Platelet Activity and Its Correlation with Inflammation and Cell Count Readings in Chronic Heart Failure Patients with Reduced Ejection Fraction

: There has been an increasing interest in the role of inflammation in thrombosis complications in chronic heart failure (HF) patients. The incidence of thrombosis in HF has been shown to be the highest in patients classified as NYHA IV (New York Heart association). It is stated that inflammation is regulated by platelet-induced activation of blood leukocytes. We aimed to compare the platelet and cell count readings in chronic HF with reduced ejection fraction (HFrEF) patients according to NYHA functional class and to evaluate the correlation between those readings. : A total of 185 patients were examined. The results of heart echoscopy (TEE) testing; fibrinogen, N-terminal pro b-type natriuretic peptide (NT-proBNP), C reactive protein (CRP), and cortisol concentrations; complete blood counts; and a 6 min walking test were assessed and platelet aggregation was determined. : Mean platelet volume (MPV) increased with deterioration of a patient's state ( < 0.005). Lymphocyte count and percentage were the lowest in the NYHA IV group ( < 0.005). Neutrophil and monocyte percentage and count were the highest ( < 0.045) in the NYHA IV group. Adenosine diphosphate (ADP)- and ADR-induced platelet aggregation was higher in the NYHA III group compared to NYHA II and I groups ( < 0.023). NYHA functional class correlated with mean platelet volume (MPV) (r = 0.311, = 0.0001), lymphocyte count (r = -0.186, = 0.026), monocyte count ( = 0.172, = 0.041), and percentage (r = 0.212, = 0.011). CRP concentration correlated with NT-proBNP (r = 0.203, = 0.005). MPV correlated with fibrinogen concentration (r = 0.244, = 0.004). : (1) MPV could be considered as an additional reading reflecting a patient's condition, however the use of MPV to identify patients at risk of hypercoagulable state should be evaluated in more extensive studies; (2) increased neutrophil and monocyte counts could indicate a higher inflammatory state in chronic HFrEF.