Prophylactic Use of an Implantable Cardioverter–Defibrillator after Acute Myocardial Infarction
Stefan H. Hohnloser, M.D., Karl Heinz Kuck, M.D., Paul Dorian, M.D., Robin S. Roberts, M.Tech., John R. Hampton, M.D., Robert Hatala, M.D., Eric Fain, M.D., Michael Gent, D.Sc., Stuart J. Connolly, M.D., for the DINAMIT Investigators
Background Implantable cardioverter–defibrillator (ICD)therapy has been shown to improve survival in patients withvarious heart conditions who are at high risk for ventriculararrhythmias. Whether benefit occurs in patients early aftermyocardial infarction is unknown.
Methods We conducted the Defibrillator in Acute Myocardial InfarctionTrial, a randomized, open-label comparison of ICD therapy (in332 patients) and no ICD therapy (in 342 patients) 6 to 40 daysafter a myocardial infarction. We enrolled patients who hadreduced left ventricular function (left ventricular ejectionfraction, 0.35 or less) and impaired cardiac autonomic function(manifested as depressed heart-rate variability or an elevatedaverage 24-hour heart rate on Holter monitoring). The primaryoutcome was mortality from any cause. Death from arrhythmiawas a predefined secondary outcome.
Results During a mean (±SD) follow-up period of 30±13months, there was no difference in overall mortality betweenthe two treatment groups: of the 120 patients who died, 62 werein the ICD group and 58 in the control group (hazard ratio fordeath in the ICD group, 1.08; 95 percent confidence interval,0.76 to 1.55; P=0.66). There were 12 deaths due to arrhythmiain the ICD group, as compared with 29 in the control group (hazardratio in the ICD group, 0.42; 95 percent confidence interval,0.22 to 0.83; P=0.009). In contrast, there were 50 deaths fromnonarrhythmic causes in the ICD group and 29 in the controlgroup (hazard ratio in the ICD group, 1.75; 95 percent confidenceinterval, 1.11 to 2.76; P=0.02).
Conclusions Prophylactic ICD therapy does not reduce overallmortality in high-risk patients who have recently had a myocardialinfarction. Although ICD therapy was associated with a reductionin the rate of death due to arrhythmia, that was offset by anincrease in the rate of death from nonarrhythmic causes.
Prophylactic use of an implantable cardioverter–defibrillator(ICD) has been shown to prolong life in several populationsof patients with serious heart disease and reduced left ventricularfunction. Previous trials, however, have included relativelyfew patients who have recently had a myocardial infarction.1,2The first 6 to 12 months after myocardial infarction constitutea period during which there is a particularly high risk of deathfrom arrhythmia,3,4,5 and pharmacologic therapies other thanbeta-blockers have not been shown to be effective in counteractingthis risk.
The Defibrillator in Acute Myocardial Infarction Trial (DINAMIT)was designed to test whether prophylactic implantation of anICD would reduce mortality in survivors of a recent myocardialinfarction who are at high risk for ventricular arrhythmias.6Because several large studies have shown that markers of impairedautonomic function are associated with increased mortality,7,8,9,10,11only survivors of infarction who had severe left ventriculardysfunction as well as depressed heart-rate variability or anelevated 24-hour heart rate were eligible for the trial.
Methods
Organization of the Trial
The DINAMIT trial was initiated by the investigators. The studyprotocol was approved by the institutional review boards ofall 73 participating investigational sites in 12 countries worldwide.All the patients gave written informed consent before randomization.An external data and safety monitoring committee independentlyreviewed the results at regular intervals throughout the trial.A description of the design and study protocol has been publishedpreviously.6
Patient Population
Patients aged 18 to 80 years were eligible if they had recentlyhad a myocardial infarction (6 to 40 days previously) and ifthey had a left ventricular ejection fraction of 0.35 or less,as assessed by angiography, radionuclide scanning, or echocardiography.Patients also had to have a standard deviation of normal-to-normalRR intervals of 70 msec or less or a mean RR interval of 750msec or less (heart rate, 80 beats per minute or greater) overa 24-hour period,8,9,10,11,12 as assessed by 24-hour Holtermonitoring performed at least three days after the infarction.
