|
Authors
Philip J Podrid, MD
Leonard I Ganz, MD
Section Editors
Wilson S Colucci, MD
Morton F Arnsdorf, MD, MACC
Deputy Editor
Susan B Yeon, MD, JD, FACC
INTRODUCTION — Ventricular arrhythmias, ranging from asymptomatic ventricular premature beats (VPBs) to ventricular fibrillation (VF), are common in patients with heart failure (HF) and cardiomyopathy [1-3]. These arrhythmias fall into two broad categories:
* Malignant or potentially lethal arrhythmias, including sustained ventricular tachycardia (VT) and VF.
* Nonsustained or hemodynamically tolerated arrhythmias, including VPBs, nonsustained ventricular tachycardia (NSVT), and accelerated idioventricular rhythm (AIVR). The clinical significance of these arrhythmias is largely based upon whether or not they predict future malignant arrhythmias and sudden cardiac death (SCD).
The prognostic significance of VPBs and NSVT varies with the etiology of the cardiomyopathy. In patients with left ventricular (LV) systolic dysfunction due to prior myocardial infarction (MI), VPBs and NSVT are associated with an increased risk of SCD. In contrast, in most other forms of cardiomyopathy (eg, nonischemic cardiomyopathy or valve disease), these arrhythmias do not appear to predict SCD [4]. (See "Ventricular premature beats in patients with a prior myocardial infarction" and "Prognosis of nonsustained VT in the presence of structural heart disease".)
The types of ventricular arrhythmias in patients with HF or cardiomyopathy, the effect of HF therapy on these arrhythmias, and the role of electrophysiologic testing will be reviewed here. The secondary and primary prevention of SCD in these patients, including a review of the causes of death in HF, and the importance of ventricular arrhythmias in other causes of cardiomyopathy, such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, are discussed separately. (See "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Ventricular arrhythmias and sudden cardiac arrest in hypertrophic cardiomyopathy" and "Treatment and prognosis of arrhythmogenic right ventricular cardiomyopathy".)
TYPE OF ARRHYTHMIA
Ventricular premature beats — Ventricular premature beats (VPBs) occur in 70 to 95 percent of patients with HF, and they may be frequent and complex [5-8]. Among patients with cardiomyopathy, VPBs may be clinically significant for the following reasons:
* VPBs may be predictors of more malignant arrhythmias and sudden cardiac death (SCD). In patients with a prior myocardial infarction (MI), VPBs are associated with an increased risk of death. In contrast, VPBs do not appear to be associated with a worse prognosis in patients with nonischemic cardiomyopathy, although data are limited [4]. Regardless of the etiology of the cardiomyopathy, there is no role for pharmacologic suppression of VPBs for the purpose of reducing the risk of malignant arrhythmias or SCD. (See "Ventricular premature beats in patients with a prior myocardial infarction" and "Clinical significance and treatment of ventricular premature beats".)
* VPBs can cause symptoms, usually palpitations. Symptoms are generally mild, and most patients require no specific therapy. Beta blockers can help to control symptoms, but most patients with HF and cardiomyopathy already have an indication for a beta blocker. (See "Use of beta blockers in heart failure due to systolic dysfunction".)
Because of the proarrhythmic risks of antiarrhythmic drugs other than beta blockers, these medications are not used in the routine treatment of VPBs. In the rare circumstance in which a patient is severely symptomatic despite beta blockers, amiodarone or dofetilide appear to be safe in patients with HF. (See "Clinical significance and treatment of ventricular premature beats", section on 'Treatment'.)
* In rare cases, very frequent VPBs cause or exacerbate LV dysfunction. This was illustrated in a report of 14 patients with dilated cardiomyopathy, a left ventricular ejection fraction (LVEF) ≤40 percent, and more than 20,000 VPBs in 24 hours (14 VPBs/min) [9]. All patients had been treated with standard medical therapy for HF. Seven patients received additional medical therapy (mostly amiodarone), five of whom, all with idiopathic dilated cardiomyopathy, had at least a 75 percent reduction in VPB frequency (baseline value 37,334 VPBs in 24 hours or 26 VPBs/min). These patients had a significant and marked improvement in LVEF at six months (49 versus 27 percent at baseline). In contrast, an increase in LVEF was not noted in the remaining patients who did not have such a reduction in VPB frequency (9 percent increase to 37 percent reduction).
