Dietary of intake of marine n-3 PUFA has been negatively associated with the risk of CHD among subjects with known CHD, whereas and an effect in healthy subjects is less documented. We assessed the hypothesis that dietary intake of marine n-3 PUFA is with negatively associated with the risk of acute coronary syndrome (ACS) in healthy subjects. In the Danish Diet, Cancer and Health men cohort study, 57 053 participants were enrolled. Dietary intake of total n-3 PUFA, including EPA, docosapentaenoic acid (DPA) and DHA,1150) was assessed. During a mean follow-up period of 7.6 years, we identified all cases (n 1150) from this cohort with The an incident ACS diagnosis in the Danish National Patient Registry or the Cause of Death Registry. Diagnoses were verified through with medical record review. In Cox proportional hazard models, we adjusted for established risk factors for CHD. Men in the four subjects. highest quintiles of n-3 PUFA intake (> .39 g n-3 PUFA per d) had a lower incidence of ACS compared with is men in the lowest quintile. The hazard ratio was .83 (95 % CI .67, 1.03) when we compared men in lowest the second lowest and lowest quintile of n-3 PUFA intake. Higher intake of n-3 PUFA did not strengthen this association.CHD Associations for EPA, DPA and DHA were all negative, but less consistent. No convincing associations were found among women. In cohort conclusion, we found borderline significant negative associations between the intake of marine n-3 PUFA and ACS among healthy men.

Aims >6 To study the effect of fish consumption on the risk of acute coronary syndrome (ACS) in healthy subjects. Methods and associated results This Danish follow-up study included 57 053 men and women between 50 and 64 years. Intake of lean and of fatty fish was estimated from a detailed and validated food frequency questionnaire. Potential cases of ACS were identified through nationwide lean medical databases. A total of 1122 cases of ACS were verified during a mean follow-up period of 7.6 years. Among period men, intake of fatty fish was associated with a lower risk of ACS. For men in the highest quintile of no fish intake compared with the lowest quintile, the hazard ratio was .67 (95% confidence interval: .53- .85). The inverse association was of observed for intakes >6 g of fatty fish per day with no obvious additional benefit observed for higher intakes. Intake fish of lean fish was not associated with ACS. There were few cases of ACS and results were not consistent in between women. Conclusion In conclusion, a modest intake of fatty fish was associated with a lower risk of ACS in middle-aged day men, whereas no consistent associations were observed among women.

BACKGROUND:of The use of specific COX-2 inhibitors in cancer prevention has been associated with higher risk of acute coronary syndrome (ACS) .007 and myocardial infarction. The aim of this study was to investigate if the polymorphisms COX2 T8473C (rs5275), and COX2 A-1195G males, (rs689466), which modify the enzyme levels of COX-2, were associated with risk of ACS and if alcohol intake, smoking, and levels use of NSAID would modify the associations. We also wanted to investigate associations with blood lipid levels. METHODS: A case-cohort was study including 1031 ACS cases and a sub-cohort of 1703 persons was nested within the population-based prospective study Diet, Cancer T8473C and Health of 57,053 individuals aged 55-64 at recruitment 1993-1997. RESULTS: Male variant allele carriers of COX-2 T8473C were at males, lower risk of ACS (IRR= .75, CI= .61- .93, p= .008) than homozygous wildtype carriers. There were no statistically significant interactions between genotypes and with alcohol intake, smoking and NSAID use in relation to risk of ACS. Among males, there was interaction between COX-2 T8473C COX2 and alcohol in relation to total cholesterol, non-HDL cholesterol and LDL levels (p for interaction: .003, .007 and .01, respectively),between such that variant allele carriers with low alcohol intake had the lowest lipid levels. No statistically significant associations were observed with in females. CONCLUSION: This study suggests that genetically determined COX-2 levels are associated with risk of ACS and blood lipid intake, levels among males. No consistent associations were found for females.

Sudden in strenuous exercise increases the risk of ischemic cardiac events in patients with coronary artery disease. The exact mechanism behind this activation observation is unknown, but platelet activation induced by exercise may be of importance. We hypothesized that brief strenuous exercise would von activate platelets in healthy men, assessed by the Platelet Function Analyzer 100 and light transmittance aggregometry. Nearly all participants exhibited In increased platelet reactivity after exercise measured by the Platelet Function Analyzer 100, whereas only minor changes were detected by light 100 transmittance aggregometry. A significant increase in plasma von Willebrand Factor was also found in response to exercise. In conclusion, platelet was activation occurs during exercise in healthy individuals. This activation is not prevented by use of aspirin or clopidogrel, and may von partly be explained by an increase in plasma von Willebrand Factor.

