Comparison of drug-eluting stents with bare metal stents in unselected patients with acute myocardial infarction.

Objectives: The aim of this study was to compare the procedural characteristics and outcomes of patients with acute myocardial infarction treated with drug-eluting stents (DES) vs. bare metal stents (BMS).

Background: DES have been shown to reduce the incidence of restenosis and target vessel revascularization (TVR) in clinical randomized studies when compared with BMS in patients undergoing elective percutaneous intervention.

Percutaneous coronary intervention in unprotected left main disease: a status report.

Percutaneous coronary intervention (PCI) of the unprotected left main (LM) artery is currently not recommended as a routine procedure based on the history of inferior outcomes of LM percutaneous transluminal coronary angioplasty and bare metal stenting. Instead, surgical revascularization (coronary artery bypass grafting, CABG) is considered to be the gold standard. There is renewed interest in LM-PCI because of improved outcomes of PCI utilizing drug eluting stents (DES) in multiple randomized trials.

Salicylic acid activates sigma factor B by rsbU-dependent and -independent mechanisms.

Salicylic acid (SAL) may impact Staphylococcus aureus virulence by activating the sigB operon (rsbU-V-W-sigB), thus leading to reductions in alpha-toxin production and decreased fibronectin binding (L. I. Kupferwasser et al.

Susceptibility to thrombin-induced platelet microbicidal protein is associated with increased fluconazole efficacy against experimental endocarditis due to Candida albicans.

Platelet microbicidal proteins (PMPs) are believed to be integral to host defense against endovascular infection. We previously demonstrated that susceptibility to thrombin-induced PMP 1 (tPMP-1) in vitro negatively influences Candida albicans virulence in the rabbit model of infective endocarditis (IE). This study evaluated the relationship between in vitro tPMP-1 susceptibility (tPMP-1s) or resistance (tPMP-1r) and efficacy of fluconazole (FLU) therapy of IE due to C.

Salicylic acid attenuates virulence in endovascular infections by targeting global regulatory pathways in Staphylococcus aureus.

Aspirin has been previously shown to reduce the in vivo virulence of Staphylococcus aureus in experimental endocarditis, through antiplatelet and antimicrobial mechanisms. In the present study, salicylic acid, the major in vivo metabolite of aspirin, mitigated two important virulence phenotypes in both clinical and laboratory S. aureus strains: alpha-hemolysin secretion and fibronectin binding in vitro.

In vitro susceptibility to thrombin-induced platelet microbicidal protein is associated with reduced disease progression and complication rates in experimental Staphylococcus aureus endocarditis: microbiological, histopathologic, and echocardiographic analyses.

Background: Mammalian platelets contain small, cationic, staphylocidal peptides, termed thrombin-induced platelet-microbicidal proteins (tPMPs). Evidence suggests that tPMPs play a key role in host defense against endovascular infections, such as infective endocarditis (IE). In the present study, we evaluated the influence of differences in staphylococcal tPMP-susceptibility profiles in vitro on disease severity in experimental IE.

[Culture-negative endocarditis: etiology, diagnosis, management and therapy].

Background: Culture-negative endocarditis is a diagnostic challenge with variable clinical presentation and protean manifestations.

Etiology And Diagnosis: The two main causes why endocarditis may be culture-negative are 1. antibiotic treatment prior to obtaining blood cultures, and 2.

Diagnosis of culture-negative endocarditis: the role of the Duke criteria and the impact of transesophageal echocardiography.

Background: The Duke criteria have been shown to be more sensitive than the von Reyn criteria in the diagnosis of culture-positive endocarditis but to date have not been fully validated for culture-negative endocarditis (CNE). The aim of this study was (1) to compare the diagnostic accuracy of the Duke criteria versus clinical judgment and the von Reyn criteria in CNE and (2) to assess the diagnostic impact of transesophageal echocardiography (TEE) on the Duke criteria in CNE.

Methods: The study group consisted of 49 patients with suspected CNE in whom the presence (n = 32) or absence (n = 17) of endocarditis was confirmed by surgery, autopsy, or both.

Expression of endothelial cell adhesion molecules on heart valves: up-regulation in degeneration as well as acute endocarditis.

Inflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha), as well as shear stress, cause endothelial cells (ECs), to undergo not only functional alterations but also structural reorganizations, which contribute to vascular leakage. Like ECs of the human aorta, ECs on heart valves are exposed to extreme shear stress. However, while ECs expression of cell adhesion molecules (CAMs) in large vessels has been widely studied, it seems that there are no such studies on ECs of heart valves, although this knowledge might be important for our understanding of the aetiological aspects of local inflammatory responses.

Plasmid-mediated resistance to thrombin-induced platelet microbicidal protein in staphylococci: role of the qacA locus.

Thrombin-induced platelet microbicidal protein 1 (tPMP-1) is a small, cationic peptide released from rabbit platelets following thrombin stimulation. In vitro resistance to this peptide among strains of Staphylococcus aureus correlates with the survival advantage of such strains at sites of endothelial damage in humans as well as in experimental endovascular infections. The mechanisms involved in the phenotypic resistance of S.

Comparative efficacies of liposomal amikacin (MiKasome) plus oxacillin versus conventional amikacin plus oxacillin in experimental endocarditis induced by Staphylococcus aureus: microbiological and echocardiographic analyses.

Optimal treatment strategies for serious infections caused by Staphylococcus aureus have not been fully characterized. The combination of a beta-lactam plus an aminoglycoside can act synergistically against S. aureus in vitro and in vivo.

Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects.

Background: Platelets are integral to cardiac vegetations that evolve in infectious endocarditis. It has been postulated that the antiplatelet aggregation effect of aspirin (ASA) might diminish vegetation evolution and embolic rates.

Methods And Results: Rabbits with Staphylococcus aureus endocarditis were given either no ASA (controls) or ASA at 4, 8, or 12 mg.

The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events.

Objectives: The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events.

Background: An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined.