Nonsustained Ventricular Tachycardia

Nonsustained ventricular tachycardia (VT) has been an intimidating diagnosis for many physicians because its presence, in general, portends an increased risk of sudden death. The management and approach has been quite diverse and inconsistent in part due to the absence of a large body of literature. There have been major developments, however, over the last two decades in better understanding the mechanism of VPCs and ventricular tachycardia as well as adopting a more systematic approach to diagnosis and management. With the publication of the results of CAST I and II, there has been a movement away from empiric treatment of asymptomatic VPCs and nonsustained VT, and an emphasis on risk stratification on the basis of the underlying heart disease. Coronary artery disease, by far, is the most common etiology for heart disease in the United States, but there are numerous other conditions such as hypertrophic and dilated cardiomyopathies, as well as right ventricular dysplasia and “normal heart” ventricular tachycardias that require a tailored approach. Noninvasive and invasive methods of risk stratification, such as measurement of heart rate variability and signal-averaged ECG's, as well as electrophysiologic testing, respectively, have enabled us to identify “high risk” patients that may benefit from therapy whether it be antiarrhythmics or implantable defibrillators. Recent and on-going prospective trials such as the CAMIAT, EMIAT, GESICA, MADIT, MUSTT, and CABG-PATCH will hopefully further our knowledge base and make the management of VPCs and nonsustained VT a more uniform process.     

Mode of Induction of Ventricular Tachycardia and Prognosis in Patients with Coronary Disease: The Multicenter UnSustained Tachycardia Trial (MUSTT)

Introduction: Programmed stimulation is an important prognostic tool in the evaluation of patients with an ejection fraction ≤40% after myocardial infarction. Many believe that ventricular tachycardia (VT) requiring 3 ventricular extrastimuli (VES) for induction is less likely to occur spontaneously and has less predictive value. However, it is unknown whether the mode of VT induction is associated with long-term prognosis.
Methods and Results: We analyzed a cohort of 371 patients enrolled in MUSTT who had inducible monomorphic VT and who were not treated with antiarrhythmic drugs or an implantable cardioverter defibrillator during the trial. Patients in whom sustained VT was induced with 1 or 2 VES or burst pacing (single VES n = 15, double VES n = 127, burst n = 7, total n = 149) were compared with those in whom VT was induced with 3 VES (n = 222). Compared with the others, patients requiring 3 VES were closer to their most recent myocardial infarction (17 vs 51 months, P = 0.035) and showed a trend toward a lower ejection fraction (26% vs 30%, P = 0.057). VT requiring 3 VES had a shorter cycle length (240 vs 260 ms, P < 0.001). Despite these findings, there was no difference in the incidence of arrhythmic death or cardiac arrest (HR 1.02; 95% CI 0.69-1.51) or all-cause mortality (HR 1.03; 95% CI 0.76-1.39) according to the mode of induction in adjusted analyses.
Conclusions: The prognostic significance of VT induced by 3 VES is similar to that of VT induced by 1 or 2 VES, or burst pacing, in patients with coronary disease and abnormal LV function.     

Wearable Cardioverter‐Defibrillator in a Patient with Left Ventricular Noncompaction/Hypertrabeculation,Coronary Artery Disease,and Polyneuropathy

A 55‐year‐old Caucasian male with coronary heart disease was admitted because of dyspnea for 4 weeks. Echocardiography showed a dilated left ventricle with an ejection fraction of 34% and apical left ventricular hypertrabeculation/noncompaction with an apical thrombus. Neurologic examination revealed positional tremor and generally reduced tendon reflexes. During 8 weeks, his condition improved under pharmacotherapy. The patient was skeptical about implantable cardioverter‐defibrillator (ICD) and expected further improvement from pharmacotherapy. Thus, he received a wearable cardioverter‐defibrillator (WCD). We conclude that a WCD might be useful in noncompaction patients in whom improvement of systolic dysfunction is expected or who are skeptical about ICDs.     

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 ).     

