Left ventricular outflow tract tachycardia originating from the right coronary cusp: identification of location of origin by endocardial noncontact activation mapping from the right ventricular outflow tract

Idiopathic left ventricular outflow tract (LVOT) tachycardia has been shown to originate from a supravalvular site in some patients. Considerable attention recently has focused on identifying this variant of LVOT tachycardia on 12-lead ECG. We report the case of 15-year-old boy in whom a noncontact three-dimensional mapping electrode deployed in the right ventricular outflow tract (RVOT) assisted in identifying a supravalvular LVOT tachycardia. Observation of two early breakthrough sites in the RVOT and right ventricular septum suggested a right aortic cusp origin of the tachycardia. Pace mapping in the right aortic cusp identified a successful ablation site.     

Successful radiofrequency catheter ablation of epicardial left ventricular outflow tract tachycardia from the anterior interventricular coronary vein

We report a case of idiopathic left ventricular outflow tract (LVOT) tachycardia that was eliminated by a radiofrequency application from the anterior interventricular coronary vein (AIV). The ECG exhibited QRS complexes with an inferior axis and atypical left bundle branch block pattern with an early transition of the precordial R waves at V3. Several radiofrequency applications from the coronary cusps and endocardial LVOT were not effective. Radiofrequency applications in the AIV, where the activation preceded the onset of the QRS by 30 msec, successfully eliminated the tachycardia. The AIV may be an optional site for radiofrequency ablation of idiopathic epicardial LVOT tachycardia.     

Percutaneous epicardial radiofrequency ablation of idiopathic ventricular tachycardia

We describe 3 patients with ventricular tachycardia in whom epicardial ablation was done after prior attempts of endocardial ablation had failed. Clinical ventricular tachycardia originated at the right ventricular outflow tract in one patient and near the mitral annulus in another patient. In these two cases ventricular tachycardia was mapped and successfully ablated with a percutaneous subxiphoid approach to the pericardial space. In the remaining patient, ventricular tachycardia originated near the mitral annulus and was ablated via a coronary vein. The two patients who presented tachycardiomyopathy recovered normal left ventricular function after successful ablation. Failure of endocardial ablation may reflect a substrate of epicardial arrhythmia. Epicardial ablation is effective and provides an alternative therapy for patients with ventricular tachycardia, including those with no structural heart disease.     

Noncontact mapping to guide ablation of right ventricular outflow tract tachycardia

OBJEWCTIVES: The aim of this study was to determine whether noncontact mapping is feasible in the right ventricle and assess its utility in guiding ablation of difficult-to-treat right ventricular outflow tract (RVOT) ventricular tachycardia (VT). BACKGROUND: In patients without inducible arrhythmia, RVOT VT may be difficult to ablate. Noncontact mapping permits ablation guided by a single tachycardia complex, which may facilitate ablation of difficult cases. However, the mapping system may be geometry-dependent, and it has not been validated in the unique geometry of the RVOT. METHODS: Ten patients with left bundle inferior axis VT, no history of myocardial infarction and normal left ventricular function underwent noncontact guided ablation; seven had failed previous ablation and three had received a defibrillator. All noncontact maps were analyzed by a blinded reviewer to determine whether the arrhythmia focus was epicardial and to predict on the basis of the map whether arrhythmia would recur. RESULTS: The procedure was acutely successful in 9 of 10 patients. During a mean follow-up of 11 months, 7 of 9 patients remained arrhythmia-free. Both patients in whom the blinded reviewer predicted failure had arrhythmia recurrence: one due to epicardial origin with multiple endocardial exit sites and one due to discordance between site of lesion placement and earliest activation on noncontact map. CONCLUSIONS: Mechanisms of ablation failure in RVOT VT include absence of sustained arrhythmia, difficulty with substrate localization and epicardial origin of arrhythmia. In this study, noncontact mapping was safely and effectively used to guide ablation of patients with difficult-to-treat RVOT VT.     

Ventricular tachycardias mimicking those arising from the right ventricular outflow tract

INTRODUCTION: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT. METHODS AND RESULTS: We reviewed the clinical, echocardiographic, and ECG findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 +/- 4 vs 83 +/- 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 +/- 1.0 vs 2.4 +/- 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, but ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted. CONCLUSION: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.     

