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51. Association between loop diuretic dose changes and outcomes in chronic heart failure: observations from the ESC-EORP Heart Failure Long-Term Registry

Author

Kapelios, C.J. Laroche, C. Crespo-Leiro, M.G. Anker, S.D. Coats, A.J.S. Díaz-Molina, B. Filippatos, G. Lainscak, M. Maggioni, A.P. McDonagh, T. Mebazaa, A. Metra, M. Moura, B. Mullens, W. Piepoli, M.F. Rosano, G.M.C. Ruschitzka, F. Seferovic, P.M. Lund, L.H. Gale, C.P. Beleslin, B. Budaj, A. Chioncel, O. Dagres, N. Danchin, N. Erlinge, D. Emberson, J. Glikson, M. Gray, A. Kayikcioglu, M. Maggioni, A. Nagy, K.V. Nedoshivin, A. Petronio, A.-S. Roos-Hesselink, J. Wallentin, L. Zeymer, U. Anker, S. Mebazaa, A. Coats, A. Filippatos, G. Ferrari, R. Maggioni, A.P. Goda, A. Diez, M. Fernandez, A. Fruhwald, F. Gatzov, P. Kurlianskaya, A. Hullin, R. Christodoulides, T. Hradec, J. Nielsen, O.W. Nedjar, R. Uuetoa, T. Jimenez, J.F.D. Harjola, V.-P. Logeart, D. Tousoulis, D. Milicic, D. Merkely, B. Amir, O. Shotan, A. Shafie, D. Mirrakhimov, E. Kavoliuniene, A. Erglis, A. Otljanska, M. Kostovska, E.S. DeMarco, D.C. Drozdz, J. Fonseca, C. Chioncel, O. Dekleva, M. Dahlstrom, U. Lainscak, M. Goncalvesova, E. Estrago, V. Bajraktari, G. Auer, J. Ablasser, K. Fruhwald, F. Dolze, T. Brandner, K. Gstrein, S. Poelzl, G. Moertl, D. Reiter, S. Muslibegovic, A. Vasilj, M. Fazlibegovic, E. Cesko, M. Zelenika, D. Palic, B. Pravdic, D. Cuk, D. Vitlianova, K. Katova, T. Kurteva, T. Gatzov, P. Kamenova, D. Antova, M. Krejci, J. Spinar, J. Krupicka, J. Malek, F. Hegarova, M. Lazarova, M. Monhart, Z. Hassanein, M. El Messiry, F. El Shazly, A.H. Elrakshy, Y. Youssef, A. Moneim, A.A. Noamany, M. Dayem, T.K.A. Farag, N. Halawa, S.I. Hamid, M.A. Saleh, A. Ebeid, H. Hanna, R. Louis, O. Enen, M.A. Ibrahim, B.S. Nasr, G. Elbahry, A. Sobhy, H. Ashmawy, M. Gouda, M. Aboleineen, W. Bernard, Y. Meneveau, N. Pillot, M. Morel, M. Seronde, M.-F. Schiele, F. Briand, F. Delahaye, F. Damy, T. Eicher, J.-C. de Groote, P. Fertin, M. Lamblin, N. Isnard, R. Thevenin, S. Hagege, A. Logeart, D. Le Marcis, V. Ly, J.-F. Coisne, D. Lequeux, B. Le Moal, V. Mascle, S. Lotton, P. Behar, N. Donal, E. Ridard, C. Reynaud, A. Basquin, A. Bauer, F. Codjia, R. Galinier, M. Tourikis, P. Stavroula, M. Stefanadis, C. Chrysohoou, C. Kotrogiannis, I. Matzaraki, V. Karavidas, A. Tsitsinakis, G. Kapelios, C. Nanas, J. Kampouri, H. Nana, E. Kaldara, E. Eugenidou, A. Vardas, P. Saloustros, I. Tsaknakis, T. Evangelou, S. Tziourganou, H. Tsaroucha, A. Papadopoulou, A. Douras, A. Polgar, L. Kosztin, A. Nyolczas, N. Nagy, A.C. Halmosi, R. Elber, J. Shotan, A. Fuhrmann, A.V. Amir, O. Romano, S. Marcon, S. Penco, M. Di Mauro, M. Lemme, E. Carubelli, V. Rovetta, R. Bulgari, M. Quinzani, F. Bosi, S. Schiavina, G. Squeri, A. Di Tano, G. Pirelli, S. Ferrari, R. Fucili, A. Passero, T. Musio, S. Di Biase, M. Correale, M. Salvemini, G. Brognoli, S. Zanelli, E. Giordano, A. Agostoni, P. Salvioni, E. Copelli, S. Modena, M.G. Valenti, C. Olaru, A. Bandino, S. Deidda, M. Mercuro, G. Marino, P.N. Di Ruocco, M.V. Piccinino, C. Parrinello, G. Licata, G. Torres, D. Giambanco, S. Busalacchi, S. Arrotti, S. Novo, S. Inciardi, R.M. Pieri, P. Galifi, M.A. Teresi, G. Buccheri, D. Minacapelli, A. Veniani, M. Frisinghelli, A. Priori, S.G. Cattaneo, S. Opasich, C. Gualco, A. Pagliaro, M. Mancone, M. Fedele, F. Cinque, A. Vellini, M. Scarfo, I. Romeo, F. Ferraiuolo, F. Sergi, D. Anselmi, M. Melandri, F. Leci, E. Iori, E. Bovolo, V. Frea, S. Bergerone, S. Botta, M. Canavosio, F.G. Gaita, F. Merlo, M. Cinquetti, M. Sinagra, G. Ramani, F. Fabris, E. Artico, J. Miani, D. Fresco, C. Daneluzzi, C. Proclemer, A. Cicoira, M. Zanolla, L. Marchese, G. Torelli, F. Vassanelli, C. Voronina, N. Tamakauskas, V. Smalinskas, V. Karaliute, R. Petraskiene, I. Rumbinaite, E. Kavoliuniene, A. Brazyte-Ramanauskiene, R. Petraskiene, D. Sinkiewicz, W. Gilewski, W. Pietrzak, J. Orzel, T. Kardaszewicz, P. Lazorko-Piega, M. Mosakowska, K. Bellwon, J. Rynkiewicz, A. Raczak, G. Lewicka, E. Dabrowska-Kugacka, A. Bartkowiak, R. Wozakowska-Kaplon, B. Krzeminski, A. Zabojszcz, M. Grzegorzko, A. Bury, K. Nessler, J. Zalewski, J. Furman, A. Poliwczak, A. Bala, A. Zycinski, P. Rudzinska, M. Jankowski, L. Kasprzak, J.D. Michalak, L. Soska, K.W. Drozdz, J. Huziuk, I. Flis, P. Weglarz, J. Bodys, A. Grajek, S. Straburzynska-Migaj, E. Dankowski, R. Szymanowska, K. Szyszka, A. Nowicka, A. Samcik, M. Wolniewicz, L. Komorowska, K. Poprawa, I. Komorowska, E. Sajnaga, D. Zolbach, A. Abdulkarim, A.-F. Lauko-Rachocka, A. Kaminski, L. Kostka, A. Cichy, A. Ruszkowski, P. Splawski, M. Fitas, G. Szymczyk, A. Serwicka, A. Fiega, A. Zysko, D. Krysiak, W. Szabowski, S. Skorek, E. Pruszczyk, P. Bienias, P. Ciurzynski, M. Welnicki, M. Mamcarz, A. Folga, A. Zielinski, T. Rywik, T. Leszek, P. Sobieszczanska-Malek, M. Kozar-Kaminska, K. Komuda, K. Wisniewska, J. Tarnowska, A. Marchel, M. Opolski, G. Kaplon-Cieslicka, A. Gil, R.J. Mozenska, O. Gil, K. Pawlak, A. Michalek, A. Krzesinski, P. Piotrowicz, K. Stanczyk, A. Skrobowski, A. Ponikowski, P. Jankowska, E. Rozentryt, P. Polonski, L. Nowalany-Kozielska, E. Kuczaj, A. Kalarus, Z. Szulik, M. Klys, J. Prokop-Lewicka, G. Kleinrok, A. TavaresAguiar, C. Ventosa, A. Pereira, S. Faria, R. Chin, J. DeJesus, I. Santos, R. Silva, P. Moreno, N. Lourenço, C. Pereira, A. Castro, A. Andrade, A. OliveiraGuimaraes, T. Martins, S. Placido, R. Lima, G. Brito, D. Francisco, A.R. Proenca, M. Araujo, I. Marques, F. Fonseca, C. Moura, B. Campelo, M. Silva-Cardoso, J. Rodrigues, J. Rangel, I. Martins, E. Peres, M. Marta, L. Severino, D. Durao, D. Leao, S. Magalhaes, P. Moreira, I. Ferreira, C. Araujo, C. Ferreira, A. Baptista, A. Radoi, M. Bicescu, G. Vinereanu, D. Sinescu, C.-J. Macarie, C. Popescu, R. Daha, I. Dan, G.-A. Stanescu, C. Dan, A. Craiu, E. Nechita, E. Christodorescu, R. Otasevic, P. Seferovic, P.M. Simeunovic, D. Ristic, A.D. Celic, V. Pavlovic-Kleut, M. Stojcevski, B. Pencic, B. Stevanovic, A. Andric, A. Simić, D. Ašanin, M. Iric-Cupic, V. Jovic, M. Milanov, S. Mitic, V. Atanaskovic, V. Antic, S. Pavlovic, M. Stanojevic, D. Stoickov, V. Ilic, S. DeljaninIlic, M. Petrovic, D. Stojsic, S. Kecojevic, S. Dodic, S. Adic, N.C. Cankovic, M. Stojiljkovic, J. Mihajlovic, B. Radin, A. Radovanovic, S. Krotin, M. Klabnik, A. Pernicky, M. Murin, J. Kovar, F. Kmec, J. Strasek, M. Iskra, M.S. Ravnikar, T. Suligoj, N.C. Fras, Z. Jug, B. Glavic, T. Losic, R. Bombek, M. Krunic, B. Horvat, S. Kovac, D. Rajtman, D. Letonja, M. Winkler, R. Melihen-Bartolic, C. Bartolic, A. Kladnik, M. Pusnik, C.S. Marolt, A. Klen, J. Drnovsek, B. Leskovar, B. Anguita, M.J.F. GallegoPage, J.C. Martinez, F.M.S. Andres, J. Bayes-Genis, A. Mirabet, S. Mendez, A. Garcia-Cosio, L. Leon, V. Gonzalez-Costello, J. Muntane, G. Garay, A. Alcade-Martinez, V. Fernandez, S.L. Rivera-Lopez, R. Fernandez-Alvarez, M. Serrano-Martinez, J.L. Grille-Cancela, Z. Marzoa-Rivas, R. Paniagua-Martin, M.J. Barge-Caballero, E. Gonzalez-Gallarza, R.D. SalvadorMontanes, O. Manjavacas, A.M.I. Conde, A.C. Araujo, A. Soria, T. Gomez-Bueno, M. Cobo-Marcos, M. Alonso-Pulpon, L. SegoviaCubero, J. Sayago, I. Gonzalez-Segovia, A. Briceno, A. Subias, P.E. Cano, M.J.R. Sanchez, M.A.G. Jimenez, J.F.D. Pinilla, J.M.G. de la Villa, B.G. Sahuquillo, A. Marques, R.B. Calvo, F.T. Perez-Martinez, M.T. Garrido-Bravo, I.P. Pastor-Perez, F. Pascual-Figal, D.A. Molina, B.D. Orus, J. Gonzalo, F.E. Bertomeu, V. Valero, R. Martinez-Abellan, R. Quiles, J. Mateo, I. ElAmrani, A. Fernandez-Vivancos, C. Valero, D.B. Almenar-Bonet, L. Sanchez-Lazaro, I.J. Marques-Sule, E. Facila-Rubio, L. Perez-Silvestre, J. Garcia-Gonzalez, P. Garcia-Escriva, D. Pellicer-Cabo, A. de laFuente Galan, L. Diaz, J.L. Platero, A.R. Arias, J.C. Blasco-Peiro, T. Julve, M.S. Sanchez-Insa, E. Portoles-Ocampo, A. Melin, M. Hägglund Lindahl, I.-M. Asserlund, B. Olsson, L. Dahlström, U. Afzelius, M. Karlström, P. Tengvall, L. Olsson, B. Kalayci, S. Cavusoglu, Y. Gencer, E. Yilmaz, M.B. Gunes, H.

