Left bundle branch block-type ventricular tachycardia originating from the left ventricular septum in a patient with cardiac sarcoidosis

This case report describes a left bundle branch block (LBBB)-type ventricular tachycardia (VT) with a unique reentrant circuit in a patient with cardiac sarcoidosis. The VT morphology and pace mapping supported an exit site of the VT from the basal posterior right ventricle (RV) septum. Nonetheless, concealed entrainment was established by pacing from a septal left ventricular (LV) site recording a diastolic potential, opposite site to the RV site. A point ablation at that LV site could successfully terminate the VT, suggesting that a critical isthmus was located on the LV side of the interventricular septum despite the demonstration of an LBBB-type VT.     

Eleven-years long follow-up in a patient after myocardial infarction, with low ejection fraction and recurrent ventricular tachycardia. The role of implantable cardioverter defibrillator and selective ablation

The selective ablation of the recurrent ventricular tachycardia (VT) in a 75-year old patient after extensive inferior myocardial infarction (24 years ago), with low ejection fraction was performed. In 1995 the cardioverter-defibrillator was implanted due to recurrent, symptomatic VT. The coronary angiography in 1995 and in 2006 revealed the occlusion of the right coronary and the circumflex arteries. One year after implantation, he had electrical storm caused by proarrhythmic effect of amiodarone with prolongation of QT/QTc interval. During follow up episodes of VT (approximately 5/year) were successfully terminated by ATP and rarely by cardioversion. Recently, the patient was admitted to the hospital because of the very frequent (25/day) episodes of slow (500-560 ms), sustained ventricular tachycardia. The pharmacological treatment was unsuccessful. CARTO mapping and entrainment pacing revealed VT circuit around mitral annulus. A few applications at the paraseptal part of the mitral isthmus terminated VT, which was no longer inducible. During following days there were no VTs requiring ICD interventions.     

CARTO标测指导心肌梗死后室性心动过速的射频消融

心肌梗死 (MI)后室性心动过速 (VT)的基质存在解剖上的复杂性并且血液动力学常常是不稳定的 ,因此射频导管消融的成功率是有限的。本研究的目的是运用电解剖标测 (CARTO)指导VT的射频消融 ,以便弄清折返环和梗死区的关键峡部 ,此可能增加临床消融的效率。 19例MI的病人 (年龄 6 6± 7岁 ,其中男性 17例 )因VT拟作 2 0次消融 [17例在服用抗心律失常药 ,7例已安装埋藏式心脏转复除颤器 (ICD) ]。所有病例均反复发作临床型VT(周期为 42 3± 87ms)。在VT时或窦律 /右室起搏 (SR/RVP)行左室CARTO标测。对 13例 14次血液动力学稳定的VT实施标测 ,包括 2例无休止性慢VT。仅 8例临床性VT ,在心动过速时完成了整个左室的重建 ,另 6例因反复机械损伤MI区内关键性峡部 ,使临床型VT不再诱发。 12例在SR/RVP时完成左室标测 ,包括 6例关键性峡部损伤及 6例血液动力学不稳定者。在 8例CARTO标测的VT中 ,有 3例呈现典型的“8字”型折返环 ,2例沿二尖瓣 (MA)激动心室。在 8例VT中 ,于关键性峡部放电消融 ,其中 6例VT终止 ,平均放电 2次 ;然后行线性消融连接两个疤痕区域或连接疤痕与MA环 ,平均放电 16次。在SR/RVP时标测 ,可见 1个或多个疤痕区域 ,4例在诱发VT时放电 ,均终止了VT ;另 8例因极不稳定的血液动力学或机械损?     

Two adults requiring implantable defibrillators because of ventricular tachycardia and left ventricular dysfunction caused by presumed Kawasaki disease.

There is an adult patient population in Japan with undiagnosed coronary artery lesions caused by Kawasaki disease (KD) occurring before 1967, the time at which KD was first described. Two adult patients presented with a low left ventricular (LV) ejection fraction and ventricular tachycardia (VT) caused by presumed KD. A 43-year-old man with rapid VT had a history of an acute febrile illness with desquamation of the fingertips at the age of 10 months. Coronary angiography (CAG) showed segmental stenosis of the right coronary artery (RCA) and occlusion of the left anterior descending artery with a giant aneurysm. The other patient was a 48-year-old man with a history of ischemic cardiomyopathy diagnosed after a previous myocardial infarction when he was 32 years old. He had segmental stenosis of the RCA on CAG. Non-sustained VT with transient unconsciousness was observed during 24-h Holter electrocardiography. Rapid VT with syncope was induced in both patients in the electrophysiologic studies and an implantable defibrillator was required to prevent sudden death. Physicians must be aware that VT can occur in older patients with LV dysfunction many years after KD.     

