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Background and Purpose: Atherosclerotic remodeling of the aneurysm wall, which could be detected as aneurysm wall enhancement (AWE) by magnetic resonance–vessel wall imaging, is a part of degenerative change of unruptured intracranial aneurysms (UIAs). The purpose of this study was to determine whether the luminal concentrations of atherosclerotic proteins in the aneurysm sac were associated with increased wall enhancement of UIAs in vessel wall imaging. Methods: We performed a prospective study of subjects undergoing endovascular treatments for UIAs. All subjects underwent evaluation using 3T–magnetic resonance imaging, including pre/postcontrast vessel wall imaging of the UIAs. Blood samples were collected from the aneurysm sac and the parent artery during endovascular procedures. Presence/absence of AWE was correlated with the delta difference in concentration for each atherosclerotic protein between the lumen of UIA and in the parent artery. Results: A total of consecutive 17 patients with 19 UIAs were enrolled. The delta difference of lipoprotein(a) was significantly higher in UIAs with AWE compared with those without AWE (−6.9±16.0 versus −45.4±44.9 μg/mL, P =0.03). Conclusions: Higher luminal concentrations of lipoprotein(a) in the aneurysm sac were significantly associated with increased wall enhancement of UIAs. A larger study is needed to confirm these findings.

Background: Current lipid guidelines suggest measurement of Lp(a) (lipoprotein[a]) and ApoB (apolipoprotein B) for atherosclerotic cardiovascular disease risk assessment. Polygenic risk scores (PRSs) for Lp(a) and ApoB may identify individuals unlikely to have elevated Lp(a) or ApoB and thus reduce such suggested testing. Methods: PRSs were developed using least absolute shrinkage and selection operator regression among 273 222 and 356 958 UK Biobank participants of white British ancestry for Lp(a) and ApoB, respectively, and validated in separate sets of 60 771 UK Biobank and 15 050 European Prospective Investigation into Cancer and Nutrition-Norfolk participants. We then assessed the proportion of participants who, based on these PRSs, were unlikely to benefit from Lp(a) or ApoB measurements, according to current lipid guidelines. Results: In the UK Biobank and European Prospective Investigation into Cancer and Nutrition-Norfolk cohorts, the area under the receiver operating curve for the PRS-predicted Lp(a) and ApoB to identify individuals with elevated Lp(a) and ApoB was at least 0.91 (95% CI, 0.90–0.92) and 0.74 (95% CI, 0.73–0.75), respectively. The Lp(a) PRS and measured Lp(a) showed comparable association with atherosclerotic cardiovascular disease incidence, whereas the ApoB PRS was in general less predictive of atherosclerotic cardiovascular disease risk than measured ApoB. In the context of the European Society of Cardiology/European Atherosclerosis Society lipid guidelines, at a 95% sensitivity to identify individuals with elevated Lp(a) and ApoB levels, at least 54% of Lp(a) and 24% of ApoB testing could be reduced by prescreening with a PRS while maintaining a low false-negative rate. Conclusions: A substantial proportion of suggested testing for elevated Lp(a) and a modest proportion of testing for elevated ApoB could potentially be reduced by prescreening individuals with PRSs.

Genetic variation in apolipoprotein E (APOE) influences Alzheimer's disease (AD) risk. APOE e4 alleles are the strongest genetic risk factor for late onset sporadic AD. The AD risk is dose dependent, as those carrying one APOE e4 allele have a 2–3-fold increased risk, while those carrying two e4 alleles have a 10–15-fold increased risk. Individuals carrying APOE e2 alleles have lower AD risk and those carrying APOE e3 alleles have neutral risk. APOE is a lipoprotein which functions in lipid transport, metabolism, and inflammatory modulation. Isoform specific effects of APOE within the brain include alterations to Aβ, tau, neuroinflammation, and metabolism. Here we review the association of APOE with AD, the APOE isoform specific effects within brain and periphery, and potential therapeutics.

