Lipid Risk Factors Research Articles

Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence

Dietary and policy recommendations frequently focus on reducing saturated fatty acid consumption for improving cardiometabolic health, based largely on ecologic and animal studies. Recent advances in nutritional science now allow assessment of critical questions about health effects of saturated fatty acids (SFA). We reviewed the evidence from randomized controlled trials (RCTs) of lipid and non-lipid risk factors, prospective cohort studies of disease endpoints, and RCTs of disease endpoints for cardiometabolic effects of SFA consumption in humans, including whether effects vary depending on specific SFA chain-length; on the replacement nutrient; or on disease outcomes evaluated. Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid. However, insufficient evidence exists for different chain-length-specific effects on other risk pathways or, more importantly, disease endpoints. Based on consistent evidence from human studies, replacing SFA with polyunsaturated fat modestly lowers coronary heart disease risk, with ~10% risk reduction for a 5% energy substitution; whereas replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.

Chronic low-grade inflammation, lipid risk factors and mortality in functionally dependent elderly

It has been proved that a highly sensitive C-reactive protein (hsCRP) can be used as an established marker of chronic inflammation for cardiovascular risk assessment. Since mean values of both low-density cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) decrease during aging, the knowledge that increased hsCRP concentration predicts mortality (Mt) would influence therapy and treatment outcome. The aim of this study was to examine importance of chronic low grade inflammation and its association with lipid risk factors for all-cause Mt in functionally dependent elderly. The participants of this longitudinal prospective study were 257 functionally dependent elderly aged 65-99 years. Baseline measurements: anthropometric measurements, blood pressure, fasting plasma total cholesterol (TC), triglyceride (TG), HDL-C, LDL-C, non-HDL-C, hemoglobin Alc (HbA1c) were recorded and different lipid ratios were calculated. Inflammation was assessed by the levels of white blood cells, fibrinogen and hsCRP. The participants with hsCRP grater than 10 mg/L were excluded from the study. The residual participants (77.4% women) were divided into three groups according to their hsCRP levels: a low (< 1 mg/L, n=70), average (1 to 3 mg/L, n=69), and high (3-10 mg/L, n=69) hsCRP group. Associations of all-cause Mt with different risk factors were examined using logistic regression analysis. The hsCRP level showed a significant positive correlation with waist (r = 0.199, p = 0.004) and hip (r = 0.187, p = 0.007) circumferences, body mass index (r = 0.143, p = 0.040) and serum triglyceride level (r = 0.139, p = 0.045) and significant negative correlation with HDL-C (r = -0.164, p = 0.018). Ratios TC/HDL-C and TG/HDL-C were significantly smaller in the low hsCRP group compared to the average hsCRP group (p = 0.019,p = 0.045, respectively) and without significant differences compared with the high hsCRP group. Two years after the baseline examination 22.1% participants died from all-cause Mt. After adjustment for other risk factors, a TC was significantly associated with all-cause Mt only in high hsCRP group: Odds ratio (OR) = 3.71 (95% confidence interval-CI: 1.09-12.63). In this study a high hsCRP was an important factor to identify functionally dependent elderly at high risk who may have more benefit from agressive lipid lowering treatment.

Biochemical markers for cardiovascular disease in recently postmenopausal women with or without hot flashes

Menopausal hot flashes may affect vascular function and perhaps explain conflicting data on cardiovascular disease (CVD) between observational and randomized hormone therapy (HT) studies. We prospectively assessed hot flash status in recently postmenopausal women and related it to a number of biochemical vascular surrogate markers for CVD. Healthy, nonsmoking women (n = 150) exhibiting a broad range (no, mild, moderate, severe) of hot flashes and an onset of menopause within the previous 0.5 to 3 years were studied with laboratory tests for lipids, lipoproteins, apolipoproteins, high-sensitivity C-reactive protein, and sex hormone-binding globulin. Apart from marked differences in hot flashes, the groups showed comparable levels of estrone, estradiol, or free estradiol index. The levels of total cholesterol (3.7-9.1 mmol/L) were similar between the groups (P = 0.744), and hypercholesterolemia (>6.5 mmol/L) was encountered equally often (P = 0.699). No difference was seen in high-, low-, or very low-density lipoproteins, triglycerides, apolipoprotein A-1, apolipoprotein B (or their ratio), or lipoprotein(a) between the groups. The levels of sex hormone-binding globulin and high-sensitivity C-reactive protein correlated negatively with each other (r = -0.204; P = 0.013) but showed no dependence on hot flashes (P = 0.531 and P = 0.215, respectively). No baseline difference in lipid or nonlipid CVD risk factors was observed between women with hot flashes (potential HT users) and women with no or mild hot flashes (potential HT nonusers). This may imply that hot flash status per se cannot explain the difference between observational and randomized trials.

