with arrhythmogenic right ventricular dysplasia (ARVD). Substrate-based mapping and ablation may overcome these limitations. We report the results and success of substrate-based VT ablation in ARVD. Twenty-two patients with ARVD were studied. Traditional mapping for VT was limited because of multiple/changing VT morphologies (n=14), nonsustained VT (n=10), or hemodynamic intolerance (n=5). Sinus rhythm CARTO mapping was performed to define areas of "scar" (<0.5 mV) and "abnormal" myocardium (0.5 to 1.5 mV). Ablation was performed in "abnormal" regions, targeting sites with good pace maps compared with the induced VT(s). Linear lesions were created in these areas to (1) connect the scar/abnormal region to a valve continuity or other scar or (2) encircle the scar/abnormal region. Eighteen patients had implanted cardioverter defibrillators, 15 had implanted cardioverter defibrillator therapies, and 7 had sustained VT (6 with syncope). VTs (3+/-2 per patient) were induced (cycle length, 339+/-94 ms), and scar was identified in all patients. Scar areas were related to the tricuspid annulus, proximal right ventricular outflow tract, and anterior/inferior-apical walls. Lesions connected abnormal regions to the annulus (n=12) or other scars (n=4) and/or encircled abnormal regions (n=13). Per patient, a mean of 38+/-22 radiofrequency lesions was applied. Short-term success was achieved in 18 patients (82%). VT recurred in 23%, 27%, and 47% of patients after 1, 2, and 3 years' follow-up, respectively. Substrate-based ablation of VT in ARVD can achieve a good short-term success rate. However, recurrences become increasingly common during long-term follow-up.

Viability pattern, mapping and ablation in patients with right ventricular cardiomyopathy and ventricular tachycardia

Objective: Ventricular tachycardia (VT) may originate from the epicardium (EPI). We hypothesized that QRS morphology and activation times might make ECG criteria that are not patient and site specific, unreliable in distinguishing EPI vs endocardial (ENDO) origin, but that site specific EPI vs ENDO QRS activation and QRS morphology differences should exist. We further hypothesized that QRS intervals would be markedly increased at EPI sites and the QRS morphology in lead I would change from r/s to QS or QR when transitioning from ENDO to EPI sites. Methods: Electroanatomic shells of ENDO and EPI were constructed in sinus rhythm. Pacing with 4 mm tip electrode was performed from 16 distinct non-septal ENDO Josephson sites and their counterpart EPI locations (cycle length: 400-600 ms; diastolic threshold) in 3 patients (pts) undergoing ablation for idiopathic VT. 12-lead ECG was recorded and analyzed for QRS morphology in lead I, widest QRS duration (QRSd) in any lead, and time to latest QRS nadir (QRS-N) in precordial leads. Results: Site to site and pt to pt overlap precluded utility of absolute QRS intervals in identifying EPI origin. Site specific (EPI vs corresponding ENDO) comparisons revealed: 1) increased QRSd 20ms for 13/16 (81%); 2) increased time to QRS-N 20ms for 11/16 (69%) and 3) initial negative forces in lead I (QS or QR) were seen in 9/16 (56%) EPI and no ENDO sites. One or more of above three criteria were seen in 15/16 (94%) EPI vs ENDO sites. In all 3 patients clinical VT was of EPI origin and consistently demonstrated above criteria compared to ENDO PMs. Identical EPI PMs were seen for all 3 VT morphologies and 2 of the VT were successfully ablated. One VT had SOO adjacent to coronary vessel and was not targeted. Conclusions: PM of EPI sites revealed wider QRS complexes with later time to QRS-N and more frequent / marked initial negative forces in lead I compared with corresponding ENDO locations. These findings are site specific. By comparing ENDO PM of comparable morphology to clinical VT, identification of an epicardial SOO is possible. A QRSd increase by 20ms, time to QRS-N in precordial lead increase 20ms and/or a QS or qr in lead I compared to ENDO PM strongly suggest an epicardial origin.

Pleomorphic Ventricular Tachycardia: An Uncommon Presentation in Idiopathic Left Ventricular Tachycardia

Idiopathic left ventricular tachycardia (ILVT) is a distinct entity that arises in the left ventricle, may have reentrant mechanism and is verapamil-sensitive. Pleomorphism as defined by multiple ventricular tachycardia morphologies is usually associated with either coronary artery disease or cardiomyopathy but very rare in cases of ILVT. In this case report, we describe an unusual case of ILVT with two ECG morphologies of the opposite axis that were successfully eliminated with radiofrequency ablation. The successful ablation sites were closely located to each other in the left lower ventricular septum.

