The role of Holter monitoring in patients with recurrent sustained ventricular tachycardia: an electrophysiologic correlation

The significance of spontaneous ventricular premature depolarization (VPD) frequency and severity in patients with sustained ventricular tachycardia undergoing serial electrophysiologic studies (EPS) are unknown. Nineteen patients with sustained ventricular tachycardia were studied with 24-hour Holter recordings prior to control EPS and prior to each drug trial. Successful drug or surgical treatment (with the exception of amiodarone) was based upon noninducibility of ventricular tachycardia in the laboratory. Among the eight noninducible and nonamiodarone medically treated patients, two (25%) had significant VPD reduction and/or Lown class improvement. The remaining six (75%) had no change or worsening of Holter findings, despite noninducibility of sustained VT. Among the six amiodarone-treated patients, five of whom were persistently inducible prior to discharge, four (66%) had improved and two (33%) had worsened Holter findings compared to control. None of the five (100%) surgically managed patients were inducible postoperatively, and three of the five (60%) had no change or worsening of Holter findings. We conclude that (1) EPS are superior to Holter findings in assessing successful management; and (2) Holter findings may be concordant or discordant during EPS serial drug trials or following surgery and therefore cannot predict the success or failure of the intervention.     

Inducible monomorphic sustained ventricular tachycardia in the conscious pig

Sustained monomorphic ventricular tachycardia (VT) is of clinical importance but has not been readily modeled in conscious animals. Eleven pigs had myocardial infarction induced by pulling snares previously placed around the left anterior descending (LAD) coronary artery. Six days after occlusion, bipolar pacing catheters were inserted in the right ventricular apex for induction of VT. Testing was repeated in conscious pigs on 6 out of 8 to 19 days after infarction. Monomorphic VT was induced in each animal during each session, using three to four extrastimuli. VT was terminated by burst pacing in 74% of trials; average VT rate was 362 +/- 26 beats/min. VT was prevented in four of eight animals by procainamide and in five of eight animals by magnesium, but was not prevented by lidocaine or metoprolol. The model may be useful in the study of potentially malignant ventricular tachyarrhythmias, important prodromes for sudden death.     

Value of electrophysiologic testing in patients with nonsustained ventricular tachycardia

This study was undertaken to determine the value of electrophysiologic testing in 61 patients with nonsustained ventricular tachycardia (VT) (3 or more beats) on ambulatory monitoring and no history of sustained ventricular arrhythmia. The study group consisted of 38 patients with coronary artery disease (CAD), 9 with idiopathic dilated cardiomyopathy and 14 with a normal heart. Nonsustained VT (at least 3 but not more than 15 beats) was induced in 46%, sustained VT (more than 15 beats) in 15% and no VT in 39%. Sustained VT was induced more frequently in the presence of left ventricular dysfunction (p = 0.005) but was not related to the presence of CAD. Over a mean follow-up of 26 months, 10 patients died from cardiac causes (4 suddenly), including 1 patient with inducible sustained VT, 2 with nonsustained VT and 7 with no inducible VT. Inducibility was not related to survival, either as a single variable or when combined with CAD, left ventricular dysfunction or recent myocardial infarction. Left ventricular function alone was a good predictor of outcome. Of 46 patients with an ejection fraction of 35% more or in New York Heart Association functional class I or II, 3 (7%) died from cardiac causes, compared with 7 of 13 patients (54%) with an ejection fraction of less than 35% or in functional class III or IV (p = 0.0001). Thus, in patients with nonsustained VT, the incidence of sustained VT during electrophysiologic testing is low and is related to the degree of left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of sustained monomorphic ventricular tachycardia in systemic sclerosis

Three patients with advanced systemic sclerosis and recurrent or incessant monomorphic ventricular tachycardia underwent cardiac electrophysiologic studies. Biventricular transcatheter mapping showed findings most compatible with a reentrant mechanism, which was effectively treated with transcatheter ablation.     

Brugada syndrome presenting with sustained monomorphic ventricular tachycardia

Typically Brugada syndrome presents with either ventricular fibrillation or polymorphic ventricular tachycardia that may result in sudden death or syncope in patients without any structural heart disease. We report the case of a patient with Brugada syndrome who presented atypically with recurrent presyncope following physical exertion due to sustained monomorphic ventricular tachycardia, which appeared to be sensitive to both adenosine and catecholamine. He refused ICD implantation but remained asymptomatic on treatment with a beta-blocker.     