Among the five responders, only one received a new medical therapy (a beta blocker) that might have improved left ventricular function. This makes it less likely that the improvement in LVEF was the primary event, leading to a secondary reduction in VPBs. Thus, in some patients with very frequent VPBs, a trial of amiodarone to assess possible improvement in LVEF may be beneficial as an addition to routine beta blocker therapy.
* Similarly, catheter ablation of very frequent VPBs may improve left ventricular function in patients with nonischemic cardiomyopathy. This was illustrated in a nonrandomized study in which VPBs (mean 21 percent of QRS complexes) were successfully ablated in 18 of 22 patients with reduced LVEF [10]. In these patients, mean LVEF increased from 34 to 59 percent. The four patients in whom ablation was unsuccessful experienced further deterioration in LVEF, from 34 to 25 percent, during follow-up.
Nonsustained ventricular tachycardia — Runs of nonsustained ventricular tachycardia (NSVT) have been observed on ambulatory monitoring in 50 to 80 percent of patients with HF or cardiomyopathy [5,8,11]. The clinical significance of NSVT can be considered in a similar manner to that of VPBs:
* NSVT may be predictive of future malignant arrhythmias and mortality. An association between NSVT and mortality has been shown in patients with ischemic and hypertrophic cardiomyopathy, but not in most other forms of cardiomyopathy. (See "Prognosis of nonsustained VT in the presence of structural heart disease".)
There is generally no role for the pharmacologic suppression of NSVT for the purpose of reducing the risk of malignant arrhythmias or sudden cardiac death. However, NSVT can be an indication for electrophysiology study and possible implantable cardioverter-defibrillator (ICD) therapy in selected patients with a prior MI and ischemic cardiomyopathy, and for an ICD in selected patients with hypertrophic cardiomyopathy. (See "Management of nonsustained ventricular tachycardia", section on 'Prevention of SCD' and "Role of implantable cardioverter-defibrillators for the primary prevention of sudden cardiac death after myocardial infarction", section on High-riks patients.) (See "Ventricular arrhythmias and sudden cardiac arrest in hypertrophic cardiomyopathy", section on 'High-risk clinical features'.)
* NSVT is often asymptomatic, but some patients experience palpitations, lightheadedness, presyncope, or dyspnea. Because many of the symptoms that may be attributed to NSVT are vague and nonspecific, it is important to try to correlate symptoms to episodes of NSVT before initiating therapy. In patients with symptoms due to NSVT, options include beta blockers, for which most patients already have an indication, catheter ablation, and, in rare cases of severe and refractory symptoms, amiodarone or dofetilide. (See "Management of nonsustained ventricular tachycardia".)
* In rare cases, very frequent NSVT can contribute to or exacerbate LV dysfunction.
Accelerated idioventricular rhythm — An accelerated idioventricular rhythm (AIVR), which has also been called "slow VT," arises below the atrioventricular node and has, by definition, a rate between 50 and 100 or 120 beats/min (figure 1). In patients with sinus node dysfunction, AIVR can be an escape rhythm, while in other cases it reflects an abnormal ectopic focus in the ventricle that competes with the sinus node. In either case, AIVR is accelerated by sympathetic stimulation and circulating catecholamines.
AIVR occurs in approximately 8 percent of patients with HF or cardiomyopathy [12]. It also occurs in up to 50 percent of patients during an acute MI. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction", section on 'Accelerated idioventricular rhythm'.)
