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223 results on '"Remme, Wj"'

1. Effects of perindopril on cardiac remodelling and prognostic value of pre-discharge quantitative echocardiographic parameters in elderly patients after acute myocardial infarction: the PREAMI echo sub-study

Author

Nicolosi GL, Golcea S, Cecopni C, Parrinello G, Decarli A, Remme WJ, Tavazzi L, Ferrari R, PREAMI I.n.v.e.s.t.i.g.a.t.o.r.s., CHIARIELLO, MASSIMO, Nicolosi, Gl, Golcea, S, Cecopni, C, Parrinello, G, Decarli, A, Chiariello, Massimo, Remme, Wj, Tavazzi, L, Ferrari, R, and Preami, I. n. v. e. s. t. i. g. a. t. o. r. s.

Subjects
Male, medicine.medical_specialty, Population, Myocardial Infarction, Diastole, Angiotensin-Converting Enzyme Inhibitors, Placebo, Double-Blind Method, Internal medicine, Perindopril, Humans, Medicine, Myocardial infarction, education, Aged, education.field_of_study, Ejection fraction, Ventricular Remodeling, business.industry, Prognosis, medicine.disease, Echocardiography, Doppler, Treatment Outcome, Heart failure, Cardiology, End-diastolic volume, Female, Cardiology and Cardiovascular Medicine, business, Echocardiography, Remodelling, circulatory and respiratory physiology, medicine.drug
Abstract

Aims To determine (i) the effect of perindopril on several geometric and functional parameters of the left and right ventricles assessed by echocardiography in the unique Perindopril and Remodelling in Elderly with Acute Myocardial Infarction (PREAMI) population of post-acute myocardial infarction (AMI) elderly patients with preserved left ventricular (LV) function; and (ii) the prognostic predictors at pre-discharge derived from echo-Doppler measurements in the same population. Methods and results PREAMI included 1252 post-AMI patients (age 73 ± 6 years, LV ejection fraction 59.1 ± 7.7%) receiving optimal therapy after AMI, randomized to perindopril 8 mg/day ( n = 631) or placebo ( n = 621); n = 896 had complete echo-Doppler data. Outcome measures were clinical [death, heart failure (HF)] and standard echo-Doppler parameters. Pre-discharge LV end-diastolic volume (LVEDV) was similar: 81.1 ± 23.1 (perindopril) and 79.6 ± 22.7 mL (placebo). At 6 months and 1 year, LVEDV remained unchanged with perindopril (81.2 ± 24.4 and 81.8 ± 26.8 mL, respectively), but increased with placebo (83.0 ± 25.3 and 83.6 ± 25.7 mL, respectively, both P < 0.001 vs. baseline). Perindopril reduced cardiac sphericity vs. placebo ( P = 0.015 at 6 months; P = 0.020 at 1 year). Classification regression tree analysis showed treatment as the most important predictor of remodelling. Multiple pre-discharge echocardiographic variables predicted the death/HF endpoint, independently of treatment ( P ≤ 0.05). Conclusion Remodelling occurs in post-AMI in elderly patients with normal LV function. Echo-Doppler variables at baseline have prognostic implications. Treatment with perindopril reduces progressive LV remodelling that can occur even in the case of small infarct size.

Published
2009

2. Investigating the stratified efficacy and safety of pharmacological blood pressure-lowering: an overall protocol for individual patient-level data meta-analyses of over 300 000 randomised participants in the new phase of the Blood Pressure Lowering Treatment Trialists' Collaboration (BPLTTC)

Author

Rahimi, K, Canoy, D, Nazarzadeh, M, Salimi-Khorshidi, G, Woodward, M, Teo, K, Davis, BR, Chalmers, J, Pepine, CJ, Agodoa, L, Algra, A, Asselbergs, FW, Beckett, N, Berge, E, Black, H, Brouwers, FPJ, Brown, M, Bulpitt, CJ, Byington, B, Cutler, J, Devereaux, RB, Dwyer, D, Fagard, R, Fox, K, Fukui, T, Gupta, AJ, Holman, RR, Imai, Y, Ishii, M, Julius, S, Kanno, Y, Kjeldsen, SE, Kostis, J, Kuramoto, K, Lanke, J, Lewis, E, Lievre, M, Lindholm, LH, Lueders, S, MacMahon, S, Matsuzaki, M, Mehlum, MH, Nissen, S, Ogawa, H, Othisgihara, T, Ohkubo, T, Palmer, C, Patel, A, Pepine, C, Pfeffer, M, Poulter, NR, Rakugi, H, Remuzzi, G, Ruggenenti, P, Saruta, T, Schrader, J, Schrier, R, Sever, P, Sleight, P, Staessen, JA, Suzuki, H, Thijs, L, Ueshima, K, Umemoto, S, Van Gilst, WH, Verdecchia, P, Wachtell, K, Yui, Y, Yusuf, S, Baigent, C, Collins, R, De Zeeuw, D, Neal, B, Perkovic, V, Rahman, M, Remme, WJ, Rodgers, A, Sundstrom, J, Turnbull, F, Foundation for Circulatory Health, Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), and Staessen, Jan

Subjects
medicine.medical_specialty, Epidemiology, Disease, REGIMENS, 030204 cardiovascular system & hematology, Research Support, Phase (combat), 03 medical and health sciences, Medicine, General & Internal, 0302 clinical medicine, General & Internal Medicine, Diabetes mellitus, Protocol, medicine, Journal Article, Humans, 030212 general & internal medicine, Intensive care medicine, Non-U.S. Gov't, Stroke, Antihypertensive Agents, Randomized Controlled Trials as Topic, RISK, Protocol (science), Medicine(all), Science & Technology, efficacy and safety of bp lowering treatment, HYPERTENSION, business.industry, Research Support, Non-U.S. Gov't, blood pressure, General Medicine, medicine.disease, PROSPECTIVELY-DESIGNED OVERVIEWS, MODEL, Treatment Outcome, MAJOR CARDIOVASCULAR EVENTS, Blood pressure, Patient level data, meta-analyses, Blood pressure lowering, business, Life Sciences & Biomedicine, Blood Pressure Lowering Treatment Trialists’ Collaboration
Abstract