The following exclusion criteria were applied: congestive heartfailure or New York Heart Association class IV at the time ofrandomization; noncardiac disease that limited life expectancy;coronary artery bypass grafting performed since the qualifyinginfarction or planned to be performed within four weeks afterrandomization; three-vessel percutaneous coronary interventionperformed since the qualifying infarction; name on a waitinglist for a heart transplant; current, ongoing ICD therapy; priorimplantation of a permanent pacemaker; requirement for an ICD(i.e., sustained ventricular tachycardia or fibrillation morethan 48 hours after the qualifying infarction); low probabilitythat the study ICD could be implanted within seven days afterrandomization; and expected poor compliance with the protocol.
Study Design
Patients were stratified according to clinical center and underwentcentral randomization, which was performed at the study coordinatingand methods center (Hamilton Civic Hospitals Research Centre,Hamilton, Ont., Canada). Patients were randomly assigned ina 1:1 ratio either to receive an ICD (the ICD group) or notto receive an ICD (the control group). The randomization sequencewas stratified according to center and balanced within randomlyvarying blocks of two, four, or six patients.
The study protocol mandated that patients receive the best conventionalmedical therapy. Investigators were encouraged to treat allstudy patients with angiotensin-converting–enzyme inhibitors,beta-blockers, aspirin, and lipid-lowering drugs, as appropriate.Reasons for not giving these medications were documented.
Patients who were randomly assigned to receive an ICD were requiredto undergo implantation of a market-approved, single-chamberICD (St. Jude Medical, Sunnyvale, Calif.) within one week afterrandomization. Implanted leads were required to achieve an Rwave of more than 4.9 mV, a pacing threshold of less than 2.1V at 0.5 msec, and a defibrillation threshold with a safetymargin of at least 10 J. Postoperatively, the ICD was set todetect ventricular tachycardia and fibrillation. The detectionrate for tachycardia was set at 175 or more beats per minutefor at least 16 beats. The device was programmed to deliverall discharges at maximal output in the ventricular-fibrillationzone (200 beats per minute or greater). Bradycardia pacing wasprogrammed for activation at a minimum of 40 beats per minute.Antitachycardia pacing within the ventricular-tachycardia zone(175 to 200 beats per minute) could be activated to deliverfour bursts of 6 to 10 beats beginning at 81 percent of thetachycardia cycle length, with 10-msec decrements between bursts.
Follow-up
Patients were followed with respect to all outcomes for a maximumof four years, beginning on the date of randomization. The studycommenced in April 1998, and follow-up ended in September 2003,about 15 months after the last patient had been recruited. Follow-upvisits were scheduled to take place three and six months afterrandomization and at six-month intervals thereafter.
Study Outcomes
The primary outcome in DINAMIT was death from any cause. Deathdue to cardiac arrhythmia was the secondary outcome. Ascertainmentof the cause of death of patients in the trial was the responsibilityof the local investigators. Documentation of the cause of deathwas based on information obtained from witnesses, family members,death certificates, hospital records, and autopsy reports, whenavailable, but not from ICD telemetry.
The blinded central validation committee independently reviewedinformation on all deaths. Classification of each death basedon the surrounding circumstances was agreed on by these reviewers.The committee classified deaths as either arrhythmic or nonarrhythmicin nature on the basis of criteria originally developed by Hinkleand Thaler12 and previously validated in the Canadian ImplantableDefibrillator Study13 and the Canadian Amiodarone MyocardialInfarction Arrhythmia Trial.14 These criteria are based on theclinical circumstances of death and do not rely on ICD information.
