Arrhythmias in Patients with Heart Failure

Opinion statement Both atrial and ventricular arrhythmias are very common in patients with congestive heart failure, and their presence is associated with symptoms, significant morbidity, and mortality. Studies have attempted to determine the prognostic significance of atrial and ventricular arrhythmias in patients with heart failure. Whether atrial fibrillation is an independent risk factor of mortality remains controversial. The presence of ventricular arrhythmias in patients with ischemic cardiomyopathy identifies patients at high risk for sudden death. However, in patients with nonischemic cardiomyopathy there is not a strong correlation between ventricular arrhythmias and increased risk for sudden death. Multiple trials using antiarrhythmic drugs, pharmacologic therapy, and implantable cardioverter defibrillators have been performed in an attempt to improve survival in patients 1) post-myocardial infarction; 2) with congestive heart failure, with and without nonsustained ventricular tachycardia; and 3) with sustained ventricular tachycardia and those who have survived an out-of-hospital cardiac arrest. The purpose of this article is to present an overview of arrhythmias in patients with heart failure and discuss the prevalence, prognostic significance, complications, mechanisms, and trials that have formed the current therapies presently used.     

Placement of moricizine in the selection of antiarrhythmic drug therapy

The selection of antiarrhythmic drug therapy requires a careful assessment of the benefits of ventricular arrhythmia suppression compared with the risks of antiarrhythmic drug use. Since reduction in sudden cardiac death from ventricular arrhythmia suppression has not been demonstrated, the only indications for antiarrhythmic drug suppression involve the reduction of hemodynamic symptoms such as syncope (a major benefit) or the reduction of nonhemodynamic symptoms such as palpitations or dizziness (a minor benefit). Noncardiac adverse effects and organ toxicity as well as cardiac side effects must be considered when antiarrhythmic drug therapy is initiated. For reduction of nonhemodynamically important symptoms in patients with benign or potentially lethal ventricular arrhythmias, beta blockers are chosen as first-line therapy. Because of moricizine's relatively high effectiveness in suppressing ventricular arrhythmias and its low potential for noncardiac adverse effects and organ toxicity as well as a low incidence of induced proarrhythmia and heart failure, moricizine is selected as the next drug in line. All other class I antiarrhythmic drugs either have been shown to have the potential for increasing sudden cardiac death or have major rates of noncardiac adverse effects or organ toxicity that preclude their use in these patient groups except in special circumstances. In patients with malignant ventricular arrhythmias who present with hemodynamic consequences such as syncope or worse, moricizine also is preferred as an initial drug for consideration. When compared to drugs with class IA and IB action, moricizine has comparable efficacy yet lower rates of noncardiac adverse effects, organ toxicity, proarrhythmia and heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Current approaches to drug treatment of ventricular arrhythmias

Ventricular arrhythmias are common and cause serious problems, ranging from symptom aggravation to sudden cardiac death. New knowledge about arrhythmias and new antiarrhythmic drugs provide greater opportunities for treatment choice and evaluations. A prognostic classification of ventricular arrhythmias helps to focus management. For benign ventricular arrhythmias, the objective of drug treatment is alleviation. The best management approach to potentially malignant ventricular arrhythmias, however, is not yet known, and data from ongoing clinical studies continue to accrue, developing the knowledge base needed to devise better regimens. Symptomatic patients can be managed either by symptom alleviation, as in benign arrhythmia, or more aggressively, as in malignant ventricular arrhythmia. Treatment is not mandatory for asymptomatic patients with potentially malignant ventricular arrhythmias, because there is no evidence that reducing arrhythmia prolongs life or effectively prevents symptomatic disease. Also, antiarrhythmic drugs have the potential for causing adverse effects, even lethal ones. For malignant ventricular arrhythmia, the objective of treatment is prevention of symptomatic ventricular arrhythmia and sudden cardiac death. Effective new methods predictive of successful drug treatment in individual patients are available; these methods remove much of the empiricism from management of patients with malignant ventricular arrhythmia. Treatment deemed effective by rigorous noninvasive evaluation or by electrophysiologic studies has a high probability of success in the long term. Drug management of malignant ventricular arrhythmia should become more effective in the future as a result of newly developing approaches to drug evaluation.     