Lipids and carotid plaque in the Northern Manhattan Study (NOMAS)

BackgroundLipids, particularly low-density (LDL) and high-density (HDL) lipoproteins, are associated with increased risk of stroke and cardiovascular disease, probably due to atherosclerosis. The objective of this cross-sectional analysis was to investigate the relation between blood lipids and carotid plaque.MethodsAs part of a prospective population-based study to determine the incidence and risk factors of stroke in a multiethnic population, we evaluated 1804 participants with lipid measurements and B-mode ultrasound of carotid arteries (mean age 69 +/- 10 years; 40% men; 51% Hispanic, 26% black, 23% white). The association between lipid parameters and carotid plaque was analyzed by multiple logistic regression.ResultsPlaque was present in 61% of participants. Mean total cholesterol was 202 +/- 41 mg/dl. After controlling for other lipid parameters, demographics, and risk factors, the only cholesterol subfraction associated with carotid plaque was LDL (OR per standard deviation (SD) = 1.14, 95% CI 1.02-1.27). Neither HDL nor triglycerides independently predicted carotid plaque. Apolipoprotein B (ApoB) was also associated with risk of plaque (OR per SD = 1.29, 95% CI 1.03-1.60). Apolipoprotein A-I (apoA-1) was associated with a decrease in multiple plaques (OR per SD = 0.76, 95% CI 0.60-0.97), while lipoprotein a was associated with an increased risk of multiple plaques (OR per SD = 1.31, 95% CI 1.03-1.66). ApoB:ApoA-I had the strongest relation with carotid plaque (OR per SD = 1.35, 95% CI 1.08-1.69).ConclusionsAmong the common lipid parameters, LDL has the strongest relation with carotid plaque. Other lipid precursor proteins such as ApoB and ApoA-I may be stronger predictors of subclinical atherosclerosis, however, and better targets for treatment to reduce plaque formation and risk of cerebrovascular disease.

Relationship of lipoprotein-associated phospholipase A2 and oxidized low density lipoprotein in carotid atherosclerosis

Plasma levels of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) and oxidized low density lipoprotein (oxLDL) have been identified as risk factors for cardiovascular disease. Lp-PLA(2) is the sole enzyme responsible for the hydrolysis of oxidized phospholipids on LDL particles in atherosclerotic plaques. We have studied the relationship between Lp-PLA(2) and oxLDL in carotid endarterectomy (CEA) tissues and in matched plasmas. In extracts from CEA anatomical segments, the levels of oxLDL were significantly associated with the levels of Lp-PLA(2) protein (r = 0.497) and activity (r = 0.615). OxLDL and Lp-PLA(2) mass/activity were most abundant in the carotid bifurcation and internal segments where plaque was most abundant. In extracts from CEA atheroma, the levels of oxLDL and Lp-PLA(2) were significantly correlated (r = 0.634). In matched plasma and atheroma extracts, the levels of Lp-PLA(2) were negatively correlated (r = - 0.578). The ratio of Lp-PLA(2) to oxLDL was higher in atheromatous tissue (277:1) than in normal tissue (135:1) and plasma (13:1). Immunohistochemical experiments indicated that in plaques, oxLDL and Lp-PLA(2) existed in overlapping but distinctly different distribution. Fluorescence microscopy showed both oxLDL and Lp-PLA(2) epitopes on the same LDL particle in plasma but not in plaque. These results suggest that the relationship between Lp-PLA(2) and oxLDL in the atherosclerotic plaque is different from that in the plasma compartment.

