对血浆Lp(a)致动脉硬化作用的再评价-9540正常人群及4055病例对照结果分析

目的 观察中国正常人群血浆Lp（a）的分布情况及特点，分析血浆Lp（a）水平的变化与心脑血管疾病危险性的关系，进一步证实血浆Lp（a）致动脉硬化的作用。方法 采用ELISA的方法检测了9540正常人群的血浆Lp（a），分析了年龄、性别与L（a）水平之间的关系。检测了530例心肌梗死患者（冠脉造影证实）及229例对照（冠脉造影阴性）和1386例脑梗死患者（头颅CT或核磁共振检查证实）及1910例对照的血浆Lp（a），分析了血浆Lp（a）变化与疾病危险性的关系。结果 （1）正常人群血浆Lp（a）呈偏态分布（P〈0．01），中位数为19．6mg／dl，全距为209．7mg／dl。不同年龄、性别血浆Lp（a）水平分布情况，除大于50岁的女性以外，其余各组之间比较均无显著性差异。正常人的Lp（a）水平主要分布在11～20mg／dl的范围；（2）疾病组血浆Lp（a）水平明显高于对照组（P〈0．001），Lp（a）〉30mg/dl者，心肌梗死组占43．4％，脑梗死组占68．5％，与对照组比较有显著性差异（P〈0．001），且随着Lp（a）浓度升高，心脑血管疾病的危险性有上升的趋势；（3）Logistic回归分析结果显示：Lp（a）〉30％者发生心肌梗死的危险性增加（OR值为2．2，95％CI：1．498—3．167，P〈0．001）和脑梗死的危险性增加（OR值为2．1，95％CI：1．767～2．489，P〈0．001）。结论 Lp（a）与动脉硬化密切相关，随着浓度升高，心脑血管疾病的危险性增加，它是一个独立的危险因子。     

血清脂蛋白a、高密度脂蛋白水平与进展性脑梗死的关系

目的探讨血清脂蛋白a[Lp（a）]、高密度脂蛋白（HDL）水平与进展性脑梗死的关系。方法选择发病3d内缺血性脑卒中患者404例,其中急性完全性脑梗死350例（A组）,进展性脑梗死54例（B组）,另选65例体检健康者作为对照组,检测3组血清Lp（a）、血脂、空腹血糖、血尿酸、纤维蛋白原,分析血清Lp（a）、HDL与进展性脑梗死的相关性。结果与A组比较,B组Lp（a）升高,HDL降低（P均〈0．01）。Logistic回归分析显示,高Lp（a）、低HDL对进展性脑梗死的OR分别为4．336、3．427,95％C1分别为2．037～9．230、1．657～7．089（P均〈0．01）。结论高Lp（a）、低HDL是进展性脑梗死重要的危险因素。     

尼麦角林治疗糖尿病性脑梗死43例

糖尿病性脑梗死患者共86例，随机分为治疗组、对照组各43例。治疗组给予尼麦角林注射液8mg加入生理盐水250ml静脉滴注，每日1次，疗程20天；对照组给予维脑路通注射液400mg。结果：治疗组总有效率显著优于对照组（P〈0．01）；神经功能缺损和日常生活能力评分优于治疗前（P〈0．01）和对照组（P〈0．05）；全血和血浆粘度、红细胞刚性指数、红细胞聚集指数和血浆比粘度的变化也优于治疗前（P〈0．01）及对照组（P〈0．05）。结论：尼麦角林治疗糖尿病性脑梗死安全有效。     

纳洛酮治疗急性脑梗死患者血浆内皮素含量变化及其临床意义

目的探讨纳洛酮治疗急性脑梗死患者血浆内皮素含量变化及其临床意义。方法观察41例纳洛酮治疗急性脑梗死患者血浆内皮素含量在入院24h内，治疗后3d，8d及2周的变化，并且以40例急性脑梗死患者按常规治疗作对照组。结果急性脑梗死患者24小时内两组患者血浆内皮素较正常人均明显升高（p〈0．01）；第3d，第8d两组患者血浆内皮素较治疗前均明显下降（p〈0．05）；但纳洛酮组比常规治疗组血浆内皮素下降更快（p〈0．05）；两周后两组患者血浆内皮素基本恢复到正常水平。结论急性脑梗死患者血浆内皮素水平均升高，与病情轻重及病情进展相关，纳洛酮治疗较常规治疗能更迅速地降低血浆内皮素水平。     

血清脂蛋白(a)与冠脉病变程度及心肌梗死的关系

目的研究血清脂蛋白（a）[Lp（a）]浓度与冠心病患者冠脉病变程度及心肌梗死发生的关系。方法选取行冠脉造影检查者384例作为研究对象,根据冠脉病变支数分为正常对照组、单支病变组、双支病变组、三支病变组,根据诊断分为正常对照组、心绞痛组、心肌梗死组,比较各组血清Lp（a）浓度。结果单支病变组、双支病变组、三支病变组的血清Lp（a）浓度均显著高于对照组（P〈0．05,〈0．01）,但三组内比较差异没有统计学意义。心绞痛组、心肌梗死组血清Lp（a）浓度亦均显著高于对照组（P〈0．01）,心绞痛组和心肌梗死组相比差异亦有统计学意义（P〈0．01）。Lp（a）与冠脉病变Gensini积分明显相关（偏相关系数r=0．143,P〈0．01）。结论血清Lp（a）浓度与冠心病冠状动脉病变程度成正相关,且与心肌梗死的发生密切相关。     

