Abstract
Cardiac vegetations result from bacterium–platelet adherence, activation and aggregation, and are associated with increased morbidity and mortality in infective endocarditis. The GPIIb/IIIa and FcγRIIa platelet receptors play a central role in platelet adhesion, activation and aggregation induced by endocarditis pathogens such as Staphylococcus aureus, but the influence of known polymorphisms of these receptors on the pathogenesis of infective endocarditis is unknown. We determined the GPIIIa platelet antigen PlA1/A2 and FcγRIIa H131R genotype of healthy volunteers (n = 160) and patients with infective endocarditis (n = 40), and investigated the influence of these polymorphisms on clinical outcome in infective endocarditis and S. aureus–platelet interactions in vitro. Platelet receptor genotype did not correlate with development of infective endocarditis, vegetation characteristics on echocardiogram or the composite clinical end-point of embolism, heart failure, need for surgery or mortality (P > 0.05 for all), even though patients with the GPIIIa PlA1/A1 genotype had increased in vivo platelet activation (P = 0.001). Furthermore, neither GPIIIa PlA1/A2 nor FcγRIIa H131R genotype influenced S. aureus-induced platelet adhesion, activation or aggregation in vitro (P > 0.05). Taken together, our data suggest that the GPIIIa and FcγRIIa platelet receptor polymorphisms do not influence S. aureus–platelet interactions in vitro or the clinical course of infective endocarditis.
Highlights
Infective endocarditis is a life-threatening condition resulting from infection of native and prosthetic heart valves, implanted medical devices and large vessels [1]
In as much as bacteriumeplatelet interactions are central to the pathogenesis of infective endocarditis, we examined the influence of the GPIIIa PlA1/A2 and the FcgRIIa H131R platelet receptor polymorphisms on S. aureus-induced platelet adhesion, activation and aggregation in vitro and clinical outcome in patients with infective endocarditis
In order to investigate the influence of platelet receptor polymorphisms on S. aureuseplatelet interactions, we examined S. aureuseplatelet adhesion, activation and aggregation in vitro using platelets from healthy volunteers of different GPIIIa PlA1/A2 and FcgRIIa H131R genotype (Table 2)
Summary
Infective endocarditis is a life-threatening condition resulting from infection of native and prosthetic heart valves, implanted medical devices and large vessels [1]. Staphylococcus aureus has overtaken viridans streptococci as the commonest causative agent, accounting for up to 49% of cases [2,3]. This is worrisome as S. aureus infective endocarditis has mortality rates as high as 56% [4], and underlying cardiac risk factors cannot be identified in over 50% of patients [2]. Bacteria stimulate platelet aggregation leading to vegetation formation through the initial binding of microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) to platelet glycoprotein receptors GPIIb/IIIa or GPIb via plasma protein cross-bridges [11]. The subsequent cross-linking of specific immunoglobulins bound to these MSCRAMMs with the FcgRIIa receptor on the platelet surface results in platelet activation, followed by
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