Prospective studies on the relationship between high-density lipoprotein cholesterol and cardiovascular risk: a systematic review

Epidemiological studies have extensively evaluated the association between high-density lipoprotein cholesterol (HDL-C) and cardiovascular disease (CVD) risk. The objective of this systematic review was to enumerate the number of original prospective studies that showed a significant association between HDL-C and CVD risk and provided evidence of the consistency of this association across other lipid risk factors. A systematic MEDLINE literature search identified 53 prospective cohort and five nested case-control studies that provided multivariate assessments of the association between HDL-C and CVD risk. Among these 58 prospective studies, 31 studies found a significant inverse association between HDL-C and CVD risk for all CVD outcomes and subpopulations studied, whereas 17 studies found a significant association for some CVD outcomes and/or subpopulations assessed. The ratio of studies that found a significant association out of the total studies identified was similar across all CVD outcomes, although there was less evidence for stroke and atherosclerotic outcomes. Only seven studies tested for the consistency of this association across other lipid risk factors, of which six studies suggested that the association was consistent across other lipid levels. In conclusion, the association between HDL-C and CVD risk is significant and strong, although further evidence may be needed to establish whether this association is consistent across other lipid risk factors. Furthermore, uncertainties remain regarding the mechanism in which HDL-C exerts its effects, suggesting a need for further research focused on new methods for reliable measurement.

MIF Deficiency Reduces Chronic Inflammation in White Adipose Tissue and Impairs the Development of Insulin Resistance, Glucose Intolerance, and Associated Atherosclerotic Disease

Chronic inflammation in white adipose tissue (WAT) is positively associated with obesity, insulin resistance (IR) and the development of type 2 diabetes. The proinflammatory cytokine MIF (macrophage migration inhibitory factor) is an essential, upstream component of the inflammatory cascade. This study examines whether MIF is required for the development of obesity, IR, glucose intolerance, and atherosclerosis in the LDL receptor-deficient (Ldlr(-/-)) mouse model of disease. Ldlr(-/-) mice develop IR and glucose intolerance within 15 weeks, whereas Mif(-/-)Ldlr(-/-) littermates are protected. MIF deficiency does not affect obesity and lipid risk factors but specifically reduces inflammation in WAT and liver, as reflected by lower plasma serum amyloid A and fibrinogen levels at baseline and under inflammatory conditions. Conversely, MIF stimulates the in vivo expression of human C-reactive protein, an inflammation marker and risk factor of IR and cardiovascular disease. In WAT, MIF deficiency reduces nuclear c-Jun levels and improves insulin sensitivity; MIF deficiency also reduces macrophage accumulation in WAT and blunts the expression of two proteins that regulate macrophage infiltration (intercellular adhesion molecule-1, CD44). Mechanistic parallels to WAT were observed in aorta, where the absence of MIF reduces monocyte adhesion, macrophage lesion content, and atherosclerotic lesion size. These data highlight the physiological importance of chronic inflammation in development of IR and atherosclerosis and suggest that MIF is a potential therapeutic target for reducing the inflammatory component of metabolic and cardiovascular disorders.

073 CLINICAL AND MICROBIOLOGICAL FEATURES OF MULTIVALVULAR INFECTIVE ENDOCARDITIS

Combination therapy is increasingly recommended for patients with multiple lipid disorders, especially those at high risk for coronary events. We investigated the long-term safety and effectiveness of a new drug formulation containing once-daily extended-release niacin and lovastatin. A total of 814 men and women (mean age 59 years) with dyslipidemia were enrolled in a 52-week multicenter, open-label study. We used 4 escalating doses (niacin/lovastatin in milligrams): 500/10 for the first month, 1,000/20 for the second, 1,500/30 for the third, and 2,000/40 for the fourth month through week 52. Dose-dependent effects were observed for all major lipid parameters. At week 16, mean low-density lipoprotein (LDL) cholesterol and triglycerides were reduced by 47% and 41%, respectively; mean high-density lipoprotein (HDL) cholesterol was increased by 30% (all p <0.001). LDL/HDL cholesterol and total/HDL cholesterol ratios were also decreased by 58% and 48%, respectively. These effects persisted through week 52, except for the mean increase in HDL cholesterol, which had increased to 41% at 1 year. Lipoprotein (a) and C-reactive protein also decreased in a dose-related manner (by 25% and 24%, respectively, on 2,000/40 mg; p <0.01 vs baseline). Treatment was generally well tolerated. The most common adverse event was flushing, which caused 10% of patients to withdraw. Other adverse events included gastrointestinal upset, pruritus, rash, and headache. Drug-induced myopathy did not occur in any patient. The incidence of elevated liver enzymes to >3 times the upper limit of normal was 0.5%. Once-daily niacin/lovastatin exhibits substantial effects on multiple lipid risk factors and represents a significant new treatment option in the management of dyslipidemia.