Low Density Lipoprotein (LDL) cholesterol is a lipoprotein compound that has low-density. Smoking activity can increase LDL cholesterol levels. The nicotine compound in cigarettes can increase the oxidation of LDL cholesterol that will cause atherosclerosis. This research used descriptive study. The purposed of this study was to known about the level of LDL cholesterol in active smoker serum at areas Banjar Taman, Darmasaba Village, Abiansemal, Badung. Sampels in this research are males active smoker aged 18 years old and over which amount to 30 sampels. That sampling using accidental sampling. Examination of LDL cholesterol using Calculated method. The result of LDL concentration on this research based on the characteristics of the respondens such as: normal concentration of LDL on the group of 18-40 years (60%), with time period of smoked less than 5 years (53.4%) and the light smokers category (36 , 7%). Concentration of LDL exceeded the normal limits found on the group of 18-40 years (23.3%), smoked with 6 until 10 years period have 16.7% and category of light smokers (26.7 %). The conclusion of this research , were: 66.7% have normal levels and 33.3% with over normal limits. Active smokers were expected to reduce or stop smoked habits for the better health quality.

Objective— Lp(a) [lipoprotein(a)] levels vary by race/ethnicity and were recently found to be associated with risk of heart failure (HF). We aimed to determine whether Lp(a)-related risk of HF is similar across different races and whether Lp(a) may further be related to HF with reduced ejection fraction or HF with preserved ejection fraction (HFpEF). Approach and Results— In 6809 participants of the MESA (Multi-Ethnic Study of Atherosclerosis), aged 45 to 84 years and free of cardiovascular disease, 308 incident HF events occurred during a median 13-year follow-up. Baseline Lp(a) concentrations were determined by immunoassay. Incident HF was adjudicated, distinguishing HF with reduced ejection fraction (ejection fraction, P =0.02); Lp(a) ≥30 mg/dL (HR, 1.69; P =0.01), Lp(a) ≥50 mg/dL (HR, 1.87; P =0.006). No significant relations were found in black, Hispanic, or Chinese participants, and significant race interactions were observed. Lp(a) was additionally related to greater risk of HFpEF in white participants: per log unit Lp(a) (HR, 1.48; P =0.001), Lp(a) ≥30 mg/dL (HR, 2.15; P =0.01), Lp(a) ≥50 mg/dL (HR, 2.60; P =0.004). Lp(a)-related risk of HF and HFpEF in whites was independent of aortic valve disease. Conclusions— In a multiethnic sample, Lp(a)-related risks of HF and HFpEF were only evident in white participants. If confirmed, these findings have implications in further Lp(a) research and clinical practice.

Lipoprotein (a) [Lp(a)] is a lipoprotein defined by presenting a specific apolipoprotein, ApoA, linked to the ApoB-100 by different types of chemical bonds, including a disulfide bridge. Despite their atherogenic mechanism is not fully understood, its importance has been demonstrated in the development of premature aterosclerosis. Multiple studies have shown its role as a cardiovascular risk factor associated with heart disease and stroke. We report the case of a patient with a diagnosis of Takayasu arteritis in which a massive elevation of Lp(a) was detected. We emphasize its diagnostic and therapeutic implications.

Lipoprotein apheresis involves the extracorporeal removal of low-density lipoprotein cholesterol and other atherogenic lipoproteins from the blood. It is a lifesaving treatment for patients with very high low-density lipoprotein levels which cannot be sufficiently lowered by lipid-lowering drugs and diet. However, it is an invasive, repetitive and chronic treatment under taken at fortnightly intervals on an outpatient basis, meaning that patients need considerable commitment to undertake the treatment. The Lipoprotein Apheresis Unit at University Hospital Llandough is one of only eight centres in the UK, and has undertaken patient research to evaluate the service, so that changes can be implemented to ensure the service meets the needs and expectations of patients. The survey showed that patients consider apheresis treatment to be an important and beneficial part of their health care. The majority of patients (68%) reported that their general health had improved since starting lipoprotein apheresis treatment and the other 32% reported that their general health remained the same.