Sinus Rhythm Electrogram Shape Measurements are Predictive of the Origins and Characteristics of Multiple Reentrant Ventricular Tachycardia Morphologies

During clinical electrophysiologic study, multiple clinical tachycardia morphologies often can be induced in the infarct border zone, and all morphologies must be targeted for ablation therapy to be successful. Analysis of sinus rhythm electrogram shape for localizing figure-of-eight reentrant circuits in cases of multiple morphologies is proposed. Sinus rhythm activation maps were constructed from bipolar electrograms acquired at 196 to 312 sites in the epicardial border zone in 10 postinfarction canine hearts. In each heart, at least two distinct figure-of-eight reentrant ventricular tachycardia morphologies were inducible by premature electrical stimulation, as determined by activation maps of sustained tachycardias. Sinus rhythm maps were used to predict the location of the isthmus (central common pathway [CCP]), which is the protected region of the circuit bounded by arcs of block (mean accuracy 76.7 +/- 4%). Although reentrant circuits differed, the positions of the entrance point of each CCP were common. The location of the line that would span the CCP at its narrowest width also was estimated (mean accuracy 91.3 +/- 5%). Ablation at this line is expected to prevent reentry recurrence. In one test experiment, ablation prevented recurrence of both sustained reentrant tachycardia morphologies. Sinus rhythm electrogram analyses are useful for (1) localizing multiple reentrant circuits with differences in morphology that are inducible by premature stimulation in the infarct border zone, and (2) locating and orienting the position of a linear lesion for preventing recurrence of all morphologies with minimal damage to the heart.

Incidence and significance of pleomorphism in patients with postmyocardial infarction ventricular tachycardia. Acute and long-term outcome of radiofrequency catheter ablation.

The prognostic significance of multiple ventricular tachycardia (VT) morphologies, whether spontaneous or induced, was investigated in patients who underwent radiofrequency catheter ablation (RFCA) for postinfarction ventricular tachycardia. We studied 137 patients with postinfarction ventricular tachycardia. Catheter ablation of all induced ventricular tachycardias was attempted. A single ventricular tachycardia morphology was documented in 102/137 patients (MONO group); 35 patients had spontaneous pleomorphism (PLEO group). Multiple VT morphologies were induced in 58/102 (57%) MONO patients and in all PLEO patients. A higher rate of arrhythmia suppression was obtained in MONO as compared to PLEO patients (162/212 [76%] vs. 43/110 [39%]). Clinical presentation (VT pleomorphism) (OR: 0.22, CI: 0.08-0.62) and the induced VT cycle (mean PLEO/MONO: 338/385 ms, OR: 1.06) were independent predictors of acute RFCA success. Among MONO patients, the procedure was successful in 75% of the patients with a single induced ventricular tachycardia compared to 64% of those with multiple tachycardias. The acute success rate was lower in PLEO patients (23%). PLEO patients had a significantly higher 3- and 5-year arrhythmia recurrence rate than MONO patients. RFCA acute success was the only independent predictor of long-term outcome in multivariate analysis. Spontaneous, but not induced, VT pleomorphism in patients with prior myocardial infarction adversely affects the acute and long-term success rate of RFCA.

Catheter ablation of ventricular tachycardia following myocardial infarction using three-dimensional electroanatomical mapping.

One challenge encountered during catheter ablation of postinfarction ventricular tachycardia (VT) is the inducibility of multiple VT morphologies associated with variable hemodynamic instability. The clinical usefulness and safety of a three-dimensional electroanatomical mapping in guiding radiofrequency (RF) catheter ablation of VT, used in parallel with a multichannel recording system, was studied in 28 men (mean age = 63.8 +/- 10.6 years, mean left ventricular ejection fraction = 28% +/- 9%). Three-dimensional voltage maps of the left ventricle were obtained in sinus rhythm with annotation of areas of fractionated or late potentials, zones of slow conduction and/or dense scar with no pacing capture at 10 mA. RF lesions were created either in sinus rhythm or during hemodynamically stable VT within reconstructed critical zones of the circuit. A total of 82 VTs were induced (mean = 2.9 +/- 1.0/patient). Hemodynamically unstable clinical VTs were induced in 5 patients, and clinical or nonclinical unstable VT in 14. Clinical VT was rendered noninducible in 24/28 (85.7%) patients, and monomorphic VT was eliminated in 16/28 (57.1%) patients. The mean procedural time was 258 +/- 82 minutes, and fluoroscopic exposure 13.5 +/- 8.8 minutes. During a mean follow-up period of 10.6 +/- 6.4 months, catheter ablation was repeated in 6 patients for VT recurrences. No significant complications occurred except for a transient cerebral ischemic attack in one patient. In conclusion, electroanatomical mapping assisted the successful and safe catheter ablation of both mappable and nonmappable VTs in a significant proportion of patients after myocardial infarction.