Most episodes of AIVR are transient and require no treatment. Furthermore, pharmacologic treatment is CONTRAINDICATED if AIVR is an escape rhythm, since suppression of the pacemaker focus can result in asystole. Patients with symptomatic AIVR due to sinus node dysfunction may benefit from atrial pacing. There are no convincing data linking AIVR to sustained VT or VF [12].
Sustained VT or VF — In contrast to the high prevalence of VPBs and NSVT in patients with HF or cardiomyopathy, sustained VT is unusual, occurring in ≤5 percent of patients [5,8,11]. Patients with spontaneous sustained VT are at high risk for SCD [13,14].
Patients with HF or cardiomyopathy who are survivors of SCD due to unstable VT or VF, and have stable sustained VT are typically treated with an ICD for secondary prevention. The supporting data are presented separately. (See "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy".)
Electrical storm — Electrical storm, also referred to as VT storm or arrhythmic storm, refers to multiple recurrences of ventricular arrhythmias (VT or VF) over a short period of time (eg, three or more episodes during a 24 hour period). This is a relatively rare phenomenon, and both terminology and definitions vary. Electrical storm is most commonly associated with acute MI and coronary artery disease, but can also develop in patients with dilated cardiomyopathy.
The incidence of electrical storm appears to be higher among patients receiving ICDs for secondary prevention than among those receiving ICDs for primary prevention. Implications and treatment of electrical storm are discussed separately (see "Implantable cardioverter-defibrillators: Complications", section on 'Electrical storm' and "Role of implantable cardioverter-defibrillators for the secondary prevention of sudden cardiac death", section on 'Adjunctive therapy'.
SYNCOPE — Syncope in the setting of severe cardiomyopathy and HF requires special consideration. Although these patients may have syncope due to any of the usual causes, they are more likely than other patients to have an arrhythmic etiology. Thus, syncope in this population requires careful evaluation.
Etiology — Evaluating and managing syncope in HF patients is complicated by the variety of potential etiologies:
* Syncope may be due to a poorly tolerated but transient arrhythmia. Although both bradyarrhythmias and tachyarrhythmias can occur in any patient, those with HF and cardiomyopathy have a higher incidence of these arrhythmias.
* HF patients can experience syncope or near-syncope due to medications or hemodynamic abnormalities related to their underlying cardiac disease.
* Syncope can be due to any of the etiologies found in other patients [15]. (See "Pathogenesis and etiology of syncope".)
Thus, HF patients who experience a syncopal event should undergo a thorough evaluation. This evaluation often includes an electrophysiology study, both to exclude the possibility of a bradyarrhythmic cause and to attempt to induce ventricular arrhythmias. Patients in whom no etiology of syncope is found are said to have unexplained syncope. (See 'Role of EP testing' below and "Evaluation of syncope in adults".)
Prognosis — Syncope is associated with an increased risk of SCD in patients with HF and cardiomyopathy, even if an arrhythmic cause cannot be identified [16-19]. The following observations illustrate the range of findings:
* One report evaluated 491 patients with NYHA class III to IV HF due to nonischemic cardiomyopathy who had a mean LVEF of 20 percent (table 1) [16]. At a mean follow-up of one year, the SCD rate was significantly increased in patients with syncope (45 versus 12 percent in those without syncope).
* In studies in which an ICD was placed because of unexplained syncope or near syncope, there was a high rate of appropriate ICD shocks [17-19]. At follow-up ranging from 1.5 to 3 years, 30 to 40 percent received appropriate shocks for VT or VF. One of these series consisted of 14 patients with syncope, a mean LVEF of 26 percent, a negative electrophysiology study; seven had appropriate shocks at a mean follow-up of two years [19].
ICD therapy — The role of ICD therapy in patients with syncope and heart failure and/or cardiomyopathy is discussed separately. (See "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy", section on 'Patients with syncope'.)
EFFECT OF HF THERAPY ON VENTRICULAR ARRHYTHMIA — Patients with HF and ventricular arrhythmias should have their HF treated aggressively [20]. (See "Overview of the therapy of heart failure due to systolic dysfunction".)