Physical Activity, Blood Lipids, and Lipoproteins

Dyslipidemia is a major modifiable cardiovascular disease (CVD) risk factor. While pharmacological treatment has been a focal point of dyslipidemia management for several years, increasing physical activity is a safe, cost-effective treatment option that should also be recommended by health care practitioners. Moderate aerobic exercise consistently increases high-density lipoprotein cholesterol (HDL-C) and reduces triglycerides (TG), independent of changes in body weight. However, reductions in total and low-density lipoprotein cholesterol are reported less often following aerobic exercise. Therefore, clinicians should understand that aerobic exercise is not likely to be an effective treatment option for their management. Recent empirical evidence also indicates that aerobic exercise may be of benefit for treating emerging lipid and lipoprotein risk factors such as lipoprotein particle size and number and triglyceride-rich lipoproteins. Further work is needed to clarify the impact of aerobic exercise on apolipoproteins. Based on current evidence, prescribing aerobic exercise as a means of increasing HDL-C and lowering TG is usually an efficacious strategy for treating these aspects of dyslipidemia. These effects are likely to be accompanied by changes in emerging lipid and lipoprotein risk factors.

Conventional Lipid Profile and Lipoprotein(a) Concentrations in Treated Patients with Rheumatoid Arthritis

Patients with rheumatoid arthritis (RA) have an increased cardiovascular risk not completely explained by traditional cardiovascular risk factors. If the proatherogenic lipid profile observed in active and untreated RA improves by effectively treating RA without the use of a lipid-lowering agent, other nonconventional cardiovascular lipid risk factors may be implicated. We evaluated conventional lipid risk factors and lipoprotein(a) in treated patients with RA. This cross-sectional study was conducted in 122 patients with RA. Lipid profiles of patients were compared with a control group, consisting of a population-based study cohort (DRECE study), matched for sex, age, menopausal status, and body mass index. Excess lipoprotein(a) was defined by a serum concentration > 0.3 g/l. High-density lipoprotein cholesterol (HDL-c) concentrations were higher in pre- and postmenopausal women with RA than in controls (p = 0.023 and p <or= 0.001, respectively). All RA patients had significantly lower levels of apolipoprotein B and apolipoprotein B/apolipoprotein A-I ratio, and postmenopausal women with RA also had significantly lower low-density lipoprotein cholesterol and total cholesterol levels than their respective controls. No differences were observed in serum levels of apolipoprotein A-I and triglyceride. All RA patients had higher lipoprotein(a) values than controls. Fourteen men (56%) and 10 (53%) and 42 (54%) pre- and postmenopausal women with RA, respectively, had hyperlipoproteinemia(a). RA patients undergoing antirheumatic therapy display a nonatherogenic conventional lipid profile, i.e., high HDL-c, low apolipoprotein B concentrations, and low apolipoprotein B/apolipoprotein A-I ratio. This may be counteracted by the high prevalence of hyperlipoproteinemia(a) observed in these patients.

High frequency of lipoprotein risk levels for cardiovascular disease in Takayasu arteritis

The objective of this study is to characterize the lipoprotein risk levels in Takayasu arteritis (TA) patients and its possible association with disease activity and glucocorticoid use. Twenty-five female TA patients were consecutively included and compared with 30 age-, gender-, and body mass index-matched healthy controls. Demographic features and the lipid profile were determined and cardiovascular risk levels were evaluated according to NCEP/ATPIII. Total cholesterol (TC), LDL-c, HDL-c, and triglycerides were determined after a 12-h overnight fast. Exclusion criteria were conditions that interfere in the lipid profile. The disease duration was 6.6 +/- 7.4 years; 30% had clinical activity and 80% had laboratory activity. Regarding NCEP/ATPIII risk levels, TA patients presented higher frequency of lipid risk compared to controls: high TC (48% vs. 20%, p = 0.04), low HDL-c (20% vs. 0%, p = 0.015), and high triglycerides (36% vs. 10%, p = 0.026). No difference was observed related to LDL-c risk levels between both groups (40% vs. 20%, p = 0.14). Remarkably, 60% of the patients had at least one lipid risk factor for cardiovascular disease. No difference in the lipids was observed between patients with and without clinical activity; however, those with laboratory activity showed lower levels of HDL-c (1.37 +/- 0.42 vs. 2.00 +/- 0.63 mmol/L, p = 0.012) than patients without this activity. A negative correlation was found between HDL-c and CRP levels (r = -0.42, p = 0.04). Lipids were similar in patients under glucocorticoid compared to those without this therapy. This is the first study to identify that TA, an inflammatory disease, has a proatherogenic lipid profile which is associated to laboratory disease activity.