Abstract

Aims: Guidelines recommend down-titration of loop diuretics (LD) once euvolaemia is achieved. In outpatients with heart failure (HF), we investigated LD dose changes in daily cardiology practice, agreement with guideline recommendations, predictors of successful LD down-titration and association between dose changes and outcomes. Methods and results: We included 8130 HF patients from the ESC-EORP Heart Failure Long-Term Registry. Among patients who had dose decreased, successful decrease was defined as the decrease not followed by death, HF hospitalization, New York Heart Association class deterioration, or subsequent increase in LD dose. Mean age was 66 ± 13 years, 71% men, 62% HF with reduced ejection fraction, 19% HF with mid-range ejection fraction, 19% HF with preserved ejection fraction. Median [interquartile range (IQR)] LD dose was 40 (25–80) mg. LD dose was increased in 16%, decreased in 8.3% and unchanged in 76%. Median (IQR) follow-up was 372 (363–419) days. Diuretic dose increase (vs. no change) was associated with HF death [hazard ratio (HR) 1.53, 95% confidence interval (CI) 1.12–2.08; P = 0.008] and nominally with cardiovascular death (HR 1.25, 95% CI 0.96–1.63; P = 0.103). Decrease of diuretic dose (vs. no change) was associated with nominally lower HF (HR 0.59, 95% CI 0.33–1.07; P = 0.083) and cardiovascular mortality (HR 0.62,. 95% CI 0.38–1.00; P = 0.052). Among patients who had LD dose decreased, systolic blood pressure [odds ratio (OR) 1.11 per 10 mmHg increase, 95% CI 1.01–1.22; P = 0.032], and absence of (i) sleep apnoea (OR 0.24, 95% CI 0.09–0.69; P = 0.008), (ii) peripheral congestion (OR 0.48, 95% CI 0.29–0.80; P = 0.005), and (iii) moderate/severe mitral regurgitation (OR 0.57, 95% CI 0.37–0.87; P = 0.008) were independently associated with successful decrease. Conclusion: Diuretic dose was unchanged in 76% and decreased in 8.3% of outpatients with chronic HF. LD dose increase was associated with worse outcomes, while the LD dose decrease group showed a trend for better outcomes compared with the no-change group. Higher systolic blood pressure, and absence of (i) sleep apnoea, (ii) peripheral congestion, and (iii) moderate/severe mitral regurgitation were independently associated with successful dose decrease. © 2020 European Society of Cardiology

Published
2020

52. Genetic risk and atrial fibrillation in patients with heart failure

Author

Kloosterman, M. Santema, B.T. Roselli, C. Nelson, C.P. Koekemoer, A. Romaine, S.P.R. Van Gelder, I.C. Lam, C.S.P. Artola, V.A. Lang, C.C. Ng, L.L. Metra, M. Anker, S. Filippatos, G. Dickstein, K. Ponikowski, P. van der Harst, P. van der Meer, P. van Veldhuisen, D.J. Benjamin, E.J. Voors, A.A. Samani, N.J. Rienstra, M.

Abstract

Aims: To study the association between an atrial fibrillation (AF) genetic risk score with prevalent AF and all-cause mortality in patients with heart failure. Methods and results: An AF genetic risk score was calculated in 3759 European ancestry individuals (1783 with sinus rhythm, 1976 with AF) from the BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT-CHF) by summing 97 single nucleotide polymorphism (SNP) alleles (ranging from 0–2) weighted by the natural logarithm of the relative SNP risk from the latest AF genome-wide association study. Further, we assessed AF risk variance explained by additive SNP variation, and performance of clinical or genetic risk factors, and the combination in classifying AF prevalence. AF was classified as AF or atrial flutter (AFL) at baseline electrocardiogram and/or a history of AF or AFL. The genetic risk score was associated with AF after multivariable adjustment. Odds ratio for AF prevalence per 1-unit increase genetic risk score was 2.12 (95% confidence interval 1.84–2.45, P = 2.15 × 10−24) in the total cohort, 2.08 (1.72–2.50, P = 1.30 × 10−14) in heart failure with reduced ejection fraction (HFrEF) and 2.02 (1.37–2.99, P = 4.37 × 10−4) in heart failure with preserved ejection fraction (HFpEF). AF-associated loci explained 22.9% of overall AF SNP heritability. Addition of the genetic risk score to clinical risk factors increased the C-index by 2.2% to 0.721. Conclusions: The AF genetic risk score was associated with increased AF prevalence in HFrEF and HFpEF. Genetic variation accounted for 22.9% of overall AF SNP heritability. Addition of genetic risk to clinical risk improved model performance in classifying AF prevalence. © 2020 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

Published
2020

53. European Society of Cardiology/Heart Failure Association position paper on the role and safety of new glucose-lowering drugs in patients with heart failure

Author

Seferović, P.M. Coats, A.J.S. Ponikowski, P. Filippatos, G. Huelsmann, M. Jhund, P.S. Polovina, M.M. Komajda, M. Seferović, J. Sari, I. Cosentino, F. Ambrosio, G. Metra, M. Piepoli, M. Chioncel, O. Lund, L.H. Thum, T. De Boer, R.A. Mullens, W. Lopatin, Y. Volterrani, M. Hill, L. Bauersachs, J. Lyon, A. Petrie, M.C. Anker, S. Rosano, G.M.C.

Abstract

Type 2 diabetes mellitus (T2DM) is common in patients with heart failure (HF) and associated with considerable morbidity and mortality. Significant advances have recently occurred in the treatment of T2DM, with evidence of several new glucose-lowering medications showing either neutral or beneficial cardiovascular effects. However, some of these agents have safety characteristics with strong practical implications in HF [i.e. dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 RA), and sodium–glucose co-transporter type 2 (SGLT-2) inhibitors]. Regarding safety of DPP-4 inhibitors, saxagliptin is not recommended in HF because of a greater risk of HF hospitalisation. There is no compelling evidence of excess HF risk with the other DPP-4 inhibitors. GLP-1 RAs have an overall neutral effect on HF outcomes. However, a signal of harm suggested in two small trials of liraglutide in patients with reduced ejection fraction indicates that their role remains to be defined in established HF. SGLT-2 inhibitors (empagliflozin, canagliflozin and dapagliflozin) have shown a consistent reduction in the risk of HF hospitalisation regardless of baseline cardiovascular risk or history of HF. Accordingly, SGLT-2 inhibitors could be recommended to prevent HF hospitalisation in patients with T2DM and established cardiovascular disease or with multiple risk factors. The recently completed trial with dapagliflozin has shown a significant reduction in cardiovascular mortality and HF events in patients with HF and reduced ejection fraction, with or without T2DM. Several ongoing trials will assess whether the results observed with dapagliflozin could be extended to other SGLT-2 inhibitors in the treatment of HF, with either preserved or reduced ejection fraction, regardless of the presence of T2DM. This position paper aims to summarise relevant clinical trial evidence concerning the role and safety of new glucose-lowering therapies in patients with HF. © 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology

Published
2020

54. Unravelling the interplay between hyperkalaemia, renin–angiotensin–aldosterone inhibitor use and clinical outcomes. Data from 9222 chronic heart failure patients of the ESC-HFA-EORP Heart Failure Long-Term Registry