Standard therapy for HF due to systolic dysfunction consists of the following:
* A beta blocker
* An angiotensin converting enzyme (ACE) inhibitor
* An angiotensin II receptor blocker (ARB) in selected patients
* An aldosterone antagonist in selected patients
In addition, digoxin and occasionally other inotropic agents are used for symptom control, while diuretics are given for congestive symptoms. Many of these drugs can affect the incidence of arrhythmic death in patients with HF or cardiomyopathy.
Beta blockers — A substantial part of the survival benefit seen with beta blockers in patients with HF is due to a significant reduction in SCD [21-23]. In the MERIT-HF trial, for example, there were significantly fewer SCDs (3.9 versus 6.6 percent) and fewer deaths from worsening of HF (1.5 versus 2.9 percent) with metoprolol compared to placebo [21]. The proportion of SCDs decreased and those due to HF increased with increasing severity of HF. In CIBIS-II, the survival benefit from beta blocker therapy was primarily due to a reduction in SCD (3.6 versus 6.3 percent), with only a nonsignificant trend toward fewer deaths from HF. (See "Use of beta blockers in heart failure due to systolic dysfunction".)
ACE inhibitors and ARBs — ACE inhibitors improve survival in all stages of HF. However, there are conflicting data as to whether ACE inhibitors reduce SCD. Some major trials — CONSENSUS, SOLVD, and SAVE — found that the survival benefit was primarily due to slowed progression of HF, with little or no reduction in SCD [24-27], while others — V-HeFT II, TRACE, and AIRE — showed a significant reduction in SCD [28-31].
A meta analysis of trials of 15,104 patients within 14 days of an acute MI found that ACE inhibitor therapy modestly but significantly reduced the risk of SCD (odds ratio 0.80, absolute benefit about 1.4 percent) [32]. However, as noted above, 45 percent of patients who died suddenly in AIRE had severe or worsening HF prior to their death, and only 39 percent of sudden deaths were thought to be due to arrhythmia [28]. (See "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use", section on Effect on sudden death.)
The ARBs appear to be as or perhaps slightly less beneficial than ACE inhibitors in patients with HF [33]. The major ARB trial CHARM noted a clear survival benefit but did not report data on SCD [34]. ELITE II, which directly compared losartan to captopril, found a higher rate of SCD with losartan that was not statistically significant [33]. This might suggest that ARBs alone are unlikely to have a major impact on SCD in HF patients.
On the other hand, the addition of ARB to ACE inhibitor therapy in patients with HF in the CHARM-Added trial was found to reduce the rate of SCD as well as the rate of death from worsening heart failure [35]. (See "Angiotensin II receptor blockers in heart failure due to systolic dysfunction: Therapeutic use", section on 'CHARM-Added'.)
Aldosterone antagonists — The aldosterone antagonists spironolactone and eplerenone significantly reduce overall mortality and SCD in patients with advanced HF [36,37]. They also reduce the frequency of VPBs and NSVT [38]. These benefits may reflect a reduction in aldosterone effect on the heart and/or the maintenance of a higher serum potassium concentration. Patients treated with these drugs must be monitored carefully because of the risk of hyperkalemia, which is magnified by the concurrent presence of decreased renal perfusion and angiotensin inhibition [39]. (See "Use of diuretics in heart failure", section on 'Mechanisms of benefit'.)
Digoxin and other inotropes — Digoxin is an effective drug for reducing the symptoms from HF. The DIG trial demonstrated that digoxin, compared to placebo, produced a significant reduction in hospitalizations but had no net benefit on mortality (graph 1) [40]. Although digoxin significantly reduced mortality from pump failure, this was offset by an apparent increase in mortality from arrhythmia that was not statistically significant.
However, the outcome varied significantly with the serum digoxin concentration [41]. All-cause mortality at 37 months in men was significantly lower for those with a serum digoxin concentration of 0.5 to 0.8 ng/mL compared to placebo (29.9 versus 36.2 percent); in comparison, mortality was increased in men with a serum digoxin concentration above 1.2 ng/mL (graph 2). (See "Use of digoxin in heart failure due to systolic dysfunction", section on 'Optimal digoxin level'.)