Analysis of Posterior Mitral Annular Activation During Entrainment and Catheter Ablation of Mitral Isthmus Ventricular Tachycardia Using a Coronary Sinus Catheter

A detailed analysis of the ventricular activation along the posterior aspect of the mitral annulus was made using a multipolar catheter positioned in the coronary sinus in a patient with mitral isthmus ventricular tachycardia (VT) associated with a remote inferior myocardial infarction and prior cryosurgical ablation for the elimination of a different preexisting VT. A change in the timing and sequence of the ventricular activation along the isthmus could be observed during induction of the VT and entrainment pacing. A radiofrequency (RF) current application directed at the posterolateral region of the isthmus successfully eliminated this tachycardia. During the RF delivery, complete conduction block was confirmed by a sudden change in the activation sequence during sinus rhythm.     

Transvenous dual site left ventricular pacing plus biventricular pacing for the management of refractory ventricular tachycardia

This is a case report of a male patient with nonischemic cardiomyopathy who had severely depressed left ventricular systolic function and functional class III congestive heart failure (CHF). He also had left bundle branch block (LBBB) and recurrent ventricular tachycardia (VT). Though the patient’s CFH functional class improved after implantation of a transvenous biventricular ICD system, recurrent VT episodes required the initiation of amiodarone. After an improved condition for 28 months, recurrent VT episodes led to multiple consecutive ICD shocks, which constituted an electrical storm and a battery status of elective replacement indicator (ERI). The recurrent VT episodes were suppressed with intravenous amiodarone and lidocaine. As Radiofrequency ablation was declined by the patient, a new left ventricular (LV) lead was transvenously added, providing biventricular and dual site LV pacing. After this intervention the arrhythmia subsided and the intravenous antiarrhythmic medications were stopped. No episodes of sustained VT leading to ICD shocks were observed for the following 9 months. The events in this case suggest that dual site LV pacing with biventricular pacing could be an alternative strategy for the management of refractory VT.     

Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathological autopsy of a patient that underwent a successful ablation of an electrical storm from the left ventricular summit

A 65-year-old man with non-ischemic cardiomyopathy, underwent an autopsy 2 months after the successful ablation of a sustained left ventricular (LV) summit ventricular tachycardia (VT). The patient died due to interstitial pneumonia from amiodarone use. The earliest activation sites of the VT were documented from both inside the anterior interventricular vein (AIV) and epicardial surface. The diameter of the AIV was 3–4 mm, and the radiofrequency (RF) lesion inside the AIV was a slight lesion due to high impedance with a high temperature. The lesion from the epicardial surface was also superficial and insufficient due to neighboring coronary arteries and the existence of epicardial fat. A successful application was performed from the LV endocardium, and diffuse myocardial fibrosis was observed in the mid-myocardium including inside the RF lesions. The actual relationship between the myocardial fibrosis and LV summit VT remains unclear, but this case showed the difficulty of achieving a successful ablation from the epicardial side, when the focus exists in the mid-myocardium around the LV summit.     

Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction.

OBJECTIVES: We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations. BACKGROUND: The nature of the reentrant circuit that underlies VT during acute MI is not well understood. METHODS: Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI. RESULTS: Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P < .01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P < .05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P < .05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P < .05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT. CONCLUSIONS: The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.     

A Rare Case of Transcatheter Closure of Both Inlet and Outlet of a Left Coronary Artery-to-Left Ventricular Fistula with Giant Coronary Artery Aneurysm

A congenital coronary artery fistula (CCAF) combined with giant coronary aneurysm (CAA) is a rare congenital cardiac abnormality. We reported an 8-year-old patient who underwent transcatheter closure of both inlet and outlet of a proximal left coronary artery (LCA)-to-left ventricular (LV) fistula with CAA of 41 mm × 28 mm in diameter, during which acute occlusion of left anterior descending coronary artery (LAD) occurred immediately after device implantation at the inlet of fistula. We managed to prevent the patient from major adverse cardiac events by conservative therapy with dual antiplatelet agents instead of surgical removal of the device. The patient recovered well and had been follow-up for 2 years with no late complications reported.     