Autonomic and pharmacological responses of idiopathic ventricular tachycardia arising from the left ventricular outflow tract

Background: It is well recognized that the mechanism of idiopathic ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) is mostly due to cyclic AMP-mediated triggered activity. The mechanism of VT arising from the left ventricular outflow tract (LVOT) has not been well clarified whether it is the same as VT of RVOT.
Methods: We studied autonomic modulations and pharmacological interventions on VT/premature ventricular contractions (PVCs) from LVOT to explore its possible mechanism in six patients (age: 49 ± 14, three males). None of them had structural heart diseases.
Results: Isoproterenol application easily induced VT and/or PVCs from LVOT. Valsalva maneuvers suppressed isoproterenol-induced VT in two and PVCs in two, and carotid sinus massage (CSM) suppressed PVCs in one patient. Adenosine triphosphate inhibited both VT and PVCs in all six patients. Propranolol, lidocaine, and procainamide eliminated VT/PVCs in four, three, and four patients, respectively. Verapamil terminated VT in one and PVCs in another one patient, but aggravated PVCs to VT in one patient.
Conclusion: The results suggest that the mechanism of VT from LVOT is mostly due to cAMP-mediated triggered activity as similar to that in VT from RVOT.     

Comparison of endocardial and epicardial programmed stimulation for the induction of ventricular tachycardia

Twenty-seven patients who had pairs of stainless steel wire electrodes placed on the right and the left ventricle during cardiac surgery underwent both epicardial and endocardial programmed ventricular stimulation to assess the inducibility of ventricular tachycardia. Twenty-six of the patients had coronary artery disease and were studied to evaluate map-guided surgery for treatment of ventricular arrhythmias. Burst ventricular pacing and up to three ventricular extrastimuli coupled to two drive train cycle lengths were delivered from the right and left ventricular epicardial wire electrodes and from endocardial catheter electrodes placed at the apex and outflow tract of the right ventricle. Ventricular tachycardia was reproducibly induced in three patients by both endocardial and epicardial stimulation. In one patient ventricular tachycardia was reproducibly induced by epicardial stimulation, but nonreproducible, nonsustained ventricular tachycardia was induced by endocardial stimulation. Ventricular tachycardia remained inducible by both endocardial and epicardial stimulation in three instances (two patients) during drug therapy. A negative study (less than 10 consecutive ventricular beats induced) was obtained in 23 patients by both endocardial and epicardial stimulation. The patients were followed up for 12 to 43 months (average 31). Sudden death or documented ventricular tachycardia occurred in two of the three patients with a positive study by both endocardial and epicardial stimulation. Nineteen (83%) of the 23 patients with concordantly negative studies remained free of arrhythmias. On the basis of concordant results of endocardial and epicardial stimulation (p = 0.001) these results suggest that epicardial stimulation of the right and the left ventricle is an acceptable method to assess the postoperative inducibility of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Layered activation of epicardial scar in arrhythmogenic right ventricular dysplasia: possible substrate for confined epicardial circuits

Background- Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results- Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm(2)) than the endocardium (57±44 cm(2); P=0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P<0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls (P=0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls (P=1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions- Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.     

Differences in arrhythmogenicity between the canine right ventricular outflow tract and anteroinferior right ventricle in a model of Brugada syndrome

BACKGROUND: The Brugada syndrome is characterized by ST-segment elevation on the ECG, especially in the right precordial leads sensitive to the right ventricular outflow tract (RVOT). OBJECTIVES: The purpose of this study was to evaluate the hypothesis that right ventricular electrophysiologic heterogeneity caused arrhythmogenicity in the Brugada syndrome. METHODS: Action potentials (APs) were mapped on the epicardium of 14 RVOT preparations and on the transmural surfaces of 15 pairs of RVOT and right ventricular anteroinferior (RVAI) preparations isolated from canine hearts. Brugada ECG and arrhythmias were induced with pilsicainide (2.5-12.5 micromol/L), pinacidil (1.25-12.5 micromol/L), and terfenadine (2.0 micromol/L). RESULTS: Low doses of drugs elevated the J-ST segment and induced APs with both short and long action potential durations (APDs) in contiguous RVOT epicardial regions. In addition, APs in the RVOT had a larger phase 1 notch and longer APD than in RVAI. The longest APDs were in the epicardium in RVOT but in the endocardium in RVAI regions. High doses of drugs eliminated the phase 2 dome of the AP and abbreviated APDs in the epicardium but not in endocardium and reduced the epicardial heterogeneity of APs but increased the transmural gradient of APD in 14 (93%) of the RVOT preparations. In contrast, abbreviations of epicardial APDs occurred in only 4 (27%) of the RVAI preparations. Ventricular tachycardia occurred more frequently in the RVOT (47%) than in paired RVAI preparations (7%). Blocking the transient outward current reduced the heterogeneity of APs and eliminated arrhythmogenicity in all preparations. CONCLUSION: Compared with the RVAI region, the RVOT has greater electrophysiologic heterogeneity that contributes to arrhythmogenicity in this model of Brugada syndrome.     