QTc interval in the assessment of cardiac risk

In the United States alone 300,000–400,000 people die of sudden cardiac death every year. Muchof this mortality is assumed to be caused by ventricular tachyarrhythmias. Prolonged QTc reflect cardiacrepolarization prolongation and/or increased repolarization inhomogenity known to be associated withincreased risk of arrhythmias. The paper gives a review of the possibilities to assess the risk ofventricular arrhythmia and/or cardiac death from QTc. Prolonged QTc may hold independent prognosticimportance for mortality in common diseases as ischemic heart disease and diabetes mellitus where as theprognostic importance in heart failure and arterial hypertension is more uncertain. In more rare diseases asthe inborn long QT syndrome the QT interval gives not only important hint to the diagnosis but the magnitudealso provides information on prognosis. QTc has probably no independent prognostic importance in hypertrophiccardiomyopathy or in the arrhythmogenic right ventricular disease. The degree of QTc prolonging duringtreatment with QTc prolonging drugs is prognostic for the risk of ventricular arrhythmia in form of torsadede pointes and QTc prolonging drugs should probably not be prescribed for patients with a QTc greater than460 ms and withdrawn if QTc exceeds 500 ms during treatment. Data from the DIAMOND study suggest that QTc canbe used to point out those heart failure patients who will benefit from antiarrhythmic therapy.     

Significance and control of cardiac arrhythmias in patients with congestive cardiac failure

A wide spectrum of ventricular and supraventricular tachyarrhythmias occurs in the setting of congestive cardiac failure. However, the two most clinically significant are atrial fibrillation and ventricular tachycardia and fibrillation.In the past there has been much emphasis on premature ventricular contractions and more recently, on nonsustained ventricular tachycardia. For the most part, these arrhythmias are asymptomatic in heart failure. They are markers of sudden arrhythmic death but their suppression by antiarrhythmic drugs have not resulted in a reduction of total mortality. Two approaches have been used to this end. The first is the use of beta-adrenergic blocking drugs and antiarrhythmic agents such as amiodarone. Beta-blockers have been shown to significantly reduce sudden death as well as total mortality, while the effects of amiodarone have been less decisive. The prospective role of the implantable cardioverter defibrillator (ICD) is undergoing critical evaluation in patients with cardiac failure at high risk for sudden death. The elective role of the ICD is well established as first-line therapy in patients with heart failure resuscitated from sudden death and in those with sustained ventricular tachycardia in conjunction with conventional therapies for cardiac decompensation.The prevalence of atrial fibrillation rises as a function of severity of cardiac failure, but it is also in known that persistent atrial fibrillation with an uncontrolled ventricular response may induce heart failure. Controlled ventricular response may prevent congestive heart failure and improve left ventricular function. The two most common causes of atrial fibrillation in cardiac failure in Europe and America are ischemic heart disease and hypertension, while mitral valve disease remains the prevalent cause elsewhere. The choice of antiarrhythmic drugs for maintaining sinus rhythm is critical in the prevention of heart failure aggravation and proarrhythmic reactions of antiarrhythmic drugs. Amiodarone and dofetilide are most widely used in this context.     