IntroductionPrevious research from the Blood Pressure Lowering Treatment Trialists’ Collaboration (BPLTTC) and others has shown that pharmacological blood pressure (BP)- lowering substantially reduces the risk of major cardiovascular events, including ischaemic heart disease, heart failure and stroke. In this new phase, the aim is to conduct individual patient-level data (IPD) meta-analyses involving eligible BP-lowering randomised controlled trials (RCTs) to address uncertainties relating to efficacy and safety of BP-lowering treatment.Methods and analysisRCTs investigating the effect of pharmacological BP-lowering, with a minimum of 1000 patient-years of follow-up in each trial arm, are eligible. Our systematic review identified 100 potentially eligible trials. We requested their investigators/sponsors to contribute baseline, follow-up and outcomes data. As of June 2018, the collaboration has obtained data from 49 trials (n=315 046 participants), with additional data currently in the process of being transferred from four RCTs (n=34 642 participants). In addition, data harmonisation has commenced. Scientific activities of the collaboration are overseen by the Steering Committee with input from all collaborators. Detailed protocols for individual meta-analyses will be developed and registered on public platforms.Ethics and disseminationEthics approval has been obtained for this new and extended phase of the BPLTTC, the largest collaboration of de-identified IPD from RCTs. It offers an efficient and ethical manner of re-purposing existing data to answer clinically important questions relating to BP treatment as well as methodological questions relating to IPD meta-analyses. Among the immediate impacts will include reliable quantification of effects of treatment modifiers, such as baseline BP, age and prior disease, on both vascular and non-vascular outcomes. Analyses will further assess the impact of BP-lowering on important, but less well understood, outcomes, such as new-onset diabetes and renal disease. Findings will be published in peer-reviewed medical journals on behalf of the collaboration.