Author

Rossignol, P. Lainscak, M. Crespo-Leiro, M.G. Laroche, C. Piepoli, M.F. Filippatos, G. Rosano, G.M.C. Savarese, G. Anker, S.D. Seferovic, P.M. Ruschitzka, F. Coats, A.J.S. Mebazaa, A. McDonagh, T. Sahuquillo, A. Penco, M. Maggioni, A.P. Lund, L.H. Christopher Peter Gale, G.B. Branko Beleslin, R.S. Andrzej Budaj, P.L. Ovidiu Chioncel, R.O. Nikolaos Dagres, D.E. Nicolas Danchin, F.R. David Erlinge, S.E. Jonathan Emberson, G.B. Michael Glikson, I.L. Alastair Gray, G.B. Meral Kayikcioglu, T.R. Aldo Maggioni, I.T. Klaudia Vivien Nagy, H.U. Aleksandr Nedoshivin, R.U. Anna-Sonia Petronio, I.T. Jolien Roos-Hesselink, N.L. Lars Wallentin, S.E. Uwe Zeymer, D.E. Anker, S. Mebazaa, A. Coats, A. Filippatos, G. Ferrari, R. Maggioni, A.P. Goda, A. Diez, M. Fernandez, A. Fruhwald, F. Fazlibegovic, E. Gatzov, P. Kurlianskaya, A. Hullin, R. Christodoulides, T. Hradec, J. Nielsen, O.W. Nedjar, R. Uuetoa, T. Hassanein, M. Jimenez, J.F.D. Harjola, V.P. Logeart, D. Chumburidze, V. Tousoulis, D. Milicic, D. Merkely, B. O'Donoghue, E. Amir, O. Shotan, A. Shafie, D. Metra, M. Matsumori, A. Mirrakhimov, E. Kavoliuniene, A. Erglis, A. Vataman, E. Otljanska, M. Kostovska, E.S. DeMarco, D.C. Drozdz, J. Fonseca, C. Chioncel, O. Dekleva, M. Shkolnik, E. Dahlstrom, U. Lainscak, M. Goncalvesova, E. Temizhan, A. Estrago, V. Bajraktari, G. Auer, J. Ablasser, K. Fruhwald, F. Dolze, T. Brandner, K. Gstrein, S. Poelzl, G. Moertl, D. Reiter, S. Podczeck-Schweighofer, A. Muslibegovic, A. Vasilj, M. Fazlibegovic, E. Cesko, M. Zelenika, D. Palic, B. Pravdic, D. Cuk, D. Vitlianova, K. Katova, T. Velikov, T. Kurteva, T. Gatzov, P. Kamenova, D. Antova, M. Sirakova, V. Krejci, J. Mikolaskova, M. Spinar, J. Krupicka, J. Malek, F. Hegarova, M. Lazarova, M. Monhart, Z. Hassanein, M. Sobhy, M. El Messiry, F. El Shazly, A.H. Elrakshy, Y. Youssef, A. Moneim, A.A. Noamany, M. Reda, A. Dayem, T.K.A. Farag, N. Halawa, S.I. Hamid, M.A. Said, K. Saleh, A. Ebeid, H. Hanna, R. Aziz, R. Louis, O. Enen, M.A. Ibrahim, B.S. Nasr, G. Elbahry, A. Sobhy, H. Ashmawy, M. Gouda, M. Aboleineen, W. Bernard, Y. Luporsi, P. Meneveau, N. Pillot, M. Morel, M. Seronde, M.-F. Schiele, F. Briand, F. Delahaye, F. Damy, T. Eicher, J.-C. de Groote, P. Fertin, M. Lamblin, N. Isnard, R. Lefol, C. Thevenin, S. Hagege, A. Jondeau, G. Logeart, D. Le Marcis, V. Ly, J.-F. Coisne, D. Lequeux, B. Le Moal, V. Mascle, S. Lotton, P. Behar, N. Donal, E. Thebault, C. Ridard, C. Reynaud, A. Basquin, A. Bauer, F. Codjia, R. Galinier, M. Tourikis, P. Stavroula, M. Tousoulis, D. Stefanadis, C. Chrysohoou, C. Kotrogiannis, I. Matzaraki, V. Dimitroula, T. Karavidas, A. Tsitsinakis, G. Kapelios, C. Nanas, J. Kampouri, H. Nana, E. Kaldara, E. Eugenidou, A. Vardas, P. Saloustros, I. Patrianakos, A. Tsaknakis, T. Evangelou, S. Nikoloulis, N. Tziourganou, H. Tsaroucha, A. Papadopoulou, A. Douras, A. Polgar, L. Kosztin, A. Nyolczas, N. Nagy, A.C. Halmosi, R. Elber, J. Alony, I. Shotan, A. Fuhrmann, A.V. Amir, O. Romano, S. Marcon, S. Penco, M. Di Mauro, M. Lemme, E. Carubelli, V. Rovetta, R. Bulgari, M. Quinzani, F. Lombardi, C. Bosi, S. Schiavina, G. Squeri, A. Barbieri, A. Di Tano, G. Pirelli, S. Ferrari, R. Fucili, A. Passero, T. Musio, S. Di Biase, M. Correale, M. Salvemini, G. Brognoli, S. Zanelli, E. Giordano, A. Agostoni, P. Italiano, G. Salvioni, E. Copelli, S. Modena, M.G. Reggianini, L. Valenti, C. Olaru, A. Bandino, S. Deidda, M. Mercuro, G. Dessalvi, C.C. Marino, P.N. Di Ruocco, M.V. Sartori, C. Piccinino, C. Parrinello, G. Licata, G. Torres, D. Giambanco, S. Busalacchi, S. Arrotti, S. Novo, S. Inciardi, R.M. Pieri, P. Chirco, P.R. Galifi, M.A. Teresi, G. Buccheri, D. Minacapelli, A. Veniani, M. Frisinghelli, A. Priori, S.G. Cattaneo, S. Opasich, C. Gualco, A. Pagliaro, M. Mancone, M. Fedele, F. Cinque, A. Vellini, M. Scarfo, I. Romeo, F. Ferraiuolo, F. Sergi, D. Anselmi, M. Melandri, F. Leci, E. Iori, E. Bovolo, V. Pidello, S. Frea, S. Bergerone, S. Botta, M. Canavosio, F.G. Gaita, F. Merlo, M. Cinquetti, M. Sinagra, G. Ramani, F. Fabris, E. Stolfo, D. Artico, J. Miani, D. Fresco, C. Daneluzzi, C. Proclemer, A. Cicoira, M. Zanolla, L. Marchese, G. Torelli, F. Vassanelli, C. Voronina, N. Tamakauskas, V. Smalinskas, V. Karaliute, R. Petraskiene, I. Kazakauskaite, E. Rumbinaite, E. Kavoliuniene, A. Vysniauskas, V. Brazyte-Ramanauskiene, R. Petraskiene, D. Stankala, S. Switala, P. Juszczyk, Z. Sinkiewicz, W. Gilewski, W. Pietrzak, J. Orzel, T. Kasztelowicz, P. Kardaszewicz, P. Lazorko-Piega, M. Gabryel, J. Mosakowska, K. Bellwon, J. Rynkiewicz, A. Raczak, G. Lewicka, E. Dabrowska-Kugacka, A. Bartkowiak, R. Sosnowska-Pasiarska, B. Wozakowska-Kaplon, B. Krzeminski, A. Zabojszcz, M. Mirek-Bryniarska, E. Grzegorzko, A. Bury, K. Nessler, J. Zalewski, J. Furman, A. Broncel, M. Poliwczak, A. Bala, A. Zycinski, P. Rudzinska, M. Jankowski, L. Kasprzak, J.D. Michalak, L. Soska, K.W. Drozdz, J. Huziuk, I. Retwinski, A. Flis, P. Weglarz, J. Bodys, A. Grajek, S. Kaluzna-Oleksy, M. Straburzynska-Migaj, E. Dankowski, R. Szymanowska, K. Grabia, J. Szyszka, A. Nowicka, A. Samcik, M. Wolniewicz, L. Baczynska, K. Komorowska, K. Poprawa, I. Komorowska, E. Sajnaga, D. Zolbach, A. Dudzik-Plocica, A. Abdulkarim, A.-F. Lauko-Rachocka, A. Kaminski, L. Kostka, A. Cichy, A. Ruszkowski, P. Splawski, M. Fitas, G. Szymczyk, A. Serwicka, A. Fiega, A. Zysko, D. Krysiak, W. Szabowski, S. Skorek, E. Pruszczyk, P. Bienias, P. Ciurzynski, M. Welnicki, M. Mamcarz, A. Folga, A. Zielinski, T. Rywik, T. Leszek, P. Sobieszczanska-Malek, M. Piotrowska, M. Kozar-Kaminska, K. Komuda, K. Wisniewska, J. Tarnowska, A. Balsam, P. Marchel, M. Opolski, G. Kaplon-Cieslicka, A. Gil, R.J. Mozenska, O. Byczkowska, K. Gil, K. Pawlak, A. Michalek, A. Krzesinski, P. Piotrowicz, K. Uzieblo-Zyczkowska, B. Stanczyk, A. Skrobowski, A. Ponikowski, P. Jankowska, E. Rozentryt, P. Polonski, L. Gadula-Gacek, E. Nowalany-Kozielska, E. Kuczaj, A. Kalarus, Z. Szulik, M. Przybylska, K. Klys, J. Prokop-Lewicka, G. Kleinrok, A. Aguiar, C.T. Ventosa, A. Pereira, S. Faria, R. Chin, J. De Jesus, I. Santos, R. Silva, P. Moreno, N. Queirós, C. Lourenço, C. Pereira, A. Castro, A. Andrade, A. Guimaraes, T.O. Martins, S. Placido, R. Lima, G. Brito, D. Francisco, A.R. Cardiga, R. Proenca, M. Araujo, I. Marques, F. Fonseca, C. Moura, B. Leite, S. Campelo, M. Silva-Cardoso, J. Rodrigues, J. Rangel, I. Martins, E. Correia, A.S. Peres, M. Marta, L. da Silva, G.F. Severino, D. Durao, D. Leao, S. Magalhaes, P. Moreira, I. Cordeiro, A.F. Ferreira, C. Araujo, C. Ferreira, A. Baptista, A. Radoi, M. Bicescu, G. Vinereanu, D. Sinescu, C.-J. Macarie, C. Popescu, R. Daha, I. Dan, G.-A. Stanescu, C. Dan, A. Craiu, E. Nechita, E. Aursulesei, V. Christodorescu, R. Otasevic, P. Seferovic, P.M. Simeunovic, D. Ristic, A.D. Celic, V. Pavlovic-Kleut, M. Lazic, J.S. Stojcevski, B. Pencic, B. Stevanovic, A. Andric, A. Simić, D. Ašanin, M. Iric-Cupic, V. Jovic, M. Davidovic, G. Milanov, S. Mitic, V. Atanaskovic, V. Antic, S. Pavlovic, M. Stanojevic, D. Stoickov, V. Ilic, S. Ilic, M.D. Petrovic, D. Stojsic, S. Kecojevic, S. Dodic, S. Adic, N.C. Cankovic, M. Stojiljkovic, J. Mihajlovic, B. Radin, A. Radovanovic, S. Krotin, M. Klabnik, A. Goncalvesova, E. Pernicky, M. Murin, J. Kovar, F. Kmec, J. Semjanova, H. Strasek, M. Iskra, M.S. Ravnikar, T. Suligoj, N.C. Komel, J. Fras, Z. Jug, B. Glavic, T. Losic, R. Bombek, M. Krajnc, I. Krunic, B. Horvat, S. Kovac, D. Rajtman, D. Cencic, V. Letonja, M. Winkler, R. Valentincic, M. Melihen-Bartolic, C. Bartolic, A. Vrckovnik, M.P. Kladnik, M. Pusnik, C.S. Marolt, A. Klen, J. Drnovsek, B. Leskovar, B. Anguita, M.J.F. Page, J.C.G. Martinez, F.M.S. Andres, J. Bayes-Genis, A. Mirabet, S. Mendez, A. Garcia-Cosio, L. Roig, E. Leon, V. Gonzalez-Costello, J. Muntane, G. Garay, A. Alcade-Martinez, V. Fernandez, S.L. Rivera-Lopez, R. Puga-Martinez, M. Fernandez-Alvarez, M. Serrano-Martinez, J.L. Grille-Cancela, Z. Marzoa-Rivas, R. Blanco-Canosa, P. Paniagua-Martin, M.J. Barge-Caballero, E. Cerdena, I.L. Baldomero, I.F.H. Padron, A.L. Rosillo, S.O. Gonzalez-Gallarza, R.D. Montanes, O.S. Manjavacas, A.M.I. Conde, A.C. Araujo, A. Soria, T. Garcia-Pavia, P. Gomez-Bueno, M. Cobo-Marcos, M. Alonso-Pulpon, L. Cubero, J.S. Sayago, I. Gonzalez-Segovia, A. Briceno, A. Subias, P.E. Hernandez, M.V. Cano, M.J.R. Sanchez, M.A.G. Jimenez, J.F.D. Garrido-Lestache, E.B. Pinilla, J.M.G. de la Villa, B.G. Sahuquillo, A. Marques, R.B. Calvo, F.T. Perez-Martinez, M.T. Gracia-Rodenas, M.R. Garrido-Bravo, I.P. Pastor-Perez, F. Pascual-Figal, D.A. Molina, B.D. Orus, J. Gonzalo, F.E. Bertomeu, V. Valero, R. Martinez-Abellan, R. Quiles, J. Rodrigez-Ortega, J.A. Mateo, I. ElAmrani, A. Fernandez-Vivancos, C. Valero, D.B. Almenar-Bonet, L. Sanchez-Lazaro, I.J. Marques-Sule, E. Facila-Rubio, L. Perez-Silvestre, J. Garcia-Gonzalez, P. Ridocci-Soriano, F. Garcia-Escriva, D. Pellicer-Cabo, A. de la Fuente Galan, L. Diaz, J.L. Platero, A.R. Arias, J.C. Blasco-Peiro, T. Julve, M.S. Sanchez-Insa, E. Aured-Guallar, C. Portoles-Ocampo, A. Melin, M. Hägglund, E. Stenberg, A. Lindahl, I.-M. Asserlund, B. Olsson, L. Dahlström, U. Afzelius, M. Karlström, P. Tengvall, L. Olsson, B. Kalayci, S. Temizhan, A. Cavusoglu, Y. Gencer, E. Yilmaz, M.B. Gunes, H.

