![]() Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Our results do not prove causality, but our findings may be used as rationale for future (mechanistic) studies on serum-free thiol modulation in heart failure.Īssociations of serum-free thiol concentrations with heart failure severity and outcomes In patients with new-onset or worsening HF, a lower serum-free thiol concentration, indicative of higher oxidative stress, is associated with increased HF severity and poorer prognosis. ![]() Lower serum-free thiol concentrations were associated with more advanced HF, as indicated by worse NYHA class, higher plasma NT-proBNP (P < 0.001 for both) and with higher rates of all-cause mortality (hazard ratio (HR) per standard deviation (SD) decrease in free thiols: 1.253, 95% confidence interval (CI): 1.171–1.341, P < 0.001), cardiovascular mortality (HR per SD: 1.182, 95% CI: 1.086–1.288, P < 0.001), and the composite outcome (HR per SD: 1.058, 95% CI: 1.001–1.118, P = 0.046). Associations between free thiol concentrations and clinical characteristics and outcomes, including all-cause mortality, cardiovascular mortality, and a composite of HF hospitalization and all-cause mortality during a 2-years follow-up, were reported. Serum-free thiol concentrations were determined by colorimetric detection in 3802 patients from the BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT-CHF). The purpose of this study was to investigate associations between serum-free thiol concentrations and disease severity and clinical outcome in patients with new-onset or worsening HF. ![]() The role of serum-free thiol concentrations, as a marker of systemic oxidative stress, in HF remains largely unknown. Oxidative stress may be a key pathophysiological mediator in the development and progression of heart failure (HF). ![]()
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