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Biomedical subjects

Jean Bergeron

Publications and source records attributed to Jean Bergeron.

At least 19 recordsLinked to original sources

Predictors of aortic stenosis in homozygous familial hypercholesterolemia: A study from the Canadian HoFH registry.

BACKGROUND: Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disease of low-density lipoprotein cholesterol (LDL-C) metabolism. This disease is associated with a major risk of both atherosclerotic cardiovascular disease and aortic stenosis (AS). The predictors of AS in this population are not well established. OBJECTIVE: To investigate the univariable and multivariable predictors of AS in patients from the Canadian HoFH registry. METHODS: Individuals from the Canadian HoFH registry were included in this retrospective longitudinal study. Clinical data were obtained from the treating physicians using a standardized questionnaire. Cox proportional hazards models were used to investigate the predictors of AS. The observed lifetime risk of AS was calculated using Kaplan-Meier estimates. RESULTS: Among the 67 patients with HoFH, 25 (37%) developed AS. The mean age at baseline was 22 ± 17 years and women represented 57% of the cohort. The independent predictors of AS were the baseline LDL-C (hazard ratio [HR] 1.22 [1.09-1.35], P = .0003) as well as the presence of at least 1 null genetic variant (HR 3.73 [1.41-9.86], P = .008). Having a baseline LDL-C value above 13 mmol/L was associated with an observed lifelong risk of developing AS approaching 100% within this cohort, whereas having a value below this threshold was associated with a risk of 27% (P = .0002). CONCLUSION: This is the first systematic evaluation within a national HoFH registry to report the univariable and multivariable predictors of AS in patients with HoFH. An external validation of our results in an international cohort of HoFH is warranted.

Aortic stenosis↗

Differential impact of plasma triglycerides on HDL-cholesterol and HDL-apo A-I in a large cohort.

OBJECTIVES: To examine the relationship between plasma triglycerides (TG) to HDL-cholesterol (HDL-C) or HDL apo A-I. DESIGN AND METHODS: Bivariate and multiple linear regression analyses in a large cohort of 1886 subjects. RESULTS: Higher plasma TG levels were associated with lower concentrations of both HDL-C and HDL-apo A-I. However, the HDL-C/HDL-apo A-I ratio was inversely correlated with plasma TG indicating that the overall composition of the HDL changed as plasma TG changed. Plasma TG levels contributed to 15.9% of the variance of the HDL-C/HDL-apo A-I ratio, whereas gender, HDL-TG, LDL-TG, body mass index and plasma apo B levels represented between 0.15% and 2.21% of this variance. CONCLUSIONS: These results indicate that increasing levels of plasma TG result in greater reduction in HDL-C levels than in HDL-apo A-I and this might explain, at least in part, the differences that have been observed in the magnitude of the association of HDL-C versus HDL-apo A-I with the risk of cardiovascular disease.

Adolescent↗

Visceral adiposity and endothelial lipase.

CONTEXT: Overexpression of endothelial lipase (EL) has been shown to reduce plasma high-density lipoprotein cholesterol levels in animal models. However, the extent to which EL contributes to modulate the deteriorated high-density lipoprotein profile observed in obesity in humans is less clear. OBJECTIVES: The objectives of this study were to investigate the association between levels of obesity and visceral adiposity in particular and plasma EL concentrations. METHODS: Postheparin plasma EL concentrations were measured by ELISA and visceral adiposity by computed tomography in a sample of 80 sedentary men in good health. EL mRNA levels in abdominal sc and omental adipose tissues obtained during abdominal hysterectomies were measured in another sample of 14 women. RESULTS: Plasma EL levels were positively correlated with body mass index (R = 0.46, P < 0.0001), visceral adipose tissue accumulation (R = 0.44, P < 0.0001), and a proatherogenic lipid profile including increased plasma cholesterol and triglycerides. However, EL mRNA levels were similar in sc and omental AT and were 10,000-fold lower than lipoprotein lipase mRNA levels in those tissues. CONCLUSIONS: Increased visceral adiposity is significantly correlated with elevated plasma EL levels, but this association is unlikely to be causal and may reflect other common metabolic alterations.