Background: Lipoprotein particle sizes and concentrations are characteristically altered in patients with insulin resistance (IR) or type 2 diabetes mellitus (T2DM). This study assessed the ability of an IR score, based on nuclear magnetic resonance (NMR)-derived lipoprotein information, to detect IR in otherwise healthy individuals.Lipoprotein subclass and size information were evaluated for strength of association with IR, as measured by homeostasis model assessment of insulin resistance (HOMA-IR) in the Multi-Ethnic Study of Atherosclerosis (MESA). To increase the likelihood of identifying subjects with IR, six lipoprotein measures were combined into a single algorithm. The resulting assay [Lipoprotein Insulin Resistance Index (LP-IR)] was developed using HOMA-IR in 4972 nondiabetic subjects from MESA and verified independently using glucose disposal rates (GDRs) measured during hyperinsulinemic-euglycemic clamps in 56 insulin-sensitive, 46 insulin-resistant, and 46 untreated subjects with T2DM.LP-IR exhibited stronger associations with HOMA-IR (r=0.51) and GDR (r=-0.53) than each of the individual lipoprotein parameters as well as the triglycerides/high-density lipoprotein cholesterol (TGs/HDL-C) ratio (r=0.41 and -0.44, respectively). In MESA, associations between the LP-IR score and HOMA-IR were strong in men (r=0.51), women (r=0.52), European Americans (r=0.58), African Americans (r=0.48), Chinese Americans (r=0.49), and Hispanic Americans (r=0.45). When LP-IR was categorized by HOMA-IR and either body mass index (BMI) or fasting plasma glucose (FPG), subgroups were revealed whose LP-IR scores were high (≥ 50), despite having normal BMIs (24 kg/m(2)) or FPG (100 mg/dL).LP-IR scores had strong associations with multiple measures, HOMA-IR, and GDR, the former being more reflective of hepatic and the latter of peripheral insulin sensitivity, and may represent a simple means to identify individuals with IR.

In high-risk patients who are already on a maximal lipid-lowering therapy, a lipoprotein apheresis is an important therapeutic option in preventing further progress of vascular complications as it may decrease both LDL-cholesterol (LDL-C) and lipoprotein(a) (Lp(a)) levels. We looked at the occurrence of cardiovascular events before apheresis and during apheresis in three groups defined by their lipid patterns at the start of an apheresis treatment: Group 1 (LDL-C ≥ 3.4 mmol/l and Lp(a) ≤ 600 mg/l; n = 35), Group 2 (LDL-C ≤ 3.4 mmol/l and Lp(a) ≥ 600 mg/l n = 37) and Group 3 (LDL-C ≥ 3.4 mmol/l and Lp(a) ≥ 600 mg/l; n = 15). Group 2 shows a time period of about 10 years from the first event until the start of apheresis treatment (compared to 2–6 years in the other two groups). Before the start of apheresis treatment 2.1 events per patient had occurred in Group 1, 3.4 events per patient in Group 2 and 1.8 events per patient in Group 3. Under apheresis therapy just 0.9 events per patient occurred in Group 1, 0.5 in Group 2 and 0.5 in Group 3. When comparing the two years before the start of apheresis treatment with the first two years under apheresis we saw the following reduction rates of cardiovascular events: Group 1–54%; Group 2–83%; Group 3–83.5%. Our results show that the reduction of cardiovascular events due to lipoprotein apheresis is especially high in patients with elevated levels of Lp(a) compared to patients with elevated LDL-C only indicating that physicians should be more focused on the risk factor elevated Lp(a).

A very strong association between phenotype Lp(a +) and presence of pre-β1-lipoprotein has been observed in two series of healthy young adults. The data are in agreement with the view that pre-β1-lipoprotein is identical to the lipoprotein carrying the Lp(a) antigen: the Lp(a) lipoprotein. Lp(a) antigen/pre-β1-lipoprotein occurred more frequently in persons with a positive than with a negative family history of coronary heart disease, though this trend was not statistically significant. Occurrence of Lp(a) antigen/pre-β1-rlipoprotein was not correlated with smoking or with the use of contraceptive pills.

Previous studies have shown that a slow-moving pre-beta-lipoprotein fraction, named the pre-beta1-lipoprotein, occurred significantly more frequently among subjects with coronary heart disease (CHD) than among healthy individuals. This lipoprotein is closely related to, and probably identical with, the Lp(a) lipoprotein. Immunological tests likewise showed that Lp(a) lipoprotein was significantly more common among patients with CHD than among controls. Mean cholesterol and triglyceride levels were higher in pre-beta1-lipoprotein positive than in pre-beta1-lipoprotein negative individuals. Lp(a+) individuals tended to have higher serum cholesterol values than did Lp(a-) persons but there was no difference in the mean triglyceride value. This apparent discrepancy seems to be due to the presence in occasional sera of lipoprotein fractions with pre-beta1-mobility, usually of a VLDL nature. These lipoproteins are not associated with the Lp(a) lipoprotein.