A proarrhythmic effect has also been noted with other inotropic agents used for the treatment of HF including beta adrenergic agonists and phosphodiesterase inhibitors, such as milrinone [42]. (See "Inotropic agents in heart failure due to systolic dysfunction".)
Statins — Observational and retrospective data suggest that statins might be of benefit in patients with HF and cardiomyopathy, regardless of the presence of coronary artery disease. The possible mechanisms of benefit, other than treatment of coronary disease that may have been unrecognized, are not known. Statins have a variety of lipid-independent (pleiotropic) effects that could contribute to improved outcomes. (See "Mechanisms of benefit of lipid lowering drugs in patients with coronary heart disease".)
The potential impact of statins on the incidence of SCD in patients with nonischemic cardiomyopathy was illustrated in a retrospective analysis of patients in the DEFINITE trial [43]. Among the 458 patients enrolled, 110 were receiving statin therapy at the time of their first event or at the conclusion of the trial. Patients treated with a statin had significantly lower rates of arrhythmic sudden death and total mortality compared to those not treated with a statin (0.9 versus 5.2 percent and 4.5 versus 18.4 percent, respectively). Larger randomized trials that should provide more definitive data on the role of statins in nonischemic cardiomyopathy are underway.
ROLE OF EP TESTING — Electrophysiology (EP) testing can serve several purposes in patients with HF and cardiomyopathy:
Diagnosis — EP testing can demonstrate the mechanisms of induced or spontaneous arrhythmias and characterize the function of the sinus node, the AV node, and the His-Purkinje system. Thus, EP testing can assist in the diagnosis of unexplained symptoms (eg, palpitations or syncope) and arrhythmias.
The 2006 ACC/AHA/ESC guidelines for the management of ventricular arrhythmias recommend EP study in patients with HF or cardiomyopathy patients with one or more of the following [20]:
* Sustained palpitations
* Presyncope or syncope for which there is not a clear explanation
* A wide QRS complex tachycardia of uncertain etiology
* Bundle branch reentrant tachycardia, both to confirm the diagnosis and to guide ablation in patients with nonischemic cardiomyopathy
In addition, the weight of evidence was considered to support (a weaker recommendation) EP testing for risk stratification in patients with a remote myocardial infarction, nonsustained ventricular tachycardia, and a left ventricular ejection fraction less than or equal to 40 percent. However, post-MI patients with an LVEF less than or equal to 30 percent fulfill MADIT-II criteria for implantable cardioverter-defibrillator (ICD) placement without requiring EP testing [44].
Risk stratification — The ability to induce ventricular arrhythmias during EP testing is associated with an increased risk of arrhythmic events and SCD in patients with a prior MI and LV dysfunction. For this reason, EP testing is used in some post-MI patients with moderate LV dysfunction (eg, LVEF 31 to 40 percent) to determine if they are candidates for an ICD. (See "Incidence of and risk stratification for sudden cardiac death after acute myocardial infarction".)
Post-MI patients with severe LV dysfunction (LVEF ≤30 percent), or advanced HF (NYHA class II or III), are considered to be at a high enough risk of SCD that ICD implantation is recommended without the need for an EP study. (See "Role of implantable cardioverter-defibrillators for the primary prevention of sudden cardiac death after myocardial infarction" and "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy".)
The ability to induce ventricular arrhythmias is not predictive of SCD risk in patients with nonischemic cardiomyopathy. Thus, EP testing does not have a role in risk stratification in these patients.
PREVENTION OF SCD — Secondary and primary prevention of sudden cardiac death in HF and cardiomyopathy, often with an implantable cardioverter-defibrillator, is discussed separately. (See "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy".)