Adiposity↗

Circulating oxidized LDL is associated with parameters of the metabolic syndrome in postmenopausal women.

UNLABELLED: Oxidized low-density lipoproteins (ox-LDL) play a significant role in the development of atherosclerosis. OBJECTIVE: To investigate the relation between circulating ox-LDL and components of the metabolic syndrome (MS) in a sample of 124 postmenopausal women with varying glucose tolerance status. METHODS: This cross-sectional study included postmenopausal women not using hormone therapy. Ox-LDL concentrations were measured in plasma by a monoclonal antibody (mAb-4E6) based competition ELISA. LDL peak particle diameter (LDL-PPD) was measured by non-denaturating polyacrylamide gradient gel electrophoresis (PAGGE). Presence of the MS was determined according to the definition of the NCEP-ATPIII. RESULTS: Circulating ox-LDL concentrations were significantly associated with some factors of the MS such as triglyceride (r=0.48; p<0.0001), high-density lipoprotein cholesterol (r=-0.34; p=0.0001) and fasting plasma glucose concentrations (r=0.21; p=0.02). Ox-LDL concentrations were also associated with LDL cholesterol (r=0.54; p<0.0001), total cholesterol (r=0.48; p<0.0001), LDL apolipoprotein B (r=0.62; p<0.0001) and LDL-PPD (r=-0.18; p<0.05). Moreover, women with the MS had significantly higher ox-LDL concentrations (79.5+/-28.3 U/l) compared to women without the MS (64.2+/-19.9 U/l) (p<0.05). CONCLUSION: Ox-LDL concentrations are associated with individual components of the MS and are significantly higher in postmenopausal women with MS compared to healthy postmenopausal women.

Apolipoproteins↗

Gene polymorphisms in the Quebec population: a risk to develop hypertriglyceridemia.

In Eastern Québec, two major lipoprotein lipase (LPL) gene mutations, P207L and G188E, lead to complete LPL deficiency in homozygote subjects and contribute to elevated predisposition to hypertriglyceridemia in heterozygotes. First, we determined the allele frequencies of LPL (D9N, G188E, P207L, D250N, N291S, and S447X), APOE (C112R and C158R), PPARalpha (L162V), and PPARgamma2 (P12A) single nucleotide polymorphisms (SNPs) in a random-based cohort of the metropolitan Québec city area. Second, we compared the LPL X447 allele frequencies observed in the random cohort and in a cohort of LPL P207L deficient patients. In the random cohort, the LPL N9 rare allele exhibited a higher prevalence than previously expected (p=0.0001). The LPL X447 allele frequency was lower in the patient cohort (Freq: 4.4%) than in the random cohort (Freq: 11.2%) (p=0.0001). These results reveal the importance of genetic screening for LPL gene mutations D9N and S447X in a population at risk to develop hypertriglyceridemia.

Cohort Studies↗

Association of heterozygous familial hypercholesterolemia with smaller HDL particle size.

Small, dense HDL particles have been associated with factors known to increase the risk of cardiovascular disease, such as obesity, hypertriglyceridemia, small dense LDL particles, decreased HDL-cholesterol levels and increased apoA-I fractional catabolic rate from plasma. In order to assess the potential contribution of HDL particle size to atherosclerosis in heterozygous familial hypercholesterolemia (FH), we examined the electrophoretic characteristics of HDL particles in a large cohort of well defined FH heterozygotes and controls. A total of 259 FH heterozygotes and 208 controls participated in the study. FH subjects were carriers of one of the nine French Canadian mutations in the LDL receptor gene. All subjects were apoE3 homozygotes. HDL particles were characterized by non-denaturing polyacrylamide gradient gel electrophoresis following a 6-week lipid-lowering drug-free baseline period. The integrated HDL size was significantly smaller in the FH group compared to controls (FH=87.3+/-5.2 Angstroms versus controls=91.6+/-4.9 Angstroms, P<0.0001). In each groups, men had smaller HDL particles than women. Multiple regression linear analyses showed that the FH/Control status accounted for 20.3% of the variance in the integrated HDL size. These results suggest that the FH/control status was independently associated with variations in HDL particle size and that these variations could contribute to the development of premature atherosclerosis in these patients.

