An Unusual Case Of Right Ventricular Outflow Tract Tachycardia

In this report, we describe an unusual case of right ventricular outflow tract (RVOT) tachycardia with episodes of repetitive monomorphic ventricular tachycardia (VT), paroxysmal sustained VT and incessant monomorphic VT of the same morphology. Diltiazem, adenosine, or metoprolol failed to interrupt these arrhythmias. However, administration of intravenous propafenone completely eliminated all ventricular ectopic activity. Electrophysiologic study performed off propafenone showed that the ventricular ectopic activity originated from a single locus at the anterior wall of the RVOT. Two radiofrequency applications at this site resulted in complete elimination of ventricular ectopic activity.     

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.     

The Relation of QT Dispersion to Spontaneous Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction

Background: QT dispersion is associated with ventricular arrhythmias and sudden death among patients with a previous myocardial infarction (Ml). The relationship between QT dispersion and ventricular arrhythmias during the acute phase of Ml is uncertain. Methods: Patients enrolled in the Multicenter Study of Silent Myocardial Ischemia who had first Q wave myocardial infarctions (n = 363) were screened for the presence of ventricular arrhythmias during the initial hospitalization. Twelve patients had ventricular fibrillation, and 18 patients had an episode of monomorphic ventricular tachycardia. Each patient who had ventricular arrhythmias was matched with four controls on the basis of age, peak creatine kinase, thrombolysis, and the presence of congestive heart failure. The final study population consisted of 150 patients: 12 patients with ventricular fibrillation (VF+) who were compared to 48 controls (VF—), and 18 patients with ventricular tachycardia (VT+) who were compared to 72 controls (VT–). The RR, QRS, and QT intervals were measured manually using standard 12-lead ECGs (25 mm/s) obtained after hospital admission. The maximal QT dispersion (maximum — minimum value) was calculated. Multivariate logistic regression analysis was performed to determine if QT dispersion was independently associated with ventricular arrhythmias during the acute phase of Ml. Results: QT dispersion was significantly greater in VF+ patients compared to VF— patients (89 ± 18 ms vs 66 ± 22 ms, P > 0.01). QT dispersion was similar in VT+ and VT— patients (68 ± 25 ms vs 68 ± 26 ms, P = NS). QT dispersion was the only variable that was independently associated with ventricular fibrillation (OR 1.7 for each 10-ms increment in QT dispersion; 95% Cl 1.2–2.6; P = 0.008). QT dispersion was not associated with monomorphic ventricular tachycardia (OR 1.0; 95% Cl 0.8–1.2; P = NS). Conclusion: QT dispersion is independently associated with ventricular fibrillation, but not monomorphic ventricular tachycardia, during the acute phase of Ml.     

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.     

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.     

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.     

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.     

Radiofrequency Ablation Guided by Mechanical Termination of Idiopathic Ventricular Arrhythmias Originating in the Right Ventricular Outflow Tract

Mapping of Idiopathic Ventricular Arrhythmias. Background: Termination of ventricular tachycardia (VT) by mechanical pressure has been described for fascicular and postinfarction VT. Mechanical interruption of idiopathic ventricular arrhythmias (VT/premature ventricular complexes [PVCs]) arising in the right ventricular outflow tract (RVOT) has not been described in systematic fashion. Methods: Eighteen consecutive patients (13 females, age 49 ± 13 years, ejection fraction 0.55 ± 0.12) underwent mapping and ablation of RVOT VT or PVCs. In 7 patients, 9 distinct VTs (mean cycle length 440 ± 127 ms), and in 11 patients, 11 distinct PVCs originating in the RVOT were targeted. Mechanical termination was considered present if a reproducibly inducible VT was no longer inducible or if frequent PVCs suddenly ceased with the mapping catheter at a particular location. Endocardial activation time, electrogram characteristics, and pace‐mapping morphology were assessed at this location. Radiofrequency energy was delivered if mechanical termination was observed. Results: All targeted arrhythmias were successfully ablated. In 7 of 18 patients (39%), catheter manipulation terminated the arrhythmia with the mapping catheter located at a particular site. Local endocardial activation time was earlier at sites of mechanical termination (?31 ± 7 ms) compared with effective sites without termination (?25 ± 3 ms, P = 0.04). The 10‐ms isochronal area was smaller in patients with mechanical interruption (0.35 ± 0.2 cm²) than in patients without mechanical termination (1.33 ± 0.9 cm², P = 0.01). At all sites susceptible to mechanical trauma, the pace map displayed a match with the targeted VT/PVC. All sites where mechanical termination of VT or PVCs occurred were effective ablation sites. Conclusions: Mechanical suppression at the site of origin of idiopathic RVOT arrhythmias frequently occurs during the mapping procedure and is a reliable indicator of effective ablation sites. Mechanical termination of RVOT arrhythmias may be indicative of a more localized arrhythmogenic substrate. (J Cardiovasc Electrophysiol, Vol. 21, pp. 42–46, January 2010)     