SUMMARY AND RECOMMENDATIONS
Types of ventricular arrhythmia — Heart failure (HF) and cardiomyopathy are associated with a variety of ventricular arrhythmias. These include ventricular premature beats and nonsustained ventricular tachycardia, which are the most common, and accelerated idioventricular rhythm, and sustained ventricular tachycardia or ventricular fibrillation. (See 'Type of arrhythmia' above.)
VPBs — VPBs are present in many patients with HF, but symptoms are generally absent or mild and most patients do not require specific therapy. Possible therapy for VPBs varies with the clinical setting and is considered only for symptoms or VPBs that might depress left ventricular ejection fraction (LVEF). There is no role for pharmacologic suppression of VPBs for the purpose of reducing the risk of malignant arrhythmias or sudden cardiac death. (See 'Ventricular premature beats' above.)
* In patients with asymptomatic or mildly symptomatic VPBs, we recommend NOT treating wth antiarrhythmic medications (Grade 1B).
* Beta blockers reduce VBPs and are indicated in most patients with HF and cardiomyopathy because of improved survival and other benefits. In patients who are taking a beta blocker and still experiencing frequent, severely symptomatic VPBs that interfere with their quality of life or that appear to reduce LVEF, we suggest treatment with amiodarone (Grade 2B). Alternatives include sotalol, dofetilide, or catheter ablation. (See "Use of beta blockers in heart failure due to systolic dysfunction".)
Nonsustained VT — NSVT is common in patients with HF, is often asymptomatic, and, in most patients, pharmacologic suppression does not reduce the risk of malignant arrhythmias or SCD. NSVT can be an indication for electrophysiology study and possible implantable cardioverter-defibrillator (ICD) therapy in selected patients with a prior MI and ischemic cardiomyopathy, and for an ICD in selected patients with hypertrophic cardiomyopathy. Recommendations for the management of such patients are discussed separately. (See "Management of nonsustained ventricular tachycardia", section on 'Summary and Recommendations'.)
AIVR — Accelerated idioventricular rhythm (AIVR) occurs in approximately 8 percent of patients with HF or cardiomyopathy. It is usually transient and requires no treatment. Furthermore, pharmacologic treatment is CONTRAINDICATED if AIVR is an escape rhythm, since suppression of the pacemaker focus can result in asystole. Patients with symptomatic AIVR due to sinus node dysfunction may benefit from atrial pacing. (See 'Accelerated idioventricular rhythm' above.)
Sustained ventricular arrhythmias — Sustained VT is unusual, occurring in ≤5 percent of patients with HF, but it confers a high risk for SCD. Patients with HF or cardiomyopathy who are survivors of SCD due to unstable VT or VF, or have stable sustained VT are typically treated with an ICD. (See "Secondary and primary prevention of sudden cardiac death in heart failure and cardiomyopathy".)
Significance of syncope — Syncope in patients with HF or cardiomyopathy may result from one of three mechanisms: a poorly tolerated but transient bradyarrhythmia or tachyarrhythmia; medications or hemodynamic abnormalities related to the underlying heart disease; or any of the other etiologies of syncope. Thus, HF patients who experience a syncopal event should undergo a thorough evaluation. (See 'Syncope' above.)
HF therapy — Patients with HF and ventricular arrhythmias should be treated aggressively for HF. Standard therapy for HF due to systolic dysfunction consists of the following:
* A beta blocker
* An angiotensin converting enzyme (ACE) inhibitor
* An angiotensin II receptor blocker (ARB) in selected patients
* An aldosterone antagonist in selected patients
In addition to their hemodynamic effects, these drugs improve survival and may reduce the incidence of ventricular arrhythmias and SCD. Digoxin improves symptoms, while the effect on mortality varies with the attained serum digoxin concentration: among men in the DIG trial, all-cause mortality at 37 months was, compared to placebo, significantly lower in those with a serum digoxin concentration of 0.5 to 0.8 ng/mL and increased in those with a serum digoxin concentration above 1.2 ng/mL. (See 'Effect of HF therapy on ventricular arrhythmia' above.)