Adult↗

Dietary contaminants and oxidative stress in Inuit of Nunavik.

The aim of the present study was to investigate the potential deleterious effects of dietary contaminants such as polychlorinated biphenyls (PCBs) and methylmercury (MeHg) on different molecules sensitive to oxidative stress, namely, plasma oxidized low-density lipoproteins (OxLDLs), plasma homocysteine (Hcy), blood glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH). We also planned to assess the potential beneficial effects of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs) and selenium (Se) that are also present in the traditional Inuit diet. A total of 99 participants were studied. Plasma levels of PCBs, blood levels of Se and MeHg, plasma lipids (triacylglycerols, total, LDL-, and high-density lipoprotein cholesterol [LDL-C and HDL-C, respectively], apolipoprotein B-LDL), erythrocyte n-3 PUFAs, OxLDL, Hcy, blood GPx, GSH, and GR have been determined. Mean concentrations of MeHg, Se, and PCBs were respectively 10- to 14-fold, 8- to 15-fold, and 16- to 18-fold higher than reported in white population consuming little or no fish. Multivariate analyses show that variance in plasma OxLDL concentrations was predicted by LDL-C (P = .007), HDL-C (P = .005), and PCBs (P = .006). The level of LDL oxidation, represented as the ratio OxLDL/apolipoprotein B-LDL, was predicted by LDL-C (P = .0002), HDL-C (P = .002), and GSH (P = .005). Concentration of plasma Hcy was positively predicted by age (P = .02) but negatively by body mass index (P = .04) and Se (P = .005). Glutathione was predicted by the smoking status (P = .004) and the level of LDL oxidation (P = .005), whereas GR was only predicted by the smoking status (P = .0009). The variance of GPx was not predicted by any contaminant or other physiological parameter. Dietary MeHg showed no association with the examined oxidative biomarkers, whereas PCB level was a predictor of the plasma concentration of OxLDL, although this concentration remained very low. The level of GPx activity in Inuit was higher than levels previously reported to be protective in whites. Homocysteine was negatively predicted by Se, suggesting a possible beneficial effect of Se. Moreover, n-3 PUFAs were highly correlated with dietary contaminants, but had no relationships with oxidative biomarkers. This study suggests that, in adult Inuit, contaminated traditional diet seems to have no direct oxidative effects on molecules involved in oxidative stress.

Adult↗

Associations between hypertriglyceridemia, dietary fat intake, oxidative stress, and endothelial activation in men.

OBJECTIVE: We examined the associations between intake of different types of dietary fat and plasma levels of oxidative stress and endothelial activation markers in men. METHODS: For that purpose, a complete physical and metabolic profile was assessed. Dietary habits of subjects were determined with a 3-d food record. We also measured fasting plasma 8-iso-prostaglandin F2alpha and oxidized low-density lipoprotein concentrations and soluble forms of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin. All these measurements were performed with commercial enzyme-linked immunosorbent assay kits and standards. RESULTS: We found that a high total dietary fat intake was associated with high plasma sICAM-1 (r = 0.40, P < 0.005), sVCAM-1 (r = 0.31, P < 0.05), and E-selectin (r = 0.28, P < 0.05) levels. We also found that in men matched for plasma triacylglycerol levels, those consuming a diet rich in total fat (>105 g/d, n = 21) were characterized by higher circulating levels of sICAM-1 (P < 0.05) and E-selectin (P < 0.05) compared with triacylglycerol-matched individuals with a low total dietary fat intake (<105 g/d, n = 21). However, no significant difference was noted in plasma oxidized low-density lipoprotein levels between groups. Further, we conducted multivariate analyses and found that saturated fatty acid intake was the only dietary variable after inclusion of other dietary variables that contributed to circulating sICAM-1 (P < 0.05) and sVCAM-1 (P < 0.05). CONCLUSION: Our study suggests that high dietary fat consumption is associated with endothelial activation in men and that this detrimental effect is likely attributable to the saturated fatty acid content of the diet.