Evaluation of antiarrhythmic therapy using Holter monitoring

Premature ventricular complexes and nonsustained ventricular tachycardia mark a person with structural cardiac disease as a high--risk candidate for sudden cardiac death. Such ventricular arrhythmias are considered potentially lethal and should be distinguished from both those that are benign and those that cause hemodynamic consequences (i.e., lethal or malignant arrhythmias). Noninvasive Holter monitoring is the principal technique for detecting and evaluating the presence of potentially lethal ventricular arrhythmias. These arrhythmias undergo a high degree of spontaneous variability. Thus, to define a therapeutic drug effect, a reduction in the frequency of premature ventricular complexes of at least 75% and a reduction in the frequency of nonsustained ventricular tachycardia by at least 90% are required to eliminate the likelihood of spontaneous variability as the cause of this change in the frequency of arrhythmia. To define proarrhythmia, a different algorithm must be applied. When using antiarrhythmic drugs, a quantitative ventricular arrhythmia baseline for both frequency and type of arrhythmia must be established so that after therapeutic intervention repeat Holter monitoring can determine whether efficacy, inefficacy or proarrhythmia had occurred. Holter monitoring clearly reveals differential antiarrhythmic response rates among classes of antiarrhythmic drugs in patients with benign or potentially lethal arrhythmias. However, preliminary data have not clearly defined the relation between antiarrhythmic pharmacotherapy and a reduction in sudden cardiac death. The results of large-scale clinical trials that have only recently been undertaken must be assessed to determine whether sudden cardiac death can be prevented by adequately suppressing potentially lethal ventricular arrhythmias.     

Comparison of ambulatory electrocardiography and exercise testing

Ambulatory electrocardiography and exercise testing are two noninvasive diagnostic procedures widely employed to evaluate patients for cardiac arrhythmias and S-T segment changes. This review addresses the differences and similarities of the two techniques, and examines the relative diagnostic and prognostic merit of the arrhythmia and S-T segment changes detected with each method.

Ambulatory electrocardiography is more sensitive than exercise testing in detecting cardiac arrhythmias. The recording of ventricular arrhythmia is of value in predicting sudden death in survivors of myocardial infarction, whereas exercise-induced ventricular arrhythmia has limited predictive value. Nevertheless, exercise-induced S-T depression is of great prognostic value in predicting mortaliy and sudden death in patients wlth acute and chronic coronary heart disease.     

Arrhythmias in heart failure: current concepts of mechanisms and therapy

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.     

Genesis of arrhythmias in the failing heart and therapeutic implications

Between 50 and 70% of patients with heart failure die suddenly and unexpectedly before they have deteriorated to New York Heart Association class IV symptoms. It has long been known that ventricular ectopy predicts sudden cardiac death in coronary heart disease, and this has also been shown in dilated cardiomyopathy. It is less certain whether antiarrhythmic drugs reduce this risk and improve prognosis. Supraventricular arrhythmias frequently develop in heart failure of all causes. They nearly always cause symptoms, and the establishment of atrial fibrillation may mark a permanent deterioration. Except for sustained ventricular tachycardia, ventricular arrhythmias are often occult. Hypokalemia and digitalis toxicity may have been precipitated by diuretics or interaction with antiarrhythmic drugs. In coronary heart failure, arrhythmias may be related to scar tissue or ischemia, which may also be responsible in dilated cardiomyopathy. Use of inotropes and inodilators may precipitate arrhythmias, whereas drugs that conserve energy or potassium, such as beta blockers and angiotensin-converting enzyme inhibitors, may prevent them. Since suppression of ventricular arrhythmias has not been shown to prevent sudden death or prolong life in patients with heart failure, it may be that such arrhythmias do not directly presage ventricular fibrillation except in so far as they are markers of a poor prognosis with a risk of sudden death. If so, such arrhythmias are most likely to be suppressed by agents that result in improvement of left ventricular function and, through that, prolongation of life.     

Ventricular arrhythmia in congestive heart failure.