A small number of recent studies have reportedly failed to detect the well-established association between a high Lp(a) lipoprotein level and coronary heart disease (CHD). This has made some workers question the importance of a high Lp(a) lipoprotein level as a CHD risk factor. However, serious problems with some of the commercially available test kits, inadequate test techniques or failure to consider the lability of the Lp(a) lipoprotein particle are more plausible explanations of the confounding results. The problems with some of the commercially available test kits include lack of standardization and validation; risk of cross-reactivity with plasminogen or other serum proteins; failure to consider potential problems when measuring samples with varying length of the Lp(a) polypeptide chain (i.e. failure to cope with the isoform variation); non-divulgence of contents of test reagents; and pretreatments of samples that drastically change the Lp(a) lipoprotein particles from their native state. Any test system should be validated at the scientific level before it is assumed to provide correct measurements of Lp(a) lipoprotein level in serum. New test kits should be safely anchored in validation in one of the research laboratories active in the area, before they are put on the market. As new batches are produced, the quality of every new batch of test kits should be monitored on a long-term basis in collaboration with a research laboratory.

To the Editor: Previous reports have demonstrated that lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzymatic inflammatory biomarker, is associated with increased risk of cardiovascular events [(1)][1]. Lp-PLA2 mediates formation of bioactive mediators (lysophosphatidyl choline and

Polyunsaturated fatty acids (PUFAs) are critical to nervous system function and structure, but their rates of incorporation from plasma into brain have not been evaluated. In the adult rat, calculations based on our model show that at least 3;-5% of esterified brain arachidonic acid (AA) and 2;-8% of esterified brain docosahexaenoic acid (DHA) are replaced daily by unesterified PUFAs in plasma. These rates, when related to unlabeled brain PUFA composition, give half-lives of 1-2 weeks for plasma-brain exchange of AA and DHA. In the human brain, the arachidonate replacement rate is 0.3% per day. Although unesterified plasma PUFA concentrations are low, their rates of incorporation into brain are sufficient to compensate for metabolic and efflux losses, so that PUFA transport from plasma into brain as a component of a lipoprotein is unnecessary. Dietary supplementation, by altering plasma unesterified PUFA concentrations, can regulate brain PUFA content and may help to treat brain diseases involving PUFA imbalance.

Summary The genetically determined Lp(a) lipoprotein whose specific apoprotein evolved from plasminogen exhibits association with atherosclerotic/thrombotic diseases including coronary heart disease (CHD). People with an Lp(a) lipoprotein concentration corresponding to the top quartile in the healthy population have a significantly increased CHD risk compared with those with a lower value, and the risk in the top decile appears to be particularly high. However, a very low Lp(a) lipoprotein level may also cause disadvantage with respect to CHD and longevity. Lp(a) lipoprotein may compromise thrombolytic processes through molecular mimicry and in vitro it stimulates vascular cells to cell division. The normal function of Lp(a) lipoprotein is unknown. It could be related to repair processes. Preliminary evidence suggests that Lp(a) lipoprotein may be involved in vascular processes in the placenta. It has been reported that Lp(a) lipoprotein increases following myocardial infarction in a way suggesting that it could possess characteristics of an acute phase reactant. In view of the strikingly high heritability of Lp(a) lipoprotein, this would a priori be unlikely. We have not been able to confirm a significant increase in Lp(a) lipoprotein following myocardial infarction. Several commercially available test kits are of a doudtful quality. At present, a highly needed, international effort at standardizing Lp(a) lipoprotein measurements is taking place.

High density lipoprotein (HDL) is a lipoprotein containing apo A-1, associated with other apolipoproteins. One of the HDL functions is as the reversed transporter of cholesterol in order to reduce cholesterol level in peripheral tissues. Low HDL cholesterol level is often related to obesity. High cholesterol level, obesity, and low HDL level are known as risk factors of coronary heart diseases. Overweight subjects have higher probabality for suffering from heart diseases and stroke. This study aimed to elaborate high density lipoprotein (HDL) levels in males aged 40-59 years with body mass index higher than 23 kg/m2. This study used consecutive sampling method. Total subjects involved in this study were 20 males who lived in Malalayang. The results showed that there were 11 subjects with normal HDL levels and nine subjects (45%) with low HDL levels (60 mg/dL). Terdapat 19 subjek (95%) dengan obesitas dan hanya satu subjek (5%) yang mengalami overweight. Simpulan: Sebagian besar laki-laki berusia 40-59 tahun yang berdomisili di Kecamatan Malalayang Manado dengan indeks massa tubuh ≥23 kg/m2 mempunyai kadar HDL normal. Kata kunci: laki-laki, high density lipoprotein, indeks massa tubuh