Adult↗

Postprandial variations of plasma inflammatory markers in abdominally obese men.

OBJECTIVE: Abdominal obesity is associated with a fasting proinflammatory condition. However, not much is known of the potential variations in circulating inflammatory markers after food intake. The purpose of the present study was to examine postprandial changes in plasma tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and C-reactive protein (CRP) concentrations in men and their potential associations with fat distribution and metabolic profile variables. RESEARCH METHODS AND PROCEDURES: Thirty-eight men were given a high-fat meal in the morning after an overnight fast, and TNF-alpha, IL-6, and CRP levels were measured in plasma at 0, 4, and 8 hours after the meal. Physical and metabolic profiles were also assessed for each participant. RESULTS: We observed a substantial increase in circulating IL-6 levels (p < 0.0001) after the meal. Although postprandial variations in circulating TNF-alpha levels across time failed to reach statistical significance (p = 0.02), we noted a significant decrease in plasma TNF-alpha concentrations 4 hours (-10%, p < 0.001 vs. 0 hours) after food intake. Plasma CRP levels were not affected by the fat load. We also noted that insulin-sensitive individuals displayed a less pronounced inflammatory response after food intake than insulin-resistant subjects. DISCUSSION: Results of the present study show that consumption of a high-fat meal leads to an increase in plasma IL-6 concentrations and transient decrease in circulating TNF-alpha levels in overweight men. Our results suggest a possible role of insulin resistance in the modulation of the postprandial inflammatory response, which could, in turn, contribute to worsen the state of insulin resistance.

Abdominal Fat↗

Baseline plasma C-reactive protein concentrations influence lipid and lipoprotein responses to low-fat and high monounsaturated fatty acid diets in healthy men.

To date, no studies have compared the effects of consuming a low-fat diet and a high monounsaturated fatty acid (MUFA) diet, under unrestricted energy intake conditions, on plasma C-reactive protein (CRP) concentrations. Men [n = 61; 37.5 +/- 11.5 y old (mean +/- SD), mean BMI 29.0 +/- 5.0 kg/m2] were randomly assigned to consume ad libitum a moderately low-fat diet (25.8% of energy intake from fat) or a high-fat diet rich in MUFA (40.1% of energy intake from fat, 22.5% from MUFA) for 6-7 wk. Plasma CRP concentrations were measured using a highly sensitive assay. Neither diet affected the plasma CRP concentration. However, baseline CRP concentrations predicted lipoprotein/lipid responsiveness to the experimental diets. After intake of the low-fat diet, plasma total and VLDL-triglyceride (TG) concentrations were increased in the subgroup with high CRP concentrations (P < 0.05 and P < 0.01, respectively) whereas they were reduced in the subgroup with low CRP concentrations at baseline (P < 0.01 for both). The high-MUFA diet reduced plasma TG, VLDL-TG, and VLDL cholesterol only in the subgroup with low CRP at baseline (P < 0.0001). In conclusion, the low-fat diet and the high-MUFA diet did not affect plasma CRP concentrations. However, baseline plasma CRP concentrations may modulate the diet-induced changes in plasma lipid and lipoprotein concentrations.

Adult↗

Metabolic profile in severely obese women is less deteriorated than expected when compared to moderately obese women.