Radiofrequency ablation for post infarction ventricular tachycardia. Report of a single centre experience of 112 cases.

This report presents the largest consecutive series to date of radiofrequency ablation in the treatment of post infarction ventricular tachycardia. One hundred and twelve consecutive patients were studied, with an average of 12 documented episodes of ventricular tachycardia in the month preceding the radiofrequency ablation. Seventy-four percent of the subjects had an ejection fraction of less than 35%; 84% had more than one morphology of ventricular tachycardia and 30% had haemodynamically unstable ventricular tachycardia. The mean follow-up period was 61 months. Complete success defined as no inducible sustained monomorphic ventricular tachycardia was achieved in 38%. Modified result, defined as ventricular tachycardia only inducible by two stimuli more aggressive than at baseline was achieved in 34%. During follow-up, ventricular tachycardia recurred in 25 patients: 22 after a failed procedure, two following a modified result and one following a complete success. Twenty-five patients died: 13 of progressive cardiac failure and four of presumed arrhythmic causes, three after a failed procedure and one following a modified result. There were no procedure-related deaths. Procedural complications occurred in seven patients. In this report, radiofrequency ablation of post infarction ventricular tachycardia is a successful procedure with a low complication rate. Acute procedural success accurately predicts long-term freedom from recurrent ventricular tachycardia.

Mapping for ventricular tachycardia.

Mapping strategies for ventricular tachycardia (VT) have evolved significantly in the past 2 decades. This review discusses mapping techniques that can help in successful VT ablation. The electrocardiogram (ECG) remains a vital component of VT mapping and can help to identify the chamber of origin of VT. The ECG morphology of VT, however, is influenced by orientation of heart and location of the scar. Activation mapping during VT is an important technique that can help in further localization. Care has to be exercised to ensure that small signals are not ignored and far-field signals are recognized. Pace-mapping to mimic the VT is another way to map exit site for scar based reentrant VT or the site of origin of triggered and automatic VT in the absence of structural heart disease. For the latter group, this technique is widely used in determining the site of ablation. It is important to ensure a complete ECG match (12 out of 12 leads) of the pace-map to the clinical arrhythmia in these patients. In patients with structural heart disease, entrainment mapping remains the gold standard for defining the protected isthmus and other components of the VT circuit. Using this technique, successful ablation of reentrant VT can be achieved in 60-90% of patients. In order to perform entrainment mapping, the VT has to be hemodynamically tolerated; this is not the case in 25% of pts with scar based reentrant VT. The development of 3-dimensional mapping systems allows for more anatomically based linear ablation in patients with poorly tolerated uniform VT. Despite these advances, there are still about 10-20% VTs that cannot be ablated successfully with the above described techniques, especially in patients with structural heart disease. Other recent advances such as percutaneous closed chest epicardial mapping technique and cooled tip ablation catheter technology have the potential to enhance mapping and successful ablation of VT.

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.

Sequential map-guided endocardial resection for ventricular tachycardia improves outcome.