Preferential Locations for Critical Reentry Circuit Sites Causing Ventricular Tachycardia After Inferior Wall Myocardial Infarction

Reentrant VT Post MI. Introduction : For relatively slow monomorphic ventricular tachycardia (VT) after myocardial infarction, entrainment can be used to identify reentry circuit "isthmus sites" (exit sites and sites proximal to the exit) where radioifrequency (RF) catheter ablation has the greatest likelihood of interrupting reentry. Similarities in coronary and ventricular anatomy may cause such sites to form in preferential locations. The objective of this study is to determine if there are preferential locations for reentry circuit isthmus regions in chronic inferior wall infarctions causing VT.
Methods and Results : Catheter mapping and RF catheter ablation was performed in 21 patients with an old inferior wall myocardial infarction and VT. The inferior wall was divided into 9 anatomic regions: 3 apical, 3 mid, and 3 basal segments. Of 46 different VTs, an endocardial isthmus site was identified in one or more zones in 28 (61%), with 10 VTs having isthmus sites in two or more adjacent regions. Isthmus zones were found in a basal region of the left ventricle in 24 (86%) of 28 VTs, in a mid segment in 9 (32%) VTs, and in an apical segment in 1 (4%) (P = 0.002). Of 30 RF current applications that terminated VT, 21 (70%) were at basal isthmus sites.
Conclusion : The high prevalence of endocardial isthmus zones near the base of the left ventricle suggests that the mitral annulus often plays a role in defining the margins of reentry circuits that cau.se relatively slow VTs after inferior wall myocardial infarction.     

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transvenous ICD implantation after artificial tricuspid valve replacement A new approach placing a transvenous ICD lead in the mid cardiac vein of the coronary sinus

Implantation of a transvenous device in patients with a tricuspid valve replacement or a complex congenital heart disease with no access to the right ventricle represents problems. The lack of access to the right ventricle might preclude transvenous placement of a defibrillation lead at ICD implantation. A young patient (21 years) with a history of severe chest trauma with rupture of the tricuspid valve as well as the right coronary artery and consecutive inferior myocardial infarction was initially treated with tricuspid valve replacement (St Jude Medical artificial prosthesis, 33 mm) and a bypass graft to the right coronary artery. Four years later, the patient was admitted with a hemodynamically not tolerated ventricular tachycardia (VT: CL 250 ms, LBBB, left axis). The VT could be reproduced during electrophysiological testing. An ICD was implanted subpectorally in combination with a transvenous active fixation ICD lead. The transvenous ICD lead was placed via a guiding catheter into a coronary sinus branch (middle cardiac vein). Acceptable pacing and sensing values could be obtained. The defibrillation threshold was 25 J. In conclusion transvenous ICD lead implantation into a side branch of the coronary sinus in combination with a pectorally implanted “active can” ICD device seems to be an alternative approach. This approach may avoid implantation of additional subcutaneous defibrillation leads or even thoracotomy for ICD implantation.     

Ventricular tachycardia induced by biventricular pacing in patient with severe ischemic cardiomyopathy

INTRODUCTION: Cardiac resynchronization therapy (CRT) is a new alternative which affords symptomatic improvement in two-thirds of patients who exhibit medically refractory congestive heart failure (CHF) as well as significant prolongation of the QRS duration (>135 msec). As more experience with CRT accrues, unexpected complications of this promising therapy may become apparent. Herein, we describe a patient with severe ischemic cardiomyopathy and refractory CHF who developed incessant ventricular tachycardia (VT) after the initiation of biventricular pacing. The patient is a 75-year-old man who suffered an inferior myocardial infarction 6 years before presenting for CRT. He underwent a three-vessel CABG in 1997. Subsequently, episodes of near syncopal sustained VT developed, for which he received a dual chamber ICD. In 2001 he developed refractory CHF and ECG revealed LBBB with a QRS duration of 195 msec. Shortly after the initiation of biventricular pacing, the patient developed multiple episodes of drug resistant monomorphic VT that could be terminated only transiently by ICD therapies. Ultimately, the only intervention, which proved to be effective in eliminating VT episodes, was inactivation of LV pacing. Despite subsequent therapeutic regimen of sotalol, lidocaine, tocainide, and quinidine all subsequent attempts to reactivate LV pacing resulted in prompt VT recurrence. CONCLUSION: This case represents a clear example of CRT induced proarrhythmia, which required inactivation of LV pacing for effective acute management. Such an intervention should be considered in CRT patients who exhibit a notable increase in drug refractory VT episodes.     