Subjects
cardiovascular diseases
Abstract

Aims: We assessed the interplay between hyperkalaemia (HK) and renin–angiotensin–aldosterone system inhibitor (RAASi) use, dose and discontinuation, and their association with all-cause or cardiovascular death in patients with chronic heart failure (HF). We hypothesized that HK-associated increased death may be related to RAASi withdrawal. Methods and results: The ESC-HFA-EORP Heart Failure Long-Term Registry was used. Among 9222 outpatients (HF with reduced ejection fraction: 60.6%, HF with mid-range ejection fraction: 22.9%, HF with preserved ejection fraction: 16.5%) from 31 countries, 16.6% had HK (≥5.0 mmol/L) at baseline. Angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) was used in 88.3%, a mineralocorticoid receptor antagonist (MRA) in 58.7%, or a combination in 53.2%; of these, at ≥50% of target dose in ACEi: 61.8%; ARB: 64.7%; and MRA: 90.3%. At a median follow-up of 12.2 months, there were 789 deaths (8.6%). Both hypokalaemia and HK were independently. associated with higher mortality, and ACEi/ARB prescription at baseline with lower mortality. MRA prescription was not retained in the model. In multivariable analyses, HK at baseline was independently associated with MRA non-prescription at baseline and subsequent discontinuation. When considering subsequent discontinuation of RAASi (instead of baseline use), HK was no longer found associated with all-cause deaths. Importantly, all RAASi (ACEi, ARB, or MRA) discontinuations were strongly associated with mortality. Conclusions: In HF, hyper- and hypokalaemia were associated with mortality. However, when adjusting for RAASi discontinuation, HK was no longer associated with mortality, suggesting that HK may be a risk marker for RAASi discontinuation rather than a risk factor for worse outcomes. © 2020 European Society of Cardiology

Published
2020

55. Cardiovascular and non-cardiovascular death distinction: the utility of troponin beyond N-terminal pro-B-type natriuretic peptide. Findings from the BIOSTAT-CHF study

Author

Ferreira, J.P. Ouwerkerk, W. Tromp, J. Ng, L. Dickstein, K. Anker, S. Filippatos, G. Cleland, J.G. Metra, M. van Veldhuisen, D.J. Voors, A.A. Zannad, F.

Abstract

Aims: Heart failure (HF) patients are at high-risk of cardiovascular (CV) events, including CV death. Nonetheless, a substantial proportion of these patients die from non-CV causes. Identifying patients at higher risk for each individual event may help selecting patients for clinical trials and tailoring cardiovascular therapies. The aims of the present study are to: (i) characterize patients according to CV vs. non-CV death; (ii) develop models for the prediction of the respective events; (iii) assess the models' performance to differentiate CV from non-CV death. Methods and results: This study included 2309 patients with HF from the BIOSTAT-CHF (a systems BIOlogy Study to TAilored Treatment in Chronic Heart Failure) study. Competing-risk models were used to assess the best combination of variables associated with each cause-specific death. Results were validated in an independent cohort of 1738 HF patients. The best model to predict CV death included low blood pressure, estimated glomerular filtration rate ≤ 60 mL/min, peripheral oedema, previous HF hospitalization, ischaemic HF, chronic obstructive pulmonary disease, elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP), and troponin (c-index = 0.73). The non-CV death model incorporated age > 75 years, anaemia and elevated NT-proBNP (c-index = 0.71). Both CV and non-CV death rose by quintiles of the risk scores; yet these models allowed the identification of patients in whom absolute CV death rates clearly outweigh non-CV death ones. These findings were externally replicated, but performed worse in a less severely diseased population. Conclusions: Risk models for predicting CV and non-CV death allowed the identification of patients at higher absolute risk of dying from CV causes (vs. non-CV ones). Troponin helped in predicting CV death only, whereas NT-proBNP helped in the prediction of both CV and non-CV death. These findings can be useful both for tailoring therapies and for patient selection in HF trials in order to attain CV event enrichment. © 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology

Published
2020

56. Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes

Author

Bakris G, Agarwal R, Anker S, Pitt B, Ruilope L, Rossing P, Kolkhof P, Nowack C, Schloemer P, Joseph A, Filippatos G, and FIDELIO-DKD Investigators

Abstract

BACKGROUND: Finerenone, a nonsteroidal, selective mineralocorticoid receptor antagonist, reduced albuminuria in short-term trials involving patients with chronic kidney disease (CKD) and type 2 diabetes. However, its long-term effects on kidney and cardiovascular outcomes are unknown. METHODS: In this double-blind trial, we randomly assigned 5734 patients with CKD and type 2 diabetes in a 1:1 ratio to receive finerenone or placebo. Eligible patients had a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of 30 to less than 300, an estimated glomerular filtration rate (eGFR) of 25 to less than 60 ml per minute per 1.73 m2 of body-surface area, and diabetic retinopathy, or they had a urinary albumin-to-creatinine ratio of 300 to 5000 and an eGFR of 25 to less than 75 ml per minute per 1.73 m2. All the patients were treated with renin-angiotensin system blockade that had been adjusted before randomization to the maximum dose on the manufacturer's label that did not cause unacceptable side effects. The primary composite outcome, assessed in a time-to-event analysis, was kidney failure, a sustained decrease of at least 40% in the eGFR from baseline, or death from renal causes. The key secondary composite outcome, also assessed in a time-to-event analysis, was death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. RESULTS: During a median follow-up of 2.6 years, a primary outcome event occurred in 504 of 2833 patients (17.8%) in the finerenone group and 600 of 2841 patients (21.1%) in the placebo group (hazard ratio, 0.82; 95% confidence interval [CI], 0.73 to 0.93; P=0.001). A key secondary outcome event occurred in 367 patients (13.0%) and 420 patients (14.8%) in the respective groups (hazard ratio, 0.86; 95% CI, 0.75 to 0.99; P=0.03). Overall, the frequency of adverse events was similar in the two groups. The incidence of hyperkalemia-related discontinuation of the trial regimen was higher with finerenone than with placebo (2.3% and 0.9%, respectively). CONCLUSIONS: In patients with CKD and type 2 diabetes, treatment with finerenone resulted in lower risks of CKD progression and cardiovascular events than placebo. (Funded by Bayer; FIDELIO-DKD ClinicalTrials.gov number, NCT02540993.).

Published
2020

57. Effects of Elamipretide on Left Ventricular Function in Patients With Heart Failure With Reduced Ejection Fraction: The PROGRESS-HF Phase 2 Trial

Author

Butler, J, Khan, M, Anker, S, Fonarow, G, Kim, R, Nodari, S, O'Connor, C, Pieske, B, Pieske-Kraigher, E, Sabbah, H, Senni, M, Voors, A, Udelson, J, Carr, J, Gheorghiade, M, Filippatos, G, Butler J, Khan MS, Anker SD, Fonarow GC, Kim RJ, Nodari S, O'Connor CM, Pieske B, Pieske-Kraigher E, Sabbah HN, Senni M, Voors AA, Udelson JE, Carr J, Gheorghiade M, Filippatos G, Butler, J, Khan, M, Anker, S, Fonarow, G, Kim, R, Nodari, S, O'Connor, C, Pieske, B, Pieske-Kraigher, E, Sabbah, H, Senni, M, Voors, A, Udelson, J, Carr, J, Gheorghiade, M, Filippatos, G, Butler J, Khan MS, Anker SD, Fonarow GC, Kim RJ, Nodari S, O'Connor CM, Pieske B, Pieske-Kraigher E, Sabbah HN, Senni M, Voors AA, Udelson JE, Carr J, Gheorghiade M, and Filippatos G

Abstract

Background: Elamipretide, a novel mitochondrial modulating agent, improves myocardial energetics; however, it is unknown whether this mechanistic benefit translates into improved cardiac structure and function in heart failure (HF) with reduced ejection fraction (HFrEF). The objective of this study was to evaluate the effects of multiple subcutaneous doses of elamipretide on left ventricular end systolic volume (LVESV) as assessed by cardiac magnetic resonance imaging. Methods: We randomized 71 patients with HFrEF (LVEF ≤ 40%) in a double-blind, placebo-controlled trial in a 1:1:1 ratio to receive placebo, 4 mg or 40 mg elamipretide once daily for 28 consecutive days. Results: The mean age (standard deviation) of the study population was 65 ± 10 years, 24% were females, and the mean EF was 31% ± 7%. The change in LVESV from baseline to week 4 was not significantly different between elamipretide 4 mg (89.4 mL to 85 mL; difference, −4.4 mL) or 40 mg (77.9 mL to 76.6 mL; difference, −1.2 mL) compared with placebo (77.7 mL to 74.6 mL; difference, −3.8 mL) (4 mg vs placebo: difference of means, −0.3; 95% CI, −4.6 to 4.0; P = 0.90; and 40 mg vs placebo: difference of means, 2.3; 95% CI, −1.9 to 6.5; P = 0.28). Also, no significant differences in change in LVESV and LVEF were observed between placebo and either of the elamipretide groups. Rates of any study drug-related adverse events were similar in the 3 groups. Conclusions: Elamipretide was well tolerated but did not improve LVESV at 4 weeks in patients with stable HFrEF compared with placebo.

Published
2020

58. Management of heart failure patients with COVID-19: a joint position paper of the Chinese Heart Failure Association & National Heart Failure Committee and the Heart Failure Association of the European Society of Cardiology

Author

Zhang, Y, Coats, A, Zheng, Z, Adamo, M, Ambrosio, G, Anker, S, Butler, J, Xu, D, Mao, J, Khan, M, Bai, L, Mebazaa, A, Ponikowski, P, Tang, Q, Ruschitzka, F, Seferovic, P, Tschöpe, C, Zhang, S, Gao, C, Zhou, S, Senni, M, Zhang, J, Metra, M, Zhang Y, Coats AJS, Zheng Z, Adamo M, Ambrosio G, Anker SD, Butler J, Xu D, Mao J, Khan MS, Bai L, Mebazaa A, Ponikowski P, Tang Q, Ruschitzka F, Seferovic P, Tschöpe C, Zhang S, Gao C, Zhou S, Senni M, Zhang J, Metra M, Zhang, Y, Coats, A, Zheng, Z, Adamo, M, Ambrosio, G, Anker, S, Butler, J, Xu, D, Mao, J, Khan, M, Bai, L, Mebazaa, A, Ponikowski, P, Tang, Q, Ruschitzka, F, Seferovic, P, Tschöpe, C, Zhang, S, Gao, C, Zhou, S, Senni, M, Zhang, J, Metra, M, Zhang Y, Coats AJS, Zheng Z, Adamo M, Ambrosio G, Anker SD, Butler J, Xu D, Mao J, Khan MS, Bai L, Mebazaa A, Ponikowski P, Tang Q, Ruschitzka F, Seferovic P, Tschöpe C, Zhang S, Gao C, Zhou S, Senni M, Zhang J, and Metra M

Abstract

The coronavirus disease 2019 (COVID-19) pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is causing considerable morbidity and mortality worldwide. Multiple reports have suggested that patients with heart failure (HF) are at a higher risk of severe disease and mortality with COVID-19. Moreover, evaluating and treating HF patients with comorbid COVID-19 represents a. formidable clinical challenge as symptoms of both conditions may overlap and they may potentiate each other. Limited data exist regarding comprehensive management of HF patients with concomitant COVID-19. Since these issues pose serious new challenges for clinicians worldwide, HF specialists must develop a structured approach to the care of patients with COVID-19 and be included early in the care of these patients. Therefore, the Heart Failure Association of the European Society of Cardiology and the Chinese Heart Failure Association & National Heart Failure Committee conducted web-based meetings to discuss these unique clinical challenges and reach a consensus opinion to help providers worldwide deliver better patient care. The main objective of this position paper is to outline the management of HF patients with concomitant COVID-19 based on the available data and personal experiences of physicians from Asia, Europe and the United States.

