The Prognostic Significance of Inducing Nonsustained Ventricular Tachycardia in Patients Presenting with Sustained Ventricular Tachycardia or Cardiac Arrest

The significance of inducing nonsustained ventricular tachycardia during baseline electrophysiological testing in patients presenting with sustained ventricular arrhythmias is unclear. In this study, 145 consecutive patients presenting with cardiac arrest or sustained ventricular tachycardia underwent electrophysiological study. Twenty five (17%) had no inducible ventricular tachycardia (group I), 33 (23%) had inducible nonsustained ventricular tachycardia (group II), and 87 (60%) had inducible sustained ventricular tachycardia (group 111). Group I was not treated with antiarrhythmic therapy. Groups II and III underwent serial drug trials guided by electrophysiological testing. Mean follow-up for all three groups was 31 ± 18 months. The actuarial rate of arrhythmia recurrence for group 1 at 12, 24, and 36 months of follow-up was 0%, 6%, and 17%, respectively. This actuarial arrhythmia recurrence rate for group I was significantly lower (P < 0.05) than that of group II (16%, 27%, and 32%) and group III (32%, 39%, and 44%). There was no significant difference between the arrhythmia recurrence rates in groups 11 and III. When groups II and III were broken down into drug responders and nonresponders, drug responders in both groups had significantly fewer arrhythmia recurrences than nonresponders (P < 0.05). The overall incidence of sudden death was low (11 of 145, 8%) and not significantly different between groups I, II, and III. In summary, among patients who present with sustained ventricular arrhythmias, those who have nonsustained ventricular tachycardia induced during baseline electrophysiological testing respond to serial drug testing and have long-term outcomes similar to those with inducible sustained ventricular tachycardia.     

Relationship Between Ventricular Rate Variability in Nonsustained Ventricular Tachycardia and Subsequent Cardiac Events

Background: Clinical and experimental observations indicate that reduced beat-to-beat changes in the cycle length of nonsustained ventricular tachycardia (NSVT) may portend malignant ventricular tachyarrhythmias and sudden cardiac death. The purpose of the study was to test the hypothesis that measures of ventricular rate variability during NSVT (VRV-NSVT) may be useful in identifying patients at high risk of life-threatening arrhythmic events. Methods: The study group consisted of 326 patients who had NSVT on 24-hour ECG recordings. Temporal changes in up to 10 beat-to-beat intervals of NSVT runs (V-V) were assessed. The following parameters of VRV-NSVT were calculated: (1) average value of successive differences in V-V intervals (ADVV); and (2) normalized average value of successive differences in V-V intervals (nADVV). Results: During a mean follow-up of 4 years, 52 (16%) patients had a documented episode of sustained VT or ventricular fibrillation. Patients with these arrhythmic events had significantly (P < 0.001) lower values of ADVV and nADVV variables in comparison to patients without arrhythmic events. The relative risk of malignant arrhythmic events for patients with ADW < 40 ms was 4.9 (P < 0.001), for patients with nADVV < 6%, the risk was 3.9 (P < 0.001). Conclusions: The results of this study indicate a strong and significant relationship between NSVT and the risk of subsequent malignant ventricular tachycardia. The assessment of VRV-NSVT may be useful for identifying patients at high and low risk for subsequent arrhythmic events.     

Prevention of Spontaneous Sustained Ventricular Tachycardia in the Postinfarction Dog by Left Stellate Ganglionectomy

Suppression of Sustained VT by Left Stellectomy. Holter monitoring and ventricular pacing were used to examine control, right stellate ganglionectomy, and left stellate ganglionectomy treatment groups, 6-24 hours after left anterior descending coronary artery ligation in dogs. In nine of 27 controls (33%), spontaneous ventricular triplets (358 ± 8 beats/min) initiated sustained monomorphic ventricular tachycardia (386 ± 16 beats/min), followed by ventricular fibrillation at 12.6 ± 1.4 hours. Ventricular pacing produced sustained monomorphic ventricular tachycardia in 13 of 18 survivors (73%) at 24 hours. Left but not right stellectomy performed 15 minutes before coronary artery ligation reduced the incidence of spontaneous sustained monomorphic ventricular tachycardia (2 of 27, 7%, P = 0.06; 7 of 27, 26%, P = 0.50, respectively) and reduced the maximal ventricular triplet rate (332 ± 12, P <0.05 and 358 ± 10 beats/min, respectively, P = NS vs control). Neither left nor right stellectomy altered the incidence of ventricular triplets during the 6-24 hour period (153 ± 58 and 222 ± 55/hour, respectively, vs control, 177 ± 59/hour, P = NS) nor prevented pacing-induced sustained monomorphic ventricular tachycardia in the survivors at 24 hours (20 of 24, 75%; and 16 of 20, 80%, P = NS). The data demonstrate that left but not right stellectomy reduces spontaneous sustained ventricular tachycardia and ventricular fibrillation during the 6-24 hour period following coronary artery ligation in the dog. Left stellectomy reduces the triggers for sustained monomorphic ventricular tachycardia (rapid ventricular triplets) without altering the underlying reentrant substrate for sustained ventricular tachycardia.     

