title: [Clinicoimmunological disorders in patients with postinfarction left ventricular remodeling and chronic cardiac failure].
abstract: OBJECTIVE
  To characterize clinical and immune disorders in patients with ischemic heart disease (IHD), postinfarction left ventricular remodeling (PLVR), clinical manifestations of chronic cardiac failure (CCF).
  
  
  METHODS
  A comparative clinical controlled trial of immune system was made. The immune system was assessed by diagnostic and prognostic significance of changes in population composition of T- and B-lymphocytes, by activation of proinflammatory cytokines (IL-1alpha, IL-2, IL-6, IL-8, Inf-alpha, TNF-alpha); high expression of circulating immune complexes (CIC), autoimmune complexes to cardiolipin (CL) in 94 CCF patients with PLVR. The patients were divided into 3 groups according to severity of CCF. Group 1 consisted of 32 patients with CCF (FCII by NYHA) and normal ejection fraction (EF) of the left ventricle (52.0 +/- 2.8%). Group 2--31 CCF (FCIII) patients with decreased EF (by 43.8%) (36 +/- 4.3%). Group 3--31 CCF (FCIV) patients with low (25 +/- 3.8%) EF of the left ventricle. The protocol required conduction of echocardiographic parameters, paired bicycle exercise tests, 6-min walk tests, 24-h ECG monitoring, population cell composition of T- and B-lymphocytes, concentrations of cytokines, IgG and IgG autoantibodies to CL.
  
  
  RESULTS
  A dominating hyperactivation of cytokines TNFalpha, IL-1alpha, IL-2, IL-6 with high expression of CIC and autoAB to CL was associated with moderate or severe CCF (FCII-IV by NYHA), declined inotropic function of the left ventricle (EF 38-23%), low exercise tolerance and remodeling of the left ventricle.
  
  
  CONCLUSIONS
  Immune disorders in the form of hyperactivation of proinflammatory cytokines (most of all TNFalpha, IL-1alpha, IL-2, IL-6), enhanced expression of CIC and autoAB to CL growing with severity of CCF and abnormal heart pump function play an important role in CCF pathogenesis in IHD patients with LCPR and can be markers of the disease progression.
authors.forename: A T
authors.initials: AT
authors.lastname: Teplliakov
authors.forename: L A
authors.initials: LA
authors.lastname: Bolotskaia
authors.forename: M M
authors.initials: MM
authors.lastname: Dibirov
authors.forename: T A
authors.initials: TA
authors.lastname: Stepacheva
authors.forename: N V
authors.initials: NV
authors.lastname: Karaman
authors.forename: T V
authors.initials: TV
authors.lastname: Vdovina
authors.forename: S N
authors.initials: SN
authors.lastname: Shilov
authors.forename: A V
authors.initials: AV
authors.lastname: Kuznetsova
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000276:immunology*; D002908:Chronic Disease; D016207:Cytokines / Q000276:immunology*; D004358:Drug Therapy; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology*; D006801:Humans; D007136:Immunoglobulins / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology*; D012720:Severity of Illness Index; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D017153:Antibodies, Anticardiolipin; D016207:Cytokines; D007136:Immunoglobulins