Published
2019

3. Eplerenone in patients with systolic heart failure and mild symptoms

Author

Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, Vincent J, Pocock SJ, Pitt B, Drexler H, McMurray J, Remme WJ, Cornel JH, Hildebrandt P, Hradec J, Mareev V, Reddy KS, Sindone A, Martinez F, Alonso Garcia A, Wilhelmsen L, Dargie HJ, Tavazzi L, Pocock S, Leizorovic A, Collier T, Nul DR, Serra JL, Thierer JM, Cross DB, Sindone AP, Singh BB, Boreux JL, Charlier FP, Dendale P, De Keulenaer G, Marchandise B, Marechal P, Marenne F, Mieghem WV, Van Dorpe AC, Vanhaecke J, Arnold JM, Dion D, Huynh T, Kouz SM, Lepage S, McKelvie RS, O'Meara E, Proulx G, Sauve C, Aschermann M, Brecka D, Filipovsky J, Groch L, Jerabek O, Jokl I, Linkova H, Motovska Z, Munz J, Penicka M, Rucka D, Mid JS, Spacek R, Spinar J, Stipal R, Vojacek J, Attali P, Bonneau A, Bousser JP, Dutoit L, Funck F, Galinier MP, Gibelin P, Hautefeuille BD, Hittinger L, Jobic Y, Jourdain P, Komajda M, Maupas E, Olive T, Philias A, Roul G, Rouleau F, Trochu JN, Boehm M, Bruch L, Engelhardt H, Erbs S, Foerster A, Franz N, Hambrecht R, Heuer H, Krueger U, Landmesser U, Leischik R, Mitrovic V, Moehlenkamp S, Monti J, Mueller Ehmsen J, Oezcelik C, Philipp S, Pieske B, Roehnisch JU, Schunkert H, Schwinger R, Wachter R, Willenbrock R, Winkelmann BR, Winkler R, Wollert KC, Adamopoulos S, Kalikazaros I, Karavidas A, Karvounis H, Kremastinos D, Manolis AJ, Nanas I, Sotirellos K, Vasiliadis K, Zaboulis C, Lee S, Yu CM, Czibok C, Édes I, Forster T, Preda I, Simon K, Takacs J, Zámolyi K, Bhagavatula KS, Chockalingam K, Desai N, Iyengar SS, Jayadev SM, Mullasari AS, Sathe SP, Sinha N, Vadagenalli PS, Wander GS, McDonald KM, Nash P, Vaughan CJ, Agostoni P, Ambrosio GB, Bittolo Bon G, Boffa G, Cacciavillani L, Capucci A, Chiariello M, Cirrincione V, Gensini GF, Masini F, Modena MG, Monte I, Rosano GM, Senni M, Sinagra G, Tamburino C, Terrosu P, Villani GQ, Volterrani M, Chae SC, Ha CW, Ha JW, Shin JH, Bayram Llamas E, Calvillo JC, Cruz Diaz A, Delgado Leal L, Estrada Gomez MM, Kosturakis D, Petersen Aranguren F, Velasco Sanchez RG, Daniëls MC, Dirkali A, Dunselman PH, de Kluiver EP, Kragten JA, Lok DJ, Maas AH, Michels HR, Nicastia DM, Stoel I, de Swart JB, Thijssen HJ, Van Kempen LH, Voors AA, Willems FF, Dluzniewski M, Gaciong Z, Kawecka Jaszcz K, Jozwa R, Korewicki J, Krzeminska Pakula M, Kurowski M, Ogorek M, Pempera M, Rynkiewicz A, Ujda M, Wierzchowiecki M, Abreu Á, Andrade A, Carrageta M, Fonseca C, Franco F, Gil VM, Lousada N, Mendonca C, Moreira I, Padua FP, Providência L, Cardoso JC, Trabulo M, Aroutyunov GP, Gindin K, Karpov YB, Kostenko VA, Nikitin YP, Obraztsova GI, Shilkina NP, Shlyakhto EV, Skvortsov A, Ding ZP, Yeo DP, Ambrovicova V, Gaspar L, Goncalvesova E, Kycina P, Litvinova J, Mikes Z, Murin J, Poliacik P, Uhliar R, Lloyd EA, Marx D, Naidoo DP, Prozesky HW, Sliwa Hahnle K, Theron H, Anguita M, De Teresa E, Galve E, Juanatey JR, Orbe PM, Vida M, Ahremark U, Andersson B, Axelsson U, Berglund S, Boman K, Dahlstrom U, Fu M, Holm Orndahl L, Johansson A, Lindgren M, Nemeczek C, Prantare H, Roussine V, Stehn G, Stenberg A, Vasko P, Bazylevych A, Dyadyk OI, Dzyak GV, Girina OM, Ignatenko GA, Kononenko LG, Kubyshkin VF, Kuryata OV, Parkhomenko AN, Perepelytsya MV, Pertseva TO, Popik GS, Rishko MV, Sakharchuk II, Tseluyko VI, Tykhonova SA, Vizir V, Voronkov LG, Al Khaja N, Almahmeed WA, Bazargani N, Adgey AA, Al Mohammad A, Banerjee P, Barlow M, Bridges AB, Brooks N, Connolly EC, Denvir MA, Egdell RM, Kardos A, Keeling PJ, Khokhar AA, Senior R, Williams SG, Anand IS, Anderson JL, Berk MR, Bertolet BD, Bisognano JD, Blonder RD, Breburda CS, Canaday DB, Capodilupo RC, Choiunard MD, Colucci WS, Dahiya RJ, Dunlap SH, Essandoh LK, Flores AR, Henderson DA, Herzog WR Jr, Katz RJ, Kosinski EJ, Labin IN, Lally FL, Lash JA, McGrew FA 3rd, Mohiuddin SM, Moraes D, Murali SC, Nallasivan M, Philbin E, Prabhu S, Primack DS, Ramani R, Rawitscher D, Sangrigoli R, Schamalfuss CM, Stoletniy L, Strong MH, Thadani U, Treasure CB 2nd, Vicari RM, Vogel CD, Wlsh MN, Wencker D, Wilson SA, Winkel E, Wiseman AH, Zoiopoulos LY, Mancebo JR, Mendoza I, Waich S.T., PERRONE FILARDI, PASQUALE, Zannad, F, Mcmurray, Jj, Krum, H, van Veldhuisen, Dj, Swedberg, K, Shi, H, Vincent, J, Pocock, Sj, Pitt, B, Drexler, H, Mcmurray, J, Remme, Wj, Cornel, Jh, Hildebrandt, P, Hradec, J, Mareev, V, Reddy, K, Sindone, A, Martinez, F, Alonso Garcia, A, Wilhelmsen, L, Dargie, Hj, Tavazzi, L, Pocock, S, Leizorovic, A, Collier, T, Nul, Dr, Serra, Jl, Thierer, Jm, Cross, Db, Sindone, Ap, Singh, Bb, Boreux, Jl, Charlier, Fp, Dendale, P, De Keulenaer, G, Marchandise, B, Marechal, P, Marenne, F, Mieghem, Wv, Van Dorpe, Ac, Vanhaecke, J, Arnold, Jm, Dion, D, Huynh, T, Kouz, Sm, Lepage, S, Mckelvie, R, O'Meara, E, Proulx, G, Sauve, C, Aschermann, M, Brecka, D, Filipovsky, J, Groch, L, Jerabek, O, Jokl, I, Linkova, H, Motovska, Z, Munz, J, Penicka, M, Rucka, D, Mid, J, Spacek, R, Spinar, J, Stipal, R, Vojacek, J, Attali, P, Bonneau, A, Bousser, Jp, Dutoit, L, Funck, F, Galinier, Mp, Gibelin, P, Hautefeuille, Bd, Hittinger, L, Jobic, Y, Jourdain, P, Komajda, M, Maupas, E, Olive, T, Philias, A, Roul, G, Rouleau, F, Trochu, Jn, Boehm, M, Bruch, L, Engelhardt, H, Erbs, S, Foerster, A, Franz, N, Hambrecht, R, Heuer, H, Krueger, U, Landmesser, U, Leischik, R, Mitrovic, V, Moehlenkamp, S, Monti, J, Mueller Ehmsen, J, Oezcelik, C, Philipp, S, Pieske, B, Roehnisch, Ju, Schunkert, H, Schwinger, R, Wachter, R, Willenbrock, R, Winkelmann, Br, Winkler, R, Wollert, Kc, Adamopoulos, S, Kalikazaros, I, Karavidas, A, Karvounis, H, Kremastinos, D, Manolis, Aj, Nanas, I, Sotirellos, K, Vasiliadis, K, Zaboulis, C, Lee, S, Yu, Cm, Czibok, C, Édes, I, Forster, T, Preda, I, Simon, K, Takacs, J, Zámolyi, K, Bhagavatula, K, Chockalingam, K, Desai, N, Iyengar, S, Jayadev, Sm, Mullasari, A, Sathe, Sp, Sinha, N, Vadagenalli, P, Wander, G, Mcdonald, Km, Nash, P, Vaughan, Cj, Agostoni, P, Ambrosio, Gb, Bittolo Bon, G, Boffa, G, Cacciavillani, L, Capucci, A, Chiariello, M, Cirrincione, V, Gensini, Gf, Masini, F, Modena, Mg, Monte, I, PERRONE FILARDI, Pasquale, Rosano, Gm, Senni, M, Sinagra, G, Tamburino, C, Terrosu, P, Villani, Gq, Volterrani, M, Chae, Sc, Ha, Cw, Ha, Jw, Shin, Jh, Bayram Llamas, E, Calvillo, Jc, Cruz Diaz, A, Delgado Leal, L, Estrada Gomez, Mm, Kosturakis, D, Petersen Aranguren, F, Velasco Sanchez, Rg, Daniëls, Mc, Dirkali, A, Dunselman, Ph, de Kluiver, Ep, Kragten, Ja, Lok, Dj, Maas, Ah, Michels, Hr, Nicastia, Dm, Stoel, I, de Swart, Jb, Thijssen, Hj, Van Kempen, Lh, Voors, Aa, Willems, Ff, Dluzniewski, M, Gaciong, Z, Kawecka Jaszcz, K, Jozwa, R, Korewicki, J, Krzeminska Pakula, M, Kurowski, M, Ogorek, M, Pempera, M, Rynkiewicz, A, Ujda, M, Wierzchowiecki, M, Abreu, Á, Andrade, A, Carrageta, M, Fonseca, C, Franco, F, Gil, Vm, Lousada, N, Mendonca, C, Moreira, I, Padua, Fp, Providência, L, Cardoso, Jc, Trabulo, M, Aroutyunov, Gp, Gindin, K, Karpov, Yb, Kostenko, Va, Nikitin, Yp, Obraztsova, Gi, Shilkina, Np, Shlyakhto, Ev, Skvortsov, A, Ding, Zp, Yeo, Dp, Ambrovicova, V, Gaspar, L, Goncalvesova, E, Kycina, P, Litvinova, J, Mikes, Z, Murin, J, Poliacik, P, Uhliar, R, Lloyd, Ea, Marx, D, Naidoo, Dp, Prozesky, Hw, Sliwa Hahnle, K, Theron, H, Anguita, M, De Teresa, E, Galve, E, Juanatey, Jr, Orbe, Pm, Vida, M, Ahremark, U, Andersson, B, Axelsson, U, Berglund, S, Boman, K, Dahlstrom, U, Fu, M, Holm Orndahl, L, Johansson, A, Lindgren, M, Nemeczek, C, Prantare, H, Roussine, V, Stehn, G, Stenberg, A, Vasko, P, Bazylevych, A, Dyadyk, Oi, Dzyak, Gv, Girina, Om, Ignatenko, Ga, Kononenko, Lg, Kubyshkin, Vf, Kuryata, Ov, Parkhomenko, An, Perepelytsya, Mv, Pertseva, To, Popik, G, Rishko, Mv, Sakharchuk, Ii, Tseluyko, Vi, Tykhonova, Sa, Vizir, V, Voronkov, Lg, Al Khaja, N, Almahmeed, Wa, Bazargani, N, Adgey, Aa, Al Mohammad, A, Banerjee, P, Barlow, M, Bridges, Ab, Brooks, N, Connolly, Ec, Denvir, Ma, Egdell, Rm, Kardos, A, Keeling, Pj, Khokhar, Aa, Senior, R, Williams, Sg, Anand, I, Anderson, Jl, Berk, Mr, Bertolet, Bd, Bisognano, Jd, Blonder, Rd, Breburda, C, Canaday, Db, Capodilupo, Rc, Choiunard, Md, Colucci, W, Dahiya, Rj, Dunlap, Sh, Essandoh, Lk, Flores, Ar, Henderson, Da, Herzog WR, Jr, Katz, Rj, Kosinski, Ej, Labin, In, Lally, Fl, Lash, Ja, McGrew FA, 3rd, Mohiuddin, Sm, Moraes, D, Murali, Sc, Nallasivan, M, Philbin, E, Prabhu, S, Primack, D, Ramani, R, Rawitscher, D, Sangrigoli, R, Schamalfuss, Cm, Stoletniy, L, Strong, Mh, Thadani, U, Treasure CB, 2nd, Vicari, Rm, Vogel, Cd, Wlsh, Mn, Wencker, D, Wilson, Sa, Winkel, E, Wiseman, Ah, Zoiopoulos, Ly, Mancebo, Jr, Mendoza, I, and Waich, S. T.

Published
2011

4. Modulation of the renin-angiotensin-aldosterone system – pivotal in heart failure treatment

Author

Remme Wj

Subjects
medicine.medical_specialty, Sympathetic nervous system, Angiotensin II receptor type 1, Aldosterone, business.industry, Aldosterone Receptor Antagonist, medicine.disease, Angiotensin II, chemistry.chemical_compound, medicine.anatomical_structure, chemistry, Internal medicine, Heart failure, ACE inhibitor, Renin–angiotensin system, medicine, Cardiology, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

The therapy of heart failure has evolved considerably over the last few decades. Whereas in the early years the focus was on improvement of cardiac pump function and symptomatic therapy by reducing overload through diuretic therapy, attention has now shifted toward prevention of (worsening of) the syndrome. This conceptual shift has been brought about by our recent understanding of the pathophysiological mechanisms underlying the progression of heart failure, in particular neurohormonal activation and cardiac remodeling, and the potential of neurohormonal antagonists such as ACE inhibitors, bblocking agents and aldosterone receptor antagonists, to modulate these processes and thereby significantly reduce or retard heart failure-related morbidity and mortality. The reninangiotensin system and aldosterone are two of the major, closely related neurohormonal systems involved in the pathogenesis of left ventricular dysfunction. Initially, ACE inhibitor therapy for heart failure was based on the concept that as, at least in more severe heart failure, circulating renin and angiotensin II levels are increased, the ACE inhibitor was considered to be a vasodilator of potential importance. Parallel to subsequent observations that ACE inhibitors beneficially affected morbidity and mortality in heart failure, this concept changed toward one in which it was realized that, in addition to the the circulating, endocrine-acting RAS, many tissues produce components of a local tissue renin-angiotensin system, and the concept that angiotensin II, in addition to being a potent vasoconstrictor, also had growth-promoting properties and was able to stimulate other neurohormonal systems, such as the sympathetic nervous system. The beneficial effects of ACE inhibitors on morbidity and mortality become apparent after a relatively long-term treatment period and are not necessarily accompanied by clear-cut hemodynamic improvement or an increase in exercise capacity. Hence, one may correctly assume that the long-term beneficial effects of these agents relate to their chronic structural effects on the heart and the vascular wall, effects which combine inhibition of cardiac and vascular remodeling, an improvement in endothelial function and a reduction in myocardial ischemia, and which all result from modulation of the local tissue renin-angiotensin system, and which relate not or significantly less to their modulating effect on the circulating renin-angiotensin levels.

Published
1999

10. Guidelines for the Diagnosis and Treatment of Chronic Heart Failure

Author

Swedberg, Karl, Cleland, J, Dargie, H, Drexler, H, Follath, F, Komajda, M, Tavazzi, L, Smiseth, OA, Gavazzi, A, Haverich, A, Hoes, A, Jaarsma, T, Korewicki, J, Levy, S, Linde, C, Lopez-Sendon, JL, Nieminen, MS, Pierard, L, and Remme, WJ

Subjects
business.industry, CONVERTING-ENZYME-INHIBITORS, RANDOMIZED CONTROLLED-TRIALS, IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR, ACUTE CORONARY SYNDROMES, ANTIARRHYTHMIC-DRUG-THERAPY, LEFT-VENTRICULAR DYSFUNCTION, EXERCISE OXYGEN-CONSUMPTION, BRAIN NATRIURETIC PEPTIDE, CARDIOVASCULAR MAGNETIC-RESONANCE, Medicine, HOME-BASED INTERVENTION, Cardiology and Cardiovascular Medicine, business, Humanities
Published
2005

32. Reduced costs with bisoprolol treatment for heart failure - An economic analysis of the second Cardiac Insufficiency Bisoprolol Study (CIBIS-II)

Author

Bacquet, P, Levy, E, Mcguire, A, Mcmurray, J, Merot, Jl, Paschen, B, Remme, Wj, Szucs, Td, Klein, W, Brunhuber, W, Hofmann, R, Kuhn, P, Nesser, Hj, Slany, J, Weihs, W, Wiedermann, C, Wimmer, H, van Mieghem, W, Boland, J, Chaudron, Jm, Jordaens, L, Melchior, Jp, Aschermann, M, Bruthansl, J, Hradec, M, Kolbel, F, Semrad, B, Haghfelt, T, Hansen, Jf, Goetzsche, Co, Hildebrandt, P, Kassis, E, Rasmussen, V, Rokkedal, J, Thomassen, A, Groundstroem, K, Uusimaa, P, Le Heuzey JY, Aumont, Mc, Aupetit, Jf, Baille, N, Baudouy, P, Belin, A, Bonneau, A, Bonneric, G, Bousser, Jp, Citron, B, Dary, P, Decoulx, E, De Groote, P, Denolle, T, Dievart, F, Duriez, P, Eicher, Jc, Enjuto, G, Ferriere, M, Fournier, E, Garandeau, M, Gauthier, J, Genest, M, Gerbe, A, Godenir, Jp, Guillot, B, Guillot, Jp, Guillot, P, Heno, P, D'Ivernois, C, Jean, M, Kacet, S, Kalle, R, Komajda, M, Lacroix, A, Lallemand, R, Lardoux, H, Marquet, M, Martin, M, Martin, O, Mery, D, Mossaz, R, Mothes, P, Olive, T, Ostorero, M, Paganelli, F, Page, E, Pauly Laubry, C, Puel, J, Rousseau, Jf, Roux, Jj, Schenowitz, A, Sourdais, K, Tremel, F, Verdun, A, Witchiz, S, Wolf, Je, Hombach, V, Assmann, I, Beyer, T, Bischoff, Ko, Darius, H, Ertl, G, Fleck, E, Forster, K, Freytag, F, Gleichmann, U, Haasis, R, Henssge, R, Hey, D, Hesse, P, Hofs, T, Keck, M, Klein, H, Kromer, Et, Kruls Munch, J, Luderitz, B, Maisch, B, Mitrovic, V, Neubauer, S, Osterziel, Kj, Simon, H, Spitzer, Sg, Stohring, R, Taubert, G, Teichmann, W, Theisen, K, Wende, W, Wieser, H, Zotz, R, Bridges, A, Adgey, J, Ambepitiya, G, Boon, N, Boyle, Rm, Cowley, Aj, Cripps, T, Davies, Mk, Dunn, F, Findlay, J, Forsey, P, Fyfe, T, Gould, B, Greenwood, Tw, Hubner, P, Khan, S, Lewis, P, Mackay, A, Maltz, M, Mcarthur, J, Mcleod, A, Mcleod, D, Metcalfe, M, Millar Craig, M, Mills, P, Nelson, Jk, Nicholls, D, Oakley, Gd, Patterson, Dlh, Pohl, Jef, Ray, S, Silke, B, Wilkinson, Pr, Preda, I, Csanady, M, Cserhalmi, L, Edes, I, Gesztesi, T, Karpati, P, Simon, K, Tarjan, J, Fogari, R, Tramarin, R, Galie, N, Giani, P, Milanese, U, Scalvini, S, Scrutinio, D, Sechi, Leonardo Alberto, Tettamanti, F, De Vito, F, Crean, P, Mccann, H, Mulcahy, D, Sugrue, D, van Hoogenhuyze DCA, van der Burgh PH, Ciampricotti, R, van Dantzig JM, Denhartog, Fr, Henneman, Ja, van Kesteren HAM, Kragten, Ja, Liem, Kl, Limburg, A, van der Linde MR, Linssen, Gcm, Pasteuning, H, Penn, Hjam, Van Rossum, P, Schaafsma, Hj, Schelling, A, Sloos, R, Wesdorp, Jcl, Korewicki, J, Achremczyk, P, Czestockowska, E, Dowgird, M, Dyduszynski, A, Gorski, J, Ilmurzynska, K, Janicki, K, Kornacewicz Jach, Z, Kraska, T, Krzeminska Pakula, M, Kuch, J, Nartowicz, E, Petelenz, T, Piwowarska, W, Rawczynska Englert, I, Ruzyllo, W, Swiatecka, G, Tendera, M, Wierzchowiecki, M, Wodniecki, J, Wojciechowoski, D, Wrabec, K, Wysocki, H, Gomes, Rs, Ceia, Mf, Lousada, N, Campos, Jmm, Providencia, La, de Moura ALZC, Marejev, Vj, Aronov, Dm, Arutjunov, Gp, Bart, Bj, Basechikin, Ss, Belenkov, Jn, Beloussov, Jb, Bokeria, Oa, Charchogljan, Ra, Doschytsin, V, Fedorova, Ta, Glezer, Mg, Gorbachenkov, A, Gorshkov, Gospodarenko, Al, Ivashkin, Vt, Ivleva, Aj, Kyrichenko, Aa, Lavrov, Aa, Lazebnik, Lb, Marynov, A, Mazaev, Vp, Polejev, Nr, Shpektor, Sidorenko, Ba, Sobolev, Ke, Starodoubtsev, Ak, Storozhakhov, Gi, Syrkin, Al, Zodionchenko, Vs, Zvereva, Tv, Murin, J, Kaliska, G, Rybar, R, Valle, V, Artaza, M, Conthe, P, Cruz, Jm, Garcia Moll, M, Lopez Sendon JL, Martinez, A, Monzon, F, Ribas, M, Roig, E, Roldan, I, Hoglund, C, Ekdahl, S, Hjelmaeus, L, Lindberg, K, Lofdahl, P, Ulvenstam, G, Warselius, L, Follath, F, Anghern, W, Dubach, P, Erne, P, Gallino, A, Moccetti, T, Jmouro, Av, Dargie, Hj, Erdmann, E, Lechat, P, Sendon, Jll, Mareyev, V, Sadowski, Z, Seabra Gomes RJ, Zannad, F, Wehrlen Grandjean, M, Funck Brentano, C, Hansen, S, Hohnloser, S, Vanoli, E, Jaillon, P, De Baker, G, Dahlstrom, U, Hill, C, Leizorovicz, A, Burgnard, F, Rolland, C, Wiemann, H, Verkenne, P, Arab, T, Cussac, N, Dussous, V, Haise, S, and Funck Brentano, C.