BACKGROUND: Obesity is well known to be associated with an increased prevalence of metabolic complications. Severe obesity is thus expected to have more important alterations of the metabolic profile than moderate obesity. This study aimed to compare the metabolic profile of pre- and postmenopausal severely obese women with moderately obese women. METHODS: First, the metabolic profile of pre- (n=165) and postmenopausal (n=43) severely obese women (body mass index (BMI) > or =40 kg/m(2)) was compared to that of pre- (n=52) and postmenopausal (n=35) moderately obese women (BMI of 30-40 kg/m(2)). Thereafter, pre- and postmenopausal severely obese women were divided into two subgroups according to the presence/absence of a dysmetabolic profile. We used for comparison, a group of pre- and postmenopausal moderately obese women without a dysmetabolic profile. RESULTS: The metabolic profile of pre- and postmenopausal severely obese women was less deteriorated than expected when compared to moderately obese women. Moreover, severely obese women with or without a dysmetabolic profile displayed comparable or even lower plasma levels of cholesterol, HDL and LDL-cholesterol, and a lower cholesterol/HDL-cholesterol ratio than moderately obese women (P< or =0.05). After menopause, the metabolic profile of severely obese women, dysmetabolic or not, was similar to that of moderately obese women. Blood pressure was, however, higher in severely obese women compared to moderately obese women, only before menopause (P< or =0.0001). CONCLUSION: These results indicate that despite their large accumulation of adipose tissue, most of the severely obese women had a metabolic profile less deteriorated than expected, when compared to moderately obese women.

Adipose Tissue↗

Circulating levels of oxidative stress markers and endothelial adhesion molecules in men with abdominal obesity.

CONTEXT: It has been suggested that oxidative stress and endothelial dysfunction could play a role in the higher cardiovascular disease risk noted in the abdominally obese population. OBJECTIVE: The objective of this study was to describe the associations between abdominal fat accumulation, oxidative stress, and endothelial dysfunction in men. DESIGN: A complete physical and metabolic profile was assessed in a group of 56 men covering a wide range of adiposity and plasma oxidized low-density lipoprotein (OxLDL), and soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, E-selectin, and C-reactive protein concentrations were determined. RESULTS: We found that abdominal visceral adipose tissue was positively associated with plasma OxLDL (r = 0.52; P < 0.0001) and C-reactive protein (r = 0.60; P < 0.0001) concentrations. We also found significant associations between plasma E-selectin levels and hyperinsulinemia (r = 0.39; P < 0.005) as well as with the homeostasis model assessment index of insulin resistance (r = 0.42; P < 0.005). CONCLUSIONS: Our study showed that plasma OxLDL levels and low-grade systemic inflammation are increased in men with a high visceral adipose tissue accumulation. Furthermore, our results support the notion that insulin resistance is associated with endothelial activation. Overall, our observations give us further insights on the increased cardiovascular disease risk frequently noted among viscerally obese, insulin-resistant individuals.

Abdominal Fat↗

Relation of high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and fibrinogen to abdominal adipose tissue, blood pressure, and cholesterol and triglyceride levels in healthy postmenopausal women.

The associations of inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin-6 [IL-6], tumor necrosis factor-alpha, and fibrinogen) with anthropometric and metabolic variables were examined in a sample of 112 postmenopausal women not receiving hormone therapy. Body fat distribution was measured by computed tomography, and insulin sensitivity was determined by an euglycemic-hyperinsulinemic clamp. hs-CRP (0.10 < or = r(2) < or =0.37) and IL-6 (0.06 < or = r(2) < or =0.31) were significantly associated with anthropometric and metabolic variables, including visceral and subcutaneous adipose tissue, systolic and diastolic blood pressure, triglycerides, high-density lipoprotein (HDL) cholesterol, and insulin sensitivity (p <0.05). Women with greater hs-CRP concentrations showed deterioration in their metabolic risk profiles, including abdominal obesity, greater triglyceride and lower HDL cholesterol concentrations, and lower insulin sensitivity compared with women with lower hs-CRP levels. Fifty-nine percent of women with high hs-CRP concentrations had the metabolic syndrome as recently defined by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. After adjustment for visceral adipose tissue, most of the differences in the plasma lipid-lipoprotein profile were eliminated between women with high hs-CRP levels and women with low hs-CRP levels, whereas some differences in blood pressure variables, insulin sensitivity, and inflammatory markers (IL-6 and fibrinogen) remained significant. In conclusion, these results suggest that increased visceral adipose tissue levels appear to be a determinant covariable of the association between high hs-CRP concentrations and alteration in the metabolic profile.

