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Primary Prevention of Sudden Cardiac Death in Idiopathic Dilated Cardiomyopathy: The Cardiomyopathy Trial (CAT)
- Dietmar Bänsch,
- Matthias Antz,
- Sigrid Boczor,
- Marius Volkmer,
- Jürgen Tebbenjohanns,
- Karlheinz Seidl,
- Michael Block,
- Frank Gietzen,
- Jürgen Berger,
- Karl Heinz Kuck
Circulation Volume 105, Issue 1226 March 2002

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Background— Patients with idiopathic dilated cardiomyopathy (DCM) and impaired left ventricular ejection fraction have an increased risk of dying suddenly.Methods and Results— Patients with recent onset of DCM (≤9 months) and an ejection fraction ≤30% were randomly assigned to the implantation of an implantable cardioverter-defibrillator (ICD) or control. The primary end point of the trial was all-cause mortality at 1 year of follow-up. The trial was terminated after the inclusion of 104 patients because the all-cause mortality rate at 1 year did not reach the expected 30% in the control group. In August 2000, the vital status of all patients was updated by contacting patients, relatives, or local registration offices. One hundred four patients were enrolled in the trial: Fifty were assigned to ICD therapy and 54 to the control group. Mean follow-up was 22.8±4.3 months, on the basis of investigators’ follow-up. After 1 year, 6 patients were dead (4 in the ICD group and 2 in the control group). No sudden death occurred during the first and second years of follow-up. In August 2000, after a mean follow-up of 5.5±2.2 years, 30 deaths had occurred (13 in the ICD group and 17 in the control group). Cumulative survival was not significantly different between the two groups (93% and 80% in the control group versus 92% and 86% in the ICD group after 2 and 4 years, respectively).Conclusions— This trial did not provide evidence in favor of prophylactic ICD implantation in patients with DCM of recent onset and impaired left ventricular ejection fraction.
Early Protection Against Sudden Death by n-3 Polyunsaturated Fatty Acids After Myocardial Infarction: Time-Course Analysis of the Results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione
- Roberto Marchioli,
- Federica Barzi,
- Elena Bomba,
- Carmine Chieffo,
- Domenico Di Gregorio,
- Rocco Di Mascio,
- Maria Grazia Franzosi,
- Enrico Geraci,
- Giacomo Levantesi,
- Aldo Pietro Maggioni,
- Loredana Mantini,
- Rosa Maria Marfisi,
- G. Mastrogiuseppe,
- Nicola Mininni,
- Gian Luigi Nicolosi,
- Massimo Santini,
- Carlo Schweiger,
- Luigi Tavazzi,
- Gianni Tognoni,
- Corrado Tucci,
- Franco Valagussa
Circulation Volume 105, Issue 1623 April 2002

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Background— Our purpose was to assess the time course of the benefit of n-3 polyunsaturated fatty acids (PUFAs) on mortality documented by the GISSI-Prevenzione trial in patients surviving a recent (<3 months) myocardial infarction.Methods and Results— In this study, 11 323 patients were randomly assigned to supplements of n-3 PUFAs, vitamin E (300 mg/d), both, or no treatment (control) on top of optimal pharmacological treatment and lifestyle advice. Intention-to-treat analysis adjusted for interaction between treatments was carried out. Early efficacy of n-3 PUFA treatment for total, cardiovascular, cardiac, coronary, and sudden death; nonfatal myocardial infarction; total coronary heart disease; and cerebrovascular events was assessed by right-censoring follow-up data 12 times from the first month after randomization up to 12 months. Survival curves for n-3 PUFA treatment diverged early after randomization, and total mortality was significantly lowered after 3 months of treatment (relative risk [RR] 0.59; 95% CI 0.36 to 0.97; P=0.037). The reduction in risk of sudden death was specifically relevant and statistically significant already at 4 months (RR 0.47; 95% CI 0.219 to 0.995; P=0.048). A similarly significant, although delayed, pattern after 6 to 8 months of treatment was observed for cardiovascular, cardiac, and coronary deaths.Conclusions— The early effect of low-dose (1 g/d) n-3 PUFAs on total mortality and sudden death supports the hypothesis of an antiarrhythmic effect of this drug. Such a result is consistent with the wealth of evidence coming from laboratory experiments on isolated myocytes, animal models, and epidemiological and clinical studies.
The Key to Unraveling the Mystery of Mortality in Heart Failure: An Integrated Approach
- Prakash C. Deedwania
Circulation Volume 107, Issue 138 April 2003