The importance of ventricular arrhythmia is based on its association with sudden death. In certain groups of patients, ventricular arrhythmia--primarily runs of nonsustained ventricular tachycardia (NSVT)--is associated with an increased risk for sudden death. Although this relationship has been most often reported in patients with recent myocardial infarction, it has also been recognized in patients with dilated cardiomyopathy, regardless of etiology. Therefore, ventricular arrhythmia is common in patients with CHF due to cardiomyopathy. A number of studies have reported that 70-95% of patients with cardiomyopathy and congestive heart failure (CHF) have frequent ventricular premature beats, and 40-80% will manifest runs of NSVT. Many factors are responsible for ventricular arrhythmia in such patients, including structural abnormalities, electrolyte imbalance, hemodynamic impairment, activation of neurohormonal mechanisms, and pharmacologic therapy. Many studies have reported a high yearly mortality in patients with cardiomyopathy and CHF; greater than 40% of deaths are sudden, most often the result of sustained ventricular tachyarrhythmia. Most studies have noted an association between presence (and frequency) of NSVT and risk of sudden cardiac death in these patients. Unfortunately, other techniques--such as the signal-averaged electrocardiogram and electrophysiologic testing--are not helpful in identifying the individual at risk. Although several drug interventions will reduce mortality from progressive CHF, these drugs have not been shown to reduce sudden death and, indeed, have a variable effect on ventricular arrhythmia. Although NSVT is a marker for increased risk for sudden death, it is uncertain if antiarrhythmic drugs will prevent this outcome. Antiarrhythmic drugs have not been shown to be effective for preventing sudden death, although there are as yet no well-controlled randomized trials. Several studies suggest that amiodarone and beta blockers are beneficial, but this requires confirmation. For patients who have been resuscitated following an episode of sudden death due to a sustained ventricular tachyarrhythmia, antiarrhythmic therapy guided by invasive and noninvasive techniques appears to reduce risk of recurrent arrhythmia. However, the response rate to antiarrhythmic agents is low and side effects are common in patients with CHF. Especially important is the increased risk of precipitating CHF and aggravating the arrhythmia being treated. For many such patients who have had serious ventricular tachyarrhythmia, the automatic implantable cardioverter defibrillator may prove a better option. Other drugs used for management of CHF reduce overall mortality, but not risk of sudden death.     

The Role of EP-Guided Therapy in Ventricular Arrhythmias: Beta-Blockers,Sotalol, and ICD's

Arrhythmic death can be reduced by antiarrhythmic drugs to a range of 2—4%. Electrophysiologic study by testing noninducibility of ventricular arrhythmia represents the classic method for evaluating the effectiveness of drug therapy.Several clinical studies have shown thaat sotalol suppresses VT induction and prevents arrhythmias recurrences at long term follow-up in 23% to 67% of patients. The efficacy of sotalol EP guided therapy in preventing VT/VF is not necessarily related to prevention of sudden death. In the ESVEM study the superiority of d,l-sotalol to other antiarrhythmic drugs was confirmed. The response to programmed ventricular stimulation was found to be strongly predictive for arrhythmia free state while the failure of sotalol therapy to suppress VT at the EP study was associated with an high recurrence rate (40%). However, EP study failes to predict freedom from sudden death. The beta-blocking activity of racemic sotalol may account for some of the observed survival benefit.Beta-blockers therapy reduces mortality in patients after myocardial infarction primarily by a reduction of sudden death. A reduction of death, worsening heart failure and life threatening ventricular arrhythmias was shown in a recent study on carvedilol. In the prospective study of Steinbeck the EP guided-therapy did not improve the overall outcome when compared to metoprolol. Suppression of inducible arrhythmias by antiarrhythmic drugs was associated with a better outcome. The effectiveness of defibrillator therapy in reducing overall mortality, has been uncertain since great clinical trials have been concluded. MADIT, AVID and CASH trials confirmed the superiority of ICD therapy over antiarrhythmic drugs therapy: ICD should be considered the first choice therapy in post-cardiac arrest patients.The ongoing BEST Trial will give us further responses about the interaction between EP study and metoprolol effect compared to ICD in patients post myocardial infarction also focusing on tolerability and compliance of the beta-blocking therapy in patients with low ejection fraction. In this study will be useful to optimize therapy in patients at high risk of sudden death     

