This Article Abstract Full Text (PDF) All Versions of this Article: 106/21/2694    most recent 01.CIR.0000038499.22687.39v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ellison, K. E. Search for Related Content PubMed PubMed Citation Articles by Ellison, K. E. Pubmed/NCBI databases Medline Plus Health Information Coronary Artery Disease Related Collections Arrhythmias, clinical electrophysiology, drugs Chronic ischemic heart disease Ablation/ICD/surgery

(Circulation. 2002;106:2694.)
© 2002 American Heart Association, Inc.

Clinical Investigation and Reports

Effect of ß-Blocking Therapy on Outcome in the Multicenter UnSustained Tachycardia Trial (MUSTT)

Kristin E. Ellison, MD; Gail E. Hafley, MS; Kathleen Hickey, ANP-C; Joyce Kellen, MSc; James Coromilas, MD; Kenneth M. Stein, MD; Kerry L. Lee, PhD; Alfred E. Buxton, MD, for the MUSTT Investigators

From Brown Medical School (K.E.E., A.E.B.), Providence, RI; Duke Clinical Research Institute (G.E.H., K.L.L.), Durham, NC; Columbia University Medical Center (K.H., J.C.), New York, NY; University of Calgary (J.K.), Calgary, Alberta, Canada; and Cornell Medical Center (K.M.S.), New York, NY.

Correspondence to Kristin E. Ellison, MD, Cardiology Division, Rhode Island Hospital, 2 Dudley St, Suite 360, Providence, RI 02905. E-mail kellison{at}lifespan.org

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
Background— ß-Blockers are known to reduce total mortality and sudden death in survivors of recent myocardial infarction. The effects of these agents in patients at high risk for sudden death with remote infarction are not clear.

Methods and Results— We analyzed the effect of ß-blockers on outcomes in 2096 patients with coronary artery disease, ejection fraction 40%, and spontaneous nonsustained ventricular tachycardia enrolled in the Multicenter UnSustained Tachycardia Trial (MUSTT). Forty-five percent of 702 patients with inducible sustained ventricular tachyarrhythmia and 35% of 1394 patients without inducible tachycardia were discharged from hospital receiving ß-blockers. Patients treated with ß-blockers were younger and had higher ejection fractions, higher rates of recent angina, and more recent infarction. ß-Blockers were associated with decreased total mortality for the entire study population (5-year mortality 50% with ß-blockers versus 66% without ß-blockers; adjusted P=0.0001). The mortality benefit associated with ß-blockers was present in patients with and without inducible tachycardia, except those treated with implantable defibrillators. There was no significant effect of ß-blocker therapy on the rate of arrhythmic death or cardiac arrest (adjusted P=0.2344).

Conclusions— ß-Blocking agents have beneficial effects on survival of patients having characteristics of those enrolled in the MUSTT trial. These effects do not appear to be due to a specific antiarrhythmic effect of ß-blockers. The beneficial effects of ß-blockers were demonstrable in all patients except those treated with implantable defibrillators.

Key Words: death, sudden • beta-blocker • myocardial infarction • implantable cardioverter defibrillator

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
ß-Blocking agents reduce total mortality by 25% to 40% in patients with a recent myocardial infarction (MI).^1–8 Pooled data from 18 000 patients show that ß-blockers reduce sudden cardiac death by 32% to 50%.⁶ These trials examined the effects of ß-blockers when initiated early after an index infarction, with follow-up ranging from 3 to 72 months. In addition, ß-blockers have been linked with a reduced risk of death for survivors of ventricular fibrillation and tachycardia.^9,10

The Multicenter UnSustained Tachycardia Trial (MUSTT) was designed to test the effectiveness of electrophysiologically guided antiarrhythmic therapy in reducing the risk of arrhythmic death, cardiac arrest, and total mortality in patients with coronary artery disease, ejection fraction 40%, and spontaneous nonsustained ventricular tachycardia (VT).¹¹ The use of ß-blockers was strongly encouraged in all patients. Patients were enrolled in the MUSTT trial a median of 39 months after their most recent acute MI, with 17% enrolled within 1 month of an acute MI. The potential benefits of ß-blocking agents at a time this far removed from infarction are not clear, nor have the effects of these agents been evaluated in a population at high risk for arrhythmic events, such as those enrolled in this trial.