Statistical Analysis
Data analysis was performed at Hamilton Civic Hospitals ResearchCenter by two of the authors (Mr. Roberts and Dr. Gent). Allinvestigators had full access to the data. The primary studyoutcome was evaluated according to the intention-to-treat principle.The cumulative risks of death from any cause and from specificcauses over time were estimated separately for each treatmentgroup with use of the Kaplan–Meier procedure15 and werecompared between groups with use of the Mantel–Haenszeltest.16 On the basis of mortality data from similar populationsof patients,9 it was anticipated that the control group wouldhave a three-year mortality rate of 30.0 percent and that 40.0percent of these deaths would be accounted for by deaths dueto arrhythmia. The net effect of preventing 80.0 percent ofthese deaths due to arrhythmia with use of an ICD would reducethe total mortality rate to 20.4 percent — a reductionconsidered biologically plausible and clinically relevant. Basedon a one-sided test at an alpha level of 0.05, we determinedthat 525 patients would be required in order for the study tohave 80 percent power to identify a difference between the groups.Because mortality rates were lower than expected during thestudy, the target enrollment was increased to 674 patients.
A single interim analysis of efficacy was performed by an externalsafety and efficacy monitoring committee after 66 deaths —about half the anticipated number — had occurred. A one-sidedP value of less than 0.001 would have resulted in early terminationof the study. Before unblinding, a decision was made to usetwo-sided statistical testing.
Results
Characteristics of the Patients
A total of 674 patients were enrolled; 332 were randomly assignedto the ICD group and 342 to the control group. Twenty of thepatients who were randomly assigned to receive an ICD subsequentlyrefused to have one implanted. The baseline demographic characteristicsof the two groups are provided in Table 1. Most patients hadnew Q-wave infarctions, and 72.1 percent were anterior in location.Two thirds of the patients had received thrombolytic therapy,had undergone acute percutaneous intervention, or both. Themean left ventricular ejection fraction was 0.28. In a subgroupof 321 patients in whom assessment of the left ventricular ejectionfraction was repeated six to eight weeks after randomization,there was a mean (±SD) increase of 0.02±0.11.The average time from myocardial infarction to randomizationwas 18 days and was similar in the two groups.
Table 1. Characteristics of the Patients at Baseline.
There was excellent adherence to optimal medical therapy (Table 1).Amiodarone was prescribed to 27 of the patients who hadbeen randomly assigned to receive an ICD (8.1 percent) and to46 of the control patients (13.5 percent) (P=0.04). During thecourse of the study, percutaneous or surgical coronary revascularizationwas performed in 33 ICD recipients (9.9 percent), as comparedwith 50 patients in the control group (14.6 percent) (P=0.08).Only partial follow-up was available for four patients (allmembers of the control group).
Death from Any Cause
The cumulative-mortality curves for the two groups are shownin Figure 1. During an average observation period of 30±13months, 120 patients died, 62 in the ICD group and 58 in thecontrol group (hazard ratio, 1.08; 95 percent confidence interval,0.76 to 1.55; two-sided P=0.66) (Table 2). The annual mortalityrates were 7.5 and 6.9 percent, respectively. The adjudicatedcauses of death are listed in Table 2. Two patients who hadbeen randomly assigned to the ICD group died before they receivedan ICD.
A set of baseline clinical features was examined for potentialsubgroup effects (Figure 2). For each feature, the ICD effectremained consistent and did not differ significantly betweenor among subgroups.
Figure 2. Hazard Ratios for Death from Any Cause, According to Selected Clinical Characteristics.
The horizontal lines represent the 95 percent confidence intervals. NYHA denotes New York Heart Association, and SD standard deviation.