The Clinical Significance of Nonsustained Ventricular Tachycardia in Patients with Sustained Ventricular Tachyarrhythmias

Background: Nonsustained ventricular tachycardia (NSVT) predicts mortality in several disorders but its significance in patients with sustained ventricular tachyarrhythmias is unknown. We analyzed the clinical features and outcome associated with NSVT (>; 3 beats at >; 100 beats/min) recorded on a 48-hour Holter in the absence of antiarrhythmic drugs. Methods: Patients enrolled in the ESVEM trial (n = 486) were grouped according to the duration of the longest recorded episode of NSVT, and in the second analysis, according to frequency of recorded episodes. Assessments were on an intention-to-treat basis. Results: Patients without NSVT were more likely to have ischemic heart disease and had significantly lower frequencies of single and paired premature ventricular complexes (PVCs). There were no significant differences with respect to age, sex, presenting arrhythmia, years since last myocardial infarction, functional class, or present ejection fraction. The cumulative probabilities of arrhythmia recurrence and all-cause mortality at 4 years in patients without NSVT (60%± 7% and 32%± 6%, respectively) were not significantly different than those of patients with NSVT (63%± 3% and 41%± 3%, respectively). Cox regression models indicated that ejection fraction and functional class were significant predictors of outcome, but variables based on the presence, duration, and frequency of recorded episodes of NSVT were not. Conclusions: NSVT is common in patients with spontaneous and inducible sustained ventricular tachyarrhythmias and at least 10 PVCs/hour (ESVEM enrollment criteria), but is not a significant predictor of arrhythmia recurrence, sudden death, or all-cause mortality in patients with these characteristics.     

Cardiac Echinococcus Complicated by Ventricular Tachycardia

Echinococcosis is a parasitic disease that usually involves lungs and liver. Occasionally, it localizes in the heart (less than 2% of cases). We present a case of an adult patient with cardiac echinococcosis complicated by ventricular tachycardia. The diagnosis, based on transthoracic two-dimensional echocardiography, magnetic resonance imaging (MRI), and computerized tomography (CT), was confirmed by surgery.     

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 ).     

Nonsurgical Transthoracic Epicardial Approach in Patients with Ventricular Tachycardia and Previous Cardiac Surgery

INTRODUCTION: The subxyphoid pericardial mapping approach can be used to facilitate catheter ablation of postmyocardial-infarction ventricular tachycardia (post-MI VT), but the presence of dense adhesions is thought to preclude this approach in patients who have previously undergone open-chest cardiac surgery. AIMS OF THE STUDY: This study reports the first use of a nonsurgical transthoracic epicardial approach in patients with scar-related VT and previous cardiac surgery. METHODS: Five patients with a mean age of 67 +/- 10 years, left ventricular ejection fraction (LVEF) of 40 +/- 4.3%) and recurrent VT occurring 7 months to 10 years after cardiac surgery underwent combined endocardial and epicardial mapping and ablation during the same session. Because pericardial adhesions were anticipated to be denser in the anterior wall, the nonsurgical transthoracic epicardial puncture was directed to the inferior wall of the left ventricle. Failure to interrupt VT with radio frequency (RF) energy pulses delivered at the best endocardial or epicardial site prompted changing from one approach to the other. RESULTS: During the epicardial puncture procedure, the contrast medium accumulated in the inferior wall instead of spreading around the cardiac silhouette. The pericardial sac could be entered in all patients, and mapping of the inferolateral epicardial wall of the left ventricle was feasible. Fourteen VTs were induced, of which 8 could not be mapped because of poor hemodynamic tolerance. Three of the remaining 6 mappable VTs were eliminated by endocardial ablation, 2 required an epicardial RF pulse to be rendered noninducible, and 1 VT was not eliminated. No intra- or postprocedural complications were noted despite full heparinization. CONCLUSION: Nonsurgical transthoracic epicardial catheter mapping and ablation of epicardial VT related to the inferolateral left ventricular wall are feasible in patients who have previously undergone open- cardiac surgery.     