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On the Reanalysis of the GISSI-Prevenzione
- Alexander Leaf
Circulation Volume 105, Issue 1623 April 2002

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Elevated C-Reactive Protein Values and Atherosclerosis in Sudden Coronary Death: Association With Different Pathologies
- Allen P. Burke,
- Russell P. Tracy,
- Frank Kolodgie,
- Gray T. Malcom,
- Arthur Zieske,
- Robert Kutys,
- Joseph Pestaner,
- John Smialek and
- Renu Virmani
Circulation Volume 105, Issue 1730 April 2002

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Background— Elevations in serum C-reactive protein measured by high-sensitivity assay (hs-CRP) have been associated with unstable coronary syndromes. There have been no autopsy studies correlating hs-CRP to fatal coronary artery disease.Methods and Results— Postmortem sera from 302 autopsies of men and women without inflammatory conditions other than atherosclerosis were assayed for hs-CRP. There were 73 sudden deaths attributable to atherothrombi, 71 sudden coronary deaths with stable plaque, and 158 control cases (unnatural sudden deaths and noncardiac natural deaths without conditions known to elevate CRP). Atherothrombi were classified as plaque ruptures (n=55) and plaque erosion (n=18); plaque burden was estimated in each heart. Total cholesterol, high-density lipoprotein cholesterol, diabetes, smoking history, and body mass index were also determined. Immunohistochemical stains for CRP and numbers of thin cap atheromas per heart were quantitated in coronary deaths with hs-CRP in the highest and lowest quintiles. The median hs-CRP was 3.2 μg/mL in acute rupture, 2.9 μg/mL in plaque erosion, 2.5 μg/mL in stable plaque, and 1.4 μg/mL in controls. Mean log hs-CRP was higher in rupture (P<0.0001), erosion (P=0.005), and stable plaque (P=0.0003) versus controls. By multivariate analysis, atherothrombi (P=0.02), stable plaque (P=0.003), and plaque burden (P=0.03) were associated with log hs-CRP independent of age, sex, smoking, and body mass index. Mean staining intensity for CRP of macrophages and lipid core in plaques was significantly greater in cases with high hs-CRP than those with low CRP (P=0.0001), as were mean numbers of thin cap atheromas (P<0.0001).Conclusions— hs-CRP is significantly elevated in patients dying suddenly with severe coronary artery disease, both with and without acute coronary thrombosis, and correlates with immunohistochemical staining intensity and numbers of thin cap atheroma.
Coronary Anomalies: Incidence, Pathophysiology, and Clinical Relevance
- Paolo Angelini,
- José Antonio Velasco and
- Scott Flamm
Circulation Volume 105, Issue 2021 May 2002

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B-Type Natriuretic Peptide Predicts Sudden Death in Patients With Chronic Heart Failure
- Rudolf Berger,
- Martin Huelsman,
- Karin Strecker,
- Anja Bojic,
- Petra Moser,
- Brigitte Stanek and
- Richard Pacher
Circulation Volume 105, Issue 2021 May 2002

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Background— Given the high incidence of sudden death in patients with chronic heart failure (CHF) and the efficacy of implantable cardioverter-defibrillators, an appropriate tool for the prediction of sudden death is desirable. B-type natriuretic peptide (BNP) has prognostic significance in CHF, and the stimuli for its production cause electrophysiological abnormalities. This study tests BNP levels as a predictor of sudden death.Methods and Results— BNP levels, in addition to other neurohormonal, clinical, and hemodynamic variables, were obtained from 452 patients with a left ventricular ejection fraction (LVEF) ≤35%. For prediction of sudden death, only survivors without heart transplantation (HTx) or a mechanical assist device and patients who died suddenly were analyzed. Up to 3 years, 293 patients survived without HTx or a mechanical assist device, 89 patients died, and 65 patients underwent HTx. Mode of death was sudden in 44 patients (49%), whereas 31 patients (35%) had pump failure and 14 patients (16%) died from other causes. Univariate risk factors of sudden death were log BNP (P=0.0006), log N-terminal atrial natriuretic peptide (P=0.003), LVEF (P=0.005), log N-terminal BNP (P=0.006), systolic blood pressure (P=0.01), big endothelin (P=0.03), and NYHA class (P=0.04). In the multivariate model, log BNP level was the only independent predictor of sudden death (P=0.0006). Using a cutoff point of log BNP <2.11 (130 pg/mL), Kaplan-Meier sudden death–free survival rates were significantly higher in patients below (99%) compared with patients above (81%) this cutoff point (P=0.0001).Conclusion— BNP levels are a strong, independent predictor of sudden death in patients with CHF.
Prospective Study of C-Reactive Protein, Homocysteine, and Plasma Lipid Levels as Predictors of Sudden Cardiac Death
- Christine M. Albert,
- Jing Ma,
- Nader Rifai,
- Meir J. Stampfer and
- Paul M. Ridker
Circulation Volume 105, Issue 224 June 2002

