Normolipidemic Individuals Research Articles

Assessment of Nutrients Intake in Pediatrics with Type 1 Diabetes and Dyslipidemia in Jordan.

Dyslipidemias are disorders of lipoprotein metabolism that occur during childhood and adolescence, often persist into adulthood, and increase the risk of developing atherosclerotic lesions. This study aimed to assess the potential association between nutrient intake and dyslipidemia in Jordanian pediatric patients diagnosed with type 1 diabetes mellitus. This cross-sectional study was conducted in Amman, Jordan, and involved 90 children and adolescents diagnosed with type 1 diabetes mellitus. Caregivers provided the following data: sex, age, type and dose of insulin, age at onset of type 1 diabetes, and level of physical activity. Anthropometric measurements were obtained using calibrated scales, and CDC growth charts were used to assess participants' body weight status. Nutrient intake was estimated using a 120-item food frequency questionnaire (FFQ) previously validated in Jordanian children and adolescents. Serum lipid levels, including total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), were measured. Binary logistic regression was used to assess the relationship between nutrient intake and dyslipidemia. The results indicated that 36.7% of study participants had dyslipidemia. There were no significant differences in nutrient intake between dyslipidemic and normolipidemic individuals, except for a significantly higher median intake of vitamin B12 in the dyslipidemic group compared to the normolipidemic group (3.6 versus 2.7 µg, P-value = 0.046). This study found no significant association between the prevalence of dyslipidemia and nutrient intake in children and adolescents diagnosed with type 1 diabetes mellitus.

A systematic review and meta-analyses on the effects of atorvastatin on blood pressure and heart rate.

Considering the inconsistencies in the literature on the atorvastatin effect on blood pressure (BP), we performed these meta-analyses. Through a search of the Excerpta Medica Database (EMBASE), PubMed, and Web of Science databases, 1412 articles were identified, from which 33 randomized clinical trials (RCT) and 44 pre-clinical were selected. Populations from RCT were stratified according to baseline BP and lipid levels. We performed meta-analyses of the effect of atorvastatin on systolic (SBP), diastolic and mean BP; heart rate (HR); HR variability, and baroreflex. Atorvastatin reduced SBP in the overall population (P=0.05 vs. placebo; P=0.03 vs. baseline), in normotensive and hyperlipidaemic (P=0.04 vs. placebo; P=0.0001 vs. baseline) and in hypertensive and hyperlipidaemic (P=0.02 vs. placebo; P=0.008 vs. baseline) individuals in parallel RCT, but it did not affect SBP in normotensive and normolipidaemic individuals (P=0.51 vs. placebo; P=0.4 vs. baseline). Although an effect of atorvastatin was detected in hyperlipidaemic individuals, the meta-regression coefficient for the association of low density lipoprotein (LDL)-cholesterol reduction with SBP reduction in the overall population demonstrated that SBP reduction is not dependent on the changes in LDL-cholesterol. A meta-analysis of preclinical reports demonstrated that SBP was reduced in atorvastatin-treated hypertensive and normolipidaemic rats (spontaneously hypertensive rats: P<0.00001), but not in normotensive and normolipidaemic rats (control rats: P=0.97). Atorvastatin also reduced the HR in spontaneously hypertensive rat. Atorvastatin lowers BP independent of LDL-cholesterol levels. Additional studies are needed to estimate the involvement of the autonomic nervous system in the BP-lowering effect of atorvastatin.

Past, Present, and Future of Familial Hypercholesterolemia Management.

