射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

Human Model Simulating Right Ventricular Outflow Tract Tachycardia by High-Frequency Stimulation in the Left Pulmonary Artery: Autonomics and Idiopathic Ventricular Arrhythmias

Introduction: Frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). An animal model simulating RVOT tachycardia by high-frequency stimulation (HFS) of the sympathetic input to the proximal pulmonary artery (PA) has been previously described. The aim of this study was to similarly induce RVOT tachycardia in humans.
Methods: In 9 patients with no history of ventricular arrhythmias, a circumferential catheter was placed in the left, main, and proximal PA to contact the endovascular circumference of the PA. A 50-ms train of HFS (200 Hz/0.3 ms pulse duration), coupled to atrial pacing, was applied at each bipolar pair of the circumferential catheter. The coupling interval was adjusted so that the 50-ms train occurred during the ventricular refractory period.
Results: In 6 out of 9 patients, HFS in the left PA during dobutamine infusion induced monomorphic PVCs and/or VT with left bundle branch block (LBBB) morphology and inferior axis at an average stimulation level of 12.5 ± 2.7 V. HFS in the main PA and in the proximal PA did not induce any ventricular arrhythmias with the highest energy of 15 V in baseline state and during dobutamine infusion. HFS in the left PA was associated with hiccough in all patients.
Conclusion: Stimulation of the sympathetic input to the left PA during dobutamine infusion induces PVCs and/or VT exhibiting LBBB-morphology and inferior axis, closely simulating clinical RVOT tachycardia in humans.     

Radiofrequency Ablation of Ventricular Fibrillation and Multiple Right and Left Atrial Tachycardia in a Patient with Brugada Syndrome

Brugada syndrome is a well-known form of idiopathic ventricular fibrillation (VF). Few data suggest that this arrhythmia may be triggered by ventricular premature beats (VPBs), and an association with other arrhythmia such as monomorphic ventricular tachycardia (VT) or supraventricular tachycardia (SVT) has been reported. In a highly symptomatic 18-year-old-male patient with this syndrome, frequent episodes of VF, fast polymorphic VT, and fast monomorphic sustained regular tachycardia were observed. The tachycardia episodes were classified as VT or VF and as a consequence received appropriate therapies with the implanted cardioverter defibrillator (ICD). Precipitating VPBs that were stored in the ICD memory and on the electrocardiogram (ECG) exhibited the same morphology as frequent isolated VPBs. During the electrophysiological study, right and left atrial tachycardia (AT) with one-to-one atrioventricular conduction were also induced and successfully ablated. VF was ablated using the same noncontact mapping (NCM) system triggering VPBs from right ventricular outflow tract (RVOT).     

Cryocatheter ablation of right ventricular outflow tract tachycardia

INTRODUCTION: Cryocatheter techniques have been successfully applied to treat supraventricular tachycardia but there are no reports on their value in treating ventricular tachycardia (VT). We present our initial experience with cryocatheter ablation of right ventricular outflow tract (RVOT) tachycardia. METHODS AND RESULTS: Cryocatheter ablation was attempted in 14 patients (13 females, age 45.9 +/- 12.7 years) who were highly symptomatic due to frequent monomorphic ventricular extrasystole (VES) or nonsustained VT originating within the RVOT. A 9-Fr, 8-mm-tip cryocatheter was used for both mapping and ablation. Cryoablation was started after localizing the arrhythmic focus by pace and activation mapping. Ablation success, defined by complete disappearance of target VES/VT acutely and during a follow-up of 9.3 +/- 1.4 weeks, was achieved in 13 of 14 patients. Ablation was successful with local activation times of 35 +/- 4 ms, 5.8 +/- 3.3 applications, 18.8 +/- 7.5 minutes total cryo time, 9.4 +/- 4.2 minutes fluoroscopy time, and 66.9 +/- 26.1 minutes total procedure time, the latter two measures showing a reduction with number of patients treated. Three patients reported slight pain related to local pressure of the catheter on the RVOT wall. No pain was described related to delivery of cryothermal energy. CONCLUSIONS: Initial experience shows that focal VES/VT originating in the RVOT can be successfully treated using cryocatheter ablation. Acute and short term success rates, fluoroscopy times, and duration of procedure are comparable to conventional ablation techniques. A major advantage seems to be the virtual absence of ablation related pain.     