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Background— Sudden cardiac death (SCD) is an important cause of mortality even among apparently healthy populations. However, our ability to identify those at risk for SCD in the general population is poor, and more specific markers are needed.Methods and Results— To compare and contrast the relative importance of C-reactive protein (CRP), homocysteine, and lipids as long-term predictors of SCD, we performed a prospective, nested, case-control analysis involving 97 cases of SCD among apparently healthy men enrolled in the Physician’s Health Study. Of these plasma markers measured, only baseline CRP levels were significantly associated with the risk of SCD over the ensuing 17 years of follow-up (P for trend=0.001). The increase in risk associated with CRP levels was primarily seen among men in the highest quartile, who were at a 2.78-fold increased risk of SCD (95% CI 1.35 to 5.72) compared with men in the lowest quartile. These results were not significantly altered in analyses that (in addition to the matching variables of age and smoking status) controlled for lipid parameters, homocysteine, and multiple cardiac risk factors (relative risk for highest versus lowest quartile 2.65, 95% CI 0.79 to 8.83; P for trend=0.03). In contrast to the positive relationship observed for CRP, neither homocysteine nor lipid levels were significantly associated with risk of SCD.Conclusions— These prospective data suggest that CRP levels may be useful in identifying apparently healthy men who are at an increased long-term risk of SCD.
Sudden Death Predictors: An Inflammatory Association
- Peter M. Spooner and
- Douglas P. Zipes
Circulation Volume 105, Issue 224 June 2002

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Clinical and Molecular Characterization of Patients With Catecholaminergic Polymorphic Ventricular Tachycardia
- Silvia G. Priori,
- Carlo Napolitano,
- Mirella Memmi,
- Barbara Colombi,
- Fabrizio Drago,
- Maurizio Gasparini,
- Luciano DeSimone,
- Fernando Coltorti,
- Raffaella Bloise,
- Roberto Keegan,
- Fernando E.S. Cruz Filho,
- Gabriele Vignati,
- Abraham Benatar and
- Angelica DeLogu
Circulation Volume 106, Issue 12 July 2002

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Background— Mutations in the cardiac ryanodine receptor gene (RyR2) underlie catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited arrhythmogenic disease occurring in the structurally intact heart. The proportion of patients with CPVT carrying RyR2 mutations is unknown, and the clinical features of RyR2-CPVT as compared with nongenotyped CPVT are undefined.Methods and Results— Patients with documented polymorphic ventricular arrhythmias occurring during physical or emotional stress with a normal heart entered the study. The clinical phenotype of the 30 probands and of 118 family members was evaluated, and mutation screening on the RyR2 gene was performed. Arrhythmias documented in probands were: 14 of 30 bidirectional ventricular tachycardia, 12 of 30 polymorphic ventricular tachycardia, and 4 of 30 catecholaminergic idiopathic ventricular fibrillation; RyR2 mutations were identified in 14 of 30 probands (36% bidirectional ventricular tachycardia, 58% polymorphic ventricular tachycardia, 50% catecholaminergic idiopathic ventricular fibrillation) and in 9 family members (4 silent gene carriers). Genotype-phenotype analysis showed that patients with RyR2 CPVT have events at a younger age than do patients with nongenotyped CPVT and that male sex is a risk factor for syncope in RyR2-CPVT (relative risk=4.2).Conclusions— CPVT is a clinically and genetically heterogeneous disease manifesting beyond pediatric age with a spectrum of polymorphic arrhythmias. β-Blockers reduce arrhythmias, but in 30% of patients an implantable defibrillator may be required. Genetic analysis identifies two groups of patients: Patients with nongenotyped CPVT are predominantly women and become symptomatic later in life; patients with RyR2 CPVT become symptomatic earlier, and men are at higher risk of cardiac events. These data provide a rationale for prompt evaluation and treatment of young men with RyR2 mutations.
Clinical Implications of Cardiac Ryanodine Receptor/Calcium Release Channel Mutations Linked to Sudden Cardiac Death
- Andrew R. Marks
Circulation Volume 106, Issue 12 July 2002