Arrhythmogene rechtsventrikuläre Kardiomyopathie

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetically determined heart muscle disease and a major cause of sudden cardiac death and ventricular tachyarrhythmia in young, apparently healthy individuals and athletes. Patients affected by ARVC should be excluded from competitive sports and vigorous training. To provide optimal treatment, early diagnosis and risk stratification are mandatory and genetic counseling of families is recommended. Tailored treatment strategies aim at the prevention of ventricular tachyarrhythmia and sudden death as well as the preclusion of disease progression and symptomatic heart failure. Patients with a low risk of sudden death need either no specific treatment or can be treated with beta blockers or antiarrhythmic drugs, depending on the clinical manifestation of the arrhythmia. Catheter ablation in ARVC constitutes a symptom-oriented and palliative approach for frequently relapsing ventricular tachycardia refractory to antiarrhythmic medication. However, despite good acute results of catheter ablation, there is a high incidence of recurrence during long-term follow-up. In patients with ARVC at high risk of sudden death, implantation of an implantable cardioverter defibrillator (ICD) improves long-term survival by detection and termination of life-threatening ventricular arrhythmias. In the long term, however, the cumulative incidence of mainly lead-related complications of ICD therapy must be considered in the young population with ARVC, particularly when the indications are for primary prevention of sudden death or life-threatening arrhythmias. The proposed algorithm of therapeutic management in ARVC is under constant validation, development and refinement.     

Implantable cardioverter defibrillator: a review.

Sudden cardiac death claims 400,000 to 450,000 lives annually. It is believed that sudden cardiac death results predominantly from ventricular fibrillation or sustained ventricular tachycardia that deteriorates into ventricular fibrillation. Conventional treatments for patients who suffer from ventricular arrhythmias have been limited to antiarrhythmic drugs or surgery. These treatments have proved ineffective to a portion of arrhythmia sufferers. The implantable cardioverter defibrillator offers hope to a segment of ventricular arrhythmia sufferers whose disease is resistant to conventional therapies.     

Antiarrhythmic Drug Therapy for Ventricular Arrhythmias: Current Perspectives

Antiarrhythmic Drug Therapy. Pharmacologic therapy for ventricular arrhythmias has undergone a remarkable change recently. Recognition of the importance of underlying structural heart disease on prognostic implications of ventricular arrhythmias has resulted in the refinement of the clinical classification of these arrhythmias. With refinement of techniques of risk stratification, it is now possible to identify patients with ventricular arrhythmias at high risk for sudden death. Retrospective analyses of prior antiarrhythmic drug trials and new data from prospective randomized trials are now available and can more directly define the risks and benefits of antiarrhythmic therapy. Prevention of sudden death, reduction in total mortality, or improvement in symptoms remain the only benefits of antiarrhythmic drugs. With inclusion of total mortality as the major endpoint for assessment of pharmacologic interventions in high-risk patients, the potential for excess mortality due to antiarrhythmic agents is now recognized. The pharmacologic diversity of newly released antiarrhythmic agents and others under development has resulted in a re-evaluation of the traditional classification of these drugs. Multiple ongoing clinical trials will define the risks and benefits of antiarrhythmic therapy and other nonpharmacologic interventions in patients with ventricular arrhythmias.     

The Clinical Significance of Nonsustained Ventricular Tachycardia

Nonsustained Ventricular Tachycardia. Nonsustained ventricular tachycardia (NSVT) is an arrhythmia not often associated with symptoms; however, its occurrence in patients with structural heart disease is a prognostic indicator of an increased risk of mortality and sudden death. The management of asymptomatic patients with NSVT should first attempt to identify which patients are at highest risk for cardiac arrest, and second, devise a treatment that can reduce the incidence and/or mortality of cardiac arrest in this group. In patients with chronic coronary artery disease (CAD) and NSVT, programmed electrical stimulation identifies both a low and high risk group with respect to occurrence of ventricular arrhythmias. The negative predictive value of programmed electrical stimulation in patients with CAD and NSVT has been well established; however, uncertainty remains as to the optimal therapy for CAD patients with inducible ventricular arrhythmias. A number of reports suggest that patients whose inducible ventricular arrhythmias are rendered noninducible with antiarrhythmic drugs have a much lower risk of sudden death. It is yet to be resolved whether arrhythmias rendered noninducible identify a subgroup at low risk for cardiac arrest, independent of treatment. There is some evidence to suggest that the frequency of NSVT in patients with nonischemic dilated cardiomyopathy identifies a group at higher risk of sudden death. Programmed electrical stimulation adds little in helping to identify which of these patients are most likely to have cardiac arrest. The presence of NSVT in asymptomatic patients with hypertrophic cardiomyopathy may identify a group at higher risk for cardiac arrest. Further clinical studies are needed to define the best management strategy for NSVT in different types of structural heart disease.     

