In Reply Heying et al proposed some mechanisms that could underlie the in vivo bactericidal activity of the antiplatelet drug ticagrelor against gram-positive bacteria.1 They speculate that these mechanisms would be common to those already observed in the presence of other platelet inhibitors, in particular in the context of Staphylococcus aureus bloodstream infection or experimental endocarditis. On the one hand, salicylic acid alters the expression of adhesins or toxins by S aureus, thereby potentially decreasing its ability to colonize damaged tissues, and acetylsalicylic conferred some protection to patients against S aureus bloodstream infection. On the other hand, by interfering with S aureus–triggered glycoprotein IIb/IIIa activation, platelet inhibitors targeting this platelet pathway might also prevent local fibrin generation that hampers bacteria eradication by immune cells. In view of the paucity of treatments against septicaemiae or infective endocarditis, more research is needed to determine whether antiplatelet agents could prove beneficial to patients with cardiovascular disease at risk of such bacterial infection. However, whether the in vivo bactericidal effect of ticagrelor is related to its antiplatelet activity and/or to its ability to inhibit platelet-leucocyte interactions2 or whether it directly targets bacteria survival mechanisms is currently unknown.
Lancellotti P, Musumeci L, Oury C. Are Antiplatelet Agents Beneficial in Prevention of Infective Endocarditis?—Reply. JAMA Cardiol. 2019;4(11):1177–1178. doi:10.1001/jamacardio.2019.3089
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