Published
2020

59. Cardiovascular and renal outcomes with empagliflozin in heart failure

Author

Packer, M, Anker, S, Butler, J, Filippatos, G, Pocock, S, Carson, P, Januzzi, J, Verma, S, Tsutsui, H, Brueckmann, M, Jamal, W, Kimura, K, Schnee, J, Zeller, C, Cotton, D, Bocchi, E, Böhm, M, Choi, D, Chopra, V, Chuquiure, E, Giannetti, N, Janssens, S, Zhang, J, Gonzalez Juanatey, J, Kaul, S, Brunner-La Rocca, H, Merkely, B, Nicholls, S, Perrone, S, Pina, I, Ponikowski, P, Sattar, N, Senni, M, Seronde, M, Spinar, J, Squire, I, Taddei, S, Wanner, C, Zannad, F, Packer M, Anker SD, Butler J, Filippatos G, Pocock SJ, Carson P, Januzzi J, Verma S, Tsutsui H, Brueckmann M, Jamal W, Kimura K, Schnee J, Zeller C, Cotton D, Bocchi E, Böhm M, Choi DJ, Chopra V, Chuquiure E, Giannetti N, Janssens S, Zhang J, Gonzalez Juanatey JR, Kaul S, Brunner-La Rocca HP, Merkely B, Nicholls SJ, Perrone S, Pina I, Ponikowski P, Sattar N, Senni M, Seronde MF, Spinar J, Squire I, Taddei S, Wanner C, Zannad F, Packer, M, Anker, S, Butler, J, Filippatos, G, Pocock, S, Carson, P, Januzzi, J, Verma, S, Tsutsui, H, Brueckmann, M, Jamal, W, Kimura, K, Schnee, J, Zeller, C, Cotton, D, Bocchi, E, Böhm, M, Choi, D, Chopra, V, Chuquiure, E, Giannetti, N, Janssens, S, Zhang, J, Gonzalez Juanatey, J, Kaul, S, Brunner-La Rocca, H, Merkely, B, Nicholls, S, Perrone, S, Pina, I, Ponikowski, P, Sattar, N, Senni, M, Seronde, M, Spinar, J, Squire, I, Taddei, S, Wanner, C, Zannad, F, Packer M, Anker SD, Butler J, Filippatos G, Pocock SJ, Carson P, Januzzi J, Verma S, Tsutsui H, Brueckmann M, Jamal W, Kimura K, Schnee J, Zeller C, Cotton D, Bocchi E, Böhm M, Choi DJ, Chopra V, Chuquiure E, Giannetti N, Janssens S, Zhang J, Gonzalez Juanatey JR, Kaul S, Brunner-La Rocca HP, Merkely B, Nicholls SJ, Perrone S, Pina I, Ponikowski P, Sattar N, Senni M, Seronde MF, Spinar J, Squire I, Taddei S, Wanner C, and Zannad F

Abstract

BACKGROUND Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of hospitalization for heart failure in patients regardless of the presence or absence of diabetes. More evidence is needed regarding the effects of these drugs in patients across the broad spectrum of heart failure, including those with a markedly reduced ejection fraction. METHODS In this double-blind trial, we randomly assigned 3730 patients with class II, III, or IV heart failure and an ejection fraction of 40% or less to receive empagliflozin (10 mg once daily) or placebo, in addition to recommended therapy. The primary outcome was a composite of cardiovascular death or hospitalization for worsening heart failure. RESULTS During a median of 16 months, a primary outcome event occurred in 361 of 1863 patients (19.4%) in the empagliflozin group and in 462 of 1867 patients (24.7%) in the placebo group (hazard ratio for cardiovascular death or hospitalization for heart failure, 0.75; 95% confidence interval [CI], 0.65 to 0.86; P<0.001). The effect of empagliflozin on the primary outcome was consistent in patients regardless of the presence or absence of diabetes. The total number of hospitalizations for heart failure was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.70; 95% CI, 0.58 to 0.85; P<0.001). The annual rate of decline in the estimated glomerular filtration rate was slower in the empagliflozin group than in the placebo group (-0.55 vs. -2.28 ml per minute per 1.73 m2 of body-surface area per year, P<0.001), and empagliflozin-treated patients had a lower risk of serious renal outcomes. Uncomplicated genital tract infection was reported more frequently with empagliflozin. CONCLUSIONS Among patients receiving recommended therapy for heart failure, those in the empagliflozin group had a lower risk of cardiovascular death or hospitalization for heart failure than those in the placebo group, regardless of the presence or absence of diabetes.

Published
2020

60. Baseline characteristics of patients with heart failure with preserved ejection fraction in the EMPEROR-Preserved trial

Author

Anker, S, Butler, J, Filippatos, G, Shahzeb Khan, M, Ferreira, J, Bocchi, E, Böhm, M, Brunner-La Rocca, H, Choi, D, Chopra, V, Chuquiure, E, Giannetti, N, Gomez-Mesa, J, Janssens, S, Januzzi, J, Gonzalez-Juanatey, J, Merkely, B, Nicholls, S, Perrone, S, Piña, I, Ponikowski, P, Senni, M, Seronde, M, Sim, D, Spinar, J, Squire, I, Taddei, S, Tsutsui, H, Verma, S, Vinereanu, D, Zhang, J, Jamal, W, Schnaidt, S, Schnee, J, Brueckmann, M, Pocock, S, Zannad, F, Packer, M, EMPEROR-Preserved Trial Committees and, I, Anker SD, Butler J, Filippatos G, Shahzeb Khan M, Ferreira JP, Bocchi E, Böhm M, Brunner-La Rocca HP, Choi DJ, Chopra V, Chuquiure E, Giannetti N, Gomez-Mesa JE, Janssens S, Januzzi JL, Gonzalez-Juanatey JR, Merkely B, Nicholls SJ, Perrone SV, Piña IL, Ponikowski P, Senni M, Seronde MF, Sim D, Spinar J, Squire I, Taddei S, Tsutsui H, Verma S, Vinereanu D, Zhang J, Jamal W, Schnaidt S, Schnee JM, Brueckmann M, Pocock SJ, Zannad F, Packer M, EMPEROR-Preserved Trial Committees and Investigators, Anker, S, Butler, J, Filippatos, G, Shahzeb Khan, M, Ferreira, J, Bocchi, E, Böhm, M, Brunner-La Rocca, H, Choi, D, Chopra, V, Chuquiure, E, Giannetti, N, Gomez-Mesa, J, Janssens, S, Januzzi, J, Gonzalez-Juanatey, J, Merkely, B, Nicholls, S, Perrone, S, Piña, I, Ponikowski, P, Senni, M, Seronde, M, Sim, D, Spinar, J, Squire, I, Taddei, S, Tsutsui, H, Verma, S, Vinereanu, D, Zhang, J, Jamal, W, Schnaidt, S, Schnee, J, Brueckmann, M, Pocock, S, Zannad, F, Packer, M, EMPEROR-Preserved Trial Committees and, I, Anker SD, Butler J, Filippatos G, Shahzeb Khan M, Ferreira JP, Bocchi E, Böhm M, Brunner-La Rocca HP, Choi DJ, Chopra V, Chuquiure E, Giannetti N, Gomez-Mesa JE, Janssens S, Januzzi JL, Gonzalez-Juanatey JR, Merkely B, Nicholls SJ, Perrone SV, Piña IL, Ponikowski P, Senni M, Seronde MF, Sim D, Spinar J, Squire I, Taddei S, Tsutsui H, Verma S, Vinereanu D, Zhang J, Jamal W, Schnaidt S, Schnee JM, Brueckmann M, Pocock SJ, Zannad F, Packer M, and EMPEROR-Preserved Trial Committees and Investigators

Abstract

Aims: EMPEROR-Preserved is an ongoing trial evaluating the effect of empagliflozin in patients with heart failure with preserved ejection fraction (HFpEF). This report describes the baseline characteristics of the EMPEROR-Preserved cohort and compares them with patients enrolled in prior HFpEF trials. Methods and results: EMPEROR-Preserved is a phase III randomized, international, double-blind, parallel-group, placebo-controlled trial in which 5988 symptomatic HFpEF patients [left ventricular ejection fraction (LVEF) >40%] with and without type 2 diabetes mellitus (T2DM) have been enrolled. Patients were required to have elevated N-terminal pro B-type. natriuretic peptide (NT-proBNP) concentrations (i.e. >300 pg/mL in patients without and >900 pg/mL in patients with atrial fibrillation) along with evidence of structural changes in the heart or documented history of heart failure hospitalization. Among patients enrolled from various regions (45% Europe, 11% Asia, 25% Latin America, 12% North America), the mean age was 72 ± 9 years, 45% were women. Almost all patients had New York Heart Association class II or III symptoms (99.6%), and 23% had prior heart failure hospitalization within 12 months. Thirty-three percent of the patients had baseline LVEF of 41–50%. The mean LVEF (54 ± 9%) was slightly lower while the median NT-proBNP [974 (499–1731) pg/mL] was higher compared with previous HFpEF trials. Presence of comorbidities such as diabetes (49%) and chronic kidney disease (50%) were common. The majority of the patients were on angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor–neprilysin inhibitors (80%) and beta-blockers (86%), and 37% of patients were on mineralocorticoid receptor antagonists. Conclusion: When compared with prior trials in HFpEF, the EMPEROR-Preserved cohort has a somewhat higher burden of comorbidities, lower LVEF, higher median NT-proBNP and greater use of mineralocorticoid receptor antagonists a

Published
2020

64. WELCOME ADDRESS

Author

Pieske, B., Cardoso, J. S., Anker, S. D., and Brito, D. A.