Electrophysiology in evaluating the treatment of sustained monomorphic ventricular tachycardia: criteria for efficacy

The authors studied the influence on recurrence and mortality of induced ventricular arrhythmias during electrophysiological studies performed to assess the efficacy of treatment of sustained monomorphic ventricular tachycardia. One hundred and twenty-six consecutive patients investigated from 1981 to 1988 were included. The underlying pathology was chronic myocardial infarction (N = 56), dilated cardiomyopathy (N = 24), right ventricular dysplasia (N = 31) and there were 15 idiopathic cases. All these tachycardias could be induced during the control study. A second test was performed after instituting treatment. This was maintained whatever the result of the electrophysiological study except in patients in whom the tachycardia rate was over 130/mn and/or poorly tolerated. Recurrences were defined as the observation of tachycardia with the same morphology and/or the occurrence of sudden death. Follow-up averaged 29 +/- 21 months. The absence of recurrence and survival were assessed by the Kaplan-Meier method and Logrank's test. It was not possible to induce any arrhythmia after treatment in 52 patients (41%). The prevalence of absence of recurrence in this group was 0.863. If the induction of ventricular fibrillation, doublets or short runs of VT (N less than 6 with no recurrences) are included, the value increased to 0.877. These patients were considered to be non-inducible. The prevalence of absence of recurrence of arrhythmia in patients in whom it was possible to induce sustained ventricular tachycardia of the same morphology as the clinical arrhythmia was 0.512 (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of therapeutic interventions of sustained monomorphic ventricular tachycardia guided by an electrophysiologic study: a case report

Therapeutic evaluation of sustained monomorphic ventricular tachycardia (VT) using electrophysiologic study (EPS) is presented in a case of refractory VT. A 54-year-old man with a history of recurring syncope underwent coronary angiography which revealed total occlusion of the posterior descending branch of the right coronary artery. Left ventriculography showed a left ventricular aneurysm at the cardiac apex. Ejection fraction of the left ventricle was 36%. He had four VTs of different QRS morphologies in 12 lead electrocardiograms. According to our programmed ventricular stimulations, single or double, and rarely triple, extra stimuli were administered after eight basic stimuli at two basic cycle lengths. Rapid ventricular pacing, up to 210 bpm, was then added. The stimuli were delivered to two different sites in the right ventricle and to at least one site in the left ventricle. When the entire protocol could not induce VT, isoproterenol was given intravenously, and the same protocol was repeated. No drug could prevent VT attacks, even after the surgical resection of two VT foci, VT was still inducible. Postoperative drug therapy could not prevent VT induction in EPS. However, changes in the mode required for VT induction were observed. Among 47 patients with sustained monomorphic VT treated in our hospital, 24 had EPS to evaluate the efficacies of therapeutic interventions, such as drugs and surgery. In 14 patients, no VT was induced by the entire VT induction protocol. Among the remaining 10 patients, four showed changes in the VT induction mode, but VT recurred in their clinical courses even after their treatments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of spontaneous occurrence of sustained monomorphic ventricular tachycardia in right ventricular dysplasia

Objectives. We sought to demonstrate the determinants of spontaneous onset of ventricular tachycardia in right ventricular dysplasia.Background. Sudden death during athletic activities has been described in patients with right ventricular dysplasia, but few data are available on the clinical circumstances of well tolerated ventricular tachycardias.Methods. The spontaneous occurrence of 43 episodes of sustained monomorphic ventricular tachycardia was recorded during ambulatory electrocardiographic (Holter) monitoring in 12 patients.Results. The ventricular tachycardia usually occurred without a significant immediate precipitating arrhythmic event: Atrial arrhythmia was never present, and long-short cycle sequences by postextrasystolic pauses or runs of polymorphic extrasystoles were also unusual (four episodes of ventricular tachycardia each). Finally, no arrhythmia was present immediately before the tachycardia in 36 (84%) of the 43 episodes and in 8 of 12 patients. Examination of the sinus rate before the initial episode of tachycardia in each patient showed a continuous increase from 30 min to the few cycles before the tachycardia (mean RR decrease from 876 ± 778 to 830.5 ± 189 ms, with a mean slope of −8.4 ms/min; both p = 0.01 by Wilcoxon test). A within-patient comparison showed that the first cycle of the ventricular tachycardia was shorter than that of runs or couplets (389 ± 88 vs. 453 ± 121 and 520 ± 133 ms, p = 0.03 and p < 0.01, respectively, by paired t test) and that the second cycle was shorter than that of runs (383 ± 96 vs. 435 ± 120 ms, p = 0.03). Sinus rate measured 15 beats before the event was higher for ventricular tachycardia than for isolated beats (mean RR interval 835 ± 184 vs. 908 ± 153 ms, p < 0.01).Conclusions. Increased heart rate and shortening of the coupling intervals of the first cycles before the tachycardia are due to a change in the vagosympathetic balance with an increased sympathetic tone. This increase appears to be the main determinant of the ventricular tachycardia in this disease in contrast to the multifactorial origin of ventricular tachycardia due to coronary heart disease. It should be considered in patients participating in strenuous athletic activities.     