Familial hypercholesterolemia (FH) is a monogenic form of severe hypercholesterolemia that, if left untreated, is associated with early onset of atherosclerosis. FH derives from genetic variants that lead to inefficient hepatic clearance of low-density lipoprotein (LDL) particles from the circulation. The FH phenotype is encountered in approximately 1 of every 300 people. The risk of atherosclerotic cardiovascular disease (ASCVD) is higher in those with FH than in normolipidemic individuals and in those with polygenic hypercholesterolemia. FH is usually diagnosed by clinical scores that consider hypercholesterolemia, family history of early ASCVD and hypercholesterolemia, and cutaneous stigmata. Genetic diagnosis is important and should be offered to individuals suspected of FH. Family cascade screening is important to identify asymptomatic hypercholesterolemic individuals. Despite the high risk of ASCVD, this risk is heterogenous in heterozygous FH and depends not only on high LDL cholesterol (LDL-C) but also on other risk biomarkers. Risk can be evaluated by considering biomarkers such as male sex, late-onset therapy (> age 40), LDL-C > 310 mg/dL, low high-density lipoprotein cholesterol, elevated lipoprotein(a), obesity, diabetes, and hypertension by using specific risk equations and by detecting subclinical coronary atherosclerosis. Statins are the main therapy for FH and change the natural history of ASCVD; however, most individuals persist with elevated LDL-C. PCSK9 inhibitors provide robust and safe LDL-C lowering in FH, although elevated costs preclude their widespread use. Newer therapies such as ANGPTL3 inhibitors add intensive LDL-C lowering for refractory forms of FH. Finally, while it is possible to normalize LDL-C in people with FH, the disease unfortunately is still severely underdiagnosed and undertreated.

2019 George Lyman Duff Memorial Lecture: Three Decades of Examining DNA in Patients With Dyslipidemia.

Dyslipidemias include both rare single gene disorders and common conditions that have a complex underlying basis. In London, ON, there is fortuitous close physical proximity between the Lipid Genetics Clinic and the London Regional Genomics Centre. For >30 years, we have applied DNA sequencing of clinical samples to help answer scientific questions. More than 2000 patients referred with dyslipidemias have participated in an ongoing translational research program. In 2013, we transitioned to next-generation sequencing; our targeted panel is designed to concurrently assess both monogenic and polygenic contributions to dyslipidemias. Patient DNA is screened for rare variants underlying 25 mendelian dyslipidemias, including familial hypercholesterolemia, hepatic lipase deficiency, abetalipoproteinemia, and familial chylomicronemia syndrome. Furthermore, polygenic scores for LDL (low-density lipoprotein) and HDL (high-density lipoprotein) cholesterol, and triglycerides are calculated for each patient. We thus simultaneously document both rare and common genetic variants, allowing for a broad view of genetic predisposition for both individual patients and cohorts. For instance, among patients referred with severe hypertriglyceridemia, defined as ≥10 mmol/L (≥885 mg/dL), <1% have a mendelian disorder (ie, autosomal recessive familial chylomicronemia syndrome), ≈15% have heterozygous rare variants (a >3-fold increase over normolipidemic individuals), and ≈35% have an extreme polygenic score (a >3-fold increase over normolipidemic individuals). Other dyslipidemias show a different mix of genetic determinants. Genetic results are discussed with patients and can support clinical decision-making. Integrating DNA testing into clinical care allows for a bidirectional flow of information, which facilitates scientific discoveries and clinical translation.

P5302Significant correlation of visceral adiposity and adipocytokines with arterial inflammation in genetic dyslipidaemias