Tachycardia-Induced Cardiomyopathy Secondary to Right Ventricular Outflow Tract Ventricular Tachycardia: Improvement of Left Ventricular Systolic Function After Radiofrequency Catheter Ablation of the Arrhythmia

Cardiomyopathy Secondary to RVOT VT. Introduction : Several reports describe development of cardiomyopathics secondary to supraventricular tachycardia. Few reports have described cardiomyopathies secondary to ventricular tachycardia.
Methods and Results : We describe a patient who presented with dilated cardiomyopathy and repetitive nonsustained monomorphic ventricular tachycardia. Cardiac cathcterization showed hemodynamically insignificant coronary artery disease. Radiofrequency ablation of a right ventricular outflow tract ventricular tachycardia resulted in improvement of the left ventricular systolic function and resolution of heart failure symptoms.
Conclusions : This report suggests that right ventricular outflow tract ventricular tachycardia may cause reversible tachycardia-induced cardiomyopathy.     

Ventricular tachycardia of right ventricular outflow tract origin during the perioperative period: A case report

Rationale:Idiopathic ventricular tachycardia (VT) occurs in individuals without structural abnormalities in the heart, accounts for approximately 10% of total VTs. Furthermore, approximately 70% of idiopathic VTs originate from Right ventricular outflow tract (RVOT). However, among perioperative arrhythmias, incidence of VT after surgery is extremely rare and most arrhythmias are atrial origin.Patient concerns:A 69-year-old man with permanent pacemaker underwent colon surgery.Diagnoses:Patient suffered from low blood pressure and dizziness, sweating at post anesthetic care unit (PACU) and heart rate (HR) increased suddenly to 200 beats/min with monomorphic VT after bolus ephedrine administration and continuous dopamine infusion.Interventions:Pacemaker interrogation followed by DC cardioversion was done.Outcomes:Patient''s vital signs became normal and symptoms are subsided.Lessons:RVOT VT can be caused by triggering activities, such as ephedrine, dopamine, and inadequate fluid management. These triggering activities are initiated by acceleration of HR from ventricles with infusion of catecholamine which lead monomorphic VT originating from RVOT.RVOT origin PVCs can be precipitated into monomorphic VT by administrating catecholamines such as ephedrine and dopamine even in patient with pacemaker. The mechanism of these VTs includes catecholamine induced acceleration of HR. Since RVOT PVCs can be recognize by 12 EKGs, we should be pay more attentions to the pre-operation EKG and be cautious using catecholamines.     

Idiopathic Reentrant Right Ventricular Outflow Tract Tachycardia With Presystolic Potential of Central Pathway

Idiopathic Reentrant RVOT VT With Presystolic Potential . A 12‐year‐old girl with recurrent palpitation due to idiopathic ventricular tachycardia (VT) with a left bundle branch block configuration and inferior axis was referred to our hospital. During the VT, a spiky presystolic potential (SP) was recorded at the septum of right ventricular outflow tract (RVOT) just below pulmonary valve. The SP was entrained with a decremental property by pacing from right ventricular apex. Concealed entrainment was observed by pacing where the SP was recorded. Delivery of radiofrequency current targeting the SP abolished the VT. The SP with the decremental property could represent the central pathway of this idiopathic RVOT reentrant VT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1174‐1177)     

Substrate in the interventricular septum for left ventricular and right ventricular outflow tract tachycardia: ablation from the right side of the septum

Simultaneous epicardial and endocardial mapping demonstrated that in a substantial number of ventricular tachycardias (VTs) endocardial, intramural, and epicardial structures are involved in the substrate of the reentrant circuits. Both right and left ventricular breakthrough has also been described during VT originating in the interventricular septum. We report the case of a patient with a nonischemic left ventricular aneurysm presenting with a left ventricular outflow tract (LVOT) tachycardia and a right ventricular outflow tract (RVOT) tachycardia. Mapping from the anterior interventricular vein and the endocardium of the RVOT revealed mid-diastolic potentials at the epicardium of the LVOT and the endocardium of RVOT, where the criteria of central isthmus sites could be demonstrated. Ablation targeting an isolated late potential during sinus rhythm in RVOT eliminated both the LVOT tachycardia and the RVOT tachycardia. In this patient with a nonischemic left ventricular aneurysm, the substrate of a LVOT tachycardia and RVOT tachycardia is described, and successful catheter ablation of the right and left ventricular tachycardia from the septal wall of RVOT is reported.     