How to diagnose,locate, and ablate coronary cusp ventricular tachycardia

INTRODUCTION: Although radiofrequency energy usually is applied to the most favorable endocardial site in patients with outflow tract ventricular tachycardia, there are still some patients in whom the tachycardia can be ablated only from an epicardial site. We established the characteristics and technique of catheter ablation from both the left and right coronary cusps to cure left ventricular outflow tract ventricular tachycardia. METHODS AND RESULTS: We studied 15 patients in whom VT was thought to originate from the coronary cusp by both activation and pace mapping after precise mapping of the right ventricle, left ventricle, pulmonary artery, coronary cusps, and anterior interventricular vein. Twelve-lead ECG analysis revealed an S wave on lead I, tall R wave on leads II, III, and aVF, and no S wave on either lead V5 or V6. Precordial R wave transition occurred on leads V1 and V2. The earliest ventricular electrogram at a successful ablation site was recorded 35+/-12 msec before QRS onset and 19+/-15 msec earlier than the earliest ventricular electrogram recorded from the anterior interventricular vein. Almost identical pace mappings were obtained from the coronary cusp. Catheter tip temperature was maintained at 55 degrees C during energy delivery, and the distance from the tip to the ostium of each left and right coronary artery was > 1.0 cm by coronary angiography. CONCLUSION: Left ventricular outflow tract VT that could not be ablated from an endocardial site could be safely eliminated by radiofrequency application to the left and right coronary cusps.     

Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism

Introduction: "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.
Methods and Results: One hundred twenty-two consecutive patients  (61 male; 50.9 ± 15.2 years)  with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT)  (RVOT = 28%, LVOT = 36%)  , nonsustained VT  (RVOT=40%, LVOT=23%)  , and premature ventricular complexes  (RVOT = 32%, LVOT = 41%) (P = 0.32)  . Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT=70%, LVOT=80%; P = 1.00) in both groups.
Conclusions: Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."     

右室心尖部起搏与右室流出道起搏对Ⅲ度房室传导阻滞患者疗效的对比研究

目的:比较右室心尖部起搏与右室流出道起搏对Ⅲ度房室传导阻滞患者心室间运动同步性及左室内运动同步性,以及对患者心功能的影响。方法:选取因Ⅲ度及高度房室传导阻滞患者置入双腔起搏器患者共38例。其中心室电极置入右室流出道者20例(RVOT组),置入右室心尖部18例(RVA组),超声心动图术前测量左室舒张末内径(LVEDD),左室收缩末内径(LVESD)、左室射血分数(LVEF)、E/A值、心室间激动延迟时间(IVMD)、室间隔与左心室后壁间收缩延迟时间(SPWMD)。术后1个月、12个月随访。结果:术后1个月,与RVOT组比较,RVA组IVMD、SPWMD明显延长[IVMD(39.83±6.01)∶(31.95±7.86)ms,P=0.02],[SP-WMD(97.83±20.81)∶(84.6±10.89)ms,P=0.023]。术后12个月,与ROVT组比较,RVA组LVEDD明显增大[(49.11±2.39)∶(47.4±1.96)mm,P=0.02],LVESD明显增大[(34.28±3.41)∶(32.5±1.5)mm,P=0.04];LVEF明显降低[(59.56±3.38)∶(62.8±2.14)%,...     

