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Background and objective: One of the reasons for thrombosis in chronic heart failure (CHF) might be reactive forms of oxygen activating platelets. The aim of this study was to evaluate the effect of oxidant hypochlorous acid (HOCl) on platelet aggregation and dityrosine concentration in CHF patients and healthy controls. Materials and Methods: CHF patients (n = 67) and healthy (n = 31) were investigated. Heart echoscopy, 6-min walking test, complete blood count, platelet aggregation, and dityrosine concentration were performed. Platelet aggregation and dityrosine concentration were measured in plasma samples after incubation with different HOCl concentrations (0.15, 0.0778, and 0.0389 mmol/L). Results: Platelet aggregation without oxidant was lower (p = 0.049) in CHF patients than in controls. The spontaneous platelet aggregation with oxidant added was higher in CHF patients (p = 0.004). Dityrosine concentration was also higher (p = 0.032) in CHF patients. Platelet aggregation was the highest in samples with the highest oxidant concentration in both healthy controls (p = 0.0006) and in CHF patients (p = 0.036). Platelet aggregation was higher in NYHA III group in comparison to NYHA II group (p = 0.0014). Concentration of dityrosine was significantly higher in CHF samples (p = 0.032). The highest concentration of dityrosine was obtained in NYHA IV group samples (p < 0.05). Intensity of platelet aggregation, analyzed with ADP, was correlated with LV EF (r = 0.42, p = 0.007). Dityrosine concentration was correlated with NYHA functional class (r = 0.27, p < 0.05). Conclusions: The increase in platelet aggregation in CHF and healthy controls shows the oxidant effect on platelets. The increase in dityrosine concentration in higher NYHA functional classes shows a higher oxidative stress in patients with worse condition.

Background and objective: An association between coronary artery disease (CAD) and agerelated macular degeneration (ARMD) has long been postulated, but exact mechanisms remain unclear. The global prevalence of CAD and ARMD increases and early biomarkers for early diagnosis of these diseases are necessary. The aim of this study was to investigate the plasma level of oxidative stress biomarker CML in patients with and without angiographic findings of atherosclerosis in the coronary arteries (CADath+ and CADath, respectively) and to assess if there was an association of CAD with ARMD. Materials and methods: The study enrolled 233 subjects. Based on cardiologic and ophthal- mologic examinations, the patients were divided into four subgroups: CADath+ARMD+, CADath+ARMD−, CADath−ARMD+, and CADath−ARMD−. The enzyme-linked immunosorbent assay was used for the measurement of plasma CML levels. Serum lipid levels were determined by an automatic analyzer using conventional enzymatic methods. Results: CADath+ patients had higher CML concentration compared to CADath subjects (1.04 ± 0.6 vs. 0.83 ± 0.4 ng/mL, P &lt, 0.001). The highest mean CML level (1.12 ± 0.7 ng/mL) was found in CADath+ARMD+ patients. The mean plasma CML concentration was higher in subjects with any of the analyzed diseases compared to CADath−ARMD− subjects. A significant positive association of CADath+ (OR = 2.50, 95% CI 1.60–3.90, P = 0.0001), ARMD (OR = 2.08, 95% CI 1.40–3.11, P = 0.0001) and both analyzed diseases (OR = 4.67, 95% CI 2.29– 9.53, P = 0.0001) with an increased level of plasma CML in a logistic regression model adjusting by age was identified. Conclusions: The level of CML, an oxidative stress biomarker, reflects the presence of atherosclerosis in coronary arteries and shows a possible link between ARMD and CADath+ via oxidative status.