Experimental model simulating right ventricular outflow tract tachycardia: a novel technique to initiate RVOT-VT

BACKGROUND: The mechanism(s) whereby a discrete area of myocardium in the RVOT becomes arrhythmogenic remains unknown. METHODS: In 13 dogs, a circular catheter was placed in the proximal pulmonary artery (PA) to contact the endovascular circumference of the PA. A 50-msec train of high-frequency stimulation (HFS, 200 Hz), coupled to atrial pacing, was applied at each bipolar pair of the circular catheter. The coupling interval was adjusted so that the 50-msec train occurred during the ventricular refractory period, that is, the QRS complex, in order to prevent stimulation of the myocardial sleeve within the proximal PA. RESULTS: In all dogs, HFS induced ventricular premature depolarizations and VTs with a left bundle branch block (LBBB) morphology and inferior axis (average 6.8 +/- 1.6 V). Earliest activation was consistently recorded from the proximal PA. Esmolol, a short-acting beta-blocker (1 mg/kg), was administered intravenously in 11 dogs. The inducible ventricular ectopy was abolished in 10 dogs (>12 V, P < 0.05) and the response to HFS was blunted in one dog (10-11 V). After 30 minutes, the response to HFS returned to pre-esmolol levels. CONCLUSIONS: Stimulation of the sympathetic input to the proximal PA induces ventricular ectopy and VTs exhibiting a left bundle branch block morphology and inferior axis, closely simulating clinical RVOT-VT. Beta-blockade either abolishes or blunts this response, corroborating the sympathetic etiology in this model and in some clinical cases of RVOT tachycardias.     

射频导管消融治疗的特发性室性心律失常心电图特征分析

目的：探讨不同起源的特发性室性期前收缩（PVCs）和（或）室性心动过速（VT）的心电图特征,提出鉴别流程。方法根据射频导管消融PVCs/VT有效靶点或心室最早激动点的X线胸片进行定位,分析不同起源PVCs/VT的12导联心电图QRS波群。结果828例接受导管消融,580例起源于右心室,248例起源于左心室,左、右心室起源者胸导联移行指数＜0的分别占97.58%及7.24%;左和右心室流出道起源者下壁导联多数呈R型,V1上,多数右心室流出道起源者呈rS型,右室间隔起源呈QS型,主动脉瓣上起源者常呈rS或RS型;下壁导联上,左前分支起源者常呈qR型,左后分支起源者常呈rS型。结论结合体表心电图胸导联移行指数、下壁导联和V1上的QRS波群特征可初步判断特发性PVCs/VT的起源部位。     

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。     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

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."     

Autonomic Modulation for the Treatment of Ventricular Arrhythmias: Therapeutic Use of Percutaneous Stellate Ganglion Blocks

Ventricular tachycardia (VT), ventricular fibrillation (VF), and electrical storm are commonly encountered emergency conditions in cardiac and surgical intensive care units. In most cases, recurrent ventricular arrhythmias or electrical storm are associated with a heightened sympathetic tone. These arrhythmias can be difficult to treat and may be refractory to beta‐blockade, antiarrhythmic therapy, sedation, and mechanical hemodynamic support. While monomorphic ventricular tachycardia and PVC‐triggered polymorphic ventricular tachycardia may sometimes be amenable to successful ablation, some patients may be too critically ill to make such an approach feasible. We present 2 cases of minimally invasive stellate ganglion blocks for the treatment of electrical storm in patients with advanced heart failure on mechanical life support. These cases are part of a collaborative initiative at our institution to use percutaneous stellate ganglion block as an adjunctive intervention to achieve control of life‐threatening ventricular arrhythmias.     

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).     