Comparison of the characteristics of nonsustained ventricular tachycardia on Holter monitoring and sustained ventricular tachycardia observed spontaneously or induced by programmed stimulation

The characteristics of nonsustained ventricular tachycardias (VT) on Holter monitor recordings were compared with the characteristics of sustained VT noted spontaneously or induced by programmed stimulation in 50 patients with a history of spontaneous sustained VT. At baseline before antiarrhythmic therapy, all patients had nonsustained VT (triplets or longer) on Holter recordings and sustained VT inducible by programmed stimulation. The mean rate of the fastest nonsustained VT on Holter monitoring (150 +/- 52 beats/min) was significantly slower that that of induced sustained VT (246 +/- 56 beats/min) (p less than 0.001). Compared with nonsustained VT on Holter monitoring, sustained VT by programmed stimulation were faster in 45 of 50 patients, similar in 2 and slower in 3. There was a poor correlation between the rates of nonsustained VT and sustained VT (r = 0.2195). The duration of the longest nonsustained VT was fewer than 6 beats in 24 patients and 6 beats or more in 26. The mean rates of induced sustained VT were not significantly different between patients with shorter (fewer than 6 beats) and longer (6 or more beats) nonsustained VT. In 12 patients, the rate of spontaneous sustained VT was available. The rate of spontaneous sustained VT (217 +/- 59 beats/min) was similar to that of sustained VT by programmed stimulation (277 +/- 60 beats/min). There was a close correlation (r = 0.8036) between the rates of spontaneous and induced sustained VT. However, the rate of nonsustained VT on Holter monitoring (151 +/- 76 beats/min) was significantly slower than the rate of spontaneous sustained VT (p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prospective comparison of Holter monitoring and electrophysiologic study in patients with coronary artery disease and sustained ventricular tachyarrhythmias

Baseline 24-hour Holter monitoring (HM) and electrophysiologic study (EPS) were compared in 43 consecutive patients with coronary artery disease who had sustained ventricular tachyarrhythmias to determine the fraction of patients in whom each could be performed and the fraction in whom each could be used to guide therapy. Patients were excluded from HM if sustained ventricular tachycardia (VT) requiring termination occurred and from EPS if heart failure was sufficiently severe to cause excessive risk. More patients completed EPS than HM (90% vs 71%), but this difference was not statistically significant (p = 0.12). Overall, HM detected arrhythmias suitable for antiarrhythmic drug assessment in 50% of patients: 30 or more ventricular premature complexes (VPCs) per hour in 50%, 10 or more VPC pairs in 44%, 5 or more runs in 19%, and 10 or more pairs and runs in 44%. Sustained monomorphic VT suitable for electropharmacologic testing was induced at EPS in 82% (p = 0.003 vs HM). Drug efficacy could be assessed in 70% of patients evaluated by HM, compared with 96% evaluated by EPS (p = 0.02). Thus, in consecutive coronary patients with sustained ventricular tachyarrhythmias, EPS could be used to guide therapy more frequently than HM.     

Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics

Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.     