Abstract Background The adipose tissue is now established as a major regulator of cardiovascular status, mediated by the secretion of several bioactive molecules, including adipocytokines. Individuals with genetic dyslipidaemias of either familial combined hyperlipidemia (FCH) or heterozygous familial hypercholesterolemia (heFH) subtype are characterized by accelerated atherosclerosis. Nonetheless, limited data exists on the relationship between adiposity and arterial inflammation, a marker of cardiovascular risk, in this setting. Purpose To investigate the relationship between adiposity indices and arterial inflammation evaluated by 18F fluorodeoxyglycose positron emission tomography (PET/CT) in patients with hereditary lipid metabolism disorders. Methods Consecutive patients with either FCH or heFH, free of statin therapy, and normolipidaemic individuals underwent PET/CT imaging. Arterial FDG uptake was estimated as the average value of target-to-background ratio (TBR) within aortic and carotid wall. Volumes of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were measured from CT images between the proximal (cephalic) end of the L1 and distal (caudal) end of the L3 vertebrae by selecting all voxels with attenuation between −190 and −30 Hounsfield Units (HU). Serum adiponectin and leptin levels were measured with ELISA by available commercial kits. For comparisons with arterial TBR, adiponectin and leptin concentrations above and below the 25th percentile, were stratified as high and low, respectively. Results In total, 60 individuals (20 FCH, 20 heFH and 20 controls) were included. A modest but significant correlation between SAT volume and arterial TBR (R=0.386, p=0.004) was detected. This relationship did not remain significant after controlling for VAT volume (p=0.303). A strong correlation between VAT volume and arterial TBR (R=0.621, p=0.001) was observed. This relationship remained significant after controlling for SAT volume (R=0.541, p&lt;0.001). Arterial TBR values were higher in individuals with low plasma adiponectin levels (p=0.010). In addition, patients with higher leptin levels exhibited increased arterial FDG uptake compared to subjects with low serum leptin concentrations (p=0.05) Conclusions Abdominal adipose tissue imaging markers and serum adipocytokines correlate with arterial inflammation as assessed by PET/CT in patients with familial dyslipidaemias highlighting the role of abdominal adipose tissue for atherosclerosis progression in this population.

Structural and Nonlinear Optical Characteristics of In Vitro Glycation of Human Low-Density Lipoprotein, as a Function of Time

Modified low-density lipoprotein (LDL) is a well-known risk marker for diabetes and cardiovascular disease. In vitro and in vivo studies have shown that native LDL particles, when modified by oxidation and/or glycation processes, become proatherogenic. Other studies have shown that high LDL concentrations also contribute to atherogenic diseases. In the present in vitro study, we investigate structural characteristics, linear and nonlinear optical properties of LDL particles modified by glycation, compared to modified-control and non-modified LDL (LDLnat). LDL particles were isolated from normolipidemic individuals and aliquots were incubated in PBS (LDLcontrol) and glycated (LDLglyc) with glycolaldehyde (GAD) from 2 to 6 days. The nonlinear optical Z-Scan experiments indicate that GAD modifies the optical properties of the LDL. These results indicate the application of a nonlinear optical technique as a tool to investigate the characteristics of LDL particles, in particular when modifications are induced in the particles by glycation.

Total lipid, phospholipid and cholesterol contents of six marine shrimps of Mumbai, Maharashtra

The total lipid, phospholipids and cholesterol contents in the muscles of six marine shrimps viz., Parapenaeopsis stylifera, Parapenaeopsis sculptilis, Metapenaeus brevicornis, Litopenaeus vannamei, Nematopalaemon tenuipes and Acetes indicus has been reported in the present study. Total lipid were significantly (p<0.05) higher in N. tenuipes and M. brevicornis, while phospholipids were significantly (p<0.05) higher in only N. tenuipes than in other shrimp species. The cholesterol contents were higher than the phospholipids in all the shrimps except N. tenuipes. Overall, the present study showed that the selected shrimps were a good source of essential lipid with nutritional values. However, due to the high cholesterol content, moderate shrimp consumption could be recommended for normolipidemic individuals

DOES ATORVASTATIN ALONE AMELIORATE CHRONIC PERIODONTITIS IN HYPERLIPIDEMIC PATIENTS? (A CROSS-SECTIONAL STUDY)