Relation between site of origin of ventricular tachycardia and relative left ventricular myocardial perfusion and wall motion

To assess the relation between the site of origin of ventricular tachycardia (VT) and relative myocardial perfusion and wall motion, 18 patients with a history of recurrent sustained VT underwent cardiac catheterization, invasive electrophysiologic study with endocardial mapping, and resting radionuclide ventriculography. In addition, 6 patients had exercise and redistribution thallium-201 scintigraphy, whereas the remaining 12 patients had resting thallium scans. The site of origin of VT (determined by catheter and intraoperative endocardial mapping) was correlated with relative myocardial perfusion (thallium) and left ventricular (LV) wall motion. All patients had significant (>50% narrowing) coronary artery disease and 16 had LV aneurysms.Twenty sites of origin of VT (28 morphologies) were identified in these 18 patients. Of the 9 patients with multiple VT morphologies, the VT originated at disparate sites in 2 patients. All 18 patients had thallium defects at rest and 3 patients had additional reversible (ischemic) defects on exercise. Of the 20 sites of origin of VT, 16 were at the periphery of the thallium defect, 1 was adjacent to it, and 3 were in the center of it. In the 16 patients with LV aneurysm, there were 18 sites of origin: 15 at the border of the aneurysm, 1 adjacent to it, and 2 within it.The data suggest that in patients with VT and coronary artery disease the site of origin is usually the periphery of a resting thallium defect, and in patients with LV aneurysm the site is the border of the aneurysm.     

Coronary venoplasty during the implantation of the cardiac resynchronisation device--a case report

We describe a case of a 76-year-old patient with advanced block in the His-Purkjnie system, who underwent implantation of a cardioverter-defibrillator with cardiac resynchronisation therapy. Complete heart block occurred during the insertion of the coronary sinus cathether. The implantation of the left ventricular (LV) lead was impossible due to difficult anatomy of the coronary venous system. The right ventricular pacing caused the further prolongation of the QRS duration and exacerbation of heart failure symptoms. Thus, the LV lead was successfully implanted during the second procedure after the balloon venoplasty of the lateral cardiac vein. The biventricular pacing was successful during 4 months follow-up.     

Transvenous ICD implantation after artificial tricuspid valve replacement. A new approach placing a transvenous ICD lead in the mid cardiac vein of the coronary sinus

Summary Implantation of a transvenous device in patients with a tricuspid valve replacement or a complex congenital heart disease with no access to the right ventricle represents problems. The lack of access to the right ventricle might preclude transvenous placement of a defibrillation lead at ICD implantation. A young patient (21 years) with a history of severe chest trauma with rupture of the tricuspid valve as well as the right coronary artery and consecutive inferior myocardial infarction was initially treated with tricuspid valve replacement (St Jude Medical artificial prosthesis, 33 mm) and a bypass graft to the right coronary artery. Four years later, the patient was admitted with a hemodynamically not tolerated ventricular tachycardia (VT: CL 250 ms, LBBB, left axis). The VT could be reproduced during electrophysiological testing. An ICD was implanted subpectorally in combination with a transvenous active fixation ICD lead. The transvenous ICD lead was placed via a guiding catheter into a coronary sinus branch (middle cardiac vein). Acceptable pacing and sensing values could be obtained. The defibrillation threshold was 25 J. In conclusion transvenous ICD lead implantation into a side branch of the coronary sinus in combination with a pectorally implanted “active can” ICD device seems to be an alternative approach. This approach may avoid implantation of additional subcutaneous defibrillation leads or even thoracotomy for ICD implantation.     