Endocardial mapping of right ventricular outflow tract tachycardia using noncontact activation mapping

INTRODUCTION: Activation mapping and pace mapping identify successful ablation sites for catheter ablation of right ventricular outflow tract (RVOT) tachycardia. These methods are limited in patients with nonsustained tachycardia or isolated ventricular ectopic beats. We investigated the feasibility of using noncontact mapping to guide the ablation of RVOT arrhythmias. METHODS AND RESULTS: Nine patients with RVOT tachycardia and three patients with ectopic beats were studied using noncontact mapping. A multielectrode array catheter was introduced into the RVOT and tachycardia was analyzed using a virtual geometry. The earliest endocardial activation estimated by virtual electrograms was displayed on an isopotential color map and measured 33 +/- 13 msec before onset of QRS. Virtual unipolar electrograms at this site demonstrated QS morphology. Guided by a locator signal, ablation was performed with a mean of 6.9 +/- 2.2 radiofrequency deliveries. Acute success was achieved in all patients. During follow-up, one patient had a recurrence of RVOT tachycardia. Compared with patients (n = 21) who underwent catheter ablation using a conventional approach, a higher success rate was achieved by noncontact mapping. Procedure time was significantly longer in the noncontact mapping group. Fluoroscopy time was not significantly different in the two groups. CONCLUSION: Noncontact mapping can be used as a reliable tool to identify the site of earliest endocardial activation and to guide the ablation procedure in patients with RVOT tachycardia and in patients with ectopic beats originating from the RVOT.     

起源于左右心室流出道心动过速和早搏的射频导管消融治疗

目的 探讨射频导管消融（RFCA）治疗心室流出道特发性室性心动过速（室速）和室性早搏（室早）的临床效果、心电图及电生理特征。方法 58例患者中室速10例,室早48例。起源于右室流出道（RVOT）43例,左室流出道（LVOT）15例,其中起源于主动脉瓣上Valsalva左冠窦（LSV）12例。5例RVOT室速是在非接触标测系统Ensite3000指导下进行消融的。结果 （1）58例患者中55例成功,3例失败,9例复发。（2）其中1例患者术中出现急性心包压塞。（3）起源心室流出道的室速和室早具有典型的心电图特征,其中Ⅱ、Ⅲ、aVF导联单向R波是流出道室性心律失常的共同特点。（4）V1或V2导联的R波时限指数与R／S波幅指数可作为区别LSV与RVOT室速和室早的有效指标。结论 射频导管消融治疗心室流出道特发性室性心律失常是一种安全、有效的方法。非接触标测系统对于血流动力学不稳定的复杂性室性心律失常的标测与治疗具有重要的意义。     

Outflow tract tachycardia with R/S transition in lead V3: six different anatomic approaches for successful ablation

OBJECTIVES: The aim of this study was to analyze different anatomic mapping approaches for successful ablation of outflow tract tachycardia with R/S transition in lead V(3). BACKGROUND: Idiopathic ventricular tachycardia can originate from different areas in the outflow tract, including the right and left ventricular endocardium, the epicardium, the pulmonary artery, and the aortic sinus of Valsalva. Although electrocardiographic criteria may be helpful in predicting the area of origin, sometimes the focus is complex to determine, especially when QRS transition in precordial leads is in V(3). METHODS: We analyzed surface electrocardiograms of 33 successfully ablated patients with outflow tract tachycardia: 20 from the right ventricular outflow tract (RVOT) and 13 from different sites. The R/S transition was determined, and the different anatomic approaches needed for successful catheter ablation were studied. RESULTS: Overall, R/S transition in lead V(3) was present in 19 (58%) of all patients. In these patients, mapping was started and successfully completed in the RVOT in 11 of 19 (58%) patients. The remaining eight patients with R/S transition in lead V(3) needed five additional anatomic accesses for successful ablation: from the left ventricular outflow tract (n = 3), aortic sinus of Valsalva (n = 2), coronary sinus (n = 1), the epicardium via pericardial puncture (n = 1), and the trunk of the pulmonary artery (n = 1), respectively. CONCLUSIONS: A R/S transition in lead V(3) is common. In patients with outflow tract tachycardia with R/S transition in lead V(3), a stepwise endocardial and epicardial mapping through up to six anatomic approaches can lead to successful radiofrequency catheter ablation.     

The influence of atrioventricular asynchronous contraction on left and right ventricular performance]

To investigate the influence of atrioventricular asynchronous contraction on left and right ventricular performance, pulsed Doppler echocardiographic studies were performed in 10 patients who received permanent pacemaker (VVI mode), but without significant heart disease except for complete heart block. After setting the pacing rate at 40 per min, the performance was analyzed during the patient's own slow ventricular rate. Flow velocity patterns at the left (LVOT) and right ventricular outflow tracts (RVOT) were recorded by pulsed Doppler echocardiography, and ejection time (EjT), acceleration time (AcT), peak velocity (PV) and flow velocity integral (FVI), which is proportional to stroke volume, were measured for each outflow tract. When the patient's own atrial contraction occurred during ventricular systole, EjT, AcT, PV and FVI of flow at the LVOT and EjT, AcT and FVI of flow at the RVOT were decreased. Percent change of the FVI of flow at the RVOT (-34.6%) was significantly greater than that of flow at the LVOT (-16.2%, p < 0.01). These results indicate that the loss of right ventricular performance might play a prominent role in the genesis of the hemodynamic deterioration with atrioventricular asynchronous contraction.     