In the present analysis, we evaluate the impact of ß-blockers on total mortality and arrhythmic events (arrhythmic death or resuscitated cardiac arrest) in patients enrolled in the MUSTT trial.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
Population
Details of the MUSTT study protocol have been described previously.¹¹ MUSTT was a prospective, randomized, controlled trial; patients who had coronary artery disease, left ventricular ejection fraction 40%, and asymptomatic nonsustained VT (defined as 3 consecutive premature ventricular contractions with a rate >100 bpm) were candidates for enrollment. Eligible patients underwent a baseline electrophysiological study in the absence of antiarrhythmic drugs with a standardized stimulation protocol. Patients with sustained monomorphic VT (induced by 1, 2, or 3 extrastimuli) and patients with sustained polymorphic VT including ventricular fibrillation and flutter (induced by 1 or 2 extrastimuli) were randomly assigned in equal proportions to antiarrhythmic therapy guided by serial electrophysiological testing or no antiarrhythmic therapy. The status of patients in whom no sustained tachyarrhythmia was induced at the baseline study and who received no antiarrhythmic therapy was recorded in a registry.¹² In the main trial and in the registry, arrhythmic death or nonfatal cardiac arrest was reported as the primary end point and all-cause mortality as a key secondary end point.

Patients assigned to electrophysiologically guided therapy underwent serial drug testing with antiarrhythmic drugs. If no drug regimen could be found that rendered the tachyarrhythmia noninducible, the investigator could discharge the patient with a prescription for a drug that was associated with hemodynamic stability during induced tachycardia. No empirical antiarrhythmic drug therapy was used. Implantation of a cardioverter/defibrillator (ICD) could be recommended after 1 unsuccessful drug trial. Patients who declined defibrillator implantation were discharged receiving no antiarrhythmic drugs.

Of the 2202 patients enrolled at 85 sites in the United States and Canada between November 1, 1990, and October 31, 1996, 2096 (702 randomized patients and 1394 registry patients) were used for the present analysis. Excluded from the analysis were 101 registry patients who had inducible VT but either refused randomization (63 patients) or had nonreproducible induction of VT (38 patients). Also excluded were 5 patients (2 randomized patients and 3 registry patients) whose ß-blocker status at hospital discharge was unknown. For the analyses in the present report, patients were considered to be in the group receiving ß-blocking therapy if they were taking ß-blockers at the time of discharge after enrollment. Patients discharged taking sotalol (n=33 randomized patients, and 3 registry patients given sotalol for atrial fibrillation) were considered in the group of patients taking ß-blocking agents for the purpose of the present analysis. We also performed the analyses excluding patients receiving sotalol from the ß-blocker group. Propafenone was not considered a ß-blocker. Patients who did not survive to hospital discharge were included in the analysis if ß-blocker use was known at the time of death.

Statistical Analysis
The distributions of baseline characteristics were summarized with medians and 25th and 75th percentiles for continuous variables and percentages for categorical variables. Group differences in baseline characteristics, medications, and ECG characteristics were assessed with the Wilcoxon rank-sum test (for continuous variables) and the ² test (for categorical variables). All tests of significance were 2-tailed. Cumulative event rates and survival curves were calculated by the Kaplan-Meier method, and outcome differences of patients treated with ß-blockers versus those not treated were assessed with the log-rank test.¹³ In addition, covariate-adjusted analyses of the effect of ß-blockers on outcomes were performed with the Cox proportional hazards model.¹⁴ Covariates included in these analyses were induction of randomizable VT, age, sex, race, ejection fraction, duration (in beats) of the longest episode of nonsustained VT, number of vessels with 75% stenosis, history of MI, prior thrombolytic therapy, left bundle-branch block, intraventricular conduction delays, use of digitalis at baseline, prior bypass surgery or angioplasty, or symptoms of angina within 6 weeks before enrollment. Hazard ratios and 95% confidence intervals (CI) were calculated with the Cox proportional hazards model.