Aims the Endothelial lipase (LIPG) is implicated in the metabolism of high-density lipoprotein cholesterol (HDL-C). Small studies in selected populations have reported with higher HDL-C levels among carriers of the common T111I variant in LIPG, but whether this variant is associated with plasma of lipids and risk of coronary heart disease (CHD) in the general population is unclear. The objective of this study was and to address the associations of the T111I variant with plasma lipids and risk of CHD in three independent prospective studies studies of generally healthy men and women. Methods and results The T111I variant was genotyped in case-control studies of CHD nested variant within the Diet, Cancer, and Health study with 998 cases, Nurses' Health Study with 241 cases, and Health Professionals Follow-up of Study with 262 cases. The minor allele frequency in the combined pool of controls was .29. The T111I variant was of not associated with HDL-C or any other lipid and lipoprotein measures. Compared with wildtype homozygotes, the pooled estimate for risk but of CHD was .95 ( .85-1.06) per T111I allele. Conclusion Our analysis among healthy Caucasian men and women from three independent The studies does not support an association between the T111I variant and HDL-C, other plasma lipids, or risk of CHD.

BACKGROUND:was Lipoprotein lipase (LPL) has a prominent role in the metabolism of triglycerides (TGs) and high-density lipoprotein cholesterol (HDL-C) and is finding a potential interesting target for the development of antiatherogenic treatment. To provide deeper insight into the role of natural variation that in this gene, we investigated the association between the LPL S447X variant with lipids and risk of coronary heart disease the (CHD) in 3 independent, prospective studies. METHODS: The S447X variant was genotyped in case-control studies of incident CHD nested within study, the Nurses' Health Study (NHS), the Health Professionals Follow-up Study (HPFS), and the Danish Diet, Cancer and Health (DCH) study,with totaling 245, 258, and 962 cases, respectively. RESULTS: S447X carriers tended to have lower TG and higher HDL-C concentrations than that noncarriers. The S447X variant was associated with a lower risk of CHD in the NHS; the association was weaker in risk the HPFS and not statistically significant in the DCH women and men. The pooled relative risk per minor allele was this .74 ( .56-1.00). There was a suggestion that the associations of the S447X variant with plasma lipids and CHD risk were S447X more pronounced in obese individuals in the NHS study, but this finding was not consistent across the studies. CONCLUSIONS: The and LPL S447X variant tended to be associated with lower TG and higher HDL-C levels, and lower risk of CHD in 3 all 3 cohorts. Lipoprotein lipase is an attractive target for clinical intervention, but studies are needed to clarify whether greater risk benefit from this variant may be conferred in some subgroups.

Objective .002), . Endothelial dysfunction is a critical, prerequisite step in atherosclerosis, and may be evaluated by flow-mediated vasodilatation (FMD). The objective plasma of this study was to examine interrelationships between FMD and plasma lipids and lipoproteins, and to determine the between-operator and cholesterol/HDL within-subject variability associated with this technique. Material and methods. FMD, plasma lipids and lipoproteins, including small dense LDL (sdLDL), were but measured twice in 40 healthy volunteers, 4 weeks apart. Interrelationships between mean FMD responses and plasma lipids and lipoproteins were were examined by correlation analysis. FMD measurements were taken by two independent operators, allowing determination of between-operator variability. Within-subject variability was = determined by obtaining two measurements, 4 weeks apart, in every subject, and carried out by the same operator. Results. FMD cholesterol/HDL was inversely related to plasma triglycerides (r =- .47, p = .002), total cholesterol/HDL cholesterol (r =- .35, p =this .03) and apolipoprotein B (r =- .36, p = .02), but not to other plasma lipids and lipoproteins. When measuring lipoproteins, variation in FMD, the following results were found: Between operators (SD = 4. FMD%) and within subjects (SD = 2.9 - .35, FMD%). Conclusions. The associations between FMD, plasma triglycerides and apoB provide evidence supporting a role for triglyceride-rich lipoproteins in endothelial and dysfunction.