A reappraisal of the impact of dairy foods and milk fat on cardiovascular disease risk

BackgroundThis review provides a reappraisal of the potential effects of dairy foods, including dairy fats, on cardiovascular disease (CVD)/coronary heart disease (CHD) risk. Commodities and foods containing saturated fats are of particular focus as current public dietary recommendations are directed toward reducing the intake of saturated fats as a means to improve the overall health of the population. A conference of scientists from different perspectives of dietary fat and health was convened in order to consider the scientific basis for these recommendations.AimsThis review and summary of the conference focus on four key areas related to the biology of dairy foods and fats and their potential impact on human health: (a) the effect of dairy foods on CVD in prospective cohort studies; (b) the impact of dairy fat on plasma lipid risk factors for CVD; (c) the effects of dairy fat on non-lipid risk factors for CVD; and (d) the role of dairy products as essential contributors of micronutrients in reference food patterns for the elderly.ConclusionsDespite the contribution of dairy products to the saturated fatty acid composition of the diet, and given the diversity of dairy foods of widely differing composition, there is no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD. Thus, recommendations to reduce dairy food consumption irrespective of the nature of the dairy product should be made with caution.

A Gene-Centric Approach to Elucidating Cardiovascular Risk

Although behavioral precedents including diet and cigarette smoking play an important role, coronary artery disease (CAD) exhibits significant heritability,1 a part of which can be attributable to genetic variants affecting known biochemical and metabolic risk factors. In the last 2 years, impressive progress has been made in understanding the genetic basis of several of these using both candidate gene and genome-wide association study (GWAS) approaches. Article see p 16 Candidate genes, coding for proteins of known biological significance in a disease process, provide a logical first step in understanding the genetics of common disease states. Populations of affected and unaffected individuals can be studied by genotyping common single-nucleotide polymorphisms (SNPs) within a gene and its regulatory sequences. Although economically attractive, this approach is acknowledged to have a number of limitations. By definition, studies are limited to genes with a known or suspected role in defining a given phenotype and do not provide new insight into biological pathways leading to disease. Furthermore, candidate gene associations often fail to replicate for multiple reasons. Sample sizes have often been inadequate to provide the statistical power required when multiple variants of small effect are tested. The original observation may have been false positive, emphasizing the need for stringent statistical thresholds. Other issues include heterogeneity of causality. For example, genetic variants affecting plasma lipid traits may have significant effects on CAD risk, but these may be less important than or interact with other risk factors including diabetes and smoking. Finally, appropriate measures must be taken to test for population stratification. Genome wide association studies (GWASs) are is an alternative approach, facilitated by the International HapMap Project and advances in genotyping technology, permitting analysis of a million or more markers across the human genome. GWASs provides an unbiased approach that has led to the identification …

Potential impact of omega-3 treatment on cardiovascular disease in type 2 diabetes