Published
2013

65. Baseline characteristics of patients in the Reduction of Events with Darbepoetin alfa in Heart Failure trial (RED-HF)

Author

McMurray, John J.V., Anand, Inder S., Diaz, Rafael, Maggioni, Aldo P., OʼConnor, Christopher, Pfeffer, Marc A., Solomon, Scott D., Tendera, Michal, van Veldhuisen, Dirk J., Albizem, Moetaz, Cheng, Sunfa, Scarlata, Debra, Swedberg, Karl, Young, James B., Amuchastegui, M., Belziti, C., Bluguermann, J., Caccavo, M., Cartasegna, L., Colque, R., Cuneo, C., Fernandez, A., Gabito, A., Goicochea, R., Gonzalez, M., Gorosito, V., Grinfeld, L., Hominal, M., Kevorkian, R., Litvak Bruno, M., Llanos, J., Mackinnon, I., Manuale, O., Marzetti, E., Nul, D., Perna, E., Riccitelli, M., Sanchez, A., Santos, D., Schygiel, P., Toblli, J., Vogel, D., Aggarwal, A., Amerena, J., De Looze, F., Fletcher, P., Hare, D., Ireland, M., Krum, H., Lattimore, J., Marwick, T., Sindone, A., Thompson, P., Waites, J., Altenberger, J., Ebner, C., Lenz, K., Pacher, R., Poelzl, G., Charlier, F., de Ceuninck, M., De Keulenaer, G., Dendale, P., Maréchal, P., Mullens, W., Thoeng, J., Vanderheyden, M., Vanhaecke, J., Weytjens, C., Wollaert, B., Albuquerque, D., Almeida, D., Aspe y Rosas, J., Bocchi, E., Bordignon, S., Clausell, N., Kaiser, S., Leaes, P., Martins Alves, S., Montera, M., Moura, L., Pereira de Castro, R., Rassi, S., Reis, A., Saraiva, J., Simões, M., Souza Neto, J., Teixeira, M., Benov, H., Chompalova, B., Donova, T., Georgiev, P., Gotchev, D., Goudev, A., Grigorov, M., Guenova, D., Hergeldjieva, V., Ivanov, D., Kostova, E., Manolova, A., Marchev, S., Nikolov, F., Popov, A., Raev, D., Tzekova, M., Czarnecki, W., Giannetti, N., Haddad, H., Heath, J., Huynh, T., Lepage, S., Liu, P., Lonn, E., Ma, P., Manyari, D., Moe, G., Parker, J., Pesant, Y., Rajda, M., Ricci, J., Roth, S., Sestier, F., Sluzar, V., Sussex, B., Vizel, S., Antezana, G., Bugueno, C., Castro, P., Conejeros, C., Manriquez, L., Martinez, D., Potthoff, S., Stockins, B., Vukasovic, J., Gregor, P., Herold, M., Jerabek, O., Jirmar, R., Kuchar, R., Linhart, A., Podzemska, B., Soucek, M., Spac, J., Spacek, R., Vodnansky, P., Bronnum-Schou, J., Clemmensen, K., Egstrup, K., Jensen, G., Kjoller-Hansen, L., Kober, L., Markenvard, J., Rokkedal, J., Skagen, K., Torp-Pedersen, C., Tuxen, C., Videbak, L., Laks, T., Vahula, V., Harjola, V., Kettunen, R., Kotila, M., Bauer, F., Cohen Solal, A., Coisne, D., Davy, J., De Groote, P., Dos Santos, P., Funck, F., Galinier, M., Gibelin, P., Isnard, R., Neuder, Y., Roul, G., Sabatier, R., Trochu, J., Anker, S., Denny, S., Dreykluft, T., Flesch, M., Genth-Zotz, S., Hambrecht, R., Hein, J., Jeserich, M., John, M., Kreider-Stempfle, H., Laufs, U., Muellerleile, K., Natour, M., Sandri, M., Schäufele, T., von Hodenberg, E., Weyland, K., Winkelmann, B., Tse, H., Yan, B., Barsi, B., Csikasz, J., Dezsi, C., Edes, I., Forster, T., Karpati, P., Kerekes, C., Kis, E., Kosa, I., Lupkovics, G., Nagy, A., Preda, I., Ronaszeki, A., Tomcsanyi, J., Zamolyi, K., Agarwal, D., Bahl, V., Bordoloi, A., Chockalingam, K., Chopda, M., Chopra, V., Dugal, J., Ghaisas, N., Ghosh, S., Grant, P., Hiremath, S., Iyengar, S., Jagadeesa Subramania, B., Jain, P., Joshi, A., Khan, A., Mullasari, A., Naik, S., Oomman, A., Pai, V., Pareppally Gopal, R., Parikh, K., Patel, T., Prakash, V., Sastry, B., Sathe, S., Sinha, N., Srikanthan, V., Subburamakrishnan, P., Thacker, H., Wander, G., Admon, D., Katz, A., Klainman, E., Lewis, B., Marmor, A., Moriel, M., Mosseri, M., Shotan, A., Weinstein, J., Zimlichman, R., Agostoni, P., Albanese, M., Alunni, G., Bini, R., Boccanelli, A., Bolognese, L., Campana, C., Carbonieri, E., Carpino, C., Checco, L., Cosmi, F., DʼAngelo, G., De Cristofaro, M., Floresta, A., Fucili, A., Galvani, M., Ivleva, A., Marra, S., Musca, G., Peccerillo, N., Perrone Filardi, P., Picchio, E., Russo, T., Scelsi, L., Senni, M., Tavazzi, L., Erglis, A., Jasinkevica, I., Kakurina, N., Veze, I., Volans, E., Bagdonas, A., Berukstis, E., Celutkiene, J., Dambrauskaite, A., Jarasuniene, D., Luksiene, D., Rudys, A., Sakalyte, G., Sliaziene, S., Aguilar-Romero, R., Cardona-Muñoz, E., Castro-Jimenez, J., Chavez-Herrera, J., Chuquiure Valenzuela, E., De la Pena, G., Herrera, E., Leiva-Pons, J., Lopez Alvarado, A., Mendez Machado, G., Ramos-Lopez, G., Basart, D., Buijs, E., Cornel, J., de Leeuw, M., Dijkgraaf, R., Dunselman, P., Freericks, M., Hamraoui, K., Lenderlink, T., Linssen, G., Lodewick, P., Lodewijks, C., Lok, D., Nierop, P., Ronner, E., Somsen, A., van Dantzig, J., van der Burgh, P., van Kempen, L., van Vlies, B., Voors, A., Wardeh, A., Willems, F., Dickstein, K., Gundersen, T., Hole, T., Thalamus, J., Westheim, A., Dabrowski, M., Gorski, J., Korewicki, J., Kuc, K., Miekus, P., Musial, W., Niegowska, J., Piotrowski, W., Podolec, P., Polonski, L., Ponikowski, P., Rynkiewicz, A., Szelemej, R., Trusz-Gluza, M., Ujda, M., Wojciechowski, D, Wysokinski, A., Camacho, A., Fonseca, C., Monteiro, P., Apetrei, E., Bruckner, I., Carasca, E., Coman, I., Datcu, M., Dragulescu, S., Ionescu, P., Iordachescu-Petica, D., Manitiu, I., Popa, V., Pop-Moldovan, A., Radoi, M., Stamate, S., Tomescu, M., Vita, I., Aroutiounov, G., Ballyuzek, M., Bart, B., Churina, S., Glezer, M., Goloshchekin, B., Ivleva, A., Kobalava, Z., Kostenko, V., Lopatin, Y., Martynov, A., Orlov, V., Semernin, E., Shogenov, Z., Sidorenko, B., Skvortsov, A., Storzhakov, G., Sulimov, V., Talibov, O., Tereshenko, S., Tsyrline, V., Zadionchenko, V., Zateyshchikov, D., Dzupina, A., Hranai, M., Kmec, J., Micko, K., Murin, J., Pella, D., Sojka, G., Spisak, V., Vahala, P., Vinanska, D., Badat, A., Bayat, J., Dawood, S., Delport, E., Ellis, G., Garda, R., Klug, E., Mabin, T., Naidoo, D., Pretorius, M., Ranjith, N., Van Zyl, L., Weich, H., Anguita, M., Berrazueta, J., Bruguera i Cortada, J., de Teresa, E., Gómez Sánchez, M., González Juanatey, J., Gonzalez-Maqueda, I., Jordana, R., Lupon, J., Manzano, L., Pascual Figal, D., Pulpón, L., Recio, J., Ridocci Soriano, F., Rodríguez Lambert, J., Roig Minguell, E., Roig Minguell, E., Romero, J., Valdovinos, P., Klintberg, L., Kronvall, T., Lycksell, M., Morner, S., Rydberg, E., Swedberg, K., Timberg, I., Wikstrom, G., Moccetti, T.4, Ashok, J., Banerjee, P., Carr-White, G., Cleland, J., Connolly, E., Francis, M., Greenbaum, R., Kadr, H., Lindsay, S., McMurray, J., Megarry, S., Memon, A., Murdoch, D., Senior, R., Squire, I., Tan, L., Witte, K., Adams, K., Adamson, P., Adler, A., Altschul, L., Altschuller, A., Amirani, H., Anand, I., Andreou, C., Ansari, M., Antonishen, M., Banchs, H., Banerjee, S., Banish, D., Bank, A., Barbagelata, A., Barnard, D., Bellinger, R., Benn, A., Berk, M., Berry, B., Bethala, V., Bilazarian, S., Bisognano, J., Bleyer, F., Blum, M., Boehmer, J., Bouchard, A., Boyle, A., Bozkurt, B., Brown, C., Burlew, B., Burnham, K., Butler, J., Call, J., Cambier, P., Cappola, T., Carlson, R., Chandler, B., Chandra, R., Chandraratna, P., Chernick, R., Colan, D., Colfer, H., Colucci, W., Connelly, T., Costantini, O., Dadkhah, S., Dauber, I., Davis, J., Davis, S., Denning, S., Drazner, M., Dunlap, S., Egbujiobi, L., Elkayam, U., Elliott, J., El-Shahawy, M., Essandoh, L., Ewald, G., Fang, J., Farhoud, H., Felker, G., Fernandez, J., Festin, R., Fishbein, G., Florea, V., Flores, E., Floro, J., Gabris, M., Garg, M., Gatewood, R., Geller, M., Ghali, J., Ghumman, W., Gibbs, G., Gillespie, E., Gilmore, R., Gogia, H., Goldberg, L., Gradus-Pizlo, I., Grainger, T., Gudmundsson, G., Gunawardena, D., Gupta, D., Hack, T., Hall, S., Hamroff, G., Hankins, S., Hanna, M., Hargrove, J., Haught, W., Hauptman, P., Hazelrigg, M., Herzog, C., Heywood, J., Hill, T., Hilton, T., Hirsch, H., Hunter, J., Ibrahim, H., Imburgia, M., Iteld, B., Jackson, B., Jaffrani, N., Jain, D., Jain, A., James, M., Jimenez, J., Johnson, E., Kale, P., Kaneshige, A., Kapadia, S., Karia, D., Karlsberg, R., Katholi, R., Kerut, E., Khoury, W., Kipperman, R., Klapholz, M., Kosinski, E., Kozinn, M., Kraus, D., Krueger, S., Krum, H., Kumar, S., Lader, E., Lee, C., Levy, W., Lewis, E., Light-McGroary, K., Loh, I., Lombardi, W., Machado, C., Maislos, F., Mancini, D., Markus, T., Mather, P., McCants, K., McGrew, F., McLaurin, B., McMillan, E., McNamara, D., Meyer, T., Meymandi, S., Miller, A., Minami, E., Modi, M., Mody, F., Mohanty, P., Moscoso, R., Moskowitz, R., Moustafa, M., Mullen, M., Naz, T., Noonan, T., OʼBrien, T., Oellerich, W., Oren, R., Pamboukian, S., Pereira, N., Pitt, W., Porter, C., Prabhu, S., Promisloff, S., Ratkovec, R., Richardson, R., Ross, A., Saleh, N., Saltzberg, M., Sarkar, S., Schmedtje, J., Schneider, R., Schuyler, G., Shanes, J., Sharma, A., Siegel, C., Siegel, R., Silber, D., Singh, V., Singh, N., Singh, J., Sklar, J., Small, R., Smith, A., Smith, E., Smith, E., Smull, D., Sotolongo, R., Staniloae, C., Stapleton, D., Steele, P., Stehlik, J., Stein, M., Tang, W., Thadani, U., Torre-Amoine, G., Trichon, B., Tsai, C., Tummala, R., Van Bakel, A., Vicari, R., Vijay, N., Vijayaraghavan, K., Vittorio, T., Vossler, M., Wagoner, L., Wallis, D., Ward, N., Widmer, M., Wight, J., Wilkins, C., Williams, C., Williams, G., Winchester, M., Winkel, E., Wittmer, B., Wood, D., Wormer, D., Wright, R., Xu, Z., Yasin, M., and Zolty, R.

Published
2013
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67. Effect of Nesiritide in Patients with Acute Decompensated Heart Failure

Author

OʼConnor, C. M., Starling, R. C., Hernandez, A. F., Armstrong, P. W., Dickstein, K., Hasselblad, V., Heizer, G. M., Komajda, M., Massie, B. M., McMurray, J. J.V., Nieminen, M. S., Reist, C. J., Rouleau, J. L., Swedberg, K., Adams, K. F., Jr., Anker, S. D., Atar, D., Battler, A., Botero, R., Bohidar, N. R., Butler, J., Clausell, N., Corbalán, R., Costanzo, M. R., Dahlstrom, U., Deckelbaum, L. I., Diaz, R., Dunlap, M. E., Ezekowitz, J. A., Feldman, D., Felker, G. M., Fonarow, G. C., Gennevois, D., Gottlieb, S. S., Hill, J. A., Hollander, J. E., Howlett, J. G., Hudson, M. P., Kociol, R. D., Krum, H., Laucevicius, A., Levy, W. C., Méndez, G. F., Metra, M., Mittal, S., Oh, B.-H., Pereira, N. L., Ponikowski, P., Wilson, W. H., Tanomsup, S., Teerlink, J. R., Triposkiadis, F., Troughton, R. W., Voors, A. A., Whellan, D. J., Zannad, F., and Califf, R. M.

Published
2011

70. Tumour biomarkers: association with heart failure outcomes

Author

Shi, C., primary, van der Wal, H. H., additional, Silljé, H. H. W., additional, Dokter, M. M., additional, van den Berg, F., additional, Huizinga, L., additional, Vriesema, M., additional, Post, J., additional, Anker, S. D., additional, Cleland, J. G., additional, Ng, L. L., additional, Samani, N. J., additional, Dickstein, K., additional, Zannad, F., additional, Lang, C. C., additional, van Haelst, P. L., additional, Gietema, J. A., additional, Metra, M., additional, Ameri, P., additional, Canepa, M., additional, van Veldhuisen, D. J., additional, Voors, A. A., additional, and de Boer, R. A., additional

Published
2020
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74. ADQI 7: the clinical management of the Cardio-Renal syndromes: work group statements from the 7th ADQI consensus conference

Author

Davenport, A., Anker, S. D., Mebazaa, A., Palazzuoli, A., Vescovo, G., Bellomo, R., Ponikowski, P., Anand, I., Aspromonte, N., Bagshaw, S., Berl, T., Bobek, I., Cruz, D.N., Daliento, L., Haapio, M., Hillege, H., House, A., Katz, N., Maisel, A., Mankad, S., McCullough, P., Ronco, F., Shaw, A, Sheinfeld, G., Soni, S., Zamperetti, N., Zanco, P., and Ronco, C.

Published
2010
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79. Effects of serelaxin in patients with acute heart failure

Author

Metra, M., Teerlink, J. R., Cotter, G., Davison, B. A., Felker, G. M., Filippatos, G., Greenberg, B. H., Pang, P. S., Ponikowski, P., Voors, A. A., Adams, K. F., Anker, S. D., Arias-Mendoza, A., Avendano, P., Bacal, F., Bohm, M., Bortman, G., Cleland, J. G. F., Cohen-Solal, A., Crespo-Leiro, M. G., Dorobantu, M., Echeverria, L. E., Ferrari, R., Goland, S., Goncalvesova, E., Goudev, A., Kober, L., Lema-Osores, J., Levy, P. D., Mcdonald, K., Manga, P., Merkely, B., Mueller, C., Pieske, B., Silva-Cardoso, J., Spinar, J., Squire, I., Stepinska, J., Van Mieghem, W., Von Lewinski, D., Wikstrom, G., Yilmaz, M. B., Hagner, N., Holbro, T., Hua, T. A., Sabarwal, S. V., Severin, T., Szecsody, P., Gimpelewicz, C, Lembo, G, and Cardiovascular Centre (CVC)

Subjects
Male, Vasodilator Agents, Vasodilation, Blood Pressure, 030204 cardiovascular system & hematology, NESIRITIDE, THERAPY, law.invention, 0302 clinical medicine, Randomized controlled trial, law, 030212 general & internal medicine, Treatment Failure, Acute Disease, Aged, Cardiovascular Diseases, Disease Progression, Double-Blind Method, Female, Heart Failure, Hospitalization, Humans, Incidence, Infusions, Intravenous, Recombinant Proteins, Relaxin, OUTCOMES, General Medicine, ASSOCIATION, ADMISSION, INSIGHTS, Cardiology, SUBSEQUENT MORTALITY, Intravenous, hormones, hormone substitutes, and hormone antagonists, medicine.drug, medicine.medical_specialty, Infusions, NO, 03 medical and health sciences, Serelaxin, Internal medicine, medicine, In patient, Nesiritide, Pregnancy, business.industry, medicine.disease, PROTECT, Heart failure, RELAX-AHF, business, Hormone
Abstract

BackgroundSerelaxin is a recombinant form of human relaxin-2, a vasodilator hormone that contributes to cardiovascular and renal adaptations during pregnancy. Previous studies have suggested that treatment with serelaxin may result in relief of symptoms and in better outcomes in patients with acute heart failure.MethodsIn this multicenter, double-blind, placebo-controlled, event-driven trial, we enrolled patients who were hospitalized for acute heart failure and had dyspnea, vascular congestion on chest radiography, increased plasma concentrations of natriuretic peptides, mild-to-moderate renal insufficiency, and a systolic blood pressure of at least 125 mm Hg, and we randomly assigned them within 16 hours after presentation to receive either a 48-hour intravenous infusion of serelaxin (30 mu g per kilogram of body weight per day) or placebo, in addition to standard care. The two primary end points were death from cardiovascular causes at 180 days and worsening heart failure at 5 days.ResultsA total of 6545 patients were included in the intention-to-treat analysis. At day 180, death from cardiovascular causes had occurred in 285 of the 3274 patients (8.7%) in the serelaxin group and in 290 of the 3271 patients (8.9%) in the placebo group (hazard ratio, 0.98; 95% confidence interval [CI], 0.83 to 1.15; P=0.77). At day 5, worsening heart failure had occurred in 227 patients (6.9%) in the serelaxin group and in 252 (7.7%) in the placebo group (hazard ratio, 0.89; 95% CI, 0.75 to 1.07; P=0.19). There were no significant differences between the groups in the incidence of death from any cause at 180 days, the incidence of death from cardiovascular causes or rehospitalization for heart failure or renal failure at 180 days, or the length of the index hospital stay. The incidence of adverse events was similar in the two groups.ConclusionsIn this trial involving patients who were hospitalized for acute heart failure, an infusion of serelaxin did not result in a lower incidence of death from cardiovascular causes at 180 days or worsening heart failure at 5 days than placebo. (Funded by Novartis Pharma; RELAX-AHF-2 ClinicalTrials.gov number, NCT01870778.)In a randomized trial, 6545 patients with acute heart failure were assigned to either serelaxin or placebo in addition to standard care. There were no significant differences between the two groups in the incidence of death from cardiovascular causes at 180 days or worsening heart failure at 5 days.

Published
2019

80. Heart failure in cardiomyopathies: a position paper from the Heart Failure Association of the European Society of Cardiology

Author

Seferović, P.M. Polovina, M. Bauersachs, J. Arad, M. Gal, T.B. Lund, L.H. Felix, S.B. Arbustini, E. Caforio, A.L.P. Farmakis, D. Filippatos, G.S. Gialafos, E. Kanjuh, V. Krljanac, G. Limongelli, G. Linhart, A. Lyon, A.R. Maksimović, R. Miličić, D. Milinković, I. Noutsias, M. Oto, A. Oto, Ö. Pavlović, S.U. Piepoli, M.F. Ristić, A.D. Rosano, G.M.C. Seggewiss, H. Ašanin, M. Seferović, J.P. Ruschitzka, F. Čelutkiene, J. Jaarsma, T. Mueller, C. Moura, B. Hill, L. Volterrani, M. Lopatin, Y. Metra, M. Backs, J. Mullens, W. Chioncel, O. de Boer, R.A. Anker, S. Rapezzi, C. Coats, A.J.S. Tschöpe, C.

Abstract

Cardiomyopathies are a heterogeneous group of heart muscle diseases and an important cause of heart failure (HF). Current knowledge on incidence, pathophysiology and natural history of HF in cardiomyopathies is limited, and distinct features of their therapeutic responses have not been systematically addressed. Therefore, this position paper focuses on epidemiology, pathophysiology, natural history and latest developments in treatment of HF in patients with dilated (DCM), hypertrophic (HCM) and restrictive (RCM) cardiomyopathies. In DCM, HF with reduced ejection fraction (HFrEF) has high incidence and prevalence and represents the most frequent cause of death, despite improvements in treatment. In addition, advanced HF in DCM is one of the leading indications for heart transplantation. In HCM, HF with preserved ejection (HFpEF) affects most patients with obstructive, and ∼10% of patients with non-obstructive HCM. A timely treatment is important, since development of advanced HF, although rare in HCM, portends a poor prognosis. In RCM, HFpEF is common, while HFrEF occurs later and more frequently in amyloidosis or iron overload/haemochromatosis. Irrespective of RCM aetiology, HF is a harbinger of a poor outcome. Recent advances in our understanding of the mechanisms underlying the development of HF in cardiomyopathies have significant implications for therapeutic decision-making. In addition, new aetiology-specific treatment options (e.g. enzyme replacement therapy, transthyretin stabilizers, immunoadsorption, immunotherapy, etc.) have shown a potential to improve outcomes. Still, causative therapies of many cardiomyopathies are lacking, highlighting the need for the development of effective strategies to prevent and treat HF in cardiomyopathies. © 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology

Published
2019

84. Sarcopenia: A Time for Action. An SCWD Position Paper

Author

Bauer, J., Morley, J. E., Schols, A. M. W. J., Ferrucci, L., Cruz-Jentoft, A. J., Dent, E., Baracos, V. E., Crawford, J. A., Doehner, W., Heymsfield, S. B., Jatoi, A., Kalantar-Zadeh, K., Lainscak, M., Landi, F., Laviano, A., Mancuso, M., Muscaritoli, M., Prado, C. M., Strasser, F., von Haehling, S., Coats, A. J. S., Anker, S. D., Landi F. (ORCID:0000-0002-3472-1389), Bauer, J., Morley, J. E., Schols, A. M. W. J., Ferrucci, L., Cruz-Jentoft, A. J., Dent, E., Baracos, V. E., Crawford, J. A., Doehner, W., Heymsfield, S. B., Jatoi, A., Kalantar-Zadeh, K., Lainscak, M., Landi, F., Laviano, A., Mancuso, M., Muscaritoli, M., Prado, C. M., Strasser, F., von Haehling, S., Coats, A. J. S., Anker, S. D., and Landi F. (ORCID:0000-0002-3472-1389)

Abstract

The term sarcopenia was introduced in 1988. The original definition was a “muscle loss” of the appendicular muscle mass in the older people as measured by dual energy x-ray absorptiometry (DXA). In 2010, the definition was altered to be low muscle mass together with low muscle function and this was agreed upon as reported in a number of consensus papers. The Society of Sarcopenia, Cachexia and Wasting Disorders supports the recommendations of more recent consensus conferences, i.e. that rapid screening, such as with the SARC-F questionnaire, should be utilized with a formal diagnosis being made by measuring grip strength or chair stand together with DXA estimation of appendicular muscle mass (indexed for height2). Assessments of the utility of ultrasound and creatine dilution techniques are ongoing. Use of ultrasound may not be easily reproducible. Primary sarcopenia is aging associated (mediated) loss of muscle mass. Secondary sarcopenia (or disease-related sarcopenia) has predominantly focused on loss of muscle mass without the emphasis on muscle function. Diseases that can cause muscle wasting (i.e. secondary sarcopenia) include malignant cancer, COPD, heart failure, and renal failure and others. Management of sarcopenia should consist of resistance exercise in combination with a protein intake of 1 to 1.5 g/kg/day. There is insufficient evidence that vitamin D and anabolic steroids are beneficial. These recommendations apply to both primary (age-related) sarcopenia and secondary (disease related) sarcopenia. Secondary sarcopenia also needs appropriate treatment of the underlying disease. It is important that primary care health professionals become aware of and make the diagnosis of age-related and disease-related sarcopenia. It is important to address the risk factors for sarcopenia, particularly low physical activity and sedentary behavior in the general population, using a life-long approach. There is a need for more clinical research into the appropriate mea

Published
2019

85. Empagliflozin in Heart Failure with a Preserved Ejection Fraction.

Author

Anker, S. D., Butler, J., Filippatos, G., Ferreira, J. P., Bocchi, E., Böhm, M., Brunner–La Rocca, H.-P., Choi, D.-J., Chopra, V., Chuquiure-Valenzuela, E., Giannetti, N., Gomez-Mesa, J. E., Janssens, S., Januzzi, J. L., Gonzalez-Juanatey, J. R., Merkely, B., Nicholls, S. J., Perrone, S. V., Piña, I. L., and Ponikowski, P.

Abstract

BACKGROUND Sodium-glucose cotransporter 2 inhibitors reduce the risk of hospitalization for heart failure in patients with heart failure and a reduced ejection fraction, but their effects in patients with heart failure and a preserved ejection fraction are uncertain. METHODS In this double-blind trial, we randomly assigned 5988 patients with class II--IV heart failure and an ejection fraction of more than 40% to receive empagliflozin (10 mg once daily) or placebo, in addition to usual therapy. The primary outcome was a composite of cardiovascular death or hospitalization for heart failure. RESULTS Over a median of 26.2 months, a primary outcome event occurred in 415 of 2997 patients (13.8%) in the empagliflozin group and in 511 of 2991 patients (17.1%) in the placebo group (hazard ratio, 0.79; 95% confidence interval [CI], 0.69 to 0.90; PcO.001). This effect was mainly related to a lower risk of hospitalization for heart failure in the empagliflozin group. The effects of empagliflozin appeared consistent in patients with or without diabetes. The total number of hospitalizations for heart failure was lower in the empagliflozin group than in the placebo group (407 with empagliflozin and 541 with placebo; hazard ratio, 0.73; 95% CI, 0.61 to 0.88; P<0.001). Uncomplicated genital and urinary tract infections and hypotension were reported more frequently with empagliflozin. CONCLUSIONS Empagliflozin reduced the combined risk of cardiovascular death or hospitalization for heart failure in patients with heart failure and a preserved ejection fraction, regardless of the presence or absence of diabetes. [ABSTRACT FROM AUTHOR]

Published
2021
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90. Phenotype of new daily persistent headache: subtypes and comparison to transformed chronic daily headache

Author

Sanjay Cheema, Anker Stubberud, Khadija Rantell, Parashkev Nachev, Erling Tronvik, and Manjit Matharu

Subjects
NDPH, Migraine, Chronic daily headache, Phenotype, Disease classification, Medicine
Abstract

Abstract Background It is unknown whether new daily persistent headache (NDPH) is a single disorder or heterogenous group of disorders, and whether it is a unique disorder from chronic migraine and chronic tension-type headache. We describe a large group of patients with primary NDPH, compare its phenotype to transformed chronic daily headache (T-CDH), and use cluster analysis to reveal potential sub-phenotypes in the NDPH group. Methods We performed a case–control study using prospectively collected clinical data in patients with primary NDPH and T-CDH (encompassing chronic migraine and chronic tension-type headache). We used logistic regression with propensity score matching to compare demographics, phenotype, comorbidities, and treatment responses between NDPH and T-CDH. We used K-means cluster analysis with Gower distance to identify sub-clusters in the NDPH group based on a combination of demographics, phenotype, and comorbidities. Results We identified 366 patients with NDPH and 696 with T-CDH who met inclusion criteria. Patients with NDPH were less likely to be female (62.6% vs. 73.3%, p

Published
2023
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94. Rationale and design of a multicentre, randomized, placebo-controlled trial of mirabegron, a Beta3-adrenergic receptor agonist on left ventricular mass and diastolic function in patients with structural heart disease Beta3-left ventricular hypertrophy (Beta3-LVH)

Author

Pouleur, A.-C. Anker, S. Brito, D. Brosteanu, O. Hasenclever, D. Casadei, B. Edelmann, F. Filippatos, G. Gruson, D. Ikonomidis, I. Lhommel, R. Mahmod, M. Neubauer, S. Persu, A. Gerber, B.L. Piechnik, S. Pieske, B. Pieske-Kraigher, E. Pinto, F. Ponikowski, P. Senni, M. Trochu, J.-N. Van Overstraeten, N. Wachter, R. Balligand, J.-L.

Abstract

Aims: Progressive left ventricular (LV) remodelling with cardiac myocyte hypertrophy, myocardial fibrosis, and endothelial dysfunction plays a key role in the onset and progression of heart failure with preserved ejection fraction. The Beta3-LVH trial will test the hypothesis that the β3 adrenergic receptor agonist mirabegron will improve LV hypertrophy and diastolic function in patients with hypertensive structural heart disease at high risk for developing heart failure with preserved ejection fraction. Methods and results: Beta3-LVH is a randomized, placebo-controlled, double-blind, two-armed, multicentre, European, parallel group study. A total of 296 patients will be randomly assigned to receive either mirabegron 50 mg daily or placebo over 12 months. The main inclusion criterion is the presence of LV hypertrophy, that is, increased LV mass index (LVMi) or increased wall thickening by echocardiography. The co-primary endpoints are a change in LVMi by cardiac magnetic resonance imaging and a change in LV diastolic function (assessed by the E/e′ ratio). Secondary endpoints include mirabegron's effects on cardiac fibrosis, left atrial volume index, maximal exercise capacity, and laboratory markers. Two substudies will evaluate mirabegron's effect on endothelial function by pulse amplitude tonometry and brown fat activity by positron emission tomography using 17F-fluorodeoxyglucose. Morbidity and mortality as well as safety aspects will also be assessed. Conclusions: Beta3-LVH is the first large-scale clinical trial to evaluate the effects of mirabegron on LVMi and diastolic function in patients with LVH. Beta3-LVH will provide important information about the clinical course of this condition and may have significant impact on treatment strategies and future trials in these patients. © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.

Published
2018

95. Novel endotypes in heart failure: effects on guideline-directed medical therapy

Author

Tromp, J. Ouwerkerk, W. Demissei, B. G. Anker, S. D. and Cleland, J. G. Dickstein, K. Filippatos, G. van der Harst, P. Hillege, H. L. Lang, C. C. Metra, M. Ng, L. L. and Ponikowski, P. Samani, N. J. van Veldhuisen, D. J. Zannad, F. Zwinderman, A. H. Voors, A. A. van der Meer, P.

Abstract

Aims We sought to determine subtypes of patients with heart failure (HF) with a distinct clinical profile and treatment response, using a wide range of biomarkers from various pathophysiological domains. Methods and results We performed unsupervised cluster analysis using 92 established cardiovascular biomarkers to identify mutually ex elusive subgroups (endotypes) of 1802 patients with HF and reduced ejection fraction (HFrEF) from the BIOSTAT-CHF project. We validated our findings in an independent cohort of 813 patients. Based on their biomarker profile, six endotypes were identified. Patients with endotype 1 were youngest, less symptomatic, had the lowest N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels and lowest risk for all-cause mortality or hospitalization for HF. Patients with endotype 4 had more severe symptoms and signs of HF, higher NT-proBNP levels and were at highest risk for all-cause mortality or hospitalization for HF [hazard ratio (HR) 1.4; 95% confidence interval (Cl) 1.1-1.8]. Patients with endotypes 2, 3, and 5 were better uptitrated to target doses of beta-blockers (P < 0.02 for all). In contrast to other endotypes, patients with endotype 5 derived no potential survival benefit from uptitration of angiotensin-converting enzyme-inhibitoriangiotensin-II receptor blocker and beta-blockers (P-interaction

Published
2018

96. P6270Empagliflozin reduces the total burden of first and recurrent hospitalisations in patients with type 2 diabetes and established cardiovascular disease

Author

McGuire, D, primary, Zinman, B, additional, Inzucchi, S E, additional, Anker, S D, additional, Wanner, C, additional, Kaspers, S, additional, Von Eynatten, M, additional, Johansen, O.-E, additional, Elsasser, U, additional, Pocock, S, additional, Fitchett, D, additional, Jamal, W, additional, Hantel, S, additional, and Lund, S S, additional

Published
2019
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98. Design and rationale of the EMPEROR trials of, empagliflozin 10 mg once daily, in patients with chronic heart failure with reduced ejection fraction (EMPEROR-Reduced) or preserved ejection fraction (EMPEROR-Preserved)

Author

Anker, S, additional, Zannad, F, additional, Butler, J, additional, Filippatos, G, additional, Salsali, A, additional, Kimura, K, additional, Schnee, J, additional, Zeller, C, additional, Pocock, S, additional, George, J, additional, Brueckmann, M, additional, and Packer, M, additional

Published
2019
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99. Design of the Effect of EMPaglifozin on ExeRcise ability and HF-symptoms, In patients with chronic heArt faiLure (EMPERIAL) trials of empagliflozin in patients with chronic heart failure with reduced or preserved ejection fraction

Author

Abraham, W, additional, Anker, S, additional, Salsali, A, additional, Peil, B, additional, Zeller, C, additional, Brun, M, additional, Macesic, H, additional, Brueckmann, M, additional, Lindenfeld, JA, additional, and Ponikowski, P, additional

Published
2019
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100. Novel endotypes in heart failure: effects on guideline-directed medical therapy

Author

Tromp, J, primary, Ouwerkerk, W, additional, Demissei, B G, additional, Anker, S D, additional, Cleland, J G, additional, Dickstein, K, additional, Filippatos, G, additional, van der Harst, P, additional, Hillege, H L, additional, Lang, C C, additional, Metra, M, additional, Ng, L L, additional, Ponikowski, P, additional, Samani, N J, additional, van Veldhuisen, D J, additional, Zannad, F, additional, Zwinderman, A H, additional, Voors, A A, additional, and van der Meer, P, additional

Published
2018
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