Out-of-Hospital Cardiac Arrest –Optimal Management

Out-of-hospital cardiac arrest (OHCA) has attracted increasing attention over the past years because outcomes have improved impressively lately. The changes for neurological intact outcomes has been poor but several areas have achieved improving survival rates after adjusting their cardiac arrest care. The pre-hospital management is certainly key and decides whether a cardiac arrest patient can be brought back into a spontaneous circulation. However, the whole chain of resuscitation including the in-hospital care have improved also. This review describes aetiologies of OHCA, risk and potential protective factors and recent advances in the pre-hospital and in-hospital management of these patients.     

Cardiac Arrest in Stockholm with Special Reference to the Ambulance Organization

ABSTRACT During a one-year period all patients with cardiac arrest (CA) taken care of by three ambulances were studied. An incidence of 110 cardiac arrests/100000 inhabitantslyear was found. The majority of CAs affected the elderly and occurred during the day in their homes. The majority of CAs were witnessed but cardiopulmonary resuscitation (CPR) had been initiated by bystanders in only a few cases. The ambulance arrived within a mean time of 7.7±4.0 min. Forty-eight per cent of the CA patients showed ventricular tachycardia or ventricular fibrillation (VT/VF) on ambulance arrival. Patients with a prolonged ambulance delay showed a lower incidence of VT/VF than patients with a short delay. Patients in whom CPR had been initiated by bystanders showed a significantly higher incidence of VT/VF (67%) than unattended patients (45%). Bystander CPR was furthermore associated with an increased incidence of VT/VF in patients with prolonged ambulance delay. VT/VF was present at the time when the ambulance arrived in 86% of the CA patients who had received CPR from a bystander and were reached within 8 min by the ambulance.     

Long-term Reproducibility of Response to Noninvasive Programmed Cardiac Stimulation in Spontaneous, Sustained Ventricular Tachycardia Treated with Amiodarone Therapy

A total of 73 noninvasive serial electrophysiological studies were carried out in 12 patients with spontaneous sustained ventricular tachycardia, inducible in spite of chronic treatment with amiodarone, in order to verify the effect of this drug on the long-term reproducibility of the test. A ventricular tachycardia was induced in 72 of 73 times; in 59% of cases, the clinical form was induced. In 8 of 12 patients, two or more types or morphologies of ventricular tachycardia could be induced. The induction modes (driving rate and number of extrastimuli) changed considerably in different studies. During a follow-up of 12 ± 6 months, 5 out of 12 patients had spontaneous relapses. We observed no differences between these patients and the others regarding inducibility, types and morphologies of the induced tachycardias, or induction modes. Therefore, when ventricular tachycardia is inducible in spite of chronic amiodarone therapy, it is always inducible during follow-up, even if a great intrapatient change of type and the morphology of induced tachycardias and induction modes is observed. However, since similar electrophysiological features are present in patients with and without spontaneous recurrence of ventricular tachycardia, serial electrophysiological studies are of little value in predicting the clinical outcome.     

Effects of Incremental Doses of Procainamide in Patients with Sustained Uniform Ventricular Tachycardia

Procainamide in Patients with Uniform VT. Introduction: Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than II) years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT). Methods and Results: Twenty-nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug-free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 ± 2, 10.5 ± 3, and 14.5 ± 3 mg/L before, and 4.7 ± 2, 9.6 ± 3, and 14.6 ± 4 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide. Conclusion: Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non-inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.     

The Duration of Induced Ventricular Tachycardia as Related to Clinically Sustained Ventricular Tachycardia

Programmed electrical stimulation has been extremely useful in the management of patients with sustained ventricular tachycardia or cardiac arrest. However, the definition of sustained ventricular tachycardia is controversial, and the relationship between the duration of induced ventricular tachycardia and the risk for spontaneous ventricular tachycardia has not been adequately defined. Thus, we examined the records of 64 patients with at least three beats of induced ventricular tachycardia during EP studies using single and double premature stimuli in sinus rhythm and during ventricular paced rhythm (two sites, up to three drive cycle lengths) and using ventricular burst pacing to correlate maximum length of induced ventricular tachycardia with the nature of their spontaneous arrhythmias. Forty-nine patients (77%) had ventricular tachycardia requiring intervention to terminate it, which we called sustained. Nine patients (14%) had ten or fewer beats of ventricular tachycardia; four patients (6%) had 11 to 20 beats of ventricular tachycardia; and two patients (3%) had more than 20 beats of ventricular tachycardia which did not require intervention for termination. Inducible sustained ventricular tachycardia had a sensitivity of 88% and a specificity of 92% for identifying patients with clinical sustained ventricular tachycardia or fibrillation. More than 20 beats of inducible ventricular tachycardia had a sensitivity of 92% and a specificity of 92%. More than 10 beats of inducible ventricular tachycardia achieved a sensitivity of 98% and a specificity of 91% for identifying patients with sustained ventricular tachycardia or fibrillation. The criteria used for the duration of inducible ventricular tachycardia are arbitrary and the interpretation of inducible nonsustained ventricular tachycardia must depend on the purpose of the test and the prior probability of each result.     