动态心电图对室性心动过速诊断价值的探讨

从１６５０例动态心电图中检出室性心动过速（室速）３３例，检出率为２％，２４ｈ室速发作频度≤１０次者２９例，多于１０次者４例，最多１例为１５６６次。３３例室速患者中患冠心病、心肌炎和心肌病等２６例（７８．８％）。室速由Ｒ落Ｐ诱发１４例（４２．４％），Ｒ落Ｔ１例（３．０％）。活动时发生室速１３例（３９．４％），其中１２例（９２．３％）有器质性心脏病。室速时频率为７４～２３０次／ｍｉｎ，平均１２９．３次／ｍｉｎ。早搏指数小于１。提示动态心电图对检出室速、尤其对患器质性心脏病者有重要临床意义，应重视Ｒ落Ｐ诱发室速现象。     

Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia

We report three cases of sustained monomorphic ventricular tachycardia(VT) in the setting of coronary artery disease,resistant to beta-blockers in two patients and to amiodarone in all,successfully terminated by low doses of intravenous(IV) epinephrine.VT was the first manifestation of coronary artery disease in one patient,whereas the other two patients had a previous history of myocardial infarction and were recipients of an implantable cardioverter-defibrillator(ICD).One of these two patients experienced an arrhythmic storm.All had hemodynamic instability at the time of epinephrine administration.A single slow administration of IV epinephrine(0.5 to 1 mg administered over 30 to 60 s) restored sinus rhythm after 30-90 s with only minor side effects.In the ICD patient with recurrent VT and several cardioversions due to transformation of VT to ventricular fibrillation,epinephrine injection led to the avoidance of further shocks.Although potentially harmful,low doses of IV epinephrine used alone or in combination with beta-blocker treatment and electrical cardioversion may be an alternative effective therapy for sustained monomorphic VT refractory to amiodarone.The role of epinephrine in the termination of VT should be studied further,especially in patients pre-treated with amiodarone in combination with beta-blockers.     

Value of Holter monitoring in identifying risk for sustained ventricular arrhythmia recurrence on amiodarone

Seventy-four patients with sustained ventricular tachyarrhythmias had 22 +/- 3 hours of Holter monitoring before and after 11 +/- 6 days of amiodarone treatment. On control Holter recordings, 55 patients (group I) had frequent (more than 10 extrasystoles per hour) and/or complex (at least couplets) ventricular ectopic activity (VEA), and 19 patients (group II) had infrequent and simple VEA. A positive Holter monitor response to amiodarone was defined as a decrease in VEA by more than 85% and abolition of all complex VEA. In group I, 34 patients (62%) had a positive Holter monitor response. In group II, 16 patients (84%) had persistent, infrequent and simple VEA and 3 had frequent and/or complex VEA. During a mean follow-up of 13 +/- 12 months, 22 patients (30%) had ventricular tachycardia (VT) or sudden death. In group I, VT or sudden death occurred in 6 of 34 (18%) patients with a positive Holter monitor response and 11 of 21 (52%) with a negative Holter monitor response (p less than 0.01), and in group II, VT or sudden death occurred in 5 of 16 patients (31%) with persistent, infrequent and simple VEA. All episodes of VT or sudden death occurred after at least 2 weeks of amiodarone therapy (mean 5 +/- 6 months). The predictive accuracy of a positive Holter monitor response as an indicator for subsequent prevention of sustained ventricular tachyarrhythmias and sudden cardiac death was 82% and for a negative Holter monitor response as an indicator of tachyarrhythmia or sudden death recurrence on therapy it was 52%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Procainamide induced sustained monomorphic ventricular tachycardia in a patient with benign premature ventricular complexes

A 59-year old female with history of benign ventricular ectopy who developed sustained monomorphic ventricular tachycardia (VT) during therapy with procainamide is reported. The tachycardia occurred 24 hours after institution of procainamide without any other evidence of drug toxicity or QT prolongation. When procainamide was withheld, VT resolved completely and no arrhythmia could be induced by programmed ventricular stimulation. When the patient was rechallenged with procainamide at therapeutic level, sustained monomorphic VT was initiated reproducibly by programmed ventricular stimulation. Without antiarrhythmic therapy, patient has been asymptomatic and free of recurrent VT after a follow-up of 9 months. This case: Demonstrates that procainamide may cause the first emergence of sustained monomorphic VT in a patient with no previous history of VT; and Emphasizes the utility of programmed ventricular stimulation in providing direct evidence for drug mediated exacerbation of the ventricular arrhythmia.