Antiarrhythmic drugs

Opinion statement Both supraventricular and ventricular arrhythmias are associated with increased mortality and morbidity. Numerous antiarrhythmics have been developed in an attempt to decrease the frequency of these arrhythmias, hoping to improve survival and improve quality of life. Antiarrhythmic agents are a diverse group of drugs that affect various cardiac ionic channels and block specific arrhythmias. However, despite the suppression of these potentially lethal cardiac arrhythmias, only the β blockers have been shown to reduce sudden arrhythmic death, especially in patients with prior myocardial infarction or heart failure. Some antiarrhythmic agents can also worsen the index arrhythmia and caution must be used especially in the compromised patient. A simple guideline is as follows: For conversion of atrial fibrillation or flutter to sinus rhythm, in the absence of structural heart disease, intravenous ibutilide or oral propafenone or flecainide are good choices. For maintenance of sinus rhythm, propafenone or flecainide are logical choices. In the presence of structural heart disease, amiodarone, dofetilide, or dl sotalol are preferred. In heart failure, dofetilide or amiodarone are the logical choices. The role of antiarrhythmic therapy for ventricular arrhythmias is questionable and may be contraindicated, except for the use of β blockers. The implantable cardioverter-defibrillator is often used in patients at high risk. At times, the addition of an antiarrhythmic agent such as amiodarone may be justified.     

Programmed stimulation in patients with malignant ventricular arrhythmias. I: Diagnostic value

Sudden cardiac death is a leading cause of death in industrially developed countries and accounts for approximately 90 000 deaths yearly in the FRG. While the majority of victims have severe coronary heart disease, sudden cardiac death is infrequently caused by acute myocardial infarction (20%) but is predominantly related to malignant ventricular arrhythmias (i.e., ventricular fibrillation or sustained ventricular tachycardia). Patients with a history of such malignant ventricular arrhythmias are at high risk for sudden death. Spontaneous occurrence of sustained ventricular tachycardia and of ventricular fibrillation is critically related to two factors: 1. trigger-arrhythmias consisting usually of complex ventricular extrasystoles (Lown classification IV to V); 2. increased vulnerability of the myocardium representing the target organ for trigger-arrhythmias. While trigger-arrhythmias can be easily recorded by noninvasive techniques including Holter monitoring or exercise and stress ECG, ventricular vulnerability is more difficult to determine and often requires ventricular stimulation with intracardiac electrocatheters. In patients with documented spontaneous malignant ventricular arrhythmias, two aspects of programmed stimulation must be considered: 1. diagnostic, and more importantly, 2. therapeutic purposes of this method. Diagnostic purposes include determination of the mode of initiation and unequivocal ventricular localization of the tachycardia excluding other arrhythmias with broad QRS complex. In patients with spontaneous sustained ventricular tachycardia, programmed stimulation can reproducibly initiate the clinical arrhythmia in 85% (sensitivity and specificity of the method approximately 90%). In patients with cardiac arrest due to ventricular fibrillation, programmed stimulation is less reliable (50%). However, the main purpose of programmed stimulation in patients with documented clinical malignant arrhythmias is not diagnostic or prognostic evaluation but is serial electrophysiological studies for individual optimization of antiarrhythmic therapy.     