糖尿病视网膜病变血小板5-HT及血浆NO、ET的变化

选择40例DR患者，35例2型糖尿病患者和42例正常人做对照组，测定的血小板5-HT、血浆NO、血浆ET水平。结果：血小板5-HTDR组低于糖尿病组（P〈0．05）及对照组（P〈0．01），糖尿病组低于正常对照组（P〈005），血浆NO水平DR组低于糖尿病组（P〈0．05）和对照组（P〈0．01），糖尿病组低于健康对照（P〈0．05）而ET水平DR组高于糖尿病组（P〈0．05）和对照组（P〈0．01），糖尿病组高于对照组（P〈0．05）。结论：DR血小板释放5-HT异常增多，血浆NO水平的降低，ET水平的升高，参与了糖尿病视网膜病变的发生发展。     

奥扎格雷对急性脑梗死患者血浆溶血磷脂酸(LPA)水平的影响

目的探讨急性脑梗死患者血浆溶血磷脂酸（LPA）水平变化，奥扎格雷对急性脑梗死患者血浆LPA水平的影响。方法84例急性脑梗死患者，随机分为2组：奥扎格雷组（44例）、阿斯匹林组（40例），奥扎格雷组给予奥扎格雷静点，阿斯匹林组给予阿斯匹林口服。两组在发病24h、1w及2w时定测定血浆LPA含量。年龄相匹配的75名健康体检者作为对照组，测定血浆LPA含量。结果脑梗死患者血浆LPA水平明显高于对照组。奥扎格雷组血浆LPA水平下降较阿斯匹林组更明显，差异有显著性（P（0．01）。结论急性脑梗死患者血浆LPA水平明显升高，奥扎格雷可降低急性脑梗死血浆LPA水平，效果优于阿斯匹林。     

急性脑梗死患者血浆脑钠肽与内皮素的关系

目的：观察急性脑梗死患者血浆脑钠肽（BNP）和内皮素（ET）水平的变化,探讨其在缺血性脑血管病发生发展及早期评估病情中的意义。方法：根据脑梗死临床神经功能缺损程度评分,将59例急性脑梗死患者分为轻型组（0～20分）36例,中型组（20～30分）14例,重型组（30～45分）9例。测定各组患者入院时、治疗第5天和第10天血浆BNP、ET水平,并与40例健康者作比较。结果：急性脑梗死患者血浆BNP、ET水平较对照组明显升高（均P〈0．01）;重型脑梗死组血浆BNP、ET水平明显高于轻、中型组（均P〈0．01）;入院时急性脑梗死组血浆BNP、ET水平开始升高,治疗第5天达高峰,治疗10d后明显下降。结论：BNP和ET参与了脑梗死的病理生理过程,其含量变化与病情严重程度呈正相关性,可作为早期判断脑梗死严重程度的指标之一。     

急性脑梗死患者血浆溶血磷脂酸变化的临床意义

用定磷法测定急性脑梗死患者（脑梗死组）发病24h内，第3、7、14、21天及健康对照组的血浆溶血磷脂酸（LPA）水平，Barthel指数（BI值），评价预后。结果脑梗死组血浆LPA水平发病24h内显著高于对照组（P〈0．01），随发病时间延长呈下降趋势，于第14天恢复至正常水平；发病24h内血浆LPA水平与BI指数呈显著负相关（r=0．607，P〈0．01）。提示血浆LPA水平与急性脑梗死患者预后密切相关。     

脂蛋白（a）、超敏C反应蛋白与2型糖尿病患者脉搏波传导速度的关系

目的探讨脂蛋白（a）[Lp（a）]、高敏C反应蛋白（hs-CRP）与2型糖尿病（T2DM）患者脉搏波传导速度（baPWV）的相关性。方法将80例T2DM患者按有无心脑血管并发症分为2组,36例无并发症者为对照组,44例合并冠心病和（或）脑血管病等为观察组,分别对2组患者Lp（a）、hs-CRP水平及baPWV进行检测并比较。结果观察组Lp（a）、hs-CRP水平及baPWV均高于对照组（P〈0.01或〈0.05）。Lp（a）、hs-CRP水平与baPWV均呈正相关（r=0.261、0.412,P〈0.05或〈0.01）。结论 T2DM合并心脑血管并发症者Lp（a）、hs-CRP水平及baPWV明显升高,联合检测Lp（a）、hs-CRP水平是预测动脉粥样硬化的敏感指标。     

Plasma resistin levels and risk of myocardial infarction and ischemic stroke

CONTEXT: Resistin is a hormone that has been linked to insulin resistance, inflammatory processes, and coronary heart disease in case-control studies; however, prospective data on the association between plasma resistin levels and future risk of cardiovascular disease are lacking. OBJECTIVE: The objective of the study was to investigate the association between plasma resistin levels and risk of future myocardial infarction (MI) and ischemic stroke (IS) in a large prospective cohort. METHODS: We investigated the association between plasma resistin levels and risk of MI and IS in a case-cohort design among 26,490 middle-aged subjects from the European Investigation into Cancer and Nutrition-Potsdam Study without history of MI or stroke at time of blood draw. Plasma resistin levels were measured in baseline blood samples of 139 individuals who developed MI, 97 who developed IS, and 817 individuals who remained free of cardiovascular events during a mean follow-up of 6 yr. RESULTS: After multivariable adjustment for established cardiovascular risk factors including C-reactive protein, individuals in the highest compared with the lowest quartile of plasma resistin levels had a significantly increased risk of MI (relative risk 2.09; 95% confidence interval 1.01-4.31; P for trend = 0.01). In contrast, plasma resistin levels were not significantly associated with risk of IS (relative risk 0.94; 95% confidence interval 0.51-1.73; P for trend = 0.88). CONCLUSION: Our data suggest that high plasma resistin levels are associated with an increased risk of MI