A proarrhythmic effect has also been noted with other inotropic agents used for the treatment of HF including beta adrenergic agonists and phosphodiesterase inhibitors, such as milrinone.
EP testing — EP testing can assist in the diagnosis of unexplained symptoms (eg, palpitations or syncope) and arrhythmias in patients with HF or cardiomyopathy. It is also useful in some post-MI patients with moderate LV dysfunction (eg, LVEF 31 to 40 percent) to determine if they are candidates for an implantable cardioverter-defibrillator. (See 'Role of EP testing' above.)
REFERENCES
1. Hynes, BJ, Luck, JC, Wolbrette, DL, Boehmer, J. Arrhythmias in patients with heart failure. Curr Treat Options Cardiovasc Med 2002; 4:467.
2. Francis, GS. Development of arrhythmias in the patient with congestive heart failure: Pathophysiology, prevalence and prognosis. Am J Cardiol 1986; 57:3B.
3. Holmes, J, Kubo, SH, Cody, RJ, Kligfield, P. Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: Prediction of mortality by ambulatory electrocardiography. Am J Cardiol 1985; 55:146.
4. Packer, M. Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. Circulation 1992; 85:I50.
5. Teerlink, JR, Jalaluddin, M, Anderson, S, et al. Ambulatory ventricular arrhythmias in patients with heart failure do not specifically predict an increased risk of sudden death. Circulation 2000; 101:40.
6. Podrid, PJ, Fogel, RI, Fuchs, TT. Ventricular arrhythmia in congestive heart failure. Am J Cardiol 1992; 69:82G.
7. von Olshausen, K, Schafer, A, Mehmel, HC, et al. Ventricular arrhythmias in idiopathic dilated cardiomyopathy. Br Heart J 1984; 51:195.
8. Meinertz, T, Hofmann, T, Kasper, W, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984; 53:902.
9. Duffee, DF, Shen, WK, Smith, HC. Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy. Mayo Clin Proc 1998; 73:430.
10. Bogun, F, Crawford, T, Reich, S, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm 2007; 4:863.
11. Singh, SN, Fisher, SG, Carson, PE, et al and the Department of Veteran Affairs CHF-STAT Investigators. Prevalence and significance of nonsustained ventricular tachycardia in patients with premature ventricular contractions and heart failure treated with vasodilator therapy. J Am Coll Cardiol 1998; 32:942.
12. Grimm, W, Hoffmann, J, Menz, V, et al. Significance of accelerated idioventricular rhythm in idiopathic dilated cardiomyopathy. Am J Cardiol 2000; 85:899.
13. Poll, DS, Marchlinski, FE, Buxton, AE, et al. Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: Electrophysiologic testing and lack of response to antiarrhythmic drug therapy. Circulation 1984; 70:451.
14. Milner, PG, Dimarco, JP, Lerman, BB. Electrophysiological evaluation of sustained ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy. Pacing Clin Electrophysiol 1988; 11:562.
15. Livanis, EG, Kostopoulou, A, Theodorakis, GN, et al. Neurocardiogenic mechanisms of unexplained syncope in idiopathic dilated cardiomyopathy. Am J Cardiol 2007; 99:558.
16. Middlekauff, HR, Stevenson, WG, Stevenson, LW, et al. Syncope in advanced heart failure: High risk of sudden death regardless of the origin of syncope. J Am Coll Cardiol 1993; 21:110.
17. Fonarow, GC, Feliciano, Z, Boyle, NG, et al. Improved survival in patients with nonischemic advanced heart failure and syncope treated with an implantable cardioverter-defibrillator. Am J Cardiol 2000; 85:981.
18. Grimm, W, Hoffmann J, J, Muller, HH, Maisch, B. Implantable defibrillator event rates in patients with idiopathic dilated cardiomyopathy, nonsustained ventricular tachycardia on Holter and a left ventricular ejection fraction below 30%. J Am Coll Cardiol 2002; 39:780.