Relationship of Reverse Anatomical Remodeling and Ventricular Arrhythmias After Cardiac Resynchronization

Introduction: Cardiac resynchronization (CRT) affects reverse anatomical remodeling in patients with heart failure. CRT has also been associated with fewer ventricular arrhythmias and reduced sudden death in some clinical trials, but the predictors and mechanism of the antiarrhythmic actions of CRT have not been well defined. The purpose of this study is to investigate the relationship of reverse anatomical remodeling to ventricular arrhythmias in CRT patients.
Methods and Results: A retrospective analysis was performed of the InSync III Marquis study, a prospective, randomized, multicenter CRT trial. Echocardiographic data from 198 patients were obtained at baseline and after 6 months of CRT, and anatomical responders were defined as a reduction in left ventricular end systolic volume (LVESV) of ≥15%. Anatomical responders (n = 71, 36%) demonstrated 29% fewer single premature ventricular contractions beats (PVCs) (P = 0.0001), 48% fewer PVC runs (p = 0.0096), and fewer treated episodes of ventricular tachycardia or fibrillation (VT/VF) (P = 0.050) than nonresponders. Multiple regression analysis demonstrated that responder status significantly predicted single PVCs and PVC runs. Gender was the most important predictor of treated VT/VF with females having no episodes over 6 months of follow-up.
Conclusions: Anatomic responders to CRT demonstrate significantly fewer single PVCs and runs of PVCs. The implication of these observations is that anatomic remodeling is linked to electrical remodeling.     

Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors

Idiopathic Ventricular Arrhythmias and Cardiomyopathy. Introduction: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia‐induced cardiomyopathy (TICMP). The aim of this study was to determine the incidence, clinical and electrophysiologic characteristics, and the predictors of TICMP in patients with idiopathic ventricular arrhythmias. Methods: Study population consisted of 249 consecutive patients (148 F/101 M, 45 ± 20 y/o) with frequent PVCs and/or VT. All patients underwent transthoracic echocardiography and 24‐hour Holter monitoring. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF ≥15% following effective treatment of index ventricular arrhythmia. Results: Seventeen (6.8%) patients had TICMP. Patients with TICMP compared to patients with preserved LVEF were more likely to be male (65% vs 39%, P = 0.043) and asymptomatic (29% vs 9%, P = 0.018), and were more likely to have higher PVC burden (29.4 ± 9.2 vs 8.1 ± 7.4, P < 0.001), persistence of PVCs throughout the day (65% vs 22%, P = 0.001), and repetitive monomorphic VT (24% vs 0.9%, P < 0.001). PVC burden of 16% by ROC curve analysis best separated the patients with TICMP compared to patients with preserved LVEF (sensitivity 100%, specificity 87%, area under curve 0.96). Conclusions: TICMP was relatively common (～1 in every 15 patients) in our study population. The predictors of TICMP were male gender, absence of symptoms, PVC burden of ≥16%, persistence of PVCs throughout the day, and the presence of repetitive monomorphic VT . (J Cardiovasc Electrophysiol, Vol. 22, pp. 663‐668, June 2011)     

The Value of Electrophysiologic Testing in Patients Resuscitated From Documented Ventricular Fibrillation

EP Study and Ventricular Fibrillation. Introduction: Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing.
Methods and Results: We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 ± 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 ± 16 years) with clinically documented VT concurrently studied using the same stimulation protocol.
Conclusion: We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.     

特发性室性心动过速及室性期前收缩的射频消融治疗

目的探讨射频导管消融(radiofrequency catheter ablation,RFCA)治疗特发性室性心动过速(idiopathic ventricular tachycardia,IVT)和室性期前收缩(premature ventricualr contraction,PVC)可行性、必要性和疗效。方法回顾性分析16例IVT、PVC患者采用激动顺序标测和起搏标测法确定室性心动过速(ventricular tachycardia,VT)、PVC的起源部位并行RFCA治疗的资料。结果 3例IVT中2例起源于左室间隔部左后分支的蒲肯野系统,1例起源于右心室流出道(right ventricular outflow tract,RVOT)游离壁,同时合并另一种游离壁起源的PVC,3例消融均成功,1例复发。13例PVC中7例起源RVOT间隔部,3例起源于RVOT游离壁,1例同时存在两种形态PVC(分别起源于ROVT间隔部和游离壁),2例起源于左心室流出道,13例消融成功,1例复发。结论 RFCA治疗IVT及特定部位的PVC是安全、有效且成功率高的一种方法。     

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。