The present study was conducted to assess whether atorvastatin (ATV) alone could improve periodontal parameters and reduce inflammation and bone resorption in generalized chronic periodontitis (gCP) patients with hyperlipidemia. One hundred and two subjects were classified into three groups: Group I included 34 gCP patients with hyperlipidemia and maintained on a daily dose of 20 mg atorvastatin at least for 6 months. Group II comprised 34 gCP patients with hyperlipidemia and not taking any hypolipidemic drugs. Group III consisted of 34 normolipidemic individuals with gCP. The periodontal parameters including plaque index (PI), bleeding on probing (BOP), gingival index (GI), probing depth (PD) and clinical attachment loss (CAL) were recorded and compared. Unstimulated whole saliva and blood samples were harvested from all subjects. Salivary levels of interleukin-1beta (IL-1β) and receptor activator of nuclear kappa B ligand (RANKL) were evaluated by enzyme-linked immunosorbent assay (ELISA) technique. The blood samples were used to assess the lipid profile for all patients including total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol (HDL-C). The results demonstrated significantly greater decrease of periodontal parameters and salivary IL-1β and RANKL levels in group I compared to other groups. BOP, PD and CAL were positively correlated with the levels of salivary IL-1β, TC, TG and LDL-C whereas HDL-C measurements were negatively associated with BOP, PD and CAL. In conclusion, ATV could be a viable therapeutic modality in gCP management, due to its anti-inflammatory and antiosteopathic effects. Salivary IL-1β and RANKL could serve as reliable biomarkers in periodontal disease.

Newly-developed De Cordova’s Formula for Calculation of LDL Cholesterol in Bangladeshi Population

Raised serum LDL cholesterol is an important modifiable risk factor for the development of atherosclerosis and cardiovascular disease. So the management of dyslipidaemia is mostly based on the concentration of LDL cholesterol. Friedewald’s formula is commonly used method to estimate LDL cholesterol in most clinical laboratories. However, this formula cannot reflect the actual figure of LDL cholesterol. In 2013, de Cordova developed a new simple formula to calculate LDL cholesterol without using serum TG which is said to be more accurate than Friedewald’s formula. The present study was designed to compare the formula-based calculated LDL cholesterol (Friedewald’s formula and de Cordova’s formula) with direct homogenous estimation. The objective of the present study was to evaluate of applicability of de Cordova’s formula for calculation of LDL cholesterol. By using non-probability sampling technique, 460 individuals were enrolled in the study who were attending in the one-point collection centre of BSMMU for lipid profile estimation. Subjects were categorized as normolipidaemic individuals and dyslipidaemic patients. Serum TC, TG, HDL cholesterol and LDL cholesterol were measured by direct automated method. LDL cholesterol was also calculated by Friedewald’s formula and de Cordova’s formula. Results were expressed as mean ± SD. Comparison was done by Pearson’s correlation test, agreement was done by BlandAltman agreement test between measured and calculated LDL cholesterol. The mean ± SD of measured LDL cholesterol was 132.99 ± 36.65 mg/ dL. LDL cholesterol calculated by Friedewald’s formula and de Cordova’s formula were 121.39 mg/dL and 116.81 mg/dL respectively. The limits of agreement between measured LDL cholesterol (direct method) and calculated LDL cholesterol by de Cordova’s formula were lowest and agreement was better for all dyslipidaemic subjects. de Cordova’s formula showed better agreement with measured LDL cholesterol (direct method) than Friedewald’s formula for approximate calculation of LDL cholesterol without using triglycerides.Keywords: LDL cholesterol, de Cordova’s formula, Friedewald’s formula

Vascular inflammation and metabolic activity in hematopoietic organs and liver in familial combined hyperlipidemia and heterozygous familial hypercholesterolemia

