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.     

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.     

Postmyocardial Infarction Patients Susceptible to Ventricular Tachycardia Show Increased T Wave Dispersion Independent of Delayed Ventricular Conduction

Arrhythmia Markers After Myocardial Infarction. Introduction: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post-MI) patients.
Methods and Results: We studied 32 post-MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post-MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve-lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (  135 ± 34  msec vs  114 ± 22  msec in the MI group;  P = 0.012  ). Mean TPE and maximum TPE in VT versus MI groups were  78 ± 9  msec versus  70 ± 6  msec (  P < 0.001  ) and  117 ± 23  msec versus  104 ± 19  msec (  P = 0.020  ), respectively. Maximum TPE did not correlate with fQRS in the VT group (  r = 0.063; P = NS  ) but did correlate in the MI group (  r = 0.396; P = 0.037  ). For identification of post-MI patients prone to VT, selection of cutoff values for fQRS > 140 msec and mean TPE > 81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity.
Conclusion: Post-MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.     

Diagnostic Clues From the Surfaee ECG to Identify Idiopathic (Fascicular) Ventricular Tachycardia: Correlation with Electrophysiologic Findings

ECG in Idiopathic Fascicular VT. Introduction : An RS interval > 100 msec in precordial leads has been recently described for the diagnosis of ventricular tachycardia (VT). The aim of this study was to assess the value of this criterion when applied to patients with right bundle branch block pattern, left-axis deviation (fascicular) VT sensitive to verapamil.
Methods and Results : Eleven patients (mean age 31 ± 11 years; range 16 to 51) had a mean heart rate of 164 ± 37 beats/min (range 107 to 230) during VT, The QRS complex axis was -92°± -15° (range -80 to -115). The mean QRS duration was 121 ± 9 msec (range 105 to 140). The mean RS interval was 67 ± 9 msec (range 60 to 80). Fusion beats were present in 2 patients (18%), and AV dissociation confirmed by electrophysiologic study was found on ECG in 8 (73%) of 11. During tachycardia, the QRS-H'interval was 19 ± 10 msec (range 10 to 30) in 6 of 11 patients. In seven patients, a fast, unique (or double) presystolic potential lasting 32 msec (range 12 to 40) occurring before the onset of the QRS complex was found at the site of origin of VT, localized in the inferior apical left ventricular septum. In all cases, VT was successfully treated by catheter ablation.
Conclusion : A wide QRS complex tachycardia with right bundle branch block and left-axis deviation sensitive to verapamil observed in a young patient without structural heart disease should not be confused with supraventricular tachycardia with aberrancy but rather suggests the presence of fascicular VT. As opposed to VT associated with structural heart disease, the RS interval is < 80 msec in all precordial leads in all cases. Independent of this parameter, AV dissociation detectable on surface ECG has a sensitivity of 73%, which increases to 82% in the presence of fusion beats.     

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.     

Management of Ventricular Fibrillation with Transvenous Defibrillators Without Baseline Electrophysiologic Testing or Antiarrhythmic Drugs

Tranvenous Defibrillators Without EP Testing. Introduction : Baseline electrophysiologic study (EPS) is routinely performed in patients resuscitated from ventricular fibrillation (VF) to risk stratify and select patients for chronic antiarrhythmic drug therapy. The role of EP testing prior to insertion of a multiprogrammable implantable cardioverter defibrillator (ICD), however, is unclear.
Methods and Results: This study was a retrospective review of outcome in 66 survivors of an initial episode of out-of-hospital VF not associated with a Q wave myocardial infarction or reversible causes, treated with transvenous ICDs as first-line therapy. Patients were excluded from the study if they had a previous history of monomorphic ventricular tachycardia (VT), a clinical history suggestive of supraventricular tachycardia, or had undergone preoperative EP testing. Fifty-two of the patients (79%) were male with an average age of 58 ± 11 years. Coronary artery disease was present in 43 patients (66%), cardiomyopathy in 15 patients (23%), and valvular heart disease in 1 patient (1.5%). Seven patients (11%) had no detectable structural heart disease. The mean left ventricular ejection fraction was 0.40 ± 0.16. With an average follow-up of 25 ± 12 months, survival free of death from any cause was 100%. Twenty-three patients (35%) experienced 48 episodes of recurrent rapid VT or VF (average cycle length: 236 ± 47 msec) treated by their device. The mean time to first therapy was 223 ± 200 days. Only one of these patients also received antitachycardia pacing for two episodes of VT. One patient (1. 5%) temporarily received amiodarone after removal of an infected device that was subsequently replaced. No other patient received antiarrhythmic drug therapy.
Conclusion : After a cardiac arrest due to primary VF, select patients treated with multiprogrammable ICDs can be managed successfully without baseline EPS or antiarrhythmic drug therapy.     