Case Report: Adenosine Induced Ventricular Fibrillation in a Patient with Stable Ventricular Tachycardia

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.     

Ventricular Tachycardia in Patients with Impaired Left Ventricular Function: The Role of Propafenone

The combined occurrence of left ventricular dysfunction and -ventricular tachyarrhythmias portends a high annual mortality. Anti arrhythmic drugs can ameliorate ventricular arrhythmia and may reduce the risk of sudden cardiac death. We administered propafenone to 15 patients with ventricular tachyarrhythmias and left ventricular ejection fractions 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in 4 of 7 patients. In 8 patients studied before and during therapy, there was no significant change in left ventricular ejection fraction as determined by nuclear ventriculography. Propafenone was discontinued in 4 patients due to side effects. Seven patients receiving continuing propafenone therapy remain alive with only one patient suffering arrhythmia recurrence. Propafenone is an effective drug for the management of ventricular tachyarrhythmias and may be used for patients with impaired left ventricular function.     

Effect of Corticosteroid Therapy on Ventricular Arrhythmias in Patients with Cardiac Sarcoidosis

Background: Ventricular arrhythmias are one of the main causes of sudden death in cardiac sarcoidosis (CS). Little is known about the efficacy of corticosteroid therapy for ventricular arrhythmias in CS. Methods: Thirty‐one CS patients presenting premature ventricular contractions (PVCs, ≥300/day) were investigated. Fourteen patients had nonsustained ventricular tachycardia (NSVT). All of patients were treated with corticosteroid, and the initial dosage is 30 mg/day of prednisone, which was tapered over a period of 6 months to a maintenance dosage of 10 mg/day. Twenty‐four hour Holter monitoring, signal averaged electrocardiography (SAECG), echocardiography, gallium‐67 scintigraphy, serum angiotensin converting enzyme (ACE) and plasma B‐type natriuretic peptide (BNP) concentrations were assessed before and after corticosteroid therapy. Results: As a whole, there were no significant differences in the number of PVCs and in the prevalence of NSVT before and after steroid therapy. However, the less advanced LV dysfunction patients (EF ≥ 35%, n = 17) showed significant reduction in the number of PVCs (from 1820 ± 2969 to 742 ± 1425, P = 0.048) and in the prevalence of NSVT (from 41 to 6%, p = 0.039). Late potentials on SAECG were abolished in 3 patients. The less advanced LV dysfunction group showed a significantly higher prevalence of gallium‐67 uptake compared with the advanced LV dysfunction group (EF < 35 %, n = 14). In the advanced LV dysfunction patients, there were no significant differences in these parameters. Conclusions: Corticosteroid therapy may be effective for ventricular arrhythmias in the early stage, but less effective in the late stage. Ann Noninvasive Electrocardiol 2011;16(2):140–147     

Sudden Cardiac Death: Future Approaches Based on Identification and Control of Transient Risk Factors

Sudden Cardiac Death . Future progress in the ability to control the problem of sudden cardiac death will require new approaches in applied epidemiology, methods of accurately evaluating therapeutic outcome, and techniques to identify and control those transient risk factors that are responsible for the initiation of fatal arrhythmias. In regard to the latter, transient risk factors are distinguished from classical risk factors in two ways: (1) they are not present continuously over time, thus confounding sampling techniques among a population; and (2) their dynamic nature suggests a proximate role in the initiation of potentially fatal arrhythmias in contrast to the role of classical risk factors in the genesis of the underlying diseases. Transient risk factors derive from the structure/function model of sudden cardiac death, which places structural abnormalities in a conditioning role, establishing the sensitivity to a transient destabilizing influence. In contrast, functional abnormalities are those conditions immediately responsible for destabilizing the system, establishing vulnerability to potentially fatal arrhythmias. They include four categories of risk: (1) transient ischemia and reperfusion; (2) systemic abnormalities, such as hemodynamic dysfunction and fluid and electrolyte imbalance; (3) autonomic fluctuations, both central and cardiac; and (4) cardiac toxic states, including proarrhythmic effects of antiarrhythmic drugs and arrhythmogenic effects of other substances. Sudden cardiac death is a dynamic problem, and its pathogenesis contains dynamic features. The ability to identify transient risk factors and to control them before they exert their influence on a conditioned electrophysiologic system will provide new inroads into the problem of sudden cardiac death.