We administered testosterone, with or without the aromatase inhibitor testolactone, to determine the effects of testosterone and its aromatization to estradiol on Lp(a) levels in normal men. Average Lp (a) values decreased by 37% during testosterone alone and by 28% when testosterone and testolactone were combined, suggesting that testosterone reduces Lp(a) in men primarily by an androgenic effect and not by its conversion to estradiol.

Two hundred and ninety four pairs of Swedish twins reared apart and twins reared together were used to evaluate the importance of genetic and environmental influences on lipoprotein(a) (Lp(a)) levels. Lp(a) levels ranged from10 mg/l to 926 mg/l with 7.9% of the sample having undetectable Lp(a) levels (i.e.10 mg/l). A substantial genetic component in Lp(a) variation was indicated by a heritability estimate of approximately 90%. No difference in heritability was found across age groups. Quantitative genetic analyses also suggest correlated environmental effects most likely composed of maternal, neonatal and postnatal environmental influences. However, these effects did not reach statistical significance, partly due to a lack of power. Results from analyses of co-twin differences in Lp(a) levels for monozygotic twins indicate that sex hormone use may be of importance for Lp(a) variation in women. There was no evidence of potential influences of alcohol consumption, beta-blocker and diuretic administration on Lp(a) levels in either men or women.

In order to evaluate whether Lp(a), a lipoprotein that is potentially thrombogenic and atherogenic, is a potential risk factor for CAD in non-insulin-dependent diabetes (NIDDM), we compared the Lp(a) and its distribution in 145 NIDDM patients with that in 94 healthy control subjects. Furthermore, we studied the effect of insulin treatment on serum Lp(a) in 108 patients with NIDDM. Male and female NIDDM patients had similar Lp(a) concentrations to healthy controls (median value 167 mg L-1, range 15-1550 mg L-1 vs. 157 mg L-1, range 15-919 mg L-1, NS and 92, range 15-1190 mg L-1 vs. 103 mg L-1, range 15-842 mg L-1, NS). Also, the cumulative distribution of Lp(a) did not differ between the NIDDM patients and healthy subjects. Insulin treatment increased Lp(a) in diabetics with a Lp(a) concentration of less than 300 mg L-1, but this effect was not related to the concomitant improvement in metabolic control (mean change (+/- SEM) of HbA1c from 9.80 +/- 0.15 to 8.00 +/- 0.12; P0.001). In subjects with elevated Lp(a) concentrations (300 mg L-1) the Lp(a) concentration was unaffected by insulin, despite a similar improvement in glycaemic control. These results suggest that insulin may modulate the concentration of Lp(a).

The serum levels of Lp(a) lipoprotein (Lp(a)) were determined preoperatively in 601 patients with coronary artery disease, undergoing bypass operations. Compared with a reference group of 99 apparently healthy individuals, the Lp(a) levels were higher in the patient group (7.7 mg dl-1 vs. 5.1 mg dl-1, p = 0.012). In the patient group, there was a weak, but significant negative correlation between the Lp(a) levels and age (r = -0.10, p = 0.017), and in both groups the women had higher Lp(a) levels than the men. In the patients we found no significant correlations between Lp(a) and other serum lipids or lipoproteins, nor between Lp(a) and variables in the fibrinolytic system. We investigated the long-term effects of supplementation with n-3 polyunsaturated fatty acids (n-3 PUFAs) on the Lp(a) concentrations. Postoperatively, in a randomized fashion, 280 of the patients received 4 g of an n-3 PUFA concentrate (containing85% of long-chain n-3 PUFAs) per day, whereas 269 patients comprised the control group. The fatty acids in serum phospholipids were monitored, and a significant increase in the phospholipid n-3 fatty acids was noted in the n-3 PUFA group, as opposed to the virtually unchanged amounts in the control group. The Lp(a) levels were determined again after 6 months, and, compared with the control group, n-3 PUFA supplementation had no overall effect on the serum Lp(a) levels.