Subjects
H Social Sciences (General), medicine.medical_specialty, Cost-Benefit Analysis, Adrenergic beta-Antagonists, METOPROLOL, Placebo, THERAPY, Indirect costs, Pharmacoeconomics, Pharmacotherapy, RANDOMIZED INTERVENTION TRIAL, PHARMACOECONOMICS, Germany, Health care, Bisoprolol, Humans, Medicine, Outpatient clinic, Prospective Studies, Intensive care medicine, health care economics and organizations, Heart Failure, CARVEDILOL, business.industry, MORTALITY, Diagnosis-related group, United Kingdom, Chemotherapy, Adjuvant, MERIT-HF, HOSPITALIZATION, MINIMIZATION, INHIBITORS, France, Quality-Adjusted Life Years, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

Background Beta-blockers, used as an adjunctive to diuretics, digoxin and angiotensin converting enzyme inhibitors, improve survival in chronic heart failure. We report a prospectively planned economic analysis of the cost of adjunctive beta-blocker therapy in the second Cardiac Insufficiency BIsoprolol Study (CIBIS II). Methods Resource utilization data (drug therapy, number of hospital admissions, length of hospital stay, ward type) were collected prospectively in all patients in CIBIS . These data were used to determine the additional direct costs incurred, and savings made, with bisoprolol therapy. As well as the cost of the drug, additional costs related to bisoprolol therapy were added to cover the supervision of treatment initiation and titration (four outpatient clinic/office visits). Per them (hospital bed day) costings were carried out for France, Germany and the U.K. Diagnosis related group costings were performed for France and the U.K. Our analyses took the perspective of a third party payer in France and Germany and the National Health Service in the U.K. Results Overall, fewer patients were hospitalized in the bisoprolol group, there were fewer hospital admissions perpatient hospitalized, fewer hospital admissions overall, fewer days spent in hospital and fewer days spent in the most expensive type of ward. As a consequence the cost of care in the bisoprolol group was 5-10% less in all three countries, in the per them analysis, even taking into account the cost of bisoprolol and the extra initiation/up-titration visits. The cost per patient treated in the placebo and bisoprolol groups was FF35 009 vs FF31 762 in France, DM11 563 vs DM10 784 in Germany and pound 4987 vs pound 4722 in the U.K. The diagnosis related group analysis gave similar results. Interpretation Not only did bisoprolol increase survival and reduce hospital admissions in CIBIS II, it also cut the cost of care in so doing. This `win-win' situation of positive health benefits associated with cost savings is Favourable from the point of view of both the patient and health care systems. These findings add further support for the use of beta-blockers in chronic heart failure.

Published
2001

34. Acute anti-ischemic effects ef perindoprilat in men with coronary artery disease and their relation with left ventricular function

Author

Bartels, GL, van den Heuvel, AFM, van Veldhuisen, DJ, van der Ent, M, Remme, WJ, and Cardiovascular Centre (CVC)

Subjects
ACE-INHIBITION, MYOCARDIAL-INFARCTION, CHRONIC STABLE ANGINA, CAPTOPRIL, TRIAL, CONVERTING ENZYME-INHIBITION, HEART-DISEASE, PECTORIS, PACING-INDUCED ISCHEMIA, DYSFUNCTION
Abstract

Long-term angiotensin-converting enzyme (ACE) inhibition may reduce ischemic events in patients with coronary artery disease, but whether it protects against acute ischemia or the effects of preexisting left ventricular (LV) dysfunction on potential anti-ischemic properties is unknown. We performed a double-blind trial in 25 patients with exercise-induced ischemia. The effects of perindoprilat on pacing-induced myocardial ischemia were examined. Fourteen patients received perindoprilat and 11 patients received placebo. Based on LV function, 2 subgroups were formed in the perindoprilat group: 7 patients with LV dysfunction (LV ejection fraction

Published
1999

35. Effects of epanolol, a selective beta(1)-blocker with intrinsic sympathomimetic activity, in patients with ischemic left ventricular dysfunction

Author

Van Den Heuvel, AFM, van der Ent, M, van Veldhuisen, DJ, Kruijssen, DACM, Bartels, GL, Remme, WJ, and Cardiovascular Centre (CVC)

Subjects
epanolol, BETA-BLOCKADE, neurohormones, METOPROLOL, heart failure, HEART-FAILURE, MYOCARDIAL-METABOLISM, DISEASE, coronary flow, PARTIAL AGONIST
Abstract

Recently, different beta-blockers have been shown to be effective in the treatment of chronic heart failure (CHF), but the importance of their ancillary properties is not clear. Epanolol is a selective beta(1)-blocker with intrinsic sympathomimetic activity, which has been shown useful in angina pectoris, but its value in patients with left ventricular (LV) dysfunction and CHF is unknown. We examined the effects of epanolol in patients with LV dysfunction (n = 8; mean LV ejection fraction, 0.33 +/- 0.08) and compared them with patients with normal LV function (n = 8; mean LV ejection fraction, 0.52 +/- 0.03). Measurement of invasive hemodynamics and neurohormones was performed at rest and during myocardial ischemia, which was induced by atrial pacing. All measurements were performed before and after epanolol. Before epanolol, pacing-induced ischemia led to a similar increase in norepinephrine and coronary sinus blood flow in both groups. After epanolol, the increase in neurohormones was more pronounced in the group with LV dysfunction (norepinephrine, 1,130 +/- 164 pg/ml for patients with LV dysfunction vs. 637 +/- 41 pg/ml for normal subjects; p

Published
1998

41. Effects of metoprolol and carvedilol on pre-existing and new onset diabetes in patients with chronic heart failure: data from the Carvedilol Or Metoprolol European Trial (COMET)

Author

Torp-Pedersen C, Metra M, Charlesworth A, Spark P, Lukas MA, Poole-Wilson PA, Swedberg K, Cleland JG, Di Lenarda A, Remme WJ, Scherhag A, and COMET investigators