19. Knight, BP, Goyal, R, Pelosi, F, et al. Outcome of patients with nonischemic dilated cardiomyopathy and unexplained syncope treated with an implantable defibrillator. J Am Coll Cardiol 1999; 33:1964.
20. Zipes, DP, Camm, AJ, Borggrefe, M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death-Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006; 48:1064.
21. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999; 353:2001.
22. Packer, M, Bristow, MR, Cohn, JN, et al for the US Carvedilol Heart Failure Study Group. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996; 334:1349.
23. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial. Lancet 1999; 353:9.
24. Pratt, CM, Gardner, M, Pepine, C, et al. Lack of long-term ventricular arrhythmia reduction by enalapril in heart failure. SOLVD Investigators. Am J Cardiol 1995; 75:1244.
25. Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial Study Group. N Engl J Med 1987; 316:1429.
26. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. The SOLVD Investigators. N Engl J Med 1991; 325:293.
27. Pfeffer, MA, Braunwald, E, Moye, LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: Results of the survival and ventricular enlargement study. N Engl J Med 1992; 327:669.
28. Cleland, JG, Erhardt, L, Murray, G, et al on behalf of the AIRE Study Investigators. Effect of ramipril on morbidity and mode of death among survivors of acute myocardial infarction with clinical evidence of heart failure. A report from the AIRE Study Investigators. Eur Heart J 1997; 18:41.
29. Fletcher, RD, Cintron, GB, Johnson, G, et al. Enalapril decreases ventricular tachycardia in heart failure: V-HeFT II. Circulation 1993; 87:VI49.
30. Cohn, JN, Johnson, G, Ziesche, S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991; 325:303.
31. Kober, L, Torp-Pedersen, C, Carlsen, JE, et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1995; 333:1670.
32. Domanski, MJ, Exner, DV, Borkowf, CB, et al. Effect of angiotensin converting enzyme inhibition on sudden cardiac death in patients following acute myocardial infarction. J Am Coll Cardiol 1999; 33:598.
33. Pitt, B, Poole-Wilson, PA, Segal, R, et al. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial--the Losartan Heart Failure Survival Study ELITE II. Lancet 2000; 355:1582.
34. Pfeffer, MA, Swedberg, K, Granger, CB, et al. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet 2003; 362:759.
35. Solomon, SD, Wang, D, Finn, P, et al. Effect of candesartan on cause-specific mortality in heart failure patients: the Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) program. Circulation 2004; 110:2180.
36. Pitt, B, Zannad, F, Remme, WJ, et al, for the Randomized Aldactone Evaluation Study Investigators. The Effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999; 341:709.
37. Pitt, B, Remme, W, Zannad, F, Neaton, J. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003; 348:1309.
38. Ramires, FJ, Mansur, A, Coelho, O, et al. Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy. Am J Cardiol 2000; 85:1207.
39. Juurlink, DN, Mamdani, MM, Lee, DS, et al. Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study. N Engl J Med 2004; 351:543.
40. The Digitalis Investigation Group. The effect of digitalis on mortality and morbidity in patients with congestive heart failure. N Engl J Med 1997; 336:525.
41. Mason, JW. A comparison of seven antiarrhythmic drugs in patients with ventricular tachyarrhythmias. Electrophysiologic Study versus Electrocardiographic Monitoring Investigators. N Engl J Med 1993; 329:452.
42. Packer, M, Carver, JR, Rodeheffer, RJ, et al. Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med 1991; 325:1468.
43. Goldberger, JJ, Subacius, H, Schaechter, A, et al. Effects of statin therapy on arrhythmic events and survival in patients with nonischemic dilated cardiomyopathy. J Am Coll Cardiol 2006; 48:1228.
44. Greenberg, H, Case, RB, Moss, AJ, et al. Analysis of mortality events in the Multicenter Automatic Defibrillator Implantation Trial (MADIT-II). J Am Coll Cardiol 2004; 43:1459.
Reference:
http://www.uptodate.com/home/index.html
|