Relationship Between Serum Potassium Concentration and Risk of Recurrent Ventricular Tachycardia or Ventricular Fibrillation

INTRODUCTION: Electrolyte abnormalities are considered a correctable cause of a life-threatening ventricular arrhythmia according to American Heart Association/American College of Cardiology Practice Guidelines, and ventricular tachycardia or ventricular fibrillation in the setting of an electrolyte abnormality is considered a class III indication for defibrillator implantation. However, there are little data to support this recommendation. The purpose of this study was to determine the risk of a recurrent sustained ventricular arrhythmia in patients with a low serum potassium concentration at the time of an initial episode of a sustained ventricular arrhythmia. METHODS AND RESULTS: One hundred sixty-nine consecutive patients who presented with a sustained ventricular arrhythmia and a serum potassium concentration determined on the day of the arrhythmia underwent defibrillator implantation. All patients had structural heart disease and left ventricular ejection fraction of 0.32+/-0.15. On the day of the index arrhythmia, 30% of the patients had a serum potassium concentration <3.5 or >5.0 mEq/L, including 7% who had a serum potassium concentration <3.0 or >6.0 mEq/L. For the entire cohort of patients, freedom from a recurrent sustained ventricular arrhythmia was 18% at 5 years and was not significantly different among patients with a serum potassium concentration <3.5 mEq/L (23%), between 3.5 and 5.0 mEq/L (16%), and >5.0 mEq/L (5%; P = 0.1). CONCLUSION: The results of the present study suggest that patients with structural heart disease and an abnormal serum potassium concentration at the time of an initial episode of sustained ventricular tachycardia or ventricular fibrillation are at high risk for a recurrent ventricular arrhythmia; therefore, implantable defibrillator therapy may be reasonable.     

Identifying the High Risk Patient with Coronary Artery Disease—Is Ejection Fraction All You Need?

Although the total number of deaths resulting from cardiovascular disease has decreased in the United States, the percentage of cardiac deaths that occur suddenly has increased. Over the past 10 years, a number of randomized clinical trials have evaluated the ability of antiarrhythmic therapy to reduce mortality in patients in patients with chronic coronary disease and abnormal left ventricular function that had not yet developed spontaneous sustained VT or VF. A majority of these trials have demonstrated that the implantable cardioverter-defibrillator (ICD) can reduce mortality compared to pharmacologic antiarrhythmic therapy, or no specific antiarrhythmic therapy. While, reduced left ventricular ejection fraction (EF) has been a major determinant for entry into these studies, in all but one case, it was not the sole entry requirement. These studies have demonstrated that a number of factors have prognostic significance, and therefore impact efficacy of the ICD. None of these studies was designed to evaluate the relative efficacy of various risk factors. Therefore, we lack adequate information today to determine the most cost-effective manner in which to assign use of ICDs for primary prevention. This article reviews the potential for using EF alone as a risk factor, as well as the efficacy of other variables for risk stratification.     

Ventricular Tachycardia in Coronary Artery Disease

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Ten-Year Follow-Up of Cardiac Sympathectomy in a Young Woman with Catecholaminergic Polymorphic Ventricular Tachycardia and an Implantable Cardioverter Defibrillator

Current recommendations for therapy of catecholaminergic ventricular tachycardia (CPVT) include beta blockade and implantable cardioverter defibrillators (ICDs). Patients may experience recurrent arrhythmias, ICD shocks and, rarely, sudden death despite optimal medical therapy. We report a young woman with CPVT who received frequent ICD shocks despite beta blockade, who subsequently underwent cardiac sympathectomy with a dramatic reduction in shocks over 10 years of follow-up.     

Prevention of sudden cardiac death: the ICD,or an electrical end-point with preceding opportunities for intervention?

Sudden cardiac death (SCD) is usually due to monomorphic ventricular tachycardia and/or ventricular fibrillation. However, in the vast majority of patients these arrhythmias are associated with advanced structural disease. In our society, this is usually due to coronary artery disease (CAD). The implantable cardioverter – defibrillator is the logical approach to management in survivors of SCD. Its rational use must be guided by electrophysiology study. However, a realistic and cost-effective approach to the prevention of a first cardiac arrest must be multifaceted and take cognisance of other aspects including primary prevention. Limitation of the size of myocardial infarction (MI) is vital. Trials already suggests that effective thrombolysis may impinge long-term on arrhythmic end-points. Following infarction, ventricular arrhythmias and sudden death may also be decreased by aspirin, beta-blockers, and possibly angiotensin converting enzyme inhibitors and amiodarone. Many post-infarction studies employ a combined end-point of death and clinical arrhythmias. However, death is usually confined to those with an ejection fraction <35%. In them, treatment of associated heart failure is often a consideration and if the ejection fraction < 15–20%, depending on donor availability, transplantation may even be the preferred therapeutic option to the cardioverter-defibrillator.     