Death from Arrhythmic and Nonarrhythmic Causes
In the ICD group, there were 12 deaths due to arrhythmia, ascompared with 29 in the control group (annual rate, 1.5 percentand 3.5 percent, respectively) (Figure 3A). This differencewas highly statistically significant (hazard ratio, 0.42; 95percent confidence interval, 0.22 to 0.83; two-sided P=0.009).There were 50 deaths due to nonarrhythmic causes in the ICDgroup, as compared with 29 in the control group (hazard ratio,1.75; 95 percent confidence interval, 1.11 to 2.76; P=0.02)(Figure 3B). Of the three prespecified subcategories of deathsfrom nonarrhythmic causes, the only one found to occur at asignificantly increased rate in the ICD group was death fromcardiac, nonarrhythmic causes (P=0.05) (Table 2). Of the 50deaths from nonarrhythmic causes in the ICD group, 39 (78 percent)were cardiovascular in nature (i.e., due to cardiac, nonarrhythmicor vascular, noncardiac causes); in the control group, 23 of29 deaths from nonarrhythmic causes (79 percent) were cardiovascularin nature.
Figure 3. Kaplan–Meier Estimates of the Cumulative Risk of Death from Arrhythmia (Panel A) and from Nonarrhythmic Causes (Panel B), According to Study Group.
The average time between randomization and ICD implantationwas 6.3±7.3 days. Of the 332 patients assigned to receivean ICD, 310 actually received a device. The time between ICDimplantation and discharge from the hospital averaged 4.7±6.4days. In-hospital device-related complications occurred in 25patients; the most common of these complications were lead dislodgment,pneumothorax, and inappropriate shocks. There were no deathsrelated to device implantation. To prevent inappropriate pacing,bradycardia pacing was typically programmed to 40 to 45 beatsper minute (maximum, 55 beats per minute).
Discussion
In this randomized trial of high-risk patients who had recentlyhad a myocardial infarction, overall survival was not improvedby prophylactic implantation of an ICD. The study groups werewell balanced with respect to their baseline clinical characteristicsand the early use of reperfusion therapy. There was a high rateof use of appropriate medical therapy. It is unlikely that thesimilarity between the two groups in the rate of death fromall causes represents a false negative result due to inadequatesample size. The 95 percent confidence interval of the hazardratio for death from any cause rules out a reduction in mortalityof 25 percent or greater.
The ICD group, as compared with the control group, had a large,statistically significant reduction (by more than 50 percent)in the risk of death due to arrhythmia; however, this effectwas offset by a significant increase, of similar magnitude,in the rate of death from nonarrhythmic causes. The ICD is expectedto reduce mortality by preventing sudden cardiac deaths dueto ventricular fibrillation without any effect on death fromnonarrhythmic causes. This pattern has been consistently observedin previous trials of ICD therapy in patients at high risk.In several trials of ICD therapy — the Canadian ImplantableDefibrillator Study, the Antiarrhythmics versus ImplantableDefibrillators trial, and the Cardiac Arrest Study Hamburg —there was a 50 percent reduction in the rate of death from arrhythmiaand almost no effect on the rate of death from other causes;the net effect was a 25 percent reduction in overall mortality.17In the Multicenter Automatic Defibrillator Implantation TrialI (MADIT I) and MADIT II,1,2 which evaluated prophylactic ICDtherapy in patients with chronic ischemic heart disease, therate of death due to arrhythmia was markedly reduced and therate of death from other causes was not increased.
In DINAMIT, the reduction in the rate of arrhythmia-relateddeath was very similar to that observed in previous trials ofICD therapy. However, in contrast to the previous trials, DINAMITrevealed a statistically significant increase in the rate ofdeath from nonarrhythmic causes among patients assigned to receivean ICD. Most of these deaths (78 percent) were cardiovascularin nature. It appears that in this trial, as in previous trialsof ICD therapy, the ICD prevented death from ventricular fibrillation.However, preventing death from ventricular fibrillation didnot reduce overall mortality in these patients.