Familial dyslipidemias of either heterozygous (heFH) or combined (FCH) type lead to accelerated atherogenesis and increased cardiovascular risk. The aim of this study was to investigate in statin-naïve adult patients with familial dyslipidemias whether inflammatory activation and liver, spleen and bone marrow metabolic activity differ compared with normolipidemic subjects and between dyslipidemic groups. Fourteen patients with FCH, 14 with heFH, and 14 normolipidemic individuals were enrolled. Serum lipids, high-sensitivity C-reactive protein, and fibrinogen levels were measured, followed by 18F-fluorodeoxyglucose positron-emission tomography/computed tomography imaging. Radiotracer uptake in the aortic wall, spleen, bone marrow, and liver was quantified as tissue-to-background ratio (TBR). Patients with heFH had significantly higher low-density lipoprotein levels compared with those with FCH and controls (P<.001). However, aortic TBRs were higher in FCH compared with heFH patients and controls (P=.02 and P<.001, respectively). FCH patients exhibited higher FDG uptake in the spleen compared with controls (P=.05). In addition, FCH exhibited higher bone marrow FDG uptake compared with heFH patients and controls (P=.03 and P=.02, respectively). FCH had higher liver uptake compared with heFH patients and controls (P<.001 for both). Significant correlations were observed between inflammatory biomarkers and imaging indices as well as between aortic TBR and FDG uptake of hematopoietic organs and liver. Systemic, as well as vascular inflammation and spleen, bone marrow, and hepatic metabolic activity are increased in patients with FCH despite lower levels of low-density lipoprotein.

Abstract 367: Extreme High-Density Lipoprotein Cholesterol Genetics: An Assortment of Large and Small Polygenic Effects

Rationale: Although HDL-C levels are known to have a complex genetic basis, most studies have focused solely on identifying rare variants with large phenotypic effects to explain extreme HDL-C phenotypes. Objective: Here we concurrently evaluate the contribution of both rare and common genetic variants, as well as large-scale copy number variations (CNVs), towards extreme HDL-C concentrations. Methods: In clinically ascertained patients with low ( N =136) and high ( N =119) HDL-C profiles, we applied our targeted next-generation sequencing panel (LipidSeq TM ) to sequence genes involved in HDL metabolism, which were subsequently screened for rare variants and CNVs. We also developed a novel polygenic trait score (PTS) to assess patients’ genetic accumulations of common variants that have been shown by genome-wide association studies to associate primarily with HDL-C levels. Two additional cohorts of patients with extremely low and high HDL-C (total N =1,746 and N =1,139, respectively) were used for PTS validation. Results: In the discovery cohort, 32.4% of low HDL-C patients carried rare variants or CNVs in primary ( ABCA1 , APOA1 , LCAT ) and secondary ( LPL , LMF1 , GPD1 , APOE ) HDL-C–altering genes. Additionally, 13.4% of high HDL-C patients carried rare variants or CNVs in primary ( SCARB1 , CETP , LIPC , LIPG ) and secondary ( APOC3 , ANGPTL4 ) HDL-C–altering genes. For polygenic effects, patients with abnormal HDL-C profiles but without rare variants or CNVs were ~2-fold more likely to have an extreme PTS compared to normolipidemic individuals, indicating an increased frequency of common HDL-C–associated variants in these patients. Similar results in the two validation cohorts demonstrate that this novel PTS successfully quantifies common variant accumulation, further characterizing the polygenic basis for extreme HDL-C phenotypes. Conclusions: Patients with extreme HDL-C levels have various combinations of rare variants, common variants, or CNVs driving their phenotypes. Fully characterizing the genetic basis of HDL-C levels must extend to encompass multiple types of genetic determinants—not just rare variants—to further our understanding of this complex, controversial quantitative trait.

Lack of effects of statins on high-density lipoprotein subfractions in HIV-1-infected patients receiving protease inhibitors

BackgroundWe evaluated the effect of 45 days of rosuvastatin or pravastatin treatment on the distribution of HDL subfractions in HIV-1-infected individuals receiving boosted protease inhibitors (PIs) with cardiovascular risk. MethodsThe distribution of HDL subclasses by gradient gel electrophoresis was blindly assessed in 74 HIV-1-infected individuals receiving boosted PIs at baseline and at day 45 of statin treatment, and compared with the distribution obtained in 63 healthy normolipidemic individuals taken as controls. ResultsNo significant modification appeared in HDL distribution between the two arms of statins for the HIV-1-infected individuals. Nevertheless, when compared to controls, HDL subfractions showed a significantly lower HDL2b proportion and significantly higher proportions of HDL2a and HDL3b (P<0.001). ConclusionNo difference was observed in HDL distribution between pravastatin and rosuvastatin after 45 days treatment, in HIV-1-infected individuals under PIs. Nevertheless, when compared to healthy normolipidemic subjects, HDL distribution is clearly different, with a distribution in HIV-infected individuals under PIs associated with an increased cardiovascular risk.