Adipose Tissue↗

Insulin resistance syndrome, body mass index and the risk of ischemic heart disease.

BACKGROUND: Many people who are not obese according to standard height and weight criteria may still display features of insulin resistance syndrome and thus be at high risk of ischemic heart disease. We sought to investigate the effect of cumulative features of insulin resistance syndrome on the risk of ischemic heart disease associated with variations in body mass index (BMI) among men who participated in the Quebec Cardiovascular Study. METHODS: A cohort of 1824 nondiabetic men free of ischemic heart disease was evaluated at the 1985 baseline evaluation and followed for a period of 13 years, during which 284 first ischemic heart disease events were recorded. Relative hazards (RHs) of ischemic heart disease in 3 BMI groups (normal weight, overweight and obese) were estimated using Cox proportional hazards regression. RESULTS: Although obese men (BMI > or = 30 kg/m2) were the most likely to accumulate features of insulin resistance syndrome, the univariate risk of ischemic heart disease in this group was not significantly increased compared with normal-weight men (BMI < 25 kg/m2) (RH 1.26, 95% confidence interval [CI] 0.88-1.80). However, obese men who accumulated more than 4 features of insulin resistance syndrome were at increased risk of ischemic heart disease (RH 1.81, 95% CI 1.02-3.19) compared with normal-weight men who had fewer than 3 features of the syndrome. Conversely, having more than 4 features of insulin resistance syndrome was associated with a 3-fold increase in the risk of ischemic heart disease among normal-weight men (RH 3.01, 95% CI 1.70-5.32). INTERPRETATION: Although obesity is an important risk factor for ischemic heart disease, variations in BMI alone poorly reflect the risk of ischemic heart disease associated with features of insulin resistance syndrome.

Adult↗

Impact of waist circumference on the relationship between blood pressure and insulin: the Quebec Health Survey.

Hyperinsulinemia has been suggested to be involved in the etiology of obesity-associated hypertension. The objective of the present study was to quantify, in a population-based study, the respective contributions of excess adiposity (body mass index [BMI]), waist circumference (WC), fasting insulin levels, and insulin sensitivity to the variation of resting blood pressure. The Quebec Health Survey was used to obtain fasting plasma insulin and glucose levels and resting blood pressure as well as anthropometric measurements in a representative sample of 907 men and 937 women. When the sample was divided into tertiles of BMI and further stratified on the basis of the 50th percentile of WC (88 cm in men), nonobese men in the first BMI tertile (<23.2 kg/m2) but with abdominal obesity were characterized by an increased systolic blood pressure (SBP) compared with nonobese men with low WC (130+/-18 versus 120+/-11 mm Hg; mean+/-SD; P=0.075). The SBP was comparable to SBP values measured among men in the top BMI tertile (129+/-14 mm Hg for BMI > or =26.6 kg/m2). When subjects were classified into tertiles of fasting insulin and WC, no association between insulin levels and blood pressure was noted, once the variation in WC was considered. Insulin sensitivity (estimated with homeostasis model assessment [HOMA]) did not explain variation in blood pressure in men, whereas the contribution of HOMA in women was of marginal clinical significance (R2 of <1.3%; P<0.0001). These results suggest that the documented association between obesity, fasting insulin, insulin sensitivity, and blood pressure is largely explained by concomitant variation in WC.