The reason for the unexpected and unprecedented increase inmortality from causes other than arrhythmia in patients assignedto receive an ICD is not clear. The most likely explanationis that the patients "saved" from an arrhythmia-related deathby ICD therapy are also at high risk for death from other cardiaccauses. There was no sign of an increased rate of death in associationwith the surgical procedure or complications with the use ofthe ICD. It is unlikely that the increased rate of deaths fromcardiac, nonarrhythmic causes were due to excessive pacing,as in the Dual-Chamber and VVI Implantable Defibrillator Trial,18because the backup pacing was programmed at a very low ratein almost all the patients in the ICD group.
It has been speculated that ICDs might, by shocking ventricularfibrillation, merely transform sudden death to eventual deathfrom pump failure, without significantly prolonging life, especiallywhen ventricular fibrillation is occurring in a patient withend-stage heart failure or a large acute myocardial infarction.There is some evidence that such a possibility may have factoredinto the results of the Coronary Artery Bypass Graft Patch Trial,19and it provides a reasonable hypothesis for the results of DINAMIT.
The mean left ventricular ejection fraction in DINAMIT was significantlyreduced (at 0.28) and did not increase appreciably six weekslater. However, the mean ejection fraction was somewhat higherthan that in MADIT II (0.23)2 — a difference that mayexplain the higher overall mortality observed in MADIT II. Themain differences between patients in DINAMIT and those in previoustrials is the temporal proximity to acute infarction and theabnormal results of autonomic-function tests at baseline. InDINAMIT, the ratio of death due to arrhythmia to death fromany cause was 34 percent, similar to the ratio in other ICDtrials. A recent analysis of the MADIT II trial, which alsoenrolled patients with a previous myocardial infarction, supportsthe main finding of DINAMIT — that patients who have recentlyhad an infarction do not benefit from ICD.20 In MADIT II, themean time from the most recent infarction to enrollment in thestudy was 6.5 years; the subgroup of patients with the mostrecent infarction did not benefit at all from ICD therapy.20This finding was in marked contrast to the outcome in patientswhose infarction had occurred in the remote past, in whom thebenefit from the ICD was large.
Although several clinical studies had indicated that the resultsof tests of autonomic function carry prognostic implicationsafter myocardial infarction,7,8,9,10,11 the recently publishedAzimilide Post Infarct Survival Evaluation,21 which provideddefinitive information on the prognostic value of heart-ratevariability, has demonstrated that impaired heart-rate variabilityis associated with increased mortality but not specificallymortality from arrhythmic causes. Nonetheless, the proportionof deaths in the DINAMIT control group that were attributableto arrhythmia was 50 percent — as high as in any previoustrial of ICD therapy for secondary or primary prevention.
Use of amiodarone was more common in the control group thanit was in the ICD group. Most likely, this difference is a reflectionof physicians' desire in this unblinded study to provide additionaloptimal therapy in the absence of an ICD. However, as recentlydemonstrated in a large, randomized trial, amiodarone does notoffer any survival benefit if given for primary prevention inpatients with ischemic or nonischemic cardiomyopathy and reducedventricular function.22 Most likely, amiodarone had no effecton survival in our trial as well.
Supported by a grant from St. Jude Medical, Sunnyvale, Calif.
Drs. Hohnloser, Kuck, Dorian, and Connolly report that theyare consultants to and have received lecture fees from St. JudeMedical. Dr. Fain reports that he is an employee of St. JudeMedical.
* The investigators and study sites participating in the Defibrillatorin Acute Myocardial Infarction Trial (DINAMIT) are listed inthe Appendix.
Source Information
From J.W. Goethe University, Frankfurt (S.H.H.), and St. Georg's Hospital, Hamburg (K.H.K.) — both in Germany; St. Michel's Hospital, Toronto (P.D.), and Hamilton Civic Hospitals Research Center (R.S.R., M.G.) and McMaster University (S.J.C.), Hamilton, Ont. — all in Canada; University Hospital, Nottingham, United Kingdom (J.R.H.); Slovak Cardiovascular Institute, Bratislava, Slovak Republic (R.H.); and St. Jude Medical, Sunnyvale, Calif. (E.F.).