Abstract

BACKGROUND: Beta blocker treatment may worsen glucose metabolism. OBJECTIVE: To study the development of new onset diabetes in a large cohort of patients with heart failure treated with either metoprolol or carvedilol. DESIGN: Prospective and retrospective analysis of a controlled clinical trial. SETTING: Multinational multicentre study. PATIENTS: 3029 patients with chronic heart failure. INTERVENTIONS: Randomly assigned treatment with carvedilol (n = 1511, target dose 50 mg daily) or metoprolol tartrate (n = 1518, target dose 100 mg daily). RESULTS: Diabetic events (diabetic coma, peripheral gangrene, diabetic foot, decreased glucose tolerance or hyperglycaemia) and new onset diabetes (clinical diagnosis, repeated high random glucose level or glucose lowering drugs) were assessed in 2298 patients without diabetes at baseline. Diabetic events occurred in 122/1151 (10.6%) patients in the carvedilol group and 149/1147 (13.0%) patients in the metoprolol group (hazard ratio (HR) = 0.78; 95% confidence interval (CI) 0.61 to 0.99; p = 0.039). New onset diabetes was diagnosed in 119/1151 (10.3%) v 145/1147 (12.6%) cases in the carvedilol and metoprolol treatment groups (HR = 0.78, CI 0.61 to 0.997; p = 0.048), respectively. Patients with diabetes at baseline had an increased mortality compared with non-diabetic subjects (45.3% v 33.9%; HR = 1.45, CI 1.28 to 1.65). Both diabetic and non-diabetic subjects at baseline had a similar reduction in mortality with carvedilol compared with metoprolol (RR = 0.85; CI 0.69 to 1.06 and RR = 0.82; CI 0.71 to 0.94, respectively). CONCLUSION: A high prevalence and incidence of diabetes is found in patients with heart failure over a course of 5 years. New onset diabetes is more likely to occur during treatment with metoprolol than during treatment with carvedilol. [ABSTRACT FROM AUTHOR]

Published
2007
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43. Congestive Heart Failure

Author

Remme Wj

Subjects
Pharmacology, Inotrope, medicine.medical_specialty, Cardiac output, business.industry, Cardiomyopathy, Blood volume, Vasodilation, medicine.disease, Blood pressure, Internal medicine, Heart failure, medicine, Cardiology, Neurotransmitter metabolism, Cardiology and Cardiovascular Medicine, business
Abstract

Although the etiology of congestive heart failure is complex, a disturbance of myocardial function due to ischemic heart disease or various forms of cardiomyopathy is by far the leading causative factor. In the early stages of failure various cardiac compensating mechanisms, such as hypertrophy, an increase in contractility and the Frank-Starling mechanism, prevent a major reduction in function. With ongoing failure, myocardial muscle function further deteriorates because of a disturbance in myocardial energy utilization, abnormalities in sympathetic neurotransmitter metabolism, a reduction in beta-receptor density, and, more importantly, a derangement of intracellular calcium transport. The subsequent reduction in cardiac output leads to activation of peripheral neurohumoral mechanisms, including sympathetic stimulation, an increase in circulating norepinephrine, stimulation of the renin-angiotensin-aldosterone system (RAAS), and increased arginine vasopressin production, which result in arterial and venous vasoconstriction, redistribution of tissue blood flow, and an increase in circulating blood volume. The adjustments, however, lead to a vicious circle, where heart function is further depressed by the increase in afterload, whereas the changes in the venous bed and the increase in circulating volume ultimately result in congestion. At this point, digitalis and diuretics alone are no longer sufficiently effective and vasodilators are indicated, possibly combined, in the later stages of failure, with positive inotropic drugs. The angiotensin converting-enzyme inhibiting agents seem particularly useful in this context, presumably because of their complex mode of action, interfering with the neurohumoral systems and peripheral vasculature at multiple sites. Particularly with these agents, a remarkable improvement in clinical condition and exercise capacity has been observed. Even so, the long-term prognosis in patients with severe congestive heart failure is still extremely poor with one-year mortality rates in New York Heart Association class III and IV patients ranging from 34% to 48%. In this article, the pathophysiology of congestive heart failure and the potential of drug therapy are further discussed.

Published
1986

44. Carvedilol Protects Better Against Vascular Events Than Metoprolol in Heart Failure Results From COMET

Author

Remme, Wj, TORP PEDERSEN, C, Cleland, Jg, POOLE WILSON PA, Metra, Marco, Komajda, M, Swedberg, K, DI LENARDA, A, Spark, P, Scherhag, A, Moullet, C, and Lukas, Ma

Subjects
cardiovascular diseases
Abstract

ObjectivesWe explored whether vascular protection by carvedilol could contribute to its superior effects in the treatment of heart failure (HF) compared with metoprolol tartrate in the COMET (Carvedilol Or Metoprolol European Trial) study.BackgroundFull adrenergic blockade by carvedilol and additional (e.g., antioxidative) properties may lead to vascular protection relative to beta-1 blockade alone, and contribute to its efficacy in HF treatment.MethodsThree thousand twenty-nine patients with HF due to ischemic (51%) or idiopathic cardiomyopathy (44%) were randomized double-blind to carvedilol (n = 1,511) or metoprolol (n = 1,518) and followed for 58 months. Vascular end points were cardiovascular death, stroke, stroke death, myocardial infarction (MI), and unstable angina.ResultsThe effect of carvedilol on cardiovascular death improved consistently in subgroups with prespecified baseline variables. Myocardial infarctions were reported in 69 carvedilol and 94 metoprolol patients (hazard ratio [HR] 0.71, 95% confidence interval [CI] 0.52 to 0.97, p = 0.03). Cardiovascular death or nonfatal MI combined were reduced by 19% in carvedilol (HR 0.81, 95% CI 0.72 to 0.92, p = 0.0009 vs. metoprolol). Unstable angina was reported as an adverse event in 56 carvedilol and in 77 metoprolol patients (HR 0.71, 95% CI 0.501 to 0.998, p = 0.049). A stroke occurred in 65 carvedilol and 80 metoprolol patients (HR 0.79, 95% CI 0.57 to 1.10). Stroke or MI combined occurred in 130 carvedilol and 168 metoprolol patients (HR 0.75, 95% CI 0.60 to 0.95, p = 0.015), and fatal MI or fatal stroke occurred in 34 carvedilol and in 72 metoprolol patients (HR 0.46, 95% CI 0.31 to 0.69, p = 0.0002). Death after a nonfatal MI or stroke occurred in 61 of 124 carvedilol and in 106 of 160 metoprolol patients (HR 0.66, 95% CI 0.48 to 0.90, p = 0.0086).ConclusionsCarvedilol improves vascular outcomes better than metoprolol. These results suggest a ubiquitous protective effect of carvedilol against major vascular events.