Treatment of choice and long-term prognosis for ventricular arrhythmias

Treatment of choice and long-term prognosis of the patients with ventricular arrhythmias are described in terms of prevention of sudden cardiac death and/or recurrence of life-threatening arrhythmias(ventricular tachycardia and ventricular fibrillation). 1) As to the long-term prognosis of ventricular tachyarrhythmias, presence of organic heart disease and degree of cardiac dysfunction are major determining factors. 2) The prognosis of patients with ventricular arrhythmias depends on how sudden cardiac death and life-threatening arrhythmias can be prevented. Among various methods, the electrophysiological test and its guided-therapy for antiarrhythmic drugs are now believed to be the most effective method for the prediction and prevention of the life-threatening events. We propose that the signal averaged electrocardiography is the best screening method as non-invasive approach for the selection of patients undergoing the electrophysiological test. 3) There are still certain limitations as to the prediction of sudden cardiac death and/or prevention of recurrent life-threatening arrhythmias by antiarrhythmic drug treatments in the certain numbers of patients depending on their basal cardiac disease and functional impairment. At present, catheter ablation procedure and implantable cardioverter defibrillator are the choice of the treatment in these cases. 4) In addition to conventional antiarrhythmic drugs, the treatment for the basal cardiac condition is mandatory for the long-term prognosis in the patients with ventricular arrhythmias.     

Treatment of ventricular arrhythmias

Within the past 20 years, our knowledge concerning the epidemiology, natural history, and treatment of VT has expanded greatly. A variety of effective pharmacologic, surgical and electrical therapies for VT are now available to the clinician. Patients who present with ventricular, tachyarrhythmias should undergo a comprehensive medical evaluation directed at identifying and treating such factors as ischemia, congestive heart failure, valvular heart disease, sensitivity to cardioactive drugs, and metabolic derangements. Many patients who present with asymptomatic ventricular arrhythmias do not require specific antiarrhythmic drug therapy. However, certain patients who have already suffered a life-threatening arrhythmia or who are at high risk for such arrhythmia should be vigorously treated with specific antiarrhythmic therapy guided for that individual patient. The efficacy of any antiarrhythmic treatment should be assessed by ECG monitoring, exercise testing, and/or electrophysiologic study. In the near future, potentially revolutionary new electrical therapies for ventricular tachyarrhythmias will be evaluated. It is to be hoped that these devices used in combination with pharmacologic and surgical therapies may dramatically reduce the incidence of sudden cardiac death in high-risk patients.     

Antiarrhythmic effects of beta-adrenergic blocking agents in benign or potentially lethal ventricular arrhythmias

Classification of ventricular arrhythmias into those that are benign, potentially lethal and lethal is based on their associated risk for producing sudden cardiac death. This classification system is useful in defining indications for the treatment of ventricular arrhythmias and predicting differential rates of antiarrhythmic drug efficacy and toxicity. Whether the reduction of potentially lethal ventricular arrhythmias will prevent sudden cardiac death remains to be determined. The class II antiarrhythmic agents--the beta-adrenergic blocking drugs--have been shown to reduce sudden cardiac death in postmyocardial infarction patients, but the precise mechanism of their effect has not been defined. beta blockers are efficacious in approximately 50% of patients with benign or potentially lethal ventricular arrhythmias. This response is comparable to that seen with the class IA agent disopyramide or the class IB agents tocainide and mexiletine. beta blockers have favorable side-effect profiles including a low incidence of proarrhythmia and a lack of organ toxicity such as hepatitis, pulmonary fibrosis or agranulocytosis, which are concerns with class I and class III antiarrhythmic drugs. The proper dosage of the beta blocker is critical in limiting adverse effects. In a study of 23 patients with benign or potentially lethal ventricular arrhythmias, 11 (48%) of the patients responded to nadolol with a reduction of greater than 75% in arrhythmia frequency, and several patients responded at nadolol dosages as low as 10 mg daily. Thus, it is plausible to consider beta blockers as first-choice antiarrhythmic therapy, even in patients with left ventricular dysfunction when sympathetic tone is not required to maintain cardiac compensation.