Key result
In vitro exposure to hypochlorous acid increased platelet aggregation in both chronic heart failure patients (p=0.036) and healthy controls (p=0.0006), with higher dityrosine concentrations in worse NYHA functional classes.
Why the study?
Reactive forms of oxygen activating platelets might contribute to thrombosis in chronic heart failure, but the effect of hypochlorous acid on platelet aggregation and dityrosine concentration required evaluation.
Does in vitro exposure to hypochlorous acid increase platelet aggregation and dityrosine concentration in chronic heart failure patients compared to healthy controls?
Case-Control (n=98)
Does in vitro exposure to hypochlorous acid increase platelet aggregation and dityrosine concentration in chronic heart failure patients compared to healthy controls?
p-value: p=0.004
Oxidative stress, simulated by hypochlorous acid, increases platelet aggregation and dityrosine concentration more in chronic heart failure patients than healthy controls, correlating with disease severity.
Hypothesis-generating for oxidative stress in heart failure platelet activation; requires in vivo confirmation before clinical relevance.
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.
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Mongirdienė et al. (2019) conducted a case-control in Chronic Heart Failure (n=98). Hypochlorous acid (HOCl) exposure vs. Healthy controls / No oxidant was evaluated on Platelet aggregation and dityrosine concentration (p=0.004). In vitro exposure to hypochlorous acid increased platelet aggregation in both chronic heart failure patients (p=0.036) and healthy controls (p=0.0006), with higher dityrosine concentrations in worse NYHA functional classes.
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