Address reprint requests to Dr. Hohnloser at the Department of Medicine, Division of Cardiology, J.W. Goethe University, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany, or at hohnloser{at}em.uni-frankfurt.de.
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Appendix
Steering committee — S.J. Connolly (Hamilton, Canada),P. Dorian (Toronto), E. Fain (Sunnyvale, Calif.), M. Gent (Hamilton,Canada), J.R. Hampton (Nottingham, United Kingdom), R. Hatala(Bratislava, Slovakia), S.H. Hohnloser (chair; Frankfurt, Germany),K.H. Kuck (Hamburg, Germany), and R.S. Roberts (Hamilton, Canada).Central validation committee — M. Gent (Hamilton, Canada),M. Gardner (Halifax, Canada), H. Kottkamp (Leipzig, Germany),and P. Blomström (Uppsala, Sweden). External safety andefficacy monitoring committee — J.T. Bigger (New York),S. Pocock (London), and H.J.J. Wellens (Maastricht, the Netherlands).Clinical study sites, Canada — Hamilton Health Sciences,Hamilton (S. Connolly); St. Michael's Hospital, Toronto (P.Dorian); Victoria Heart Institute, Victoria (L.D. Sterns); Institutde Cardiologie de Montréal, Montréal (D. Roy);Queen Elizabeth II Health Sciences Centre, Halifax (M. Gardner);Cambridge Memorial Hospital, Cambridge (S. Vizel); Campus Notre-Damedu Centre Hospitalier Universitaire de Montréal, Montréal(C. Guimond); Montréal General Hospital, Montréal(T. Hadjis); Hôpital Cité de la Santé deLaval, Vimont (R. Gendreau); Welland County General Hospital1, Welland (E.G. Abraham); Guelph General Hospital, Guelph (J.Misterski); Toronto East General Hospital, Toronto (G. Rewa);Kawartha Cardiology Clinic, Peterborough (W.G. Hughes); HôpitalLaval, Sainte-Foy (F. Philippon); Oakville Trafalgar MemorialHospital, Oakville (D.R. McConachie); Welland County GeneralHospital 2, Welland (J. Vedova); Hôpital du SacréCoeur, Montréal (T.K. Kus); Foothills Hospital, Calgary(L.B. Mitchell); Ottawa Heart Institute, Ottawa (M. Green);Hôtel-Dieu De Lévis, Lévis (F. Grondin);Sunnybrook Health Science Centre, Toronto (Z. Wulffhart); UniversityHospital, Edmonton (S.K.M. Kimber); Centre Hospitalier Universitaire,Sainte-Foy (M. Samson); Hôpital de L'Enfant Jésus,Québec City (G. Houde); and Healthcare Corporation ofSt. John's, St. John's (S. Connors). Clinical study sites, Germany— Allgemeines Krankenhaus St. Georg, Hamburg (K.H. Kuck);Johann Wolfgang Goethe Universität, Frankfurt (S.H. Hohnloser);Städtische Kliniken, Kassel (J. Neuzner); UniversitätsklinikHerzzentrum, Leipzig (H. Kottkamp); St. Josefs-Hospital, Wiesbaden(W. Kasper); Städtisches Klinikum, Brandenburg (M. Oeff);Kreiskrankenhaus, Leer (E. Stammwitz); Kerckhoff Klinik, BadNauheim (J. Sperzel); Robert-Bosch-Krankenhaus, Stuttgart (U.Sechtem); Kliniken der Medizinischen Hochschule, Hannover (H.Drexler); Klinikum Weisser Hirsch, Dresden (S.G. Spitzer); ZentralkrankenhausLinks der Weser, Bremen (J. Siebels); Westfälische Wilhelms-Universität,Münster (G. Breithardt); Herzzentrum, Bad Krozingen (D.Kalusche); Universitätsklinikum, Aachen (P.Hanrath); Krankenhausder Barmherzigen Brüder, Trier (C. Drobig); MedizinischeKlinik und Poliklinik, Homburg–Saar (J. Jung); Friederich-Wilhelms-Universität,Bonn (B. Lüderitz); Julius-Maximilians-Universität,Würzburg (W. Bauer); Klinikum Süd, Nürnberg (K.J.Göhl); and Klinikum Konstanz, Zentrum für Innere Medizin,Konstanz (F. Haman). Other clinical study sites — UnitedKingdom: Wordsley Hospital, Stourbridge (P. Forsey); the GlenfieldHospital National Health Service Trust, Leicester (W.D. Toff);Regional Medical Cardiology Centre, Belfast, Northern Ireland(P.P. McKeown); and the Queen Elizabeth Hospital, Birmingham(M.J. Griffith); Slovakia: Slovak Cardiovascular Institute,Bratislava (R. Hatala); and F.D. Roosevelt Hospital, BanskáBystrica (G. Kaliska); Poland: Grochowski Hospital, Warsaw (L.Ceremuzynski); I Klinika Kardiologii, Katowice (M. Trusz-Gluza);Institute of Cardiology, Warsaw (H. Szwed); and I PomeranianAcademy of Medicine, Szczecin (Z. Kornacewicz); France: HôpitalLouis Pradel, Lyons (P. Touboul); Centre Hospitalier UniversitaireNancy, Nancy (E. Aliot); Centre Hospitalier Universitaire deRennes, Rennes (P. Mabo); Hôpital Arnaud de Villeneuve,Montpellier (J. Davy); Centre Hospitalier Bon Secours, Bon Secours(K. Khalife); Hôpital Lariboisiere, Paris (A. Leenhardt);Hôpital Maillot, Briey (M. Parisot), and Centre HospitalierGénéral, Bodlio (J. Le Potier); Czech Republic:Institute for Clinical and Experimental Medicine, Prague (J.Bytesnik); Austria: Rehabilitationszentrum Grossgmain, Grossgmain(F. Schnöll); and Wilhelminenspital der Stadt Wien, Wien(G. Jakl); Switzerland: Kantonspital Basel, Basel (S. Osswald);Sweden: University Hospital, Uppsala (P. Blomström); andHuddinge University Hospital, Huddinge (B. Eriksson); Italy:Ospedale di Bentivoglio, Bologna (B. Sassone); and United States:Fort Sanders Parkwest Hospital, Knoxville, Tenn. (J.R. Gimbel);and North Mississippi Medical Center, Tupelo (K. Crossen).
Authors/Task Force Members, , Dickstein, K., Cohen-Solal, A., Filippatos, G., McMurray, J. J.V., Ponikowski, P., Poole-Wilson, P. A., Stromberg, A., van Veldhuisen, D. J., Atar, D., Hoes, A. W., Keren, A., Mebazaa, A., Nieminen, M., Priori, S. G., Swedberg, K., ESC Committee for Practice Guidelines (CPG), , Vahanian, A., Camm, J., De Caterina, R., Dean, V., Dickstein, K., Filippatos, G., Funck-Brentano, C., Hellemans, I., Kristensen, S. D., McGregor, K., Sechtem, U., Silber, S., Tendera, M., Widimsky, P., Zamorano, J. L., Document Reviewers, , Tendera, M., Auricchio, A., Bax, J., Bohm, M., Corra, U., della Bella, P., Elliott, P. M., Follath, F., Gheorghiade, M., Hasin, Y., Hernborg, A., Jaarsma, T., Komajda, M., Kornowski, R., Piepoli, M., Prendergast, B., Tavazzi, L., Vachiery, J.-L., Verheugt, F. W. A., Zamorano, J. L., Zannad, F.
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