Aspirin to prevent growth of vegetations and cerebral emboli in infective endocarditis

Taha, TH; Durrant, S.; Mazeika, P; Nihoyannopoulos, Petros; Oakley, Celia M.

doi:10.1111/j.1365-2796.1992.tb00971.x

Cited by 55 publications

(24 citation statements)

References 14 publications

(7 reference statements)

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“…Acetylsalicylic acid (ASA, aspirin) has been used in vitro and in a number of experimental models to reduce vegetation sizes and to mitigate the course of disease (23)(24)(25). Similar effects have also been observed by Kupferwasser et al (26).…”

Section: Importance Of Staphylococcal Attachment and Invasion In Endosupporting

confidence: 53%

Salicylic acid: an old dog, new tricks, and staphylococcal disease

Herrmann¹

2003

J. Clin. Invest.

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Aspirin has been shown to cause a reduction in the virulence of Staphylococcus aureus–associated endocarditis. A new study reveals that salicylic acid, the major metabolite of aspirin, acts at the level of transcription to downregulate the production of fibrinogen, fibronectin, and α-hemolysin — virulence factors necessary for bacterial replication in host tissues and, now, potential therapeutic targets

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Section: Importance Of Staphylococcal Attachment and Invasion In Endosupporting

confidence: 53%

Salicylic acid: an old dog, new tricks, and staphylococcal disease

Herrmann¹

2003

J. Clin. Invest.

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“…Although these observations may be due in part to ASA's direct effect on platelets, it is likely that this agent's effect on prostacyclin and mediators of adherence, such as thrombospondin and fibronection, also contributes to the observed reduction in both bacterial density and vegetation weight. In addition, the reduction in vegetation weight observed with ASA therapy may have other important clinical implications, such as decreasing the incidence of embolic phenomena that are commonly experienced with endocarditis (13). Although many questions remain and other investigations are required to determine the mechanism responsible for our observations, this study provides encouraging data regarding the role of ASA therapy in the treatment of infective endocarditis.…”

Section: Discussionmentioning

confidence: 49%

Influence of aspirin on development and treatment of experimental Staphylococcus aureus endocarditis

Nicolau

Marangos

Nightingale

et al. 1995

Antimicrob Agents Chemother

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Previously, we have shown that a 5-mg/kg of body weight daily dose of aspirin (ASA) caused reductions in the bacterial densities and weights of aortic vegetations in a rabbit model of Staphylococcus aureus endocarditis. We sought to determine (i) whether ASA dosage influences the development of vegetations and (ii) whether ASA given with antimicrobial therapy improves the treatment outcome of infective endocarditis. To study the influence of ASA dosage, animals received either no ASA (control) or oral doses of 2.5, 10, 20, and 50 mg/kg daily. The 2.5-and 10-mg/kg groups had statistically significant reductions in vegetation weight compared with untreated controls. The 10-mg/kg dose also resulted in a significant decrease in bacterial densities compared with those of the controls. Although reductions in weight and bacterial density were observed in other ASA-treated groups, these did not achieve statistical significance. To study the influence of ASA and antimicrobial therapy, the animals received either vancomycin alone or vancomycin with ASA. When ASA was given prior to and during antimicrobial therapy, a significant reduction in vegetation weight was observed. Additionally, the rate of sterilization was directly proportional to this observed reduction in weight. ASA's impact on the reduction of both the bacterial density and the weight of aortic vegetations is a dose-dependent phenomenon. When given with antimicrobial therapy, ASA not only reduces vegetation weight but also improves the rate of sterilization. This study provides additional data regarding the role of ASA in the treatment of endocarditis.The pathogenesis of infective endocarditis is complex and requires the interaction of bacteria, platelets, numerous plasma factors, and integrin-binding proteins on the surface of the damaged endothelium. Once the consolidation of the vegetation components has become complete, the infecting organisms exist at high densities in fibrin and platelet meshwork (1, 2). This meshwork not only provides bacterial protection from the host defenses but also creates an environment in which the bacteria exist in a state of reduced metabolic activity and are, therefore, less susceptible to antimicrobial therapy. Because platelets are an integral component of the vegetation, plateletinduced dysfunction may offer a target site for limiting the induction and progression of this disease.Aspirin (ASA) has long been recognized as an agent that produces platelet dysfunction when it is taken orally. Within platelets, ASA blocks the synthesis of thromboxane A 2 , which is a vasoconstrictor and a promoter of platelet aggregation, by irreversibly inhibiting the cyclooxygenase and hydroperoxidase reactions needed for the production of thromboxane A 2 (15). Once induced, this defect cannot be repaired during the life span of the platelets because these cells lack the necessary biosynthetic machinery to produce new protein. As a result, the only way for the cyclooxygenase to recover is via the production of new platelets, which also explai...

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“…These animal studies prompted two clinical trials of aspirin as adjunctive therapy in the treatment of IE in humans. The first was a small, prospective, observational study of nine patients with IE who were randomly assigned to either lowdose aspirin or no aspirin [22]. This study found two symptomatic cerebral infarcts and one myocardial infarct in the patient group that received no aspirin (n=5) and no embolic events in those who received aspirin (n=4) [22].…”

Section: Introductionmentioning

confidence: 99%

“…The first was a small, prospective, observational study of nine patients with IE who were randomly assigned to either lowdose aspirin or no aspirin [22]. This study found two symptomatic cerebral infarcts and one myocardial infarct in the patient group that received no aspirin (n=5) and no embolic events in those who received aspirin (n=4) [22]. Given the extremely small numbers of patients in this pilot study, the authors rightly suggested further studies were needed to evaluate the role of aspirin in IE [22].…”

Section: Introductionmentioning

confidence: 99%

Is There a Role for Antiplatelet Therapy in Infective Endocarditis? A Review of Current Scientific Evidence

Anavekar

Murphy

2010

Curr Infect Dis Rep

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Recently, interest has emerged regarding adjuvant antiplatelet therapy in infective endocarditis (IE) and its impact on clinical outcomes. Despite ongoing research, the role of antiplatelet therapy in this setting remains unclear. Generally, investigations of IE are limited by the low incidence of the disease, practical issues related to diagnosis, and the highly variable latency period between symptom onset and definitive diagnosis. This article reviews the rationale for using antiplatelet therapy in the setting of IE and the contemporary literature that investigates its use.

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Aspirin to prevent growth of vegetations and cerebral emboli in infective endocarditis

Cited by 55 publications

References 14 publications

Salicylic acid: an old dog, new tricks, and staphylococcal disease

Salicylic acid: an old dog, new tricks, and staphylococcal disease

Influence of aspirin on development and treatment of experimental Staphylococcus aureus endocarditis

Is There a Role for Antiplatelet Therapy in Infective Endocarditis? A Review of Current Scientific Evidence

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