Hypothesis-generating systematic review of the impact of marine-derived omega-3 polyunsaturated fatty acids (PUFAs) on lipid, glycemic and hematological risk factors in type 2 diabetes using pooled data from randomized controlled trials searched up to 20 September 2008. Seven new trials in 2007 and 2008 were identified from 206 abstracts to give a total of 24 trials between 1966 and 2008 involving 1533 participants that could be pooled. The mean omega-3 PUFAs dose and duration of treatment in the new trials was 2.4 g/day and 24 weeks, respectively. Compared with placebo, omega-3 PUFAs supplementation decreased triglycerides by 7% (mean -0.17 mmol/l, 24 trials, 1530 participants), fibrinogen by 10% (mean -0.96 micromol/l, three trials, 159 participants), ADP platelet aggregation to ADP by 22% (mean -10.30%, two trials, 64 participants) and to collagen by 21% (mean -10.55%, two trials, 64 participants), with an LDL-cholesterol increase of 3% (mean 0.08 mmol/l, 21 trials, 1104 participants). None of the following risk factors appeared to be beneficially influenced: HDL-cholesterol, LDL particle size, glycemia, insulinemia, inflammatory biomarkers, blood pressure. However for some of these risk factors (such as inflammatory biomarkers) the number of trial patients was small Higher doses of omega-3 PUFAs (>or=2 g/day) may have greater triglyceride lowering effects. This systematic review and meta-analysis confirms the triglyceride lowering effects of omega-3 PUFAs, demonstrates potential dose-response effects and shows improvements in thrombogenesis. Omega-3 PUFAs raise LDL levels without concomitant changes in lipid particle size. Changes seen in conventional risk factors are insufficient to explain the cardiovascular disease risk reductions suggested to occur with omega-3 PUFAs.

National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Emerging Biomarkers for Primary Prevention of Cardiovascular Disease

Heart disease and stroke continue to be the leading causes of death in the US. As a result, investigators continue to look for new and emerging biomarkers of disease risk. Because many of these emerging biomarkers are not as well documented as those of conventional lipid and lipoprotein risk factors, their value in clinical practice needs to be critically appraised and appropriate guidelines developed for their proposed use. The National Academy of Clinical Biochemistry (NACB) convened a multidisciplinary expert panel to develop laboratory medicine practice guidelines for a selected subset of these emerging risk factors as applied in a primary prevention setting of heart disease and stroke. The NACB expert panel selected lipoprotein subclasses and particle concentration, lipoprotein(a), apolipoproteins A-I and B, high sensitivity C-reactive protein (hsCRP), fibrinogen, white blood cell count, homocysteine, B-type natriuretic peptide (BNP), N-terminal proBNP (NT-proBNP), and markers of renal function as biomarkers that fell within the scope of these guidelines. Based on a thorough review of the published literature, only hsCRP met all of the stated criteria required for acceptance as a biomarker for risk assessment in primary prevention.

Evaluation of lipid profiles and the use of omega-3 essential Fatty Acid in professional football players.

Background:Recent research showed 82% of 233 retired National Football League players under age 50 had abnormal narrowing and blockages in arteries compared to the general population of the same age. It has been suggested that early screening and intervention in this at-risk population be a priority.Hypothesis:Omega-3 essential fatty acid has been shown to improve cardiovascular lipid risk factors and should improve lipid profiles in professional football players to help reduce their recently shown accelerated risk of developing cardiovascular disease.Methods:A total of 36 active national football players were randomly assigned to 2 groups: the first group (n = 20) was provided fish oil capsules (2200 mg of mixed docosahexaenoic acid and eicosapentaenoic acid and 360 mg of other omega-3s), and the second group (n = 16) served as controls during a 60-day trial. Vertical Auto Profile cholesterol tests directly measuring serum low-density lipoprotein, high-density lipoprotein, and other subfractions were performed. Compliance, side effects, and seafood consumption data were also collected. Baseline, midpoint, and poststudy blood work measured plasma docosahexaenoic acid and eicosapentaenoic acid.Results:Treatment increased high-density lipoprotein (average percent change: +25.96, control +14.16), decreased triglycerides treatment (–8.06, control +43.98), very low-density lipoprotein treatment (–13.98, control +23.18), intermediate density lipoprotein (–27.58, control +12.07), remnant lipoproteins (–23.86, control +8.33), and very low-density lipoprotein-3 (–17.10, control +7.77). An average increase of 106.67% for docosahexaenoic acid and 365.82% for eicosapentaenoic acid compared to control was also shown.Conclusion:Omega-3 supplementation significantly improved the lipid profile of active players randomized to treatment. These results suggest that fish oil supplementation is an effective way to increase eicosapentaenoic acid and docosahexaenoic acid levels in plasma and should be considered as a method to improve modifiable cardiovascular risk lipid factors in professional football players.Clinical Relevance:A prospective study examining the effects of 60 days of a highly purified fish oil supplementation in professional football players.