Abdomen↗

Inflammatory markers and long-term risk of ischemic heart disease in men A 13-year follow-up of the Quebec Cardiovascular Study.

We tested the hypothesis that elevated plasma interleukin-6 (IL-6), C-reactive protein (CRP) and fibrinogen concentrations are independent risk factors and interact in increasing the long-term risk of ischemic heart disease (IHD) in men. A total of 1982 IHD-free men from the Quebec Cardiovascular Study were followed over a period of 13 years during which 210 first fatal IHD events and non-fatal myocardial infarctions were recorded. Increased CRP levels (4th versus 1st quartile) were not associated with an increased risk of IHD after adjustment for non-lipid risk factors (age, body mass index, systolic blood pressure, diabetes, smoking and medication use at baseline), lipid risk factors (LDL and HDL cholesterol and triglyceride levels) and for IL-6 and fibrinogen (RR=0.70, 95% CI=0.43-1.13). High plasma IL-6 levels (4th versus 1st quartile) were associated with a 70% greater risk of IHD independent of confounding risk factors and of the other 2 inflammatory markers (RR=1.71, 95% CI=1.07-2.75). The relationship between high fibrinogen levels (4th versus 1st quartile) and IHD risk was borderline significant in multivariate analyses (RR=1.53, 95% CI=0.97-2.43). An inflammation score based on plasma IL-6 and fibrinogen levels improved the IHD risk predictive value of a multivariate model of traditional risk factors (p=0.03). Including plasma CRP levels into the inflammatory score provided no additional predictive value. In conclusion, elevated plasma IL-6 concentrations are more strongly related to IHD risk than CRP and fibrinogen. An inflammation score based on high plasma IL-6 and fibrinogen levels used in combination with traditional risk factors may improve our ability to adequately identify high risk individuals.

Adult↗

Influence of apolipoprotein E genotype on the reliability of the Friedewald formula in the estimation of low-density lipoprotein cholesterol concentrations.

Lipoprotein data and apolipoprotein (apo) E genotype from 1302 participants, covering a wide range of total plasma cholesterol levels, were used to examine the impact of apo E genotype on the estimation of low-density lipoprotein cholesterol (LDL-C0 concentrations by the Friedewald formula using high-density lipoprotein cholesterol and triglyceride (TG) concentrations as compared with the beta -quantification reference procedure. The results showed that participants with apo E2/E2 genotype had significantly higher very low-density lipoprotein cholesterol (VLDL-C) concentrations and VLDL-C/TG ratio as well as lower LDL-C concentrations than participants with other apo E genotypes. Heterozygous carriers of the epsilon 2 allele had significantly higher VLDL-C than participants with apo E3/E3 and E4/E3 genotypes. The mean absolute error and the mean percentage of bias in calculated LDL-C according to all apo E genotypes, except E2/E2 genotype, were less than 0.16 mmol/L and 4.4%, respectively. Indeed, the mean error and the mean percentage of bias associated with the LDL-C calculated by the Friedewald formula in the apo E2/E2 group were 0.93 mmol/L and 40.6%, respectively. However, participants with the apo E2/E2 genotype and a type III phenotype showed a mean error and a mean percentage of bias reaching 1.53 mmol/L and 63.5%, respectively, whereas E2/E2 participants with a non-type III phenotype had a mean error and a mean percentage of bias of 0.18 mmol/L and 11.0%, respectively. Moreover, 41.9% to 57.1% of the participants had an absolute bias higher than 5% according to the apo E genotype, except for the apo E2/E2 genotypic group where 88.6% of the participants had an absolute bias higher than 5%. Stepwise multiple linear regression analyses revealed that the apo E genotype contributed to 39.0% of the VLDL-C/TG ratio variance, whereas sex, age, and high-density lipoprotein cholesterol explained between 0.5% and 3.2% of the variance. These results indicate that the apo E genotype exerts a significant influence on the estimation of LDL-C concentrations by the Friedewald formula as compared with the beta-quantification.

Adolescent↗