Can the effects of gender, menopause and ageing on lipid levels be differentiated?

The menopause, as well as ageing in both genders, can influence cardiovascular disease (CVD) risk1. An atherogenic lipoprotein profile, including small dense low density lipoprotein (sdLDL) particles, can be present even in normolipidaemic healthy young individuals (about 6%)2. If confirmed by larger studies, it will be necessary to consider different risk stratifications for those with atherogenic normolipidaemia and those with non-atherogenic hypercholesterolaemia. Furthermore, other changes associated with the menopause (increase in lipoprotein (a) [Lp(a)] levels, central obesity, endothelial dysfunction and systemic inflammation) may contribute to pro-atherogenic changes, while ethnicity and lifestyle habits (diet and exercise) cannot be ignored3. This article is protected by copyright. All rights reserved.

Effects of the peanut oil on blood lipid and blood pressure of healthy normolipidemic individuals

Effects of the peanut oil on blood lipid and blood pressure of healthy normolipidemic individuals

Periodontal Status and Hyperlipidemia: Statin Users Versus Non‐Users

The association between serum lipids and periodontal disease has been studied predominantly in patients with chronic periodontitis with limited data available regarding periodontal status of patients with hyperlipidemia. Meanwhile, the impact of statins on the periodontal health of the population also remains largely underexplored. This study aims to assess the periodontal status among patients with hyperlipidemia and users of statins. In this cross-sectional study, 94 patients with hyperlipidemia (50 receiving statins and 44 receiving non-pharmacologic therapy) and 46 control individuals who were normolipidemic underwent periodontal examination (plaque index, gingival index [GI], probing depth [PD], and clinical attachment level [CAL]). Biochemical parameters measured included serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein cholesterol levels. PD and GI were significantly higher in patients with hyperlipidemia who were non-statin users compared with the normolipidemic individuals (P <0.001 [PD] and P <0.05 [GI]) and the statin group (P = 0.001 [PD] and P <0.05 [GI]). Periodontal parameters between statin users and the normolipidemic group did not differ significantly. After adjusting for confounders, positive and significant correlations were observed between PD and TG, and TC and LDL, whereas CAL shared correlation with TC and LDL. GI was correlated with TG and TC. Regression analyses revealed that whereas TC was associated significantly with PD (P <0.001), LDL showed significant association with CAL (P = 0.013). TG showed significant association with GI (P = 0.020). Our findings suggest that relative to the general population, patients with hyperlipidemia are more prone to periodontal disease. Also, within the limits of this study, statins have a positive impact on periodontal health.

Mass spectrometry based strategies in the mapping of modified LDL

The asymptomatic nature of atherosclerosis is prompting the biomedical community to develop methods that can identify patients with high risk of cardiovascular incidents before any clinical symptoms develop. Current opinion is that oxidative modifications to circulating LDL particles (oxLDL) under inflammatory conditions are responsible for mediating fusion/aggregation events and conferring its atherogenicity. LDL particles are complex in nature, being composed of a hydrophobic outer layer of phospholipids wrapped by glycosylated Apo B-100 protein, and any of these biomolecules located at the surface of the particle may be a target of oxidative damage. The relevance, together or individually, of different modifications in oxLDL is not yet clear, with the additional challenge that the structural features inherent in each of the modification play a significant role in the complexity of setting up MS based strategies for their detection. Protocols based on mass spectrometry (MS) coupled with reverse phase LC were applied to the structural characterisation of LDL protein (Apo B-100) from normolipidemic individuals. Protein sequence coverage ≥70% was routinely achieved. In this work we describe the applicability of different MS scanning methods targeted towards the detection of oxidised amino acids, and modifications by oxidised phospholipids and sugar moieties, in providing information about the structural modifications in ApoB-100 protein from oxLDL and their location within the protein. Changes in these during oxidative stress and in diseased states are currently being investigated and correlated with lipid profile data. The development of advanced and targeted methods that allow the mapping of modifications in protein, lipid and glycan moieties of LDL particles by MS-based approaches is expected to provide a broader insight on the role that these modifications may have in the development of atherosclerosis.

Prehypertension in dyslipidemic individuals; relationship to metabolic parameters and intima-media thickness

Like hypertension, prehypertension is associated with cardiovascular disease. The aim of this study was to evaluate: a) the prevalence of prehypertension/hypertension in individuals with various dyslipidemic phenotypes; b) the relation between blood pressure (BP) and other risk factors for atherosclerosis; c) atherogenic potential of prehypertension by the assessment of intima-media thickness of the arteria carotis communis (IMT). 667 clinically asymptomatic subjects were divided into four dyslipidemic phenotypes (DLP) according to apolipoprotein B (apoB) and triglycerides (TG): DLP1 (n=198, normo-apoB/normo-TG), DLP2 (n=179, normo-apoB/hyper-TG), DLP3 (n=87, hyper-apoB/normo-TG), DLP4 (n=203, hyper-apoB/hyper-TG). DLP1 served as a control group. There was significantly higher prevalence of prehypertension and hypertension in subjects with dyslipidemia (DLP2 43.0%, 41.3%; DLP3 42.5%, 29.9%; DLP4 42.4%, 47.8%) than in normolipidemic individuals (DLP1 32.8%, 20.2%). Systolic and diastolic blood pressure (SBP + DBP) correlated with age, total cholesterol, TG, non-HDL-cholesterol, body mass index and waist circumference; SBP additionally with C-peptide, fasting glycemia; DBP additionally with apoB, homeostasis model assessment (HOMA) and plasminogen activator inhibitor-1. The IMT of hypertensive and of prehypertensive subjects was higher than that of subjects with normal BP in all DLPs. The prevalence of prehypertension was higher in all dyslipidemic patients. The common prevalence of prehypertension/hypertension was highest in the hypertriglyceridemic subjects. Prehypertensive and hypertensive patients had higher IMT than normotensive individuals in all DLPs.

Acute impact of apheresis on oxidized phospholipids in patients with familial hypercholesterolemia

We measured oxidized phospholipids (OxPL), lipoprotein (a) [Lp(a)], and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) pre- and postapheresis in 18 patients with familial hypercholesterolemia (FH) and with low(∼10 mg/dl; range 10-11 mg/dl), intermediate (∼50 mg/dl; range 30-61 mg/dl), or high (>100 mg/dl; range 78-128 mg/dl) Lp(a) levels. By using enzymatic and immunoassays, the content of OxPL and Lp-PLA(2) mass and activity were quantitated in lipoprotein density fractions plated in microtiter wells, as well as directly on apoB-100, Lp(a), and apoA-I immunocaptured within each fraction (i.e., OxPL/apoB and Lp-PLA(2)/apoB). In whole fractions, OxPL was primarily detected in the Lp(a)-containing fractions, whereas Lp-PLA(2) was primarily detected in the small, dense LDL and light Lp(a) range. In lipoprotein capture assays, OxPL/apoB and OxPL/apo(a) increased proportionally with increasing Lp(a) levels. Lp-PLA(2)/apoB and Lp-PLA(2)/apoA-I levels were highest in the low Lp(a) group but decreased proportionally with increasing Lp(a) levels. Lp-PLA(2)/apo(a) was lowest in patients with low Lp(a) levels and increased proportionally with increasing Lp(a) levels. Apheresis significantly reduced levels of OxPL and Lp-PLA(2) on apoB and Lp(a) (50-75%), particularly in patients with intermediate and high Lp(a) levels. In contrast, apheresis increased Lp-PLA(2)-specific activity (activity/mass ratio) in buoyant LDL fractions. The impact of apheresis on Lp(a), OxPL, and Lp-PLA(2) provides insights into its therapeutic benefits beyond lowering apoB-containing lipoproteins.

Abstract P348: The Effects of High Saturated Fat Intake on LDL and HDL Subclasses in Individuals with Atherogenic Dyslipidemia

Previous observations in normolipidemic individuals have indicated that the increase in LDL cholesterol (C) resulting from substitution of dietary saturated fat for carbohydrate or unsaturated fat is primarily due to higher plasma levels of large cholesterol-enriched LDL particles, with minimal effects on smaller LDL, as well as apolipoprotein (apo) B and total-C/HDL-C ratio. In the present study, we tested whether similar effects of saturated fat are observed in individuals with atherogenic dyslipidemia characterized by a preponderance of small LDL particles (LDL phenotype B). Fifty-three phenotype B participants consumed a baseline diet (55% carbohydrate, 15% protein, 30% fat, 8% saturated fat) for 3 weeks, after which they were randomized to either a moderate carbohydrate, high saturated fat diet (HSF; 39% carbohydrate, 25% protein, 36% fat, 18% saturated fat) or a moderate carbohydrate, low saturated fat diet (LSF; 37% carbohydrate, 25% protein, 37% fat, 9% saturated fat) for 3 weeks. The difference in saturated fat was derived primarily from dairy sources. Plasma lipids and lipoproteins were measured after the baseline and randomized diets. Compared to the LSF diet, participants who consumed the HSF diet had a greater percent increase in total-C (p&lt;0.0001), LDL-C (p=0.0002), total-C/HDL-C ratio (p=0.0004) and apoB (p&lt;0.0001) from the baseline diet, with no significant differences in HDL-C or apoAI. The HSF group had a greater percent increase in medium (p=0.05) and small (p=0.02) LDL particle concentrations from baseline compared to the LSF group, with no differences in large and very small LDL. There were also no significant differences in large and small HDL subclasses. The activities of both hepatic lipase (p=0.05) and cholesteryl ester transfer protein (p=0.04) were increased in the HSF group compared to the LSF group. Because medium and small LDL particles have been found to be more highly associated with CVD risk than larger LDL particles, the present results, in conjunction with our previous findings, suggest that adverse effects of very high saturated fat intake on CVD risk may be greater in phenotype B individuals than in those with normal lipoprotein profiles.

Effects of two different exercise trainings on plasma homocysteine levels and other cardiovascular disease risks

Purpose: To investigate the influences of regular sub-maximal aerobic and resistance exercise trainings for 3 months on plasma homocystenie level and other CVD risks (lipid profile, body mass index, etc.) and compare the effects of these two different types of exercise training on these parameters. Method: Thirty-eight individuals mean aged 21.68±1.38 years were included. Participants were divided into three groups as aerobic exercise (AE) (n=13), resistance exercise (RE) (n=13) and control group (CT) (n=12). Exercises were done four times a week during 12 weeks. CT (n=12) didn’t do any exercise. Blood analyses (plasma homocystenie, vitamin and lipid levels) and anthropometric measurements were performed, maximum aerobic capacity was assessed. Results: It was found that plasma homocystenie level and lipid profile didn’t change in exercise groups and CT group after 12 weeks (p>0.05). Body mass index and waist circumference decreased in both exercise groups (p 0.05). Homocystenie level has positive correlation with waist circumference (r=0,392,p=0.22) and waist-to-hip ratio (r=0,501,p=0.02),and has negative correlation with folic acid level (r=-0,447,p=0.01). Folic acid level was the essential factor for homocystenie level respect to multiple regression analysis (p=0.03,R 2 =0.60). Conclusion: Sub-maximal aerobic or resistance exercise training didn’t change homocysteine level when folic acid level at normal values in blood. Independent from the type of exercise, chronic exercise didn’t considerably change lipid profiles in normolipidemic individuals. Aerobic capacity didn’t change after 12 weeks exercise training whereas body composition improved.