Apolipoprotein E gene polymorphism and polycystic ovary syndrome patients in Western Anatolia, Turkey

Dyslipidemia, cardiovascular disease and hypertension are more frequently seen in patients with PCOS than in normal patients. We aimed at evaluating the distribution of Apo E alleles that can influence cardiovascular risk of the PCOS patients and control subjects. In this study, 129 young women with PCOS and 91 healthy women were included. In all subjects we performed hormonal, biochemical and Apo E genetic analysis. The Apo E3 allele was found at a significantly higher frequency in the PCOS patient group compared with the control group. The Apo E2 allele was found at a significantly higher frequency in the control group compared with the patient group with PCOS. Although there were genotype and allele differences between control and patient groups in this study, no statistically significant change was determined in lipid and other cardiovascular risk factors in connection with allele and genotype.

Review of the Effect of Dairy Products on Non-Lipid Risk Factors for Cardiovascular Disease

The association between dairy food consumption and the risk of cardiovascular disease (CVD) has been a topic of intense debate over the years. Recent data suggest that individuals who consume dairy foods, particularly low fat products, are less likely to develop CVD than those who have a lower intake of these foods. We are also just beginning to understand how various components of the complex dairy food matrix affect several risk factors for CVD. The objective of this review is to provide an overview of the effects of dairy foods per se and of some of their components on non lipid CVD risk factors. Focus will be on blood pressure, inflammation, insulin resistance and type 2 diabetes, obesity and the metabolic syndrome. While the impact of dairy foods on blood pressure appears to be beyond debate, their effects on body weight and other non lipid risk factors need to be further substantiated. However, the purported inverse association between dairy foods, particularly low fat dairy products, and the metabolic syndrome is suggestive of cardiovascular benefits that may go well beyond the effect of dairy fat on blood cholesterol.

Managing hypercholesterolemia and its correlation with carotid plaque morphology in patients undergoing carotid endarterectomy

Hypercholesterolemia is a critical problem in patients with carotid atherosclerosis. The adequacy of attention to lipid risk factors in patients with carotid stenosis awaiting carotid endarterectomy (CEA) has rarely been studied. We also assessed patient awareness of hypercholesterolemia and carotid plaque morphology. A prospective study was conducted of 141 consecutive patients admitted electively for CEA. Each patient's medical history was taken. Plasma cholesterol concentrations were determined. Plaque histology was scored according to American Heart Association criteria and their modification. Of patients who were aware of their hypercholesterolemia and who were receiving treatment, 28.6% had total cholesterol levels > or =5 mmol/L. Among those patients who had been told that they had no problem with hypercholesterolemia, 32.5% had plasma cholesterol concentrations > or =5 mmol/L. Among those patients who had never had their plasma cholesterol measured, 48.4% had total cholesterol levels > or =5 mmol/L. Patients in this last group tended to have more severe types of plaque pathology than those in other groups (12.9% plaque rupture). Hypercholesterolemia does not seem to be well managed in patients awaiting CEA.

Prevalence of Emerging Cardiovascular Risk Factors in Younger Individuals with a Family History of Premature Coronary Heart Disease and Low Framingham Risk Score

The purpose of this study was to assess the prevalence of emerging cardiac risk factors in individuals with a family history of premature coronary heart disease (CHD) and who were predicted to be low-risk for cardiovascular (CV) disease based on their Framingham risk score. We prospectively evaluated 89 younger men and women with a family history of premature CHD and who had a low Framingham risk score. Patients with CHD or CHD equivalents were excluded. All patients were screened for emerging clinical and lipid risk factors. Coronary calcium was present in 38% of patients and C-reactive protein > 3 mg/dl was present in 24% of patients. Low levels of high-density lipoprotein (HDL2) cholesterol were the most prevalent emerging lipid risk factor and was present in 72% of the study group. More individuals had low levels of HDL2 than total HDL (34% versus 71%; p-value =0.001). Triglyceride- (TG)-rich remnant lipoproteins were present in 49% of patients. The Framingham risk score poorly predicts CV risk in younger healthy persons with a family history of premature CHD. The prevalence of subclinical CHD and emerging clinical and lipid risk factors is high in these patients. The most prevalent lipid risk factor was low levels of HDL2. Individuals with a family history of premature CHD may benefit from screening for emerging risk factors to better assess their CV risk.