Gender-related and depot-specific differences exist in the expansion of the adipose tissue mass. The distribution of body fat, has important implications for metabolic health. Obese individuals with an upper body fat distribution have increased health complications and risks of cardiovascular diseases. Functional differences between fat depots may explain their differential involvement in metabolic obesity-related complications. The peculiarities of these adipose tissues are exposed. We will retain the following major differences.The visceral fat cells are smaller than the subcutaneous fat cells and are characterized by an increased lipolytic capacity. The visceral fat is also characterized by a lipoprotein lipase activity lower than that of the subcutaneous fat. By contrast, the subcutaneous fat cells have an enhanced capacity of fat uptake than the visceral fat cells. The non-esterified fatty acids and the adipokines (IL-6 in particular) stemming from visceral fat play an important role in the induction of liver insulin resistance. Finally, an innovative aspect of adipose tissue biology is the discovery of its infiltration by a number of immune cells in obese subjects. Infiltrating macrophages and lymphocytes are higher in visceral adipose than in the abdominal subcutaneous depots of obese subjects.

血液透析患者のLp(a) リポタンパク (Lp(a)) は高値であることが知られており, Lp(a) のプラスミノーゲンとの構造的相同性から, 血液凝固・線溶系に対する影響が示唆されている. しかし透析患者における凝固・線溶系とLp(a) との関連性についての報告はほとんどみられない.我々は人間ドック受診コントロール群 (C群, n=40), 慢性糸球体腎炎による透析導入患者 (A1群, n=25), 糖尿病性腎症による透析導入患者 (A2群, n=15), さらに血液透析歴10年以上の維持透析患者 (B群, n=21) のそれぞれにおける血清Lp(a) および凝固・線溶系因子を測定し, その関連性について検討を加えた.C群に比較してLp(a) はA1群 (p

慢性血液透析 (HD) 患者の脂質代謝異常が動脈硬化症の進展に関与していることが報告されているが, 持続性自己管理腹膜透析 (CAPD) 患老ではHD患者の脂質代謝異常の特徴である高中性脂肪 (TG) 血症, 低HDL-コレステロール (HDL-C) 血症に透析膜によるブドウ糖の負荷と透析膜としての腹膜の特性が加味された病態が予想される.本研究ではIgA腎症, HD患者を対照にCAPD患者の脂質代謝異常について検討した. また高脂血症, 血栓症, 動脈硬化症との関係から注目されているLp(a) についても検討し, 以下の結論が得られた.CAPD患者では, IgA腎症, HD患者に比較して総コレステロール (TC), TG, LDL-コレステロール (LDL-C), 動脈硬化指数, アポリポタンパクB (Apo B), Apo B/A-Iが高く, HDL-CはHD患者と同様に低値を示した. またCAPD患者のLp(a) は高値を示し, 血清アルブミンと逆相関を認めたことから, 肝での合成亢進による可能性が考慮されるが, その機序の詳細は不明である. なおペルサンチン負荷心筋タリウムシンチグラムで心筋虚血が認められたCAPD患者のLp(a) は認められなかった患者に比較して高値を示さなかった.以上よりCAPD患者はIgA腎症, HD患者に比較して脂質代謝の面より動脈硬化促進的であることが示唆された.

In a 3-year follow-up study of 761 elderly men and 983 elderly women, total plasma cholesterol levels predicted fatal coronary heart disease (CHD) in men but not women. Low-density lipoprotein level was no better a predictor of fatal CHD than total cholesterol in either sex. Women had higher levels of high-density lipoprotein than men, which explains most of their usual higher total cholesterol levels. These data suggest that cholesterol screening of elderly women would have little value without a lipoprotein evaluation.

Serum lipoprotein(a) [Lp(a)] was determined in 205 patients (71 ± 10 years; mean age ± SD) with acute stroke and in 204 nonhospitalized referent subjects in the 60- to 80-year age range. Lp(a) levels

Purpose Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis. Materials and Methods Studies were performed in male Sprague-Dawley rats. The atherosclerosis rats were prepared by feeding them with a high-cholesterol diet for 10 weeks. Low-dose darapladib (25 mg·kg-1·d-1) and high-dose darapladib (50 mg·kg-1·d-1) interventions were then administered over the course of 2 weeks. Results The serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP), and Lp-PLA2, significantly increased in atherosclerosis model groups, as did Rho kinase activity and cardiomyocyte apoptosis (p0.05). Conclusion Darapladib, a Lp-PLA2 inhibitor, leads to cardiovascular protection that might be mediated by its inhibition of both Rho kinase and Lp-PLA2 in atherosclerosis.

Objective to evaluate the association between Lp(a) lipoprotein levels, other serum lipids and the presence of lower limb atherosclerotic occlusive disease. Materials and methods angiographic findings in 36 patients were related to serum Lp(a). Total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol and Lp(a) levels were compared with those of 73 age- and sex-matched healthy controls. Results atheromatous lesions were localised in the femoropopliteal (≈60%) and aortoiliac (≈40%) segments. The number of stenosed arteries was ≥2 and the range of stenosis severity was between 40% and 100%. There was a significant increase in serum Lp(a) ( p = 0.000001) and a decrease in serum HDL ( p = 0.000009) levels in patients compared to controls. No difference was observed in total cholesterol, LDL-cholesterol or triglyceride. However, the ratio of total cholesterol/HDL-cholesterol was significantly higher ( p = 0.005) in patients. Conclusion a dyslipidaemic serum profile, characterised by increased Lp(a) levels and decreased HDL-cholesterol levels, is associated with atherosclerotic occlusive disease of the lower extremities.

This is the fourth year of competition for ATVB New Investigator Awards. The Awards recognize articles published in ATVB in 2008 that were submitted by new investigators and judged to be the most outstanding in the Atherosclerosis and Lipoproteins, Thrombosis, and Vascular Biology sections of the journal. The three awards are named for Dr Daniel Steinberg, who devised a method to determine the site of degradation of the proteins and lipids of a lipoprotein, …

This is the eighth year of competition for Atherosclerosis/Lipoprotein, Thrombosis, and Vascular Biology (ATVB) Early Career Awards. The awards recognize articles published in ATVB in 2012 that were submitted by new investigators and judged to be the most outstanding in the ATVB sections of the journal. The 3 awards are named for Dr Daniel Steinberg, who devised a method to determine the site of degradation of the proteins and lipids of a lipoprotein, which led to …

We undertook the present study to evaluate the lipid profile in 82 (51 male, 31 female) Greek individuals with heterozygous familial hypercholesterolemia (FH), aged 13-61 years from 22 families. FH heterozygotes had significantly elevated serum Lp(a) levels in comparison with 82 normal controls. Serum Lp(a) levels were also increased in FH probands compared to their controls. Additionally, serum Lp(a) concentration was elevated in the FH heterozygotes compared to their unaffected first degree relatives.

Summary: Several studies indicate the relevance of lipoprotein(a ) (Lp(a)) in the genesis of premature coronary artery disease. A simple method for determining the concentration of Lp(a) is therefore of great interest for assessing the risk of coronary artery disease in patients. We compared a new latex-enhanced immunonephelometric assay (Behringwerke AG, Marburg, Germany), using the Behring Nephelometer System 100, with an established immunoenzymometric assay (Immuno, Heidelberg, Germany). A total of 163 patients was studied. Intra- and inter-assay coefficients of variation were between 2.2% and 7.1%, and between 3.4% and 8.6%, depending on the concentration of Lp(a). The correlation between the studied assays was excellent (r = 0.93, y = 0.98x -1.57, Spearman rank, Passing & Bablok). When values above 1000 mg/1 for Lp(a) were excluded, the correlation was even higher. Increased light scattering with particle size, which hitherto has been a disadvantage of the nephelometric technique, seems to be negligible using the improved latex-enhanced approach. In patients with triacylglycerol values above 4.5 mmol/1 (n = 19) there was no interference with the Behring system, i. e. the results of the nephelometric method were not increasing, and they agreed with those of the immunoenzymometric assay. In conclusion, this new latexenhanced nephelometric immunoassay represents a rapid and precise method for the quantification of Lp(a).

In persons who are fasting, lipids circulate in the plasma as constituents of lipoprotein particles that are defined on the basis of their density as very-low-, intermediate-, low-, and high-densit...

