[A role of activation of proinflammatory cytokines and production of autoimmune complexes in the pathogenesis of chronic heart failure in patients with postinfarct cardiac dysfunction].
A comparative randomized clinical study was conducted to evaluate the diagnostic and prognostic value of the activation of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-2, IL-6, IL-8)] and the increased production of autoimmune complexes in the pathogenesis of chronic heart failure (CHF) in patients with coronary heart disease (CHD). The study included 47 patients with CHD who had a more than 6-month history of Q-forming myocardial infarction. The patients were randomized into 3 groups: 1) 21 patients with NYHA Functional Class (FC) II heart failure (HF); 2) 16 patients with FC III HF; and 3) 10 with FC IV HF. Basic therapy involved angiotensin-converting enzyme (ACE) inhibitors, nitrates, diuretics, beta-adrenoblockers; 27.6% received digoxin, disaggregatory agents. A study protocol involved the estimation of the parameters of EchCG, paired bicycle ergometric tests, 6-min walking test, ECG daily monitoring, the levels of proinflammatory cytokines in the serum and IgG autoantibodies to cardiolipin. The findings suggest that with the higher expression of autoimmune complexes, the activation of cytokines (primarily TNF-alpha, IL-1alpha, IL-2) plays an important role in the pathogenesis of CHF in patients with postinfarct cardiac dysfunction: the high activation of cytokines and the elevated level of autoimmune complexes are associated with moderate or severe NYHA FC II-IV HF, depressed left ventricular contractility (ejection fraction, 23-38%), low exercise tolerance, and cardiac remodeling.