CMR–Based Identification of Critical Isthmus Sites of Ischemic and Nonischemic Ventricular Tachycardia

ObjectivesThis study evaluates whether contrast-enhanced (CE) cardiac magnetic resonance (CMR) can be used to identify critical isthmus sites for ventricular tachycardia (VT) in ischemic and nonischemic heart disease.BackgroundFibrosis interspersed with viable myocytes may cause re-entrant VT. CE-CMR has the ability to accurately delineate fibrosis.MethodsPatients who underwent VT ablation with CE-CMR integration were included. After the procedure, critical isthmus sites (defined as sites with a ≥11 of 12 pacemap, concealed entrainment, or VT termination during ablation) were projected on CMR-derived 3-dimensional (3D) scar reconstructions. The scar transmurality and signal intensity at all critical isthmus, central isthmus, and exit sites were compared to the average of the entire scar. The distance to >75% transmural scar and to the core-border zone (BZ) transition was calculated. The area within 5 mm of both >75% transmural scar and the core-BZ transition was calculated.ResultsIn 44 patients (23 ischemic and 21 nonischemic, left ventricular ejection fraction 44 ± 12%), a total of 110 VTs were induced (cycle length 290 ± 67 ms). Critical isthmus sites were identified for 78 VTs (71%) based on ≥11 of 12 pacemaps (67 VTs), concealed entrainment (10 VTs), and/or termination (30 VTs). The critical isthmus sites, and in particular central isthmus sites, had high scar transmurality and signal intensity compared with the average of the entire scar. Of the pacemap, concealed entrainment, and termination sites, 74%, 100%, and 84% were within 5 mm of >75% transmural scar, and 67%, 100%, and 94% were within 5 mm of the core-BZ transition, respectively. The areas within 5 mm of both >75% transmural scar and the core-BZ transition (median 13% of LV) contained all concealed entrainment sites and 77% of termination sites.ConclusionsBoth in ischemic and nonischemic VT, critical isthmus sites are typically located in close proximity to the CMR-derived core-BZ transition and to >75% transmural scar. These findings suggest that CMR-derived scar characteristics may guide to critical isthmus sites during VT ablation.     

Limited predictive value of inducible sustained ventricular tachycardia for future occurrence of spontaneous ventricular tachycardia in patients with coronary artery disease and relatively preserved cardiac function

To evaluate the significance of inducible sustained ventricular tachycardia (VT) in patients with coronary artery disease and relatively preserved cardiac function, 33 patients who met the following criteria were studied; documented nonsustained VT but no history of life-threatening arrhythmia, inducible sustained VT at electrophysiologic study, and implantation of a cardioverter-defibrillator. Eighteen patients developed clinical sustained VT within 2 years. By univariate analysis, left ventricular ejection fraction (EF) and the cycle length of induced VT were associated with clinical VT occurrence. By multivariate analysis, however, EF was the only independent predictor. Among 23 patients with EF 40% (P <.01). In coronary artery disease patients with relatively preserved EF, the incidence of clinical VT is considerably low even though sustained VT is inducible. Inducible VT is therefore not appropriate for risk stratification in this patient population.     

Gitelman's syndrome with exercise-induced ventricular tachycardia.

A 62-year-old female with palpitations was admitted to hospital where she recorded 12,299 monofocal ventricular premature contractions (VPCs) in 24 h and nonsustained ventricular tachycardia (VT) on exertion. She had hypokalemia with renal potassium wasting, a chloride-resistant metabolic alkalosis, elevated plasma renin, elevated plasma aldosterone (relative to the serum K concentration), hypomagnesemia with renal magnesium wasting, decreased urine calcium excretion, and normal blood pressure. The hypokalemia and hypomagnesemia were thought to have precipitated the VT. The coronary angiogram showed normal coronary arteries; however, the left ventriculogram revealed akinesis of the posterolateral wall. Because the VT could not be induced by programmed electrical stimulation either before or during intravenous administration of isoproterenol, the VPC with the same QRS morphology as the VT became the target of radiofrequency catheter ablation (RF-CA). Intracardiac mapping showed that the earliest activation site was situated in the asynergic area of the left ventricle (LV) and radiofrequency catheter ablation directed at the LV asynergy area completely eliminated the VPCs without any complications. During the follow-up period (6 months), she was free from palpitation and VT was not clinically documented.