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45. A Comparison of the Effects of Carvedilol and Metoprolol on Well-Being, Morbidity, and Mortality (the 'Patient Journey') in Patients With Heart Failure A Report From the Carvedilol Or Metoprolol European Trial (COMET)

Author

Cleland, JGF, Charlesworth, A, Lubsen, J (Jacob), Swedberg, K, Remme, WJ, Erhardt, L, di Lenarda, A, Komajda, M, Metra, M, Torp-Pedersen, C, Poole-Wilson, PA, and Epidemiology

Abstract

ObjectivesThis study was designed to investigate the loss of well-being, in terms of life-years, overall and in patients randomized to metoprolol versus carvedilol in the Carvedilol Or Metoprolol European Trial (COMET).BackgroundThe ultimate objectives of treating patients with heart failure are to relieve suffering and prolong life. Although the effect of treatment on mortality is usually described in trials, the effects on patient well-being throughout the trials’ courses are rarely reported.MethodsA total of 3,029 patients randomized in the COMET study were included in the analysis. “Patient journey” was calculated by adjusting days alive and out of hospital over four years using a five-point score completed by the patient every four months, adjusted according to the need for intensification of diuretic therapy. Scores ranged from 0% (dead or hospitalized) to 100% (feeling very well).ResultsOver 48 months, 17% of all days were lost through death, 1% through hospitalization, 23% through impaired well-being, and 2% through the need for intensified therapy. Compared with metoprolol, carvedilol was associated with fewer days lost to death, with no increase in days lost due to impaired well-being or days in hospital. The “patient journey” score improved from a mean of 54.8% (SD 26.0) to 57.4% (SD 26.3%) (p < 0.0068).ConclusionsDespite treatment with beta-blockers, heart failure remains associated with a marked reduction in well-being and survival. Loss of quality-adjusted life-years through death and poor well-being seemed of similar magnitude over four years, and both were much larger than the loss that could be attributed to hospitalization.

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46. Amiodarone. Haemodynamic profile during intravenous administration and effect on pacing-induced ischaemia in man

Author

van Hoogenhuyze Dc, Remme Wj, Storm Cj, Kruyssen Da, and Krauss Xh

Subjects
Inotrope, medicine.medical_specialty, Cardiac output, Hemodynamics, Amiodarone, Polysorbates, Coronary Disease, Oxygen Consumption, Afterload, Internal medicine, Heart rate, medicine, Animals, Humans, Pharmacology (medical), Benzofurans, business.industry, Arrhythmias, Cardiac, medicine.disease, Myocardial Contraction, medicine.anatomical_structure, Heart failure, Cardiology, Vascular resistance, business, medicine.drug
Abstract

The haemodynamic changes during intravenous amiodarone administration in laboratory animals and human studies are reviewed and compared with the results from our investigations. While the results of previous human studies have been rather variable, our investigations suggest that the cardiovascular changes following intravenous amiodarone include an early and usually short reduction of systemic and coronary vascular resistance, which may be partially due to the vasodilating properties of the solvent, polysorbate 80. As a result, a decrease in afterload and cardiac work and increases in cardiac output and coronary blood flow occur. Contrary to the observations in the animal experiments, heart rate increases in man, presumably as a result of the relatively greater fall in afterload which occurs. However, in spite of this increase in heart rate, contractility is reduced at the end of amiodarone administration and remains depressed after the infusion, resulting in a significant increase in left ventricular filling pressure. Neither myocardial oxygen demand nor consumption change during amiodarone administration. Although the intrinsic negative inotropic effects of amiodarone warrant a cautious approach in patients with left ventricular dysfunction, worsening of heart failure or the occurrence of myocardial ischaemia has been reported in only very few cases so far. In contrast, the drug was demonstrated to protect against pacing-induced myocardial ischaemia, in patients with both normal and depressed left ventricular function. These anti-ischaemic properties of amiodarone were investigated in a second study using a double pacing stress test protocol. Overall myocardial oxygen consumption did not change during pacing after amiodarone, but it clearly reduced (regional) myocardial ischaemia, as demonstrated by a reduction of ST-segment changes and anginal pain, and in particular by the absence of myocardial lactate production during pacing after amiodarone. These anti-ischaemic properties are mainly based on a reduction of myocardial oxygen demand, rather than on an improvement in coronary flow. It is concluded then, that amiodarone has significant haemodynamic effects as manifested by an early reduction in vascular resistance and a late negative inotropic effect. Although vasodilatation of short duration caused by its solvent, polysorbate 80, also occurs, the overall cardiovascular changes are caused by the direct, intrinsic haemodynamic effects of amiodarone alone. The important anti-ischaemic properties of amiodarone appear to result primarily from these cardiovascular actions and the inherent reduction in myocardial oxygen demand.

Published
1985

49. Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial.

Author

Poole-Wilson PA, Swedberg K, Cleland JGF, Di Lenarda A, Hanrath P, Komajda M, Lubsen J, Lutiger B, Metra M, Remme WJ, Torp-Pedersen C, Scherhag A, Skene A, COMET (Carvedilol Or Metoprolol European Trial) Investigators, Poole-Wilson, Philip A, Swedberg, Karl, Cleland, John G F, Di Lenarda, Andrea, Hanrath, Peter, and Komajda, Michel

Abstract

Background: Beta blockers reduce mortality in patients who have chronic heart failure, systolic dysfunction, and are on background treatment with diuretics and angiotensin-converting enzyme inhibitors. We aimed to compare the effects of carvedilol and metoprolol on clinical outcome.Methods: In a multicentre, double-blind, and randomised parallel group trial, we assigned 1511 patients with chronic heart failure to treatment with carvedilol (target dose 25 mg twice daily) and 1518 to metoprolol (metoprolol tartrate, target dose 50 mg twice daily). Patients were required to have chronic heart failure (NYHA II-IV), previous admission for a cardiovascular reason, an ejection fraction of less than 0.35, and to have been treated optimally with diuretics and angiotensin-converting enzyme inhibitors unless not tolerated. The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality or all-cause admission. Analysis was done by intention to treat.Findings: The mean study duration was 58 months (SD 6). The mean ejection fraction was 0.26 (0.07) and the mean age 62 years (11). The all-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard ratio 0.83 [95% CI 0.74-0.93], p=0.0017). The reduction of all-cause mortality was consistent across predefined subgroups. The composite endpoint of mortality or all-cause admission occurred in 1116 (74%) of 1511 on carvedilol and in 1160 (76%) of 1518 on metoprolol (0.94 [0.86-1.02], p=0.122). Incidence of side-effects and drug withdrawals did not differ by much between the two study groups.Interpretation: Our results suggest that carvedilol extends survival compared with metoprolol. [ABSTRACT FROM AUTHOR]

Published
2003
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