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Hypercoagulability plays a key role in the progression of cardiovascular disease (CVD). Although omega-3 polyunsaturated fatty acid (PUFA) intake has been inversely related to the risk of cardiovascular events, the mechanisms are not fully understood. The aim of this study was to investigate the effects of omega-3 on novel markers of global coagulation. The generation of fibrin and thrombin, measured via overall hemostasis potential (OHP) assay and calibrated automated thrombography, respectively, was determined in 40 healthy subjects and 16 patients with CVD at baseline and after 4 weeks of 640 mg/day omega-3 PUFA. In healthy subjects, fibrin generation was significantly reduced, as measured by overall coagulation potential (p = 0.013), OHP (p < 0.001), velocity of fibrin polymerization (p = 0.002), and significant increase in delay to fibrin generation (p = 0.002). The peak of generated thrombin was significantly reduced (p = 0.043). In subjects with CVD, omega-3 PUFA significantly reduced OHP and significantly increased the lag time to thrombin generation (both p < 0.001). Treatment with omega-3 PUFA had no effect on other fibrin and thrombin generation parameters in CVD patients. Four-week omega-3 PUFA supplementation reduced thrombotic potential in healthy subjects, as shown by reduced fibrin generation and peak thrombin. There was a greater effect on fibrin generation in healthy subjects compared with those with CVD., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Purpose: Diabetes and cardiovascular disease are major public health concerns worldwide and are leading causes of morbidity and mortality. People with type 2 diabetes are at an increased risk for cardiovascular disease. Diet has a substantial affect on the progression of many diseases, including diabetes, cardiovascular disease, osteoporosis, and arthritis. Omega-3 polyunsaturated fatty acids (long-chain polyunsaturated fatty acids [LC-PUFA]) have long been attributed to the maintenance of health and may be of benefit in reducing cardiovascular risk. The purpose of this review is to investigate the possible roles of omega-3 in reducing cardiovascular risk in patients with diabetes., Methods: A literature search was conducted from the Medline, EBSCO, and EMBASE databases. Articles that addressed diabetes, cardiovascular disease, or omega-3 were included., Results: Reviews and studies reported an association with fish and omega-3 LC-PUFA consumption and decreased total cardiovascular mortality (approximately 15%-19%), along with decreased platelet activation and aggregation, improved lipid profiles, including reduction of triglycerides and very low-density lipoprotein (VLDL), decreased inflammation, and lowered blood pressure., Conclusion: Diets higher in fish and omega-3 LC-PUFA may reduce cardiovascular risk in diabetes by inhibiting platelet aggregation, improving lipid profiles, and reducing cardiovascular mortality. Fish and omega-3 LC-PUFA can be recommended to people with diabetes and included into a diabetes management program.

Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin use. IgG antibodies to complexes of platelet factor 4 (PF4) and heparin trigger the clinical manifestations of HIT. Only a subset of these antibodies will activate platelets and these can only be identified with platelet aggregation (functional) assays. Heparin-induced platelet aggregation (HIPA) and (14)C-serotonin release (SRA) assays for HIT are time-consuming and complex to perform. We have developed a whole blood impedance (WBI) test using the new Multiplate analyser. All samples referred to our laboratory over a 10 month period were screened for heparin-PF4 antibodies by an ELISA method (Zymutest HIA IgG). The 4T's score was used to assess HIT pretest probability. Twenty antibody positive samples were further tested by all three functional assays: light transmission aggregometry (LTA), SRA and WBI. Thirteen out of twenty samples were positive by LTA (10 patients) and 15 by WBI (11 patients). SRA, considered to be the gold standard, was used as a confirmatory test and 11 were found to be positive (10 patients); four discrepant samples were weakly positive by WBI. The prevalence of a positive functional test was strongly correlated with the 4T's clinical risk score, but a small number of low-risk patients had positive functional assays. In this study, the WBI assay detected all SRA positive patients and was positive for two others suggesting greater sensitivity. The rapid and easy to perform assay may be a useful tool for haematology laboratories to detect platelet-activating HIT antibodies., (Copyright (c) 2009 Elsevier Ltd. All rights reserved.)

Smoking is a risk factor for periodontitis but there are conflicting reports about the relationship between the severity of periodontitis and smoking behaviour, in part because self-reported smoking status may be inaccurate. Cotinine, a major metabolite of nicotine with a longer half-life (17 h versus 30 min), may be a more useful biochemical marker of smoking status. Smoking behaviour, plasma cotinine levels, and measures of periodontitis severity in 135 adults with moderate-advanced periodontitis were studied. Smokers had comparable periodontitis at a younger age than non-smokers. Smoking, as measured by cigarettes smoked per day and plasma cotinine levels, was significantly related to the severity of periodontitis.

Bernard-Soulier syndrome (BSS) is an extremely rare hereditary bleeding disorder, caused by mutations occurring in the Glycoprotein (GP) Ibalpha, GPIbbeta and GP9 genes that encode for the corresponding subunits of platelet GPIb-V-IX adhesion receptor complex. BSS has been reported in many populations, mostly behaving in an autosomal-recessive manner.While the great majority of BSS mutations are unique to a single individual or family, the GP9 1828A>G Asn45Ser mutation, which we have identified in an undocumented Australian Caucasian, has already been reported in multiple unrelated Caucasian families from various Northern and Central European countries. Haplotype analysis of 19 BSS patients from 15 unrelated Northern European families (including 2 compound heterozygote siblings from a British family previously published, and 17 1828A>G Asn45Ser homozygotes), showed that 14 of these BSS patients from 11 of the 1828A>G Asn45Ser homozygote families share a common haplotype at the chromosomal region 3' to the GP9 gene. Hence, the results suggest that the GP9 1828A>GAsn45Ser mutation in these families is ancient, and its frequent emergence in the European population is the result of a founder effect rather than recurrent mutational events. Association of the 1828A>G Asn45Ser mutation with variant haplotypes in 4 other Northern European BSS families raised the possibility of a second founder event, or rare recombinations in these families. Additional members from these 'atypical' lineages would need to be screened to resolve this question.