	Results

Top Abstract Introduction Methods Results Discussion References

 
Of the 2096 patients in the present analysis, 799 (38%) received ß-blockers at the time of hospital discharge after enrollment in the trial (Table 1). Of 702 patients with inducible sustained VT, 314 (45%) received ß-blockers. At last follow-up, 67% of these patients were still taking ß-blockers. Of the patients with inducible tachycardia who were not treated with specific antiarrhythmic therapy, 51% received ß-blockers versus 37% (65 of 177) of ICD-treated patients versus 39% (62 of 159) of patients treated with pharmacological antiarrhythmic therapy. A total of 7 patients randomized to electrophysiologically guided therapy were discharged taking ß-blocking agents in addition to amiodarone, sotalol, or propafenone. Of the 1394 registry patients, 485 (35%) were taking ß-blockers at the time of hospital discharge, and 65% of this group of patients were still taking ß-blockers at last follow-up.

View this table: [in this window] [in a new window]   TABLE 1. Baseline Characteristics

Patients treated with ß-blockers were younger and had higher ejection fractions, higher rates of recent angina, and more recent infarction (Table 1). This patient group was more likely to have received thrombolytic therapy and to have previously undergone angioplasty. A greater percentage of patients treated with ß-blockers were in New York Heart Association (NYHA) class I and had lower rates of congestive heart failure than the patients not taking ß-blockers at discharge. All patients discharged taking ß-blockers had lower rates of digitalis and ACE inhibitor use at baseline. Registry patients discharged taking ß-blockers also had a lower rate of calcium channel blocker use at baseline (Table 2). A comparison of baseline ECG characteristics showed that patients receiving ß-blockers at discharge had lower rates of left ventricular hypertrophy, left bundle-branch block, and intraventricular conduction delays than patients not taking ß-blockers (Table 3).

View this table: [in this window] [in a new window]   TABLE 2. Cardiac Medications Used at Baseline

View this table: [in this window] [in a new window]   TABLE 3. Baseline ECG Characteristics

The 2- and 5-year total mortality rates of 16% and 34% for patients receiving ß-blockers at discharge were significantly lower than the total mortality rates of 27% and 50% for patients not receiving ß-blockers at discharge (unadjusted P=0.0001 and covariate-adjusted P=0.0001; Figure 1; Table 4). The mortality benefit of ß-blockers was consistent across the spectrum of study patients (adjusted hazard ratios from 0.63 to 0.72), except for randomized ICD-treated patients (Table 4). The latter group of 177 patients (65 receiving ß-blockers and 112 not taking ß-blockers) demonstrated a 5-year mortality rate of 23% in patients taking ß-blockers and 27% in those who were not.

View larger version (16K): [in this window] [in a new window]   Figure 1. Mortality rates related to use of ß-blockers or lack of ß-blockers over course of trial. Both unadjusted mortality rate and mortality rate adjusted for covariates were significantly lower in patients treated with ß-blockers. Covariates included in analysis were induction of randomizable VT, age, sex, race, ejection fraction, duration (in beats) of longest episode of nonsustained VT, number of vessels with 75% stenosis, history of MI, prior thrombolytic therapy, left bundle-branch block, intraventricular conduction delays, use of digitalis at baseline, prior bypass surgery or angioplasty, or symptoms of angina within 6 weeks before enrollment. Hazard ratios and 95% CIs were calculated with Cox proportional hazards model.

View this table: [in this window] [in a new window]   TABLE 4. Effects of ß-Blocker Use on Total Mortality Rates and Arrhythmic Death/Cardiac Arrest Rates

In contrast to the beneficial effect of ß-blockers on total mortality, there was no significant benefit of ß-blocker therapy on the primary end point of arrhythmic death or cardiac arrest, after adjustment for the previously mentioned differences in baseline factors (Figure 2; Table 4). The adjusted hazard ratios, however, did show a trend toward a benefit of ß-blockers in decreasing arrhythmic events (adjusted hazard ratios from 0.81 to 0.88) for all subgroups except the randomized ICD-treated patients.

View larger version (15K): [in this window] [in a new window]   Figure 2. Rates of arrhythmic death or cardiac arrest related to use of ß-blockers or lack of ß-blockers over course of trial. Unadjusted event rates were significantly lower in patients treated with ß-blockers. After adjustment for covariates noted in Figure 1, event rates were not significantly lower in patients treated with ß-blockers.

When we performed the above analyses excluding patients from the ß-blocker group who were receiving sotalol, there was no significant difference in the results.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
The present study demonstrates that ß-blocker use is associated with improved survival in all subgroups of patients enrolled in the MUSTT trial, with the exception of those treated with ICDs. This benefit extended to patients with and without inducible ventricular tachyarrhythmias. Although there are abundant data substantiating the beneficial effects of ß-blockers on survival in patients with recent MI, our results extend these benefits to a high-risk subgroup of patients, the majority of whom had a remote infarction. The median time from infarction to enrollment was 39 months, which suggests that the beneficial effects of ß-blockers persist for long periods after MI. The protective mechanism of ß-blockers is unclear but likely relates to a combination of their anti-ischemic, antiarrhythmic, antihypertensive, and antiadrenergic properties.

In the European Myocardial Infarction Amiodarone Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), high-risk patients with recent MI were randomly assigned to either amiodarone or placebo.^15,16 In both of these trials, amiodarone therapy appeared to have a greater effect on reducing mortality in those patients taking ß-blocking agents. The results of these trials were published after enrollment in the MUSTT trial had been completed.

ß-Blockers have also been shown to reduce mortality by 26% to 65% in patients with symptomatic heart failure.^17–22 The results of the major heart failure trials were not available at the onset of the MUSTT trial; therefore, the significant benefit of ß-blocker therapy in patients with congestive heart failure was not established. This is the likely cause of the low overall use of ß-blockers in this trial. In the MUSTT trial, 25% of patients were categorized in NYHA class III and 39% in NYHA class II.

ICD therapy has been shown to provide a significant mortality benefit in patients who have survived cardiac arrest, in those with depressed left ventricular function secondary to coronary artery disease with spontaneous nonsustained VT and inducible sustained VT that is not suppressed by pharmacological antiarrhythmic therapy.^11,23,24 In addition, a recent trial demonstrated that ICDs can reduce mortality in patients with prior MI who have an ejection fraction 30%, regardless of the presence or absence of documented spontaneous nonsustained VT.²⁵

In two recent trials comparing ICDs with empiric pharmacological antiarrhythmic therapy for primary and secondary prevention of sudden death, ICD therapy demonstrated a significant mortality benefit in patients at high risk for death or recurrent arrhythmias.^23,24 However, in those trials, patients randomly assigned to ICD therapy were also given ß-blockers significantly more often than patients receiving pharmacological antiarrhythmic treatment, which has led some to question the contribution of ß-blockers to the observed superiority of ICD therapy. The benefit of ICDs in the MADIT-II (Multicenter Automatic Defibrillator Implantation Trial II) study was observed even though 70% of patients in both the ICD and control arms received ß-blocker therapy.²⁵ Of note, MUSTT patients discharged with ICDs received ß-blockers significantly less often than patients randomized to no antiarrhythmic therapy. Thus, the favorable effect of ICD therapy on survival in the MUSTT trial cannot be explained by bias in ß-blocker usage, as occurred in the other trials.

Our findings are consistent with the ß-blocker substudy of the AVID (Antiarrhythmics Versus Implantable Defibrillators) trial, in which ß-blocker use was not associated with improved survival in patients with ventricular fibrillation or symptomatic VT treated with amiodarone or ICD therapy.²⁶ ß-Blocker use in AVID patients was associated with an independent mortality reduction in eligible, nonrandomized patients who were not treated with amiodarone or ICD therapy. However, the AVID data contrasted with those obtained from EMIAT and CAMIAT, in which the benefit of ß-blockers appeared to be more significant in patients with elevated resting heart rates.^15,16 We did not collect information on the resting heart at entry into the present study. In the MUSTT trial, there was a trend toward fewer arrhythmic events and improved survival in those treated with antiarrhythmic drugs in combination with ß-blocker therapy compared with antiarrhythmic therapy alone. This trend was not observed in patients who received ICD therapy. This is likely a reflection of the significant impact of ICD therapy on sudden cardiac death and the difficulty in further decreasing event rates.

Study Limitations
Administration of ß-blocker therapy was left to the discretion of the referring physicians and therefore was not randomized. The effects of ß-blockers in patients who received pharmacological antiarrhythmic therapy may also be obscured because several of these agents possess some ß-blocker activity. The small number of patients given individual antiarrhythmic drugs also limits the power to detect differences of the effect of ß-blockers depending on the particular antiarrhythmic drug used.

Conclusions
Although the MUSTT trial was not designed to test the efficacy of ß-blocking therapy, our analysis suggests benefit in the study population except those treated with ICDs. This analysis demonstrates that the survival benefit observed in patients treated with ICD therapy is not a reflection of bias in ß-blocker use. Given that multiple studies have demonstrated beneficial effects of ß-blocker therapy in patients with coronary disease and abnormal ventricular function, and given our failure to find evidence of adverse effects of ß-blockers, it is appropriate to prescribe these drugs in patients with the characteristics of those enrolled in the MUSTT trial.

	Acknowledgments

 
This study was supported by grants UO1 HL 45700 and UO1 HL 45726 from the National Heart, Lung, and Blood Institute; C.R. Bard; Berlex Laboratories; Boehringer-Ingelheim Pharmaceuticals; Guidant Corporation; Knoll Pharmaceuticals; Medtronic; Searle; Ventritex-St. Jude Medical; Wyeth-Ayerst Laboratories; and Merck and Company.

Received June 10, 2002; revision received August 28, 2002; accepted September 2, 2002.

	References

Top Abstract Introduction Methods Results Discussion References

 

1. ß-Blocker Heart Attack Trial Research Group. A randomized trial of propranolol in patients with acute myocardial infarction, I: mortality results. JAMA. 1982; 247: 1707–1714.[Abstract]
   
2. The Norwegian Multicenter Study Group. Timolol-induced reduction in mortality and reinfarction in patients surviving acute myocardial infarction. N Engl J Med. 1981; 304: 801–807.[Abstract]
   
3. Yusuf S, Wittes J, Friedman L. Overview of results of randomized clinical trials in heart disease. I. Treatments following myocardial infarction. JAMA. 1988; 260: 2088–2093.[CrossRef][Medline] [Order article via Infotrieve]
   
4. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction: an overview of results from randomized controlled trials. JAMA. 1993; 270: 1589–1595.[Abstract]
   
5. Lau J, Antman EM, Jimenez-Silva J, et al. Cumulative meta-analysis of therapeutic trials for myocardial infarction. N Engl J Med. 1992; 327: 248–254.[Abstract]
   
6. Yusuf S, Peto R, Lewis J, et al. Beta-blockade during and after myocardial infarction: an overview of randomized trials. Prog Cardiovasc Dis. 1985; 27: 335–371.[Medline] [Order article via Infotrieve]
   
7. Kendall MJ, Lynch KP, Hjalmarson A, et al. Beta-blockers and sudden cardiac death. Ann Intern Med. 1995; 123: 358–367.[Abstract/Free Full Text]
   
8. Hennekens CH, Albert CM, Godfried SL, et al. Adjunctive drug therapy of acute myocardial infarction: evidence from clinical trials. N Engl J Med. 1996; 335: 1660–1667.[Free Full Text]
   
9. Hallstrom AP, Cobb LA, Yu BH, et al. An antiarrhythmic drug experience in 941 patients resuscitated from an initial cardiac arrest between 1970 and 1985. Am J Cardiol. 1991; 68: 1025–1031.[CrossRef][Medline] [Order article via Infotrieve]
   
10. Szabo BM, Crijns HJ, Wiesfeld AC, et al. Predictors of mortality in patients with sustained ventricular tachycardias or ventricular fibrillation and depressed left ventricular function: importance of beta-blockade. Am Heart J. 1995; 130: 281–286.[CrossRef][Medline] [Order article via Infotrieve]
    
11. Buxton AE, Lee KL, Fisher JD, et al, for the Multicenter Unsustained Tachycardia Trial Investigators. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Engl J Med. 1999; 341: 1882–1890.[Abstract/Free Full Text]
    
12. Buxton AE, Lee KL, DiCarlo L, et al, for the Multicenter Unsustained Tachycardia Trial Investigators. Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. N Engl J Med. 2000; 342: 1937–1945.[Abstract/Free Full Text]
    
13. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958; 53: 457–481.[CrossRef]
    