Radiofrequency catheter ablation of idiopathic left ventricular outflow tract tachycardia: utility of intracardiac echocardiography

INTRODUCTION: The site of origin of idiopathic ventricular tachycardia (VT) arising from the left ventricular outflow tract (LVOT) may be closely related to the aortic valve leaflets, and radiofrequency (RF) delivery potentially can damage them. Intracardiac echocardiography (ICE) can identify accurately the ablation electrode and anatomic landmarks, and contact with the endocardium can be easily assessed. The aim of this study was to define the utility and the accuracy of ICE in guiding RF ablation of idiopathic VT of the LVOT. METHODS AND RESULTS: Five consecutive patients (all men; mean age 20.4 years, range 16 to 25) symptomatic for idiopathic VT underwent RF ablation. A 9-French, in-sheath catheter with a 9-MHz ultrasound transducer was inserted through the femoral vein and positioned in the His-bundle region or right ventricular outflow tract to provide a clear view of the aortic root. Local earliest ventricular activation during tachycardia and pace mapping were used to identify the ablation site. Idiopathic VT was ablated successfully in all patients using a median of two RF pulses, delivered during tachycardia. High-resolution images of the aortic valve and ablation electrode were achievable in all cases. Direct vision of ablation electrode-endocardial contact in the outflow tract was assessed easily in all patients. CONCLUSION: Idiopathic VT of the LVOT can be treated successfully with RF ablation. ICE can accurately guide catheter ablation and identify anatomic landmarks, endocardial contact, and ablation electrode movement.     

Morphological changes in correlation with so-called idiopathic ventricular tachycardias from the right ventricular outflow tract

"Idiopathic" ventricular tachycardia is an exclusion diagnosis. The underlying reasons and mechanisms of "idiopathic" ventricular tachycardias are still not completely understood. Recent investigations showed a high prevalence of morphological abnormalities in the right ventricle of patients with "idiopathic" ventricular tachycardia out of the right ventricular outflow tract, which could often be correlated with the origin of the ventricular tachycardia. These described abnormalities were not uniform. Here we report about a patient suffering from drug-refractory "idiopathic" ventricular tachycardia for 10 years. This is the first report in which the origin of an "idiopathic" ventricular tachycardia could be localized by right-ventricular angiography, magnetic resonance tomography and electrophysiological study in the area of an interventricular septal thickening of the right ventricular outflow tract and cured by radiofrequency catheter ablation.     

Left Ventricular Outflow Tract Tachycardia Including Ventricular Tachycardia from the Aortic Cusps and Epicardial Ventricular Tachycardia

Idiopathic outflow tract ventricular tachycardia (VT) can arise from the right (RVOT) or left ventricular outflow tract (LVOT). The electrocardiographic (ECG) pattern of RVOT VT is typical in most patients, showing a monomorphic left bundle branch block (LBBB) QRS morphology with an inferior axis. Radiofrequency catheter ablation can be performed with a high success rate and provides a curative therapeutic approach. However, not all VTs with LBBB and inferior axis can be ablated from the RVOT. It has become apparent that LVOT VTs including VT originating from the aortic sinus of Valsalva or epicardium represent underrecognized VT entities which are also amenable to successful catheter ablation. Twelve-lead ECG criteria can contribute to distinguish between sites of VT origin.LVOT arrhythmias represent an increasingly recognized VT entity which can be safely and successfully treated by catheter ablation. Identification of VT origin using ECG criteria and differentiation of LVOT versus RVOT origin is essential in the careful planning of the ablation strategy.     

Acute coronary artery occlusion and ischemia-related ventricular tachycardia during catheter ablation in the right ventricular outflow tract

Coronary artery injury is a rare complication of catheter ablation in the right ventricular outflow tract (RVOT). Furthermore, acute myocardial ischemia usually causes polymorphic ventricular tachycardia (VT) or ventricular fibrillation. We herein describe a case in which catheter ablation for VT originating from the RVOT provoked ischemia-related VTs due to acute occlusion of the left anterior descending artery.