Surgery for ventricular tachycardias late after myocardial infarction is frequently associated with high mortality including sudden death, and arrhythmia recurrences. We examined our results of sequential map-guided endocardial resection at normothermia in patients with ventricular tachyarrhythmias late after myocardial infarction to assess the efficacy of this technique as well as the early and long-term outcome. From 1995 to 1999, 22 patients underwent normothermic sequential map-guided endocardial resection for ventricular tachyarrhythmias late after myocardial infarction. Mean age was 61.2+/-6.5 years and left ventricular ejection fraction 32.5+/-8.7%. Adjunctive procedures included endoventricular patch repair of left ventricular aneurysm in 21 patients, coronary artery bypass grafting in 15 patients, and mitral valve replacement in one patient. Inducibility of ventricular tachycardia was evaluated postoperatively and patients were treated with sotalol or defibrillator implantation. The intraoperative number of inducible different ventricular tachycardia morphologies was 4.0+/-2.7. More than one mapping-resection sequence was needed in ten patients. In only one patient, sustained ventricular tachycardia was induced postoperatively, sotalol was not tolerated and a defibrillator was implanted. Five patients with inducible non-sustained ventricular tachycardia became non-inducible while on sotalol. There was one operative death (4.5%). During a median follow-up of 26 (1--62) months, there were neither cardiac deaths nor ventricular tachycardia recurrences. Two patients died from non-cardiac causes. Cumulative probability of survival at 5 years was 0.83+/-0.09. Sequential map-guided endocardial resection at normothermia was associated with low operative mortality and low postoperative inducibility of sustained ventricular tachycardia. The selected therapeutic approach resulted in freedom of arrhythmia recurrence and cardiac mortality including sudden death, during long-term follow-up.

Cryoablation of ventricular tachycardia guided by return cycle mapping after entrainment

Background: Although the implantable cardioverter-defibrillator effectively prevents sudden cardiac death, patients are still prone to recurrence of ventricular tachyarrhythmias. Electrophysiologically guided surgery is the most effective modality in abolishing ventricular tachycardia, having a lower recurrence rate than pharmacologic therapy or catheter ablation. Return cycle mapping after entrainment has been shown to localize the central common pathway, which is the target region for ablation, without pacing at the pathway or recording the potentials from the pathway. Methods: To determine the accuracy and usefulness of return cycle mapping in surgery for ventricular tachycardia, we cryoablated 8 morphologies of ventricular tachycardia induced in postinfarction dogs with the guidance of return cycle mapping. The ventricular tachycardia was entrained from 3 to 5 different epicardial sites at a paced cycle length 10 to 20 ms shorter than the ventricular tachycardia cycle length and the epicardium was mapped with 61 unipolar electrodes during cessation of entrainment to construct return cycle maps. The return cycle was determined by subtracting the first activation time from the second activation time after the last stimulus in each electrode location, and the maps were then displayed on a computer. Results: The total analysis process was completed within 3 minutes by means of a computer with custom-made programs. The activation map during ventricular tachycardia did not localize the central common pathway in any morphology of ventricular tachycardia, because the pattern of activation was concentric and diastolic potentials were not recorded. Cryoablation of the region where the isotemporal lines of the return cycle equal to the ventricular tachycardia cycle length intersected resulted in termination of ventricular tachycardia in all morphologies. The intersection was 26 ± 9 mm from the earliest activation site. Epicardial mapping with 253 electrodes during cryothermia showed that the region localized by return cycle mapping was the central common pathway sandwiched between the lines of conduction block and that the cryolesion connected the lines of block, blocked the rotating wave front, and resulted in termination of the ventricular tachycardia. Conclusion: Return cycle mapping provides an accurate and rapid means of localizing the central common pathway without the need for recording potentials from the pathway or pacing at the pathway in ablation for ventricular tachycardia. (J Thorac Cardiovasc Surg 2001;121:249-58)