J‐Wave Disappearance Immediately After an Episode of Ventricular Fibrillation in a Patient With Resuscitated Sudden Cardiac Death and Brugada Syndrome

J‐Wave Disaapearance After an Episode of Ventricular Fibrillation . Early repolarization (ER) abnormalities in the inferior‐lateral leads are a matter of intense scientific debate because of their demonstrated association with Brugada syndrome (BS) and idiopathic ventricular fibrillation (VF). To add fuel to the fire, we present a case in which ER abnormalities are associated with BS but in which, more importantly, they were shown to be transient and strictly correlated with an episode of VF. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1413‐1415, December 2010)     

Long‐Term Outcomes of Inducible Very Fast Ventricular Tachycardia (Cycle Length 200–250 ms) in Patients With Ischemic Cardiomyopathy

Very Fast Ventricular Tachycardia. Background: The long‐term outcomes of patients with inducible very fast ventricular tachycardia (VFVT) of cycle length (CL) 200 to 250 ms have not been well studied. Methods: Consecutive patients with ischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of ≤40% (n = 300) underwent programmed ventricular stimulation (PVS) and were divided into 4 groups based on results of the study. Group A were noninducible, had induced ventricular fibrillation (VF), or polymorphic VT (CL < 200 ms); group B had inducible VFVT (200–250 ms); group C had inducible fast ventricular tachycardia (FVT; CL 251–320 ms); and group D had inducible slow VT (CL >320 ms). The primary endpoint was spontaneous ventricular arrhythmia or sudden death. Results: The mean age was 63 ± 12 years and mean LVEF was 29 ± 7%. At mean follow‐up of 38 ± 25 months (median 30 months), the primary endpoint rate was 6.6%, 34%, 44%, and 71% in groups A, B C, and D, respectively (P < 0.001). Neither mode of induction of VT nor LVEF altered the observed pattern in the primary endpoint. There was no significant difference in the primary endpoint among implanted cardioverter defibrillator recipients in groups B and C (38% vs 45%, P = 0.43). Adjusted hazard ratios for the primary endpoint compared to group A were 3.2, 3.5, and 7.0 in groups B, C, and D, respectively (P < 0.05). Conclusions: Inducible VFVT (200–250 ms) is a clinically significant arrhythmia with adverse long‐term outcomes and should not be considered a nonspecific finding of PVS. (J Cardiovasc Electrophysiol, Vol. 21, pp. 262–269, March 2010)     

左心室射血分数在心脏性猝死危险分层中的价值

心脏性猝死是世界上发达国家中最常见的死因,因此有效的识别高危患者并进行积极有效的预防和治疗有着重要意义。现有多项临床试验表明,左心室射血分数与心脏性猝死有密切关系,其在识别心脏性猝死高危人群及埋藏式心律转复除颤器植入对象的筛选中将具有重要的价值。     

Contemporary Clinical Trials in Ventricular Tachycardia and Fibrillation: Implications of ESVEM, CASCADE, and CASH for Clinical Management

Trials in Ventricular Tachycardias. Recent clinical trials in patients with ventricular tachycardia (VT) or fibrillation (VF) have occurred in the setting of the disappointing results of postinfarction secondary prevention studies using Class I antiarrhythmics (e.g., CAST). ESVEM addressed in a randomized trial whether electrophysiologic study (EPS) or Hotter monitoring (HM) is a more accurate predictor of long-term antiarrhythmic drug efficacy in VT/VF patients (N = 486) and what the relative efficacy of various antiarrhythmic agents is for VT/VF. Surprisingly, arrhythmia recurrence rates were not significantly different by the method of determining an efficacy prediction. However, arrhythmia recurrence and mortality were lower (by about 50% at 1 year) in patients treated with sotalol (a mixed Class II/III agent) than with other drugs (Class I). CASCADE evaluated empiric amiodarone versus guided (EPS or HM) standard (Class I) therapy in survivors of out-of-hospital cardiac arrest due to VF. The primary endpoint of cardiac death, resuscitated VF, or syncopal shock (in ICD patients) was reduced by amiodarone compared with conventional therapy (9% vs 23% at 1 year). An interim report of the ongoing CASH study suggested in 230 survivors of cardiac arrest that propafenone (Class IC) provided less effective prophylaxis (approximately 20% 1-year mortality) compared with randomly assigned therapies with amiodarone, metoprolol, or an ICD (approximately 14% mortality rates) and was excluded from further study. These studies have led to a paradigm shift in the approach to antiarrhythmic therapy of VT/VF: drugs with antisympathetic plus Class III (refractoriness prolonging) action (i.e., sotalol, amiodarone) are superior to traditional drugs with Class I (conduction slowing) effects, even when guided by EPS or HM.     

