Is Oxidative Stress–Driven Platelet Activation Associated with Echocardiographic Vegetations in Infective Endocarditis?

Infective endocarditis (IE) is a severe condition requiring both bacteremia and host predisposition. Platelets contribute by forming sterile thrombi that facilitate bacterial adhesion. Experimental evidence suggests oxidative stress–driven platelet activation, but its clinical relevance in endocarditis remains unclear. We compared markers of oxidative stress and platelet activation in patients with echocardiographic vegetations (VEG+) versus those without (VEG–). Consecutive patients undergoing transthoracic and transoesophageal echocardiography for suspected IE were prospectively enrolled. Blood samples were collected on the day of imaging to assess hydrogen peroxide (H ₂ O ₂ ), soluble NOX2–derived peptide (sNOX2-dp), P-selectin, CD40 ligand (CD40L), and tumor necrosis factor-alpha (TNF-α). Patients receiving intravenous antibiotics >7 days were excluded. Ninety patients were enrolled (49 VEG+, 41 VEG–). VEG+ patients showed higher levels of sNOX2-dp ( p = 0.002), P-selectin ( p < 0.001), and TNF-α ( p = 0.033) compared with controls, whereas H ₂ O ₂ and CD40L did not reach statistical significance ( p = 0.125 and p = 0.089, respectively). Univariate analysis associated VEG+ with sNOX2-dp ( p = 0.005), P-selectin ( p < 0.001), and TNF-α ( p = 0.038); multivariate analysis identified P-selectin ( p = 0.01) as the only independent predictor of vegetation. These findings support the hypothesis that patients with IE who develop vegetations exhibit enhanced platelet activation and oxidative stress compared with VEG– patients. Antioxid. Redox Signal. 00, 000–000.