CATHETER ABLATION OF VENTRICULAR TACHYCARDIA - LONG-TERM RESULTS

Ventricular tachycardia represents life-threatening cardiac rhythm disturbance and catheter ablation using radiofrequency current provides powerful means for definitive cure of almost all monomorphic tachyarrhythmias. Presence and extent of underlying structural heart disease is important for further prognosis of the patients, who undergo catheter ablation of ventricular tachycardia. Long-term results of catheter ablation for ventricular tachycarida in patients with and without structural heart disease are presented. Patients and results: Twenty three patients (9 females) aged 49.1 ± 15.6 (18–72) years underwent catheter ablation for monomorphic (resp. polymorphic in one patient) ventricular tqachycardia in 30 ablation procedures. Patients with structural heart disease: Seven patients (2 females) aged 54.2 ± 19.8 (21–72) years had structural heart disease (5 patients – post myocardial infarction, 1 patient – arrhythmogenic right ventricular dysplasia, 1 patient – surgically corrected transposition of great arteries). All sustained monomorphic ventricular tachycardias were eliminated during the catheter ablation and no ventricular tachycardia recurred during the follow-up period in 4 patients. In two patients sustained monomorphic ventricular tachycardia was not eliminated with radiofrequency current. One of the patients remains free of ventricular tachycardia and one patient experienced one recurrence of slowed ventricular tachycardia. Thus long-term clinical success was achieved in 4 patients and some clinical benefit probably also in the latter two patients. A different ablation strategy targeting large arrhythmogenic area at the border of postmyocardial infarction scar was employed in the last patient with frequent ICD discharges for polymorphic ventricular tachycardia associated with hemodynamic deterioration. This procedure brought immediate and long-term significant reduction of ICD shocks and rehospitalizations and probably was life-saving. Patients without structural heart disease: In sixteen patients (7 females) aged 44.2 ± 12.8 (18–66) years no structural heart disease was found. These patients presented with documented ventricular ectopy in different forms from incessant ventricular premature beats through repetitive nonsustained ventricular tachycardia to paroxysmal sustained ventricular tachycardia. The arrhythmia originated in the right ventricle in 11 patients (right ventricular outflow tract in 10 patients and basolateral wall in 1 patient) and in the left ventricle in 5 patients (inferoapicoseptal region in 4 patients and basoinferoseptal region in 1 patient). Eleven patients (68.7 %) had the arrhythmia eliminated or markedly suppressed during the ablation procedure and remain free of palpitations and antiarrhythmic drugs. Two patients with partial suppression of the ectopic rhythm are less symptomatic and the antiarrhythmic drugs could be reduced. In one patient one ventricular tachycardia morphology from the right ventricular outflow tract was eliminated while the second ventricular tachycardia morphology was not targeted (and was suppressed by antiarrhythmic drug) for close vicinity of the arrhythmogenic focus to the left anterior descending artery. Thus the clinical benefit of the ablation procedure is enhanced to 14 (87.5 %) patients. Ablation completely failed in two patients. Conclusion: Radiofrequency catheter ablation of ventricular tachycardia is highly effective and safe and results in long-term arrhythmia elimination. In patients with underlying structural heart disease it should be currently viewed as a adjunctive therapy to a complex management of the patient, while in otherwise healthy patients it can be considered a method for permanent cure.

Strategies for catheter ablation of scar-related ventricular tachycardia

Ventricular tachycardia (VT) due to reentry in and around regions of ventricular scar from an old myocardial infarction or cardiomyopathic process is often a difficult management problem. Radiofrequency catheter ablation is an option for controlling frequent VT episodes. Patient and VT characteristics determine the mapping and ablation approach and efficacy. In patients with a VT that is hemodynamically tolerated to allow mapping, prevention of recurrent VT is achieved in 54% to 66% of patients with a procedure related mortality of 1% to 2.7%. Multiple morphologies of monomorphic VT and circuits that are located deep to the endocardium are common problems that reduce efficacy. Mapping to identify target regions for ablation can be difficult if VT is rapid and not tolerated, or not inducible. Ablation of these "unmappable VTs" by designing ablation lines or areas based on the characteristics of the scar as assessed during sinus rhythm, and using approaches to assess global activation from a limited number of beats has been shown to be feasible. Ablation of multiple VTs, epicardial VTs, and poorly tolerated VTs are feasible. Future studies defining efficacy and risks are needed.

Antitachycardia burst pacing for pleomorphic reentrant ventricular tachycardias associated with non-coronary artery diseases: a morphology specific programming for ventricular tachycardias.

To study the role of antitachycardia burst pacing in patients with reentrant pleomorphic ventricular tachycardia (VT) associated with non-coronary artery diseases, the efficacy of antitachycardia pacing and appropriate antitachycardia pacing cycle length were evaluated in each pleomorphic VT morphology of seven patients. Seven patients were included in this study. Clinically documented pleomorphic VTs were reproduced in an electrophysiologic study. For each VT, rapid ventricular pacing was attempted from the apex of the right ventricle at a cycle length which was 20 ms shorter than that of VT and repeated after a decrement of the cycle length in steps of 10 ms until the VT was terminated or accelerated. All 16 VTs could be entrained by the rapid pacing, and 13 of the 16 VTs (81%) were terminated, whereas pacing-induced acceleration was observed in the other 3 VTs of the 3 patients. VT cycle length (VTCL), block cycle length (BCL) which was defined as the longest VT interrupting paced cycle length, %BCL/VTCL and entrainment zone which was defined as VTCL minus BCL, varied in each VT morphology of each patient. In two patients, antitachycardia pacing was effective in all VT morphologies and the maximum difference of the %BCL/VTCL among the pleomorphic VTs was less than 10%. Thus, antitachycardia pacing seemed to be beneficial for these patients. In the other 5 patients, a difference of more than 10% in %BCL/VTCL was observed among the pleomorphic VT morphologies and/or at least one VT morphology showed pacing-induced acceleration. Compared to the 13 terminated VTs, three accelerated VTs had a wide entrainment zone [160 +/- 44 vs 90 +/- 48 ms, p < 0.04] and small %BCL/VTCL [61 +/- 6 vs 77 +/- 11%,p<0.03]. In pleomorphic VTs associated with non-coronary artery diseases, responses to rapid pacing was not uniform; VT might be terminable or accelerated even in the same patient. We need to pay close attention when programming antitachycardia pacing in patients with pleomorphic VT.

