Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology.
The increasing prevalence of heart failure poses enormous challenges for health care systems worldwide. Despite effective medical interventions that target neurohumoral activation, mortality and morbidity remain substantial. Evidence for inflammatory activation as an important pathway in disease progression in chronic heart failure has emerged in the last two decades. However, clinical trials of 'anti-inflammatory' therapies (such as anti-tumor necrosis factor-alpha approaches) have to date failed to show benefit in heart failure patients. The Heart Failure Association of the European Society of Cardiology recently organized an expert workshop to address the issue of inflammation in heart failure from a basic science, translational and clinical perspective, and to assess whether specific inflammatory pathways may yet serve as novel therapeutic targets for this condition. This consensus document represents the outcome of the workshop and defines key research questions that still need to be addressed as well as considering the requirements for future clinical trials in this area.
Heymans
Stephane
S
Experimental & Molecular Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER Maastricht, The Netherlands. s.heymans@cardio.unimaas.nl
Hirsch
Emilio
E
Anker
Stefan D
SD
Aukrust
Pal
P
Balligand
Jean-Luc
JL
Cohen-Tervaert
Jan W
JW
Drexler
Helmut
H
Filippatos
Gerasimos
G
Felix
Stephan B
SB
Gullestad
Lars
L
Hilfiker-Kleiner
Denise
D
Janssens
Stefan
S
Latini
Roberto
R
Neubauer
Gitte
G
Paulus
Walter J
WJ
Pieske
Burkert
B
Ponikowski
Piotr
P
Schroen
Blanche
B
Schultheiss
Heinz-Peter
HP
Tschöpe
Carsten
C
Van Bilsen
Marc
M
Zannad
Faiez
F
McMurray
John
J
Shah
Ajay M
AM
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000975:Antioxidants / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use; D007249:Inflammation; D037601:Mannose-Binding Lectin / Q000378:metabolism; D061965:Matrix Metalloproteinase Inhibitors; D000081082:Phosphoinositide-3 Kinase Inhibitors; D000683:Serum Amyloid P-Component / Q000627:therapeutic use; D000099153:Pentraxins
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D002097:C-Reactive Protein; D007155:Immunologic Factors; D037601:Mannose-Binding Lectin; D061965:Matrix Metalloproteinase Inhibitors; D000081082:Phosphoinositide-3 Kinase Inhibitors; D000683:Serum Amyloid P-Component; D000099153:Pentraxins