14. Cox DR. Regression models and life-tables. J R Stat Soc. 1972; 34: 187–220.
    
15. Julian DG, Camm AJ, Frangin G, et al, for the European Myocardial Infarction Amiodarone Trial Investigators. Randomized trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet. 1997; 349: 667–674.[CrossRef][Medline] [Order article via Infotrieve]
    
16. Cairns JA, Connolly SJ, Roberts R, et al, for the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Randomized trial of outcomes after myocardial infarction in patients with frequent or repetitive ventricular premature depolarizations: CAMIAT. Lancet. 1997; 349: 675–682.[CrossRef][Medline] [Order article via Infotrieve]
    
17. Heidenreich PA, Lee TT, Massie BM. Effect of beta-blockade on mortality in patients with heart failure: a meta-analysis of randomized clinical trials. J Am Coll Cardiol. 1997; 30: 27–34.
    
18. Packer M, Bristow MR, Cohn JN, et al, for the U S 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: 1349–1355.[Abstract/Free Full Text]
    
19. The Cardiac Insufficiency Bisoprolol Investigators, and Committees. Cardiac Insufficiency Bisoprolol Study (CIBIS II): a randomized trial. Lancet. 1999; 353: 9–13.[CrossRef][Medline] [Order article via Infotrieve]
    
20. Australia/New Zealand Heart Failure Research Collaborative Group. Randomized, placebo-controlled trial of carvedilol in patients with congestive heart failure due to ischemic heart disease. Lancet. 1997; 349: 375–380.[CrossRef][Medline] [Order article via Infotrieve]
    
21. Packer M, Coats AJ, Fowler MB, et al. Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med. 2001; 344: 1651–1658.[Abstract/Free Full Text]
    
22. The Beta-blocker Evaluation of Survival Trial Investigators. A trial of the beta-blocker bucindolol in patients with advanced chronic heart failure. N Engl J Med. 2001; 344: 1659–1667.[Abstract/Free Full Text]
    
23. Moss AJ, Hall WJ, Cannom DS, et al, for the Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med. 1996; 335: 1933–1940.[Abstract/Free Full Text]
    
24. The Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997; 337: 1576–1583.[Abstract/Free Full Text]
    
25. Moss AJ, Zareba W, Hall WJ, et al, for the Multicenter Automatic Defibrillator Implantation Trial II Investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346: 877–883.[Abstract/Free Full Text]
    
26. Exner DV, Reiffel JA, Epstein AE, et al. Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic ventricular tachycardia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial. J Am Coll Cardiol. 1999; 34: 325–333.[Abstract/Free Full Text]
    

This article has been cited by other articles:

				Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, 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., September 5, 2006; 48(5): 1064 - 1108. [Full Text] [PDF]

				Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: 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., September 5, 2006; 48(5): e247 - e346. [Full Text] [PDF]

				D. P. Zipes, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, 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) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur. Heart J., September 1, 2006; 27(17): 2099 - 2140. [Full Text] [PDF]

				Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: 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) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]

				J. P. Singh, W. J. Hall, S. McNitt, H. Wang, J. P. Daubert, W. Zareba, J. N. Ruskin, A. J. Moss, and and the MADIT-II Investigators Factors Influencing Appropriate Firing of the Implanted Defibrillator for Ventricular Tachycardia/Fibrillation: Findings From the Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II) J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1712 - 1720. [Abstract] [Full Text] [PDF]

				J. A. Reiffel Drug and Drug-Device Therapy in Heart Failure Patients in the Post-COMET and SCD-HeFT Era Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 2005; 10(4_suppl): S45 - S58. [Abstract] [PDF]

				H. Lorenz, C. Junger, K. Seidl, A. Gitt, S. Schneider, R. Schiele, H. Wienbergen, R. Winkler, M. Gottwik, W. Delius, et al. Do statins influence the prognostic impact of non-sustained ventricular tachycardia after ST-elevation myocardial infarction? Eur. Heart J., June 1, 2005; 26(11): 1078 - 1085. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) All Versions of this Article: 106/21/2694    most recent 01.CIR.0000038499.22687.39v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ellison, K. E. Search for Related Content PubMed PubMed Citation Articles by Ellison, K. E. Pubmed/NCBI databases Medline Plus Health Information Coronary Artery Disease Related Collections Arrhythmias, clinical electrophysiology, drugs Chronic ischemic heart disease Ablation/ICD/surgery