The estimation of intensity of inflammatory alterations of blood in early postinfarction remodeling

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Structural postinfarction abnormalities is connected with inflammation. For better understanding pathogenesis remodeling, it was studied the intensity inflammatory disorders in early period. Purpose Research response remodeling. Materials and methods 772 patients myocardial infarction (MI) were examined. Clinical blood analysis performed at admission on 5th day MI, as well immunological examination, Echocardiography. Results In end-diastolic diameter (EDD) left ventricle (LV) ≥ 55 mm, 5 MI white cells (WBC) level (8,0 ±2,1*109/l vs 7,3 ± 1,9*109/l, p = 0,0001), absolute number neutrophils (5,0 1,7* 109/l 4,5 1,4*109/l, 0,0006) monocytes (0,64 0,30*109/l 0,57 0,30*109/l, 0,005) higher compared EDD ≤ mm. The alterations increased volume (EDV) end-systolic (ESV) similar. LV correlated WBC (r 0,3; 0,00002), also 0,0002) 0,007). positive connection EDV LF P 0,007) revealed. ESV 0,3, р=0,04; accordingly). It should be noted that increase ESD more 37mm not accompanied by authentic factors, but Il-6 (ρ=0,3; р=0,03). As far contractive function myocardium declined, registered (neutrophils EF 55% - 55-40% 4,8 1,5*109/l, less 40% 5,1 2,1*109/l, 0,002), formation areas akinesia 1 days 9,2 3,3*109/l 8,3 3,1*109/l, р=0,05) aneurysm (5,08 1,71*109/l 4,52 1,48*109/l, р=0,0006). noticed functional activity aneurism lower than without (CD14 0,035 0,02*109/l 0,049 0,02*109/l, р=0,05). appears important obtained data hypertrophy diastolic disfunction lymphocytes, expressing marker apoptosis CD95 (0,458 0,276*109/l 0,335 0,155*109/l, р=0,05; 0,441 0,26*109/l 0,342 0,21*109/л, р=0,01, Conclusion markers, decline monocytes, elevation marker, associated bigger remodeling processes. acute phase inflammation necessary stage healing, long-term clinical case, excessive activation or alteration leukocytes can lead to growth structural electrical