Shock-Induced Dispersion of Ventricular Repolarization:

Shock-induced Dispersion and VF Induction. Introduction: Shock-induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction: however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear.
Methods and Results: In eight Langendorff-perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV. SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 ± 15 msec for sbocks inducing VF. SIDR was 41 ± 17 msec for shocks delivered above the ULV, and 33 ± 14 and 27 ± 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P < 0.01 vs VF-inducing shocks). Although SIDR was larger for shocks delivered below the LLV(93 ± 24 msec, P < 0.01 vs VF-inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3%± 3.9% vs 16.3%± 4.9%, P < 0.01).
Conclusion: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.     

Analysis of the pattern of initiation of sustained ventricular arrhythmias in patients with implantable defibrillators

INTRODUCTION: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease. METHODS AND RESULTS: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating beat of all ventricular arrhythmias was 523 +/- 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty-two (85%) of the arrhythmia episodes were initiated by a late-coupled premature beat, 33 (13%) were initiated by an early-coupled premature beat, and 5 episodes (2%) were initiated with a short-long-short sequence. The pattern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias. CONCLUSION: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late-coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia.     

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)     

Spontaneous Variability of Ventricular Ectopic Activity in Patients with Sustained Ventricular Tachycardia and in Survivors of Cardiac Arrest

Background: Spontaneous variability of ventricular arrhythmia has been described in patients with chronic stable ventricular arrhythmias and in patients with chronic heart failure. However, no data are available on spontaneous variability in patients with sustained ventricular tachyarrhythmias. Thus, the present study was designed to prospectively determine the extent of spontaneous variability of ventricular arrhythmia in patients with sustained ventricular tachyarrhythmias and in survivors of cardiac arrest. Methods: Ventricular arrhythmia variability was determined in 470 patients (413 men, 57 women), age (mean ± SD) 64.6 ± 9.5 years with documented ventricular tachycardia (VT), cardiac arrest, or syncope who were prospectively enrolled in a randomized trial of the comparison of electrophysiological testing with Holter monitoring to predict antiarrhythmic drug efficacy. Coronary artery disease was present in 398 (85%) patients, and the mean left ventricular ejection fraction was 0.32 ± 0.13. They underwent two 24-hour ambulatory recordings separated by 1 day. Spontaneous variability was determined for total premature ventricular complexes (PVCs), pairs, and VT events. Results: Arithmetic mean of hourly total PVCs on day 1 was 315 ± 425. The 95% confidence limit of spontaneous reduction in total PVC count was 71%. Corresponding values for pairs, VT events of 3–15 beats, < 15 beats, or < 15 seconds were 72%, 80%, 94%, and 95%, respectively. The percentage increases in total PVCs, pairs, and VT events 3–15 beats, < 15 beats, and < 15 seconds were 243%, 259%, 397%, 1553%, and 1756%, respectively. The percentage reduction required to show a true drug effect was 63% for patients with an ejection fraction > 0.32 and 76% for those with an ejection fraction ltm 0.32 (P = 0.024). Patients who presented with unmonitored syncope showed less spontaneous variability than either patients with documented, sustained VT or cardiac arrest. Conclusions: Marked spontaneous variability of ventricular arrhythmias is observed in patients with sustained ventricular tachyarrhythmias. Variability is affected by the degree of left ventricular dysfunction. The lowest variability was observed in patients presenting with unmonitored syncope. Thus, large changes in arrhythmia frequency must be observed in this population, as in others, to be ascribed to drug effect.     