Influence of right ventricular site of stimulation and infarct location on the inducibility of ventricular tachycardia in patients with coronary artery disease

No prior studies have evaluated the relationship between the site of right ventricular stimulation, the site of prior infarction, and the inducibility of ventricular tachycardia (VT). This study was performed to determine if the location of pathologic Q waves influences the inducibility of VT at various right ventricular sites in patients with coronary artery disease (CAD) and a history of myocardial infarction (MI). In 30 patients with a history of sustained, monomorphic VT, CAD, prior MI, and pathologic Q waves, programmed ventricular stimulation was performed at the right ventricular apex, septum, and outflow tract, in random order. There was electrocardiographic evidence of an MI that was inferior in 11 patients, anterior in 10 patients, and both inferior and anterior in 9 patients. Sustained, monomorphic VT was induced in 27 of 30 patients (90%). There were no significant differences among the three sites in the rate of inducibility of VT. The rate of inducible VT at each of the three right ventricular sites was not affected by the location of prior infarction. In conclusion, among patients with sustained, monomorphic VT, CAD, and a history of MI, the incidence of inducible sustained, monomorphic VT is not influenced by the location of prior infarction, regardless of whether programmed ventricular stimulation is performed at the right ventricular apex, septum, or outflow tract.     

Mechanistic subtypes of focal right ventricular tachycardia

Idiopathic sustained focal right ventricular tachycardia (VT) is most frequently due to outflow tract (OT) tachycardia. This arrhythmia is recognized by its characteristic ECG pattern and sensitivity to adenosine. However, there are other forms of idiopathic, focal sustained VT that originate from the right ventricle (RV), which are less well appreciated and easily overlooked. This review will identify the characteristic features and electrophysiologic properties of these forms of RV VT, including those originating from the tricuspid annulus, right ventricular papillary muscles, and moderator band as well as variants of classic RVOT tachycardia and those due to microreentry in the presence of preclinical disease. Recognition of these subtypes of focal RV tachycardia should facilitate targeted therapy.     

Adenosine-Sensitive Ventricular Tachycardia:

Adenosine-Sensitive VT. Idiopathic ventricular tachycardia (VT) is a term that refers to tachycardia that arises from ventricles devoid of apparent structural abnormalities. This form of VT is now recognized to be related to several distinct entities and includes a reentrant form typically located in the region of the left posterior fascicle, an automatic form that may originate from either ventricle, and a form that originates from the right ventricular outflow tract. This last type can account for up to 80% of cases of idiopathic VT and with few exceptions can be further subdivided into repetitive monomorphic VT and paroxysmal stress-induced VT, Evidence has accumulated suggesting that both forms of VT are related to cAMP-mediated triggered activity. The experimental underpinnings of this conclusion as well as the clinical characteristics of this form of idiopathic VT are elucidated in this review.     

Radiofrequency Catheter Ablation of Sustained Monomorphic Ventricular Tachycardia in Hypertrophic Cardiomyopathy

Monomorphic VT in HCM. Introduction : Incessant monomorphic ventricular tachycardia (VT) with a right bundle branch block morphology and a northwest axis is a rare arrhythmic complication in a patient with hypertrophic cardiomyopathy and apical left ventricular aneurysm.
Methods and Results : The origin of this VT was localized using the following criteria: the presence of entrainment without fusion, equal internals from the stimulus to the beginning of the QRS complex and from the electrogram to the QRS complex during VT, and the first postpacing interval identical to the tachycardia cycle length. Radiofrequency energy applied to the septoapical part of the apical left ventricular aneurysm terminated the tachycardia within 2 seconds.
Conclusion : Using criteria to guide radiofrequency (RF) ablation of VT in patients with coronary artery disease, an incessant monomorphic VT in a patient with hypertrophic cardiomyopathy was successfully ablated.     

