Тканевой Ингибитор Матриксных Металлопротеиназ-1 (TIMP-1) Как Независимый Маркер Ишемического Ремоделирования Миокарда При Хронической Сердечной Недостаточности

It has been reported that the increased expression of natural inhibitors of the matrix metalloproteinases is associated with the high risk of mortality and heart failure progression. The aim of the study was to estimate the diagnostic value of tissue inhibitor of metalloproteinase-1 (TIMP-1) for the diagnosis of heart failure in patients with myocardial ischemia and/or post-myocardial infarction remodeling. A total of 52 patients with heart failure NYHA classes II, III, and IV were enrolled in the study. Diagnostic value and prognosis for adverse cardiovascular events were analyzed in the prospective 6-month observation. The patients were divided into three groups according to heart failure severity: group 1 included patients with NYHA class II (n=18) with preserved left ventricular (LV) ejection fraction (EF) (>45%), group 2 included patients with NYHA class III (n=23) with decreased LV EF, and group 3 included patients with the most severe NYHA class IV chronic heart failure (n=11) and LV EF of <32.5%. The age of the patients was 60.6+0.92 years. The TIMP-1 level in blood was determined by hard phase immunoenzyme analysis. All-cause mortality, cardiovascular mortality, nonfatal myocardial infarction (MI), need for revascularization, need for hospitalization, and definite progression of heart failure were the clinical endpoints with 6-month follow-up. The TIMP-1 level in patients of group 1 ranged from 181 to 375.9 ng/ml (Me=278.45 ng/ml); patients in group 2 had TIMP-1 levels ranging from 376.6 to 897.8 ng/ml (Me=637.2 ng/ml), and the levels of TIMP in patients of group 3 were significantly higher, ranging from 903.6 to 1687.9 ng/ml (Me=1295.8 ng/ml). Two patients with end-stage heart failure from group 2 and group 3 died during the study; their TIMP-1 levels were 1289.9 and 1687 ng/ml, respectively. In patients with ischemic heart disease, heart failure, and postmyocardial infarction remodeling, TIMP-1 can be considered a new independent predictor of ischemic myocardial dysfunction and LV fibrosis.