The “Short‐Coupled” Variant of Right Ventricular Outflow Ventricular Tachycardia: A Not‐So‐Benign Form of Benign Ventricular Tachycardia?

Idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT-VT) and idiopathic RVOT-extrasystoles are generally considered benign arrhythmias. We described three cases who originally presented with typical "benign looking" RVOT-extrasystoles or RVOT-VT but developed malignant polymorphic VT during follow-up. The unusual aspect of their RVOT-extrasystoles was their coupling interval, which appears to be intermediate between the ultra-short coupling interval of idiopathic VF and the long coupling interval seen in the truly benign RVOT-VT.     

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)     

Ventricular flutter induced during electrophysiologic studies in patients with old myocardial infarction: clinical and electrophysiologic predictors,and prognostic significance

INTRODUCTION: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias. METHODS AND RESULTS: We conducted a cohort study of all patients with myocardial infarction (MI) undergoing EP studies at our institution. Of 344 consecutive patients, 181 had previously documented spontaneous sustained ventricular arrhythmias, 61 had suspected ventricular arrhythmias, and 102 had neither. Ventricular flutter was induced in 65 (19%) of the patients. Left ventricular ejection fraction was highest among patients with inducible VF (35 +/- 13), lowest for patients with inducible sustained monomorphic ventricular tachycardia (SMVT; 27 +/- 9), and intermediate for patients with inducible ventricular flutter (30 +/- 10). Similarly, the coupling intervals needed to induce the arrhythmia were shortest for VF (200 +/- 28 msec), intermediate for ventricular flutter (209 +/- 27 msec), and longest for SMVT (230 +/- 35 msec). During 5 +/- 8 years of follow-up, the risk for ventricular tachycardia/VF was high for patients with SMVT and ventricular flutter and low for patients with inducible VF and noninducible patients (46%, 34%, 17%, and 14%, P < 0.005).CONCLUSION: Patients with inducible ventricular flutter appear to be "intermediate" between patients with inducible VF and patients with SMVT in terms of clinical and electrophysiologic correlates. However, the prognostic value of inducible ventricular flutter is comparable to that of SMVT.     

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.     

Idiopathic Ventricular Tachycardia and Fibrillation

Idiopathic Ventricular Tachycardia and Fibrillation. Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long-term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healthy patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long-term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellentJfy Cardiovasc Electrophysiol, Vol. 4, pp. 356–368, June 1993 ).     

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。     

Endocardial and Epicardial Ablation Guided by Nonsurgical Transthoracic Epicardial Mapping to Treat Recurrent Ventricular Tachycardia

Nonsurgical Epicardial Ablation. Introduction : An epicardial site of origin of ventricular tachycardia (VT) may explain unsuccessful endocardial radiofrequency (RF) catheter ablation. A new technique to map the epicardial surface of the heart through pericardial puncture was presented recently and opened the possibility of using epicardial mapping to guide endocardial ablation or epicardial catheter ablation. We report the efficacy and safety of these two approaches to treat 10 consecutive patients with VT and Chagas' disease.
Methods and Results : Epicardial mapping was carried out with a regular steerable catheter introduced into the pericardial space. An epicardial circuit was found in 14 of 18 mapable VTs induced in 10 patients. Epicardial mapping was used to guide endocardial ablation in 4 patients and epicardial ablation in 6. The epicardial earliest activation site occurred 107 ± 60 msec earlier than the onset of the QRS complex. At the epicardial site used to guide endocardial ablation, earliest activation occurred 75 ± 55 msec before the QRS complex. Epicardial mid-diastolic potentials and/or continuous electrical activity were seen in 7 patients. After 4.8 ± 2.9 seconds of epicardial RF applications, VT was rendered noninducible. Hemopericardium requiring drainage occurred in 1 patient; 3 others developed pericardial friction without hemopericardium. Patients remain asymptomatic 5 to 9 months after the procedure. Interruption during endocardial pulses occurred after 20.2 ± 14 seconds (P = 0.004), hut VT was always reinducible and the patients experienced a poor outcome.
Conclusion : Epicardial mapping does not enhance the effectiveness of endocardial pulses of RF. Epicardial applications of RF energy can safely and effectively treat patients with VT and Chagas' disease.     

Clustering of ventricular tachyarrhythmias in heart failure patients implanted with a biventricular cardioverter defibrillator

Background: Temporal patterns of ventricular tachyarrhythmia (VT/VF) have been studied only in patients who have received implantable cardioverter defibrillators (ICD) for secondary prevention of sudden death, and mainly in ischemic patients. The aim of this study was to evaluate VT/VF recurrence patterns in heart failure (HF) patients with biventricular ICD and to stratify results according to HF etiology and ICD indication.
Methods and Results: We studied 421 patients (91% male, 66 ± 9 years). HF etiology was ischemic in 292 patients and nonischemic in 129. ICD indication was for primary prevention in 227 patients and secondary prevention in 194. Baseline left ventricular ejection fraction (LVEF) was 26 ± 7%, QRS duration 168 ± 32 msec, and NYHA class 2.9 ± 0.6. In a follow-up of 19 ± 11 months, 1,838 VT/VF in 110 patients were appropriately detected. In 59 patients who had ≥4 episodes, we tried to determine whether VT/VF occurred randomly or rather tended to cluster by fitting the frequency distribution of tachycardia interdetection intervals with exponential functions: VT/VF clusters were observed in 46 patients (78% of the subgroup of patients with ≥4 episodes and 11% of the overall population). On multivariate logistic analysis, VT/VF clusters were significantly (P < 0.01) associated with ICD indication for secondary prevention (odds ratio [OR]= 3.12; confidence interval [CI]= 1.56–6.92), nonischemic HF etiology (OR = 4.34; CI = 2.02–9.32), monomorphic VT (OR = 4.96; CI = 2.28–10.8), and LVEF < 25% (OR = 3.34; CI = 1.54–7.23). Cardiovascular hospitalizations and deaths occurred more frequently in cluster (21/46 [46%]) than in noncluster patients (63/375 (17%), P < 0.0001).
Conclusions: In HF patients with biventricular ICDs, VT/VF clusters may be regarded as the epiphenomenon of HF deterioration or as a marker of suboptimal response to cardiac resynchronization therapy.     

Ventricular tachycardia with participation of the left bundle-Purkinje system in patients with structural heart disease: identification of slow conduction during sinus rhythm

Introduction: Idiopathic left ventricular tachycardia (VT) originating from the left posterior fascicle can be eliminated by ablation at sites with abnormal diastolic potentials (DPs) during sinus rhythm. We investigated whether such DPs can also be recorded in patients with structural heart disease and VT involving the left bundle-Purkinje system.
Methods and Results: Eight patients (mean age 67 ± 11 years) with nonischemic cardiomyopathy (n = 5) or prior myocardial infarction (n = 3) presented with VT involving the left bundle-Purkinje system (cycle length 376 ± 45 ms). Three types of VT were observed: macroreentrant VT with participation of both left bundle fascicles in three patients, fascicular VT involving the left posterior fascicle in two patients, and scar-related VT with Purkinje fibers as part of the reentrant circuit in three patients. In all patients, abnormal isolated DPs of low amplitude with a QRS—earliest DP interval of 374 ± 86 ms were found during sinus rhythm in the mid- or inferior left ventricular septum in areas with Purkinje potentials. The abnormal DPs during sinus rhythm coincided or were in proximity to DPs during the VT in six patients. VT ablation targeting the sites with the earliest abnormal DPs during sinus eliminated the VT in 7 of 8 patients with freedom from VT recurrence in six patients during the follow-up of 11 ± 5 months.
Conclusions: Isolated DPs during sinus rhythm were found in proximity to the posterior Purkinje network in patients with VT involving the left bundle-Purkinje system associated with heart disease and can be used to guide successful catheter ablation.     

Postextrasystolic Repolarization Abnormalities in ST‐U Segment in Patients with Ventricular Arrhythmias

Background: Changes in U‐wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST‐U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST‐U segment configurations were taken from the 24‐hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT‐nsVT) tnon‐VT/VF group). Results: We found T‐wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U‐wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T‐U‐wave changes, that the occurrence of U‐wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U‐wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U‐wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST‐U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U‐wave changes more frequently appeared in patients with malignant arrhythmias. Follow‐up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21