MADIT-II: Substudies and Their Implications

In MADIT-II, prophylactic ICD therapy was effective in improving survival in patients with prior myocardial infarction and an ejection fraction 相似文献   

Heart Rate Variability Before Ventricular Arrhythmias in Patients with Coronary Artery Disease and an Implantable Cardioverter Defibrillator

Background: Changes in autonomic regulation of the heart may be responsible for the occurrence of arrhythmias. Although a decrease in 24‐hour heart rate variability is a strong predictor of subsequent arrhythmias in patients with heart disease, many questions remain unanswered concerning changes in heart rate and heart rate variability in the minutes or hours preceding an arrhythmia. The aim of our study was to analyze changes in heart rate and heart rate variability occurring during the 90 minutes preceding an arrhythmia, in patients with coronary heart disease and an implantable defibrillator. Materials and Methods: Thirty‐eight patients, with a total of 93 episodes of ventricular arrhythmia, were included in the study. Heart rate and heart rate variability were measured in three 30‐minute and five 2‐minute periods preceding the arrhythmia. Heart rate variability was assessed using measurements of Poincaré plots. Results: The results show a gradual increase in heart rate before the arrhythmia, from 73 ± 13/min , to 75 ± 14/min , and finally 78 ± 15/min in the 90 minutes preceding the arrhythmia (P < 0.05) . Conclusion: Measurements of Poincaré plots showed a significant increase in their length and no significant change in their width. These results suggest that sympathetic activation is the predominant change in autonomic nervous system before a ventricular arrhythmia in patients with coronary heart disease. This change may occur as early as one hour and a half before the arrhythmia.     

Bundle Branch Reentrant Tachycardia in a Patient with Normal Ventricular Function

We report an unusual case of bundle branch reentrant tachycardia, in a patient with normal left ventricular function, cured by radiofrequency catheter ablation. However, the long-term prognosis of these patients is uncertain. We discuss the indications for an implantable defibrillator in this group.     

Arrhythmogenic Right Ventricular Cardiomyopathy 2012: Diagnostic Challenges and Treatment

ARVC 2012 . The most common presentation of arrhythmogenic right ventricular cardiomyopathy (ARVC) is palpitations or ventricular tachycardia (VT) of left bundle branch morphology in a young or middle‐aged individual. The 12‐lead electrocardiogram may be normal or have T‐wave inversion beyond V₁ in an otherwise healthy person who is suspected of having ARVC. The most frequent imaging abnormalities are an enlarged right ventricle, decrease in right ventricular (RV) function, and localized wall motion abnormalities. Risk factors for implantable cardioverter defibrillator include a history of aborted sudden death, syncope, young age, decreased left ventricular function, and marked decrease in RV function. Recent results of treatment with epicardial ablation are encouraging. (J Cardiovasc Electrophysiol, Vol. 23 pp. 1149‐1153, October 2012)     

New Family With Catecholaminergic Polymorphic Ventricular Tachycardia Linked to the Triadin Gene

We describe a new family with cathecholaminergic polymorphic ventricular tachycardia (CPVT) linked to the Triadin gene. This is the second report of such a CPVT of autosomal recessive inheritance. Using an NGS panel including 42 genes involved in cardiac sudden death, 2 heterozygous pathogenic mutations (c.613C> T/p.Gln205* and c.22 + 29 A>G) were identified in the Triadin gene in 2 sibs who experienced early severe arrhythmias without evidence of CPVT diagnosis at first cardiac evaluation. However, significant arrhythmias occurred after catecholaminergic stimulation. Each of the TRDN mutations was inherited from a healthy parent. In this family, genetic studies permit confirmation of the CPVT diagnosis in the 2 affected sibs and permit the early diagnosis of the third asymptomatic child. It also helped guide the therapeutic strategy in this family.     

Vasospastic Angina with J‐Wave Pattern and Polymorphic Ventricular Tachycardia Effectively Treated with Quinidine

Background: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J‐wave pattern was suggested to be a marker of a disorder associated with life‐threatening arrhythmias. Results: We report the case of a patient with vasospastic angina and J‐wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine—vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. Conclusion: The J‐wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina—quinidine can effectively prevent such arrhythmias in these patients.