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.     

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.     

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.     

Successful ablition of aortic cusp tachycardia from right ventricle outflow tract using a superior approach

We report a case of successful radiofrequency catheter ablation of idiopathic aortic cusp tachycardia arising close to right coronary artery ostium performed safely from the right ventricular outflow tract (RVOT) by unconventional superior approach. As both activation mapping and pace mapping of the tachycardia were suboptimal from transfemoral RV endocardial approach, retrograde aortic mapping was performed. This revealed that the site of ventricular tachycardia (VT) origin to be on the right coronary sinus. Due to close proximity of VT site of origin and the right coronary ostium, an alternate approach to ablation was considered. We approached this area easily and successfully ablated the VT with an ablation catheter introduced from a right-sided superior approach (jugular vein). The patient has remained free from recurrences over an 18 month follow-up period.     

特发性右室流出道室性早搏触发多形性室性心动过速或心室颤动四例的临床特点

目的报道4例特发性右室流出道(RVOT)室性早搏(PVC)触发多形性室性心动过速/心室颤动(PVT/VF)的临床特点。方法 76例起源于RVOT的VT患者,其中4例为PVC触发PVT/VF,总结4例的临床资料并与另72例有关资料相比较。结果所有4例触发PVT/VF时的PVC与孤立PVC的形态一致,但2种PVC的联律间期发生了明显改变,其改变幅度均≥70 ms,其中2例缩短,2例延长。1例孤立PVC时的联律间期亦不恒定。72例PVC触发的单形VT患者每天PVC次数为15 427±1 109,QT间期为404±15 ms,孤立PVC联律间期为419±22ms。4例PVC触发PVT/VF患者中3例1天的PVC次数与72例PVC触发的单形VT患者平均PVC次数相当。4例患者的QT间期及孤立PVC联律间期与另72例患者相当。而4例PVT/VF的周长均小于280 ms,明显短于72例VT的平均周长(324±59 ms)。72例单形VT患者发生晕厥比率4.1%;4例PVT/VF患者中发生晕厥者2例。采用激动标测和起搏标测证实4例患者PVC均起源于RVOT间隔侧,经射频导管消融PVC取得成功。结论起源于RVOT的PVC触发PVT/VF具有PVC联律间期不恒定及PVT/VF的周长短的临床特征,射频导管消融治疗有效。     

Exercise-induced ventricular tachycardia associated with J point ST-segment elevation in inferior leads in a patient without apparent heart disease: a variant form of Brugada syndrome?

Exercise-induced monomorphic ventricular tachycardia originating in the right ventricular outflow tract without evidence of structural heart disease can be idiopathic or can be the harbinger of structural abnormalities such as arrhythmogenic right ventricular dysplasia. Recently, the so-called variant Brugada syndrome has been reported in very few cases in the literature and is much less electrophysiologically defined in terms of its clinical significance. We present the case of a 21-year-old man with exercise-induced monomorphic ventricular tachycardia (left bundle-branch block/right axis deviation), without detectable structural heart disease, with evidence of J point and ST-segment elevation in electrocardiogram leads II, III, and aVF after intravenous administration of propafenone. This is followed by a brief discussion on the new concept of “variant Brugada syndrome,” drug-induced electrocardiographic changes, normal-variant repolarization abnormality, and idiopathic right ventricular outflow tract tachycardia.     

Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia

Coupling Intervals and Polymorphic QRS Morphologies . Introduction: Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF. Methods and Results: The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT‐group) and 21 with monomorphic VT arising from the RVOT (MVT‐group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT‐group than in the MVT‐group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT‐group than that for the VT in the MVT‐group (P < 0.01). In the PVT‐group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321–3.659; P = 0.002). Conclusion: The smaller PIs of the first VT beat may result in a polymorphic QRS morphology. (Cardiovasc Electrophysiol, Vol. 23, pp. 521‐526, May 2012)     

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."