Does Unipolar Recording Predict Successful Ablation Site in Idiopathic Left Ventricular Tachycardia?

Background:Unipolar electrogram was reported to be useful for localization of manifest accessory pathway conduction during surgical or transcatheter ablation. However, it is not clear whether the unipolar electrogram would also be useful for localizing the origin of idiopathic left ventricular tachycardia (ILVT) in which pace mapping, activation time and recording of Purkinje (P)-potential have been used for guiding the successful ablation. Methods:In patients who underwent catheter ablation for ILVT, bipolar and unipolar electrograms were recorded at the sites of current delivery. We analysed the time from P-potential to QRS onset (P-QRS time), time from local ventricular electrogram to QRS onset (V-QRS time) and the morphology and slope of rapid downstroke of unipolar electrograms (Uni-slope) during induced ILVT both at successful and unsuccessful sites. Results:In 14 consecutive patients (11M/3F, mean age 29.3)with ILVT and successful ablation, QRS morphology of ventricular tachycardia was of right bundle branch block (RBBB) with left axis deviation and right axis deviation in 11 and 3 patients, respectively. The average number of current delivery was 4.5 (range 2–12). P-potential was observed in 10/14 (71%) successful sites and 37/47 (79%) unsuccessful ablation sites. The morphology of unipolar electrogram was QS pattern in 12 and QrS pattern in 2 successful sites but rS pattern was not observed at successful sites. P-QRS time was 26.5±12.4 and 26.6±14.9 msec (p=ns), VQRS time 3.9±7.7 and 0.2±8.9 msec (p=ns), Uni-slope 7.1±3.1 and 7.3±4.5 mV/10 msec (p=ns) at successful and unsuccessful sites, respectively, showing no significant differences between successful and unsuccessful sites. Conclusions:The slope of rapid downstroke in unipolar electrogram was not useful as a guide for localization of successful ablation in patients with ILVT. However, absence of initial ‘r’ wave in 논문접수일:1999년 8월 19일 심사완료일:2000년 2월 17일 교신저자:김유호, 138-736 서울 송파구 풍납동 388-1 울산대학교 의과대학 서울중앙병원 심장내과학교실 전화:(02) 2224-3161·전송:(02) 486-5918 E-mail:youho@www.amc.seoul.kr

Dual morphology of idiopathic ventricular tachycardia.

Idiopathic ventricular tachycardia (VT) typically has a single morphology originating either in the right ventricular outflow tract (RVOT) or near the posterior fascicle of the left ventricle (LV) in most instances. We present our observations in six patients with idiopathic VT in whom two morphologies were present. Of 55 patients with idiopathic VT who underwent radiofrequency (RF) ablation, 44 had LV "fascicular" tachycardia, whereas 11 had RVOT tachycardia. During RF energy delivery, there was a change in VT morphology in two patients with idiopathic LV tachycardia. This second morphology was not ablated initially, recurred at follow-up, and was reablated successfully. In two additional patients with idiopathic LV tachycardia, a second VT was inducible after ablation of the "clinical" VT. This second morphology recurred at follow-up and was ablated successfully in one patient. The site where the second VT was ablated in all the three patients was remote from that of the first VT. In two patients with RVOT tachycardia, a second VT, originating from a different area of the RVOT, was induced after RF ablation of the "clinical" VT. This second VT recurred at follow-up and was reablated successfully in one patient. Idiopathic VT is a more heterogenous entity than hitherto believed. A second VT was seen in 11% of patients during or after RF ablation of the "clinical" VT. The appearance of a second VT suggests either a different exit site of the same circuit or another site of origin.