As part of a longitudinal study--the Kristianstad Survey--we measured plasma cholesterol, HDL- and LDL-cholesterol, triglycerides and lipoprotein (a) in a reference group consisting of 203 men and women aged 20-80, randomly sampled from a well-defined area in the southernmost part of Sweden. The selection of reference individuals and the collection of specimens for assay of the constituents were performed in accordance with current recommendations. The results were subjected to statistical analyses both with and without application of exclusion criteria. Application of the theoretical exclusion criteria resulted in the exclusion of 22% of the participants; however, this procedure had a remarkably weak impact on the results: the mean values and the standard deviations were almost unaltered. The mean (standard deviation) for cholesterol was 5.9 (1.3) mmol l-1, for HDL-C 1.1 (0.3) mmol l-1, and for LDL-C 4.3 (1.2) mmol l-1. Women had higher values than men. Plasma triglycerides were positively skewed; their median and Q3-Q1-values were 1.0 and 0.5 mmol l-1 respectively, men higher than women. There was an increase with age for cholesterol and LDL-C in both sexes and for triglycerides in women. The steepest increase of cholesterol values with age in women coincided with menopause, which have a more clear-cut separation between high and low cholesterol values than did any age limit.

1. The atherosclerotic process begins in childhood and is influenced by genetics, diet, and lifestyle. Abnormal cholesterol levels are not uncommon in children. 2. The NIH Expert Panel on Blood Cholesterol Levels in Children and Adolescents recommends heart healthy eating for all children over the age of 2 years. This eating pattern is nutritionally adequate and lowers amounts of saturated fatty acids and total fat in the diet. 3. Children with a family history of premature coronary heart disease or elevated cholesterol levels should have a lipoprotein analysis to assess for abnormal levels. 4. The occupational health nurse has an important role in assisting families in which parents and children have lipid disorders.

The Lp(a) lipoprotein, a distinct class of serum lipoproteins, was detected in 1962. It consists of an LDL particle to which a long polypeptide chain is attached by a disulfide bridge. The level of Lp(a) lipoprotein is genetically determined. Single locus control was suggested already in the very first report, and this has been conclusively confirmed by the demonstration of absolute genetic linkage to the plasminogen gene, from which the LPA gene is likely to have evolved. The detection in 1974 of an association between Lp(a) lipoprotein and coronary heart disease has been confirmed in numerous studies. The Lp(a) lipoprotein may have atherogenic as well as thrombogenic properties and thus form the bridge between atherogenesis and thrombogenesis. Genes determining a moderate level of Lp(a) lipoprotein may be longevity genes, and it seems possible that Lp(a) lipoprotein, because of its affinity to vessel walls, may also influence placental function. Lp(a) lipoprotein measurements should be included in the diagnostic work-up of people with premature coronary heart disease or with such disease in close relatives.

The Lp(a) lipoprotein1 is a distinct class of serum lipoprotein particles which was detected because of its immunological properties. It consists of a low density lipoprotein (LDL) particle to which a long polypeptide chain has been attached (the Lp(a) polypeptide chain, the Lp(a) apolipoprotein or apolipoprotein(a)). It is the Lp(a) polypeptide chain that confers the unique antigenic properties to the Lp(a) lipoprotein particle.

SUMMARY The interest in Lp(a) lipoprotein [Lp(a)] has increased dramatically during the last few years due to the documented strong association between high Lp(a) levels and early atherosclerosis and its sequelae and the probable additional thrombogenic effect of inherited high Lp(a) levels. However, some paradoxes still remain to be solved in Lp(a) research. This pilot study was performed to test whether some criteria could be found for an association between Lp(a) levels, HLA genotype, and early coronary heart disease. If so, it could help to explain why some individuals with high Lp(a) levels get atherosclerosis while others with comparable lipid levels do not. It would also indicate that immunological processes could be involved in Lp(a) associated atherosclerosis. In this case-control study the HLA-DR genotypes 13 or 17 were significantly more frequently encountered in 30 male patients with early coronary heart disease than in 30 sex and age matched healthy controls (P = 0.012). These HLA-DR specificities were especially frequent in male patients with high Lp(a) levels. The same HLA-DR genotype pattern was not seen in 30 female patients, although there was a trend towards more frequent 13a genotype.

Lipoprotein(a), or Lp(a), is a lipoprotein having lipid composition similar to that of LDL, but a protein moiety consisting of ApoB 100 linked by disulfide bridge to apo(a), a glycoprotein with structural similarity to plasminogen. Lp(a) can be both atherogenic and thrombogenic. These two actions are likely to be mutually operative, a fact that on a molar basis makes Lp(a) more of a cardiovascular pathogen than LDL.