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The article focuses on a study which examined the effect of an additional loading dose of 250 milligrams (mg) aspirin at the onset of acute coronary syndrome in patients who are already on chronic therapy with 100 mg aspirin. The study included consecutive patients with symptoms suggestive of acute coronary syndrome, including a cohort already under chronic aspirin therapy. It found that the addition of aspirin in patients taking chronic therapy with 100 mg aspirin decreased platelet hyperfunction and thromboxane B2.

The article presents a prospective observational study on pronounced platelet hyperfunction in patients with cardiac arrest achieving restoration of spontaneous circulation. It concludes that patients with myocardial ischemia-triggered cardiac arrest had the most eminent degree of platelet hyperfunction below high shear rate. It observes that succeeding trials are essential to elucidate whether rapid, more aggressive antiplatelet therapy improves outcome after cardiac arrest.

To gain insight into molecular mechanisms of anti-inflammatory effects of statins, we have studied global gene expression in circulating leucocytes in an in-vivo model of acute inflammation following statin administration.For this purpose, a randomized, double-blind, placebo-controlled, crossover study was conducted in six healthy male volunteers, who received simvastatin (80 mg/day), rosuvastatin (40 mg/day) or placebo before infusion of E. coli lipopolysaccharide (LPS). Leucocyte RNA isolated before and after statin treatment, and after LPS-infusion was subjected to GeneChip transcript profiling (n=42).Data analysis revealed that statins exert little effect on leucocyte gene expression. Statin-responsive genes included several immune response genes and the cholesterol efflux transporter (ABCA1). Rosuvastatin appeared to moderately downregulate expression of the genes encoding the inflammatory response proteins orosomucoid (ORM1) and interleukin 18 receptor accessory protein (IL18RAP). LPS-infusion induced a pronounced response of the leucocyte transcriptome, notably affecting transcripts related to immune regulation, cell proliferation and motility. While the majority of LPS-induced changes were not modulated by either statin, few select genes responded differently after statin treatment, such as the genes encoding the CD32 receptor (FCGR2A) or the protein geranylgeranyltransferase 1b subunit (PGGT1B).We found that few ‘inflammatory’ genes appeared to be moderately down regulated during rosuvastatin administration, such as the ORM1 or IL18RAP genes. The small number of statin-induced differences, both during treatment and after LPS-induced inflammation, however, suggests that statins might exert their anti-inflammatory action mainly at the posttranscriptional level rather than at the level of gene transcription. [ABSTRACT FROM AUTHOR]

The article presents a study which examines the influence of the Duffy receptor on human inflammation in vivo. There were 16 Duffy-positive white subjects and 16 Duffy-negative subjects of African descents included in the study. It was found that the Duffy antigen altered chemokine concentrations in blood.

von Willebrand factor (VWF) plays a pivotal role in platelet adhesion and aggregation at sites of high shear rates (eg, in coronary arteries that have stenotic or ruptured atherosclerotic plaque lesions). Numerous studies have investigated the relationship between VWF plasma levels and thromboembolic cardiovascular events. In contrast to the rather weak association in the general population, in patients with preexisting vascular disease, VWF is significantly predictive for adverse cardiac events, including death. Likewise, VWF typically rises during the course of acute coronary syndrome, and the extent of this VWF release is an independent predictor of adverse clinical outcome in these patients. Various lines of evidence indicate that VWF is not only a marker but also actually an important effector in the pathogenesis of myocardial infarction. This central role of VWF in thrombogenesis has made it a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in acute coronary syndrome and further outlines the relevance of therapeutic interventions targeting VWF for acute coronary syndrome patients.