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Effects of Ventricular Premature Stimulus Coupling Interval on Blood Pressure and Heart Rate Turbulence
- Mari A. Watanabe,
- Joseph E. Marine,
- Robert Sheldon and
- Mark E. Josephson
Circulation Volume 106, Issue 316 July 2002

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Background— Heart rate turbulence (HRT) is a promising noninvasive risk stratifier for mortality after myocardial infarction. On the basis of a study of ventricular premature complex coupling interval and sympathetic nerve burst amplitude, we hypothesized that measures of HRT would increase with increased prematurity of the coupling interval.Methods and Results— Twenty-eight patients undergoing programmed electrical stimulation were studied (12 with prior myocardial infarction, aged 60±18 years). An extrastimulus was delivered from the right ventricular apex after 20 sinus beats with a V-S₂ coupling interval decremented by 20 to 30 ms until refractoriness was reached. Turbulence slope (TS), turbulence timing (TT), and turbulence onset were calculated for each extrastimulus, and the linear regressions of these parameters on coupling interval and compensatory pause were calculated. Arterial blood pressure was measured with arterial catheter or a noninvasive continuous blood pressure transducer (Buffington cuff). TS and turbulence onset were abnormal in 4 and 13 patients, respectively. HRT parameters were significantly correlated with coupling interval or compensatory pause in only 2 or 3 patients for a given regression analysis. This absence of correlation was found likely to be due to lack of correlation between compensatory pause and systolic blood pressure after the compensatory pause. Heart rate and TS were correlated: Patients with high heart rate had low TS and late TT (TS=−2.7+0.01×sinus cycle length, P=0.018; TT=8.8 to 0.005×sinus cycle length, P=0.013).Conclusions— HRT can be induced by programmed stimulation. In this setting, heart rate affects HRT but not ventricular premature complex prematurity. Induced HRT seems to be a valid method for measuring HRT parameters in patients with few ventricular premature complexes.
Mapping and Ablation of Idiopathic Ventricular Fibrillation
- Michel Haïssaguerre,
- Morio Shoda,
- Pierre Jaïs,
- Akihiko Nogami,
- Dipen C. Shah,
- Josef Kautzner,
- Thomas Arentz,
- Dietrich Kalushe,
- Dominique Lamaison,
- Mike Griffith,
- Fernando Cruz,
- Angelo de Paola,
- Fiorenzo Gaïta,
- Mélèze Hocini,
- Stéphane Garrigue,
- Laurent Macle,
- Rukshen Weerasooriya and
- Jacques Clémenty
Circulation Volume 106, Issue 820 August 2002

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Background— Ventricular fibrillation is the main mechanism of sudden cardiac death. The feasibility of eliminating recurrent episodes by catheter ablation has not been reported.Methods and Results— Twenty-seven patients without known heart disease (13 men, 14 women, 41±14 years of age) were studied after being resuscitated from recurrent (10±12) episodes of primary idiopathic ventricular fibrillation; 23 had received a defibrillator. The first initiating beat of ventricular fibrillation had an identical electrocardiographic morphology and coupling interval (297±41 ms) to preceding isolated premature beats typically noted in the aftermath of resuscitation. These triggers were localized by mapping the earliest electrical activity and ablated by local radiofrequency delivery. Outcome was assessed by Holter and defibrillator memory interrogation. Premature beats were elicited from the Purkinje conducting system in 23 patients: from the left ventricular septum in 10, from the anterior right ventricle in 9, and from both in 4. The interval from the Purkinje potential to the following myocardial activation varied from 10 to 150 ms during premature beat but was 11±5 ms during sinus rhythm, indicating location at peripheral Purkinje arborization. The premature beats originated from the right ventricular outflow tract muscle in 4 patients. The accuracy of mapping was confirmed by acute elimination of premature beats during local radiofrequency delivery. During a follow-up of 24±28 months, 24 patients (89%) had no recurrence of ventricular fibrillation without drug.Conclusions— Primary idiopathic ventricular fibrillation is a syndrome characterized by dominant triggers from the distal Purkinje system. These sources can be eliminated by focal energy delivery.
Exercise-Induced Increase in Baroreflex Sensitivity Predicts Improved Prognosis After Myocardial Infarction
- Maria Teresa La Rovere,
- Chiara Bersano,
- Marco Gnemmi,
- Giuseppe Specchia and
- Peter J. Schwartz
Circulation Volume 106, Issue 820 August 2002

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Background— Despite the rational expectation for a survival benefit produced by exercise training among post–myocardial infarction (MI) patients, direct evidence remains elusive. Clinically, changes in autonomic balance toward lower vagal activity have consistently been associated with increased mortality risk; conversely, among both control and post-MI dogs, exercise training improved vagal reflexes and prevented sudden death. Accordingly, we tested the hypothesis that exercise training, if accompanied by a shift toward increased vagal activity of an autonomic marker such as baroreflex sensitivity (BRS), could reduce mortality in post-MI patients.Methods and Results— Ninety-five consecutive male patients surviving a first uncomplicated MI were randomly assigned to a 4-week endurance training period or to no training. Age (51±8 versus 52±8 years), site of MI (anterior 41% versus 43%), left ventricular ejection fraction (52±13 versus 51±14%), and BRS (7.9±5.4 versus 7.9±3.4 ms/mm Hg) did not differ between the two groups. After 4 weeks, BRS improved by 26% (P=0.04) in trained patients, whereas it did not change in nontrained patients. During a 10-year follow-up, cardiac mortality among the 16 trained patients who had an exercise-induced increase in BRS ≥3 ms/mm Hg (responders) was strikingly lower compared with that of the trained patients without such a BRS increase (nonresponders) and that of the nontrained patients (0 of 16 versus 18 of 79 [23%], P=0.04). Cardiac mortality was also lower among responders irrespective of training (4% versus 24%, P=0.04).Conclusions— Post-MI exercise training can favorably modify long-term survival, provided that it is associated with a clear shift of the autonomic balance toward an increase in vagal activity.
Impact of Community-Wide Police Car Deployment of Automated External Defibrillators on Survival From Out-of-Hospital Cardiac Arrest
- Robert J. Myerburg,
- Jeffrey Fenster,
- Mauricio Velez,
- Donald Rosenberg,
- Shenghan Lai,
- Paul Kurlansky,
- Starbuck Newton,
- Melenda Knox and
- Agustin Castellanos
Circulation Volume 106, Issue 927 August 2002

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Background— Disappointing survival rates from out-of-hospital cardiac arrests encourage strategies for faster defibrillation, such as use of automated external defibrillators (AEDs) by nonconventional responders.Methods and Results— AEDs were provided to all Miami-Dade County, Florida, police. AED-equipped police (P-AED) and conventional emergency medical rescue (EMS) responders are simultaneously deployed to possible cardiac arrests. Times from 9-1-1 contact to the scene were compared for P-AED and concurrently deployed EMS, and both were compared with historical EMS experience. Survival with P-AED was compared with outcomes when EMS was the sole responder. Among 420 paired dispatches of P-AED and EMS, the mean±SD P-AED time from 9-1-1 call to arrival at the scene was 6.16±4.27 minutes, compared with 7.56±3.60 minutes for EMS (P<0.001). Police arrived first to 56% of the calls. The time to first responder arrival among P-AED and EMS was 4.88±2.88 minutes (P<0.001), compared with a historical response time of 7.64±3.66 minutes when EMS was the sole responder. A 17.2% survival rate was observed for victims with ventricular fibrillation or pulseless ventricular tachycardia (VT/VF), compared with 9.0% for standard EMS before P-AED implementation (P=0.047). However, VT/VF benefit was diluted by the observation that 61% of the initial rhythms were nonshockable, reducing the absolute survival benefit among the total study population to 1.6% (P-AED, 7.6%; EMS, 6.0%).Conclusions— P-AED establishes a layer of responders that generate improved response times and survival from VT/VF. There was no benefit for victims with nonshockable rhythms.
Spatial Inhomogeneity of Sympathetic Nerve Function in Hibernating Myocardium
- Andrew J. Luisi,
- James A. Fallavollita,
- Gen Suzuki and
- John M. Canty
Circulation Volume 106, Issue 713 August 2002

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Background— Although humans and swine with hibernating myocardium have an increased risk of sudden death, the contribution of chronic alterations in sympathetic nerve function is unknown. Acute transmural ischemia causes inhomogeneity in sympathetic innervation that may lead to lethal arrhythmias, but it is unclear whether similar abnormalities develop in response to chronic reversible ischemia.Methods and Results— Swine were chronically instrumented with a left anterior descending coronary artery (LAD) stenosis that produced hibernating myocardium after 3 months. Resting subendocardial flow (LAD 0.75±0.14 versus 1.19±0.14 mL · min⁻¹ · g⁻¹, P<0.05) and wall thickening (LAD 15±3% versus 40±2%, P<0.05) were reduced compared with normal remote regions, without triphenyltetrazolium chloride evidence of necrosis. ¹³¹I-meta-iodobenzylguanidine (MIBG) was used to assess integrity of the norepinephrine uptake-1 mechanism, and the spatial and transmural distributions were quantified by ex vivo counting. In hibernating myocardium, MIBG deposition was decreased in each layer, with the greatest reduction in the subendocardium (LAD subendocardium 0.28±0.02 versus 0.42±0.04 mL · g⁻¹ · min⁻¹ in normal, P<0.05; LAD subepicardium 0.31±0.03 versus 0.38±0.04 mL · g⁻¹ · min⁻¹ in normal, P<0.05). In contrast, there were no spatial alterations of MIBG deposition in sham-instrumented animals.Conclusions— The sympathetic norepinephrine uptake-1 mechanism is impaired in hibernating myocardium. These findings raise the possibility that chronic alterations in sympathetic innervation contribute to the excess mortality seen in the setting of hibernating myocardium.
Automated External Defibrillator Use by Police Responders: Where Do We Go From Here?
- José A. Joglar and
- Richard L. Page
Circulation Volume 106, Issue 927 August 2002

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Proposed Diagnostic Criteria for the Brugada Syndrome: Consensus Report
Circulation Volume 106, Issue 195 November 2002

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Relation of Ejection Fraction and Inducible Ventricular Tachycardia to Mode of Death in Patients With Coronary Artery Disease: An Analysis of Patients Enrolled in the Multicenter Unsustained Tachycardia Trial
- Alfred E. Buxton,
- Kerry L. Lee,
- Gail E. Hafley,
- D. George Wyse,
- John D. Fisher,
- Michael H. Lehmann,
- Luis A. Pires,
- Michael R. Gold,
- Douglas L. Packer,
- Mark E. Josephson,
- Eric N. Prystowsky,
- Mario R. Talajic
Circulation Volume 106, Issue 195 November 2002

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Background— Fifty percent of deaths in patients with coronary disease occur suddenly. Although many factors correlate with increased mortality, there is little information regarding the influence of these factors on mode of death. As such, optimum methods to determine patients most likely to benefit from implantable defibrillator therapy are unclear.Methods and Results— We analyzed the relation of ejection fraction and inducible ventricular tachyarrhythmias to mode of death in all 1791 patients enrolled in the Multicenter Unsustained Tachycardia Trial who did not receive antiarrhythmic therapy. Total mortality and arrhythmic deaths/cardiac arrests occurred more frequently in patients with ejection fraction <30% than in those with ejection fraction of 30% to 40%. The percentage of deaths classified as arrhythmic was similar in patients with ejection fraction <30% or ≥30%. The relative contribution of arrhythmic events to total mortality was significantly higher in patients with inducible tachyarrhythmia (58% of deaths in inducible patients versus 46% in noninducible patients, P=0.004). The higher percentage of events that were arrhythmic among patients with inducible tachyarrhythmia appeared more distinct among patients with an ejection fraction ≥30% (61% of events were arrhythmic among inducible patients with ejection fraction ≥30% and only 42% among noninducible patients, P=0.002).Conclusions— Both low ejection fraction and inducible tachyarrhythmias identify patients with coronary disease at increased mortality risk. Ejection fraction does not discriminate between modes of death, whereas inducible tachyarrhythmia identifies patients for whom death, if it occurs, is significantly more likely to be arrhythmic, especially if ejection fraction is ≥30%.
Effect of β-Blocking Therapy on Outcome in the Multicenter UnSustained Tachycardia Trial (MUSTT)
- Kristin E. Ellison,
- Gail E. Hafley,
- Kathleen Hickey,
- Joyce Kellen,
- James Coromilas,
- Kenneth M. Stein,
- Kerry L. Lee,
- Alfred E. Buxton
Circulation Volume 106, Issue 2119 November 2002

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Background— β-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 β-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 β-blockers. Patients treated with β-blockers were younger and had higher ejection fractions, higher rates of recent angina, and more recent infarction. β-Blockers were associated with decreased total mortality for the entire study population (5-year mortality 50% with β-blockers versus 66% without β-blockers; adjusted P=0.0001). The mortality benefit associated with β-blockers was present in patients with and without inducible tachycardia, except those treated with implantable defibrillators. There was no significant effect of β-blocker therapy on the rate of arrhythmic death or cardiac arrest (adjusted P=0.2344).Conclusions— β-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 β-blockers. The beneficial effects of β-blockers were demonstrable in all patients except those treated with implantable defibrillators.

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