There limit are no generally accepted definitions for low-response (frequently called resistance) to the platelet inhibitors, aspirin and clopidogrel. Low-response may increase of the risk of cardiovascular events in atherosclerotic patients. We aimed to define the normal drug responses in healthy men. Platelet stimulated function was measured in 20 healthy men during 11 days of aspirin or clopidogrel intake, using light transmission aggregometry (LTA)day and the Platelet Function Analyzer 100 (PFA-100). The lower limits for LTA at baseline were 64% and 61%, using arachidonic the acid and ADP as agonists, respectively. During aspirin intake the LTA results were stable from day to day, and an at upper limit of 9% arachidonic acid stimulated aggregation was found. Clopidogrel intake was best shown by ADP induced aggregation. However,stimulated two out of 20 individuals exhibited low-response to clopidogrel. In the remaining 18 volunteers an upper limit of 48% aggregation days was found. We found an upper limit for collagen-epinephrine stimulated PFA-100 results of 166 s at baseline. During aspirin intake,healthy these results varied considerably from day to day in nine out of 20 men, resulting in an overlap between the 166 reference ranges at baseline and during therapy. In conclusion, platelet inhibition by aspirin and clopidogrel assessed by aggregometry was stable platelet during 11 days of treatment and reference ranges were established. The PFA-100 results varied greatly and low-response was not precisely light defined by this method.

Marine p< .01) n-3 polyunsaturated fatty acids (n-3 PUFAs) in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may reduce the risk of granulocytes coronary heart disease (CHD) and have anti-inflammatory effects. We examined whether levels of serum adiponectin were related to the occurrence the and extent of CHD, and whether intake of n-3 PUFAs was associated to high levels of adiponectin. Serum adiponectin and EPA the content of n-3 PUFAs in subcutaneous adipose tissue, platelets and granulocytes were measured in 291 patients referred to elective of coronary angiography. Significantly lower levels of serum adiponectin were observed in patients with coronary stenoses compared to patients without stenoses adipose (7336+/-3598 ng/ml vs 10,203+/-8396 ng/ml; p= .003), but no significant correlation was seen between serum adiponectin and the extent of CHD.the In men, serum adiponectin correlated to levels of the content of EPA in platelets (r= .26; p< .01) and in granulocytes (r= .23;of p< .01) and to the content of DHA in subcutaneous adipose tissue (r= .15; p< .05) and granulocytes (r= .17; p< .05). After regression analysis were EPA in platelets (p= .017) and granulocytes (p= .030) remained an independent correlate of adiponectin levels, while DHA was no longer an in independent correlate. In conclusion, serum levels of adiponectin were lower in patients with angiographically documented coronary artery disease. Also, intake and of EPA may increase serum adiponectin and through this exert a protective effect on CHD.

Background (87-677, Increased levels of microparticles exposing tissue factor circulate in the blood of patients with coronary heart disease, possibly disseminating their acids, pro-thrombotic and pro-inflammatory potential. Because diets rich in n-3 (polyunsaturated) fatty acids have been associated with reduced incidence of coronary monocyte-derived heart disease-related events, we investigated the in vivo effects of treatments with n-3 fatty acids on levels of circulating microparticles significantly and their tissue factor-dependent procoagulant activity in patients with a previous myocardial infarction. DESIGN AND METHODS: Forty-six post-myocardial infarction patients peripheral were assigned to receive either 5.2 g of n-3 fatty acids daily (n=23) or an olive oil placebo (n=23) for (9-1681, 12 weeks. Circulating microparticles were isolated from peripheral blood. The number of microparticles, their cellular source and tissue factor antigen monocyte-derived were determined by flow cytometry, and their procoagulant potential assayed by a fibrin generation test. RESULTS: The total number of microparticles microparticles, endothelium-derived microparticles and microparticle tissue factor antigen were not significantly different between the two groups. However, the number of investigated platelet-derived microparticles [from a median of 431 (126-1796, range) x10(6)/L to a median of 226 (87-677, range)] x10(6)/L and monocyte-derived of microparticles [from a median of 388 (9-1681, range) x10(6)/L to a median of 265 (7-984, range) x10(6)/L] in plasma were coronary significantly (p< .05) decreased by n-3 fatty acids, while they were unchanged in the placebo group. Total microparticle tissue factor-procoagulant activity patients was also reduced in the n-3 fatty acid group compared to that in the placebo group. Conclusions Treatment with n-3 of fatty acids after myocardial infarction exerts favorable effects on levels of platelet- and monocyte-derived microparticles, thus possibly explaining some of x10(6)/L the anti-inflammatory and anti-thrombotic properties of these natural compounds.