Staphylococcus aureus increases platelet reactivity in patients with infective endocarditis

Area of Science:

• Cardiology
• Infectious Diseases
• Hematology

Background:

• Thromboembolism is a common complication of infective endocarditis (IE).
• Staphylococcus aureus (SA) is the primary cause of IE and is associated with increased platelet reactivity.
• The optimal antithrombotic strategy for IE remains undetermined.

Purpose of the Study:

• To investigate whether platelet reactivity is elevated in patients with SA-IE.
• To determine if antiplatelet medication, specifically aspirin (ASA), can mitigate this increased reactivity.
• To assess the safety of ASA in SA-IE patients regarding bleeding events.

Main Methods:

• A prospective, observational, single-center cohort study involving 114 IE patients.
• Patients were categorized into four groups based on SA status (coagulase-positive vs. coagulase-negative) and ASA use.
• Platelet function was assessed using Multiplate electrode aggregometry, and blood clotting was evaluated with ROTEM thromboelastometry. Bleeding was assessed using TIMI criteria.

Main Results:

• ASA-naïve patients with SA-positive IE exhibited significantly higher platelet aggregation (ADP stimulation) compared to those with coagulase-negative IE.
• Aspirin medication effectively abrogated this increased platelet reactivity in both SA-positive and coagulase-negative IE groups.
• Aspirin did not increase bleeding risk in SA-positive IE patients, although it was associated with increased red blood cell transfusions in SA-negative patients.

Conclusions:

• Staphylococcus aureus IE is linked to heightened platelet reactivity.
• Aspirin effectively reduces platelet reactivity in SA-IE patients without a significant increase in bleeding risk.
• These findings suggest a potential therapeutic role for aspirin in managing SA-positive IE, warranting further investigation in clinical trials.