title: Alterations of soluble TWEAK and CD163 concentrations in patients with chronic heart failure.
abstract: Inflammatory activation plays a pivotal role in chronic heart failure with reduced ejection fraction (HF-REF). A novel mediator from TNF family: soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) along its soluble decoy receptor CD163 (sCD163) recently has been investigated in other cardiovascular pathologies. We aimed to evaluate sTWEAK and sCD163 concentrations in HF-REF patients. The study enrolled 79 patients with stable HF-REF, EF < 35%. The control population without history of heart failure included two groups: 26 comorbidities matched patients and 27 healthy volunteers. sTWEAK and sCD163 serum concentrations were determined using ELISA kits. Univariate and multivariate analysis was performed to assess variables affecting concentration of sTWEAK and sCD163. HF-REF patients were characterized by higher sTWEAK (median 374 IQR: 321-429 vs 201 IQR: 145-412pg/ml, P=0.005), sCD163 (median 744 IQR: 570-1068 vs 584 IQR: 483-665pg/ml, P=0.03) concentrations and sTWEAK/sCD163 ratio (median 0.53 IQR: 0.32-0.7 vs 0.3 IQR: 0.22-0.37, P=0.001) comparing to healthy volunteers. Comparing to comorbidities matched controls, HF-REF patients had lower sTWEAK levels (median 374 IQR: 321-429 vs 524 IQR: 384-652pg/ml; P=0.002), while sCD163 and sTWEAK/sCD163 ratio didn't differ. Concentration of sTWEAK in HF-REF was affected by white blood cell count and aspirin intake, while sCD163 by exercise capacity, LV diastolic volume, CRP and presence of arterial hypertension.
  
  
  CONCLUSIONS
  HF-REF patients present increased sTWEAK and sCD163 levels as well as sTWEAK/sCD163 ratio when compared to healthy subjects, however CHF itself appears to be associated with down-regulation of sTWEAK.
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Ptaszynska-Kopczynska
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Marta
authors.initials: M
authors.lastname: Marcinkiewicz-Siemion
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Lisowska
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Ewa
authors.initials: E
authors.lastname: Waszkiewicz
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Marcin
authors.initials: M
authors.lastname: Witkowski
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Jasiewicz
authors.affiliation: Department of Regenerative Medicine and Immune Regulation, Medical University of Bialystok, Poland.
authors.forename: Paula
authors.initials: P
authors.lastname: Miklasz
authors.affiliation: Department of Cardiology, Internal Affair and Administration Ministry Hospital, Bialystok, Poland.
authors.forename: Piotr
authors.initials: P
authors.lastname: Jakim
authors.affiliation: Department of Cardiology, Internal Affair and Administration Ministry Hospital, Bialystok, Poland.
authors.forename: Bogdan
authors.initials: B
authors.lastname: Galar
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland.
authors.forename: Wlodzimierz Jerzy
authors.initials: WJ
authors.lastname: Musial
authors.affiliation: Department of Cardiology, Medical University of Bialystok, Poland; Department of Community Medicine and Civilization Disease Prevention, Medical University of Bialystok, Poland. Electronic address: fizklin@wp.pl.
authors.forename: Karol Adam
authors.initials: KA
authors.lastname: Kaminski
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood*; D015214:Antigens, Differentiation, Myelomonocytic / Q000097:blood*; D001241:Aspirin / Q000031:analogs & derivatives / Q000627:therapeutic use; D016022:Case-Control Studies; D000074049:Cytokine TWEAK; D015536:Down-Regulation; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D007958:Leukocyte Count; D008239:Lysine / Q000031:analogs & derivatives / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011956:Receptors, Cell Surface / Q000097:blood*; D012307:Risk Factors; D048069:Tumor Necrosis Factors / Q000097:blood*; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D000074049:Cytokine TWEAK; D011956:Receptors, Cell Surface; C109743:TNFSF12 protein, human; D048069:Tumor Necrosis Factors; D008239:Lysine; D001241:Aspirin; C010395:acetylsalicylic acid lysinate
keywords: Chronic heart failure; Inflammation; Soluble receptor CD163 (sCD163); Soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK)