Clinical effectiveness in everyday practice: improving outcomes for all patients through a national acute coronary syndrome data collaborative.

The management of acute coronary syndromes (ACS) has an extensive and impressive evidence-base with which to guide clinical practice. Despite this, translation to the clinical environment has proved to be challenging and incomplete and can be attributed to patient, provider and system factors. Causes of suboptimal guideline adherence relate to diverse issues, including patient complexity, barriers in knowledge translation of guideline recommendations and a limited capacity within health services. Addressing these factors may enable more effective guideline implementation. In Australia, the infrastructure for clinical data management is fragmented, uncoordinated and often administratively driven, compromising access to important information, which might improve clinical effectiveness. An integrated approach is required to improve clinical effectiveness in ACS care in Australia. Greater access to information both to assist in clinical decision-making and monitoring outcomes may help direct the focus towards understudied populations and improve performance and clinically relevant outcomes. A peer-led initiative based on common datasets, providing rapid feedback, while developing and disseminating a 'toolbox' of proven and sustainable interventions, could improve clinical effectiveness in the Australian management of ACS and provides a rationale for a national ACS registry.

Current guidelines for the management of unstable angina: a new diagnostic and management paradigm.

The new guidelines reflect a worldwide change to more sensitive diagnostic strategies and more aggressive management of unstable angina. Stratification to high risk now includes those patients with only a minor degree of electrocardiographic ST depression (0.5 mm) or a significant elevation of cardiac troponin. High-risk patients are recommended to be treated with intensive medical and invasive management. Intermediate-risk patients may be best evaluated using an accelerated diagnostic strategy over an 8-12 h period before being reclassified as high or low risk.

The effects of RU 41.740, a glycoprotein immunomodulating agent derived from Klebsiella pneumoniae, on intra-abdominal abscess formation in mice.

The prophylactic and therapeutic efficacies of the immunomodulating agent RU 41.740 (a glycoprotein extract from Klebsiella pneumoniae) were studied in a murine model of intra-abdominal abscess formation with Bacteroides fragilis, Escherichia coli, and bran as an abscess-potentiating agent. Parenteral injection of RU 41.740, either before or after injection of an abscess-inducing mixture (AIM), was associated with significantly diminished incidence and size of abscesses. Abscess incidence and size were significantly decreased by oral administration of RU 41.740 after, but not before, AIM injection. Abscess formation and resolution are the results of complex interactions of host defence mechanisms with bacteria and potentiating agent, and RU 41.740 has been shown previously to activate both macrophage and neutrophil function. These results indicate that activation of non-specific defences may protect against abscess development in chronic sepsis.

Abscess induction in beige (bg/bg) mutant mice.

Humans with Chediak-Higashi Syndrome (CHS) and several animal species with similar defects have been reported to have increased susceptibility to infection, including abscess formation, associated with granulocyte abnormalities. These defects were investigated by comparing mice of the SB/Le strain, homozygous for the beige mutation, with their heterozygous littermates and with normal BALB/c mice with respect to the ability to form intraabdominal abscesses. Mice were autopsied 7 days after the intraperitoneal inoculation of a mixture of Bacteroides fragilis, Escherichia coli and an abscess-potentiating agent, bran. Although homozygous beige mice formed more numerous abscesses than controls, the total abscess sizes and bacterial contents were not significantly different. Histopathologically, the abscesses resembled those in normal mice. Phagocytic killing assays using granulocytes from beige mice of the SB/Le and C57BL/6J strains showed no significant differences between homozygous beige mice and controls. Within the context of these experiments in which neutrophil function in vivo and in vitro was examined with respect to anaerobic and facultative Gram-negative bacteria, it is concluded that beige mice can respond adequately to an infectious bacterial challenge. The increased susceptibility to an infection seen in various species with CHS-like disease may relate to virulence factors of the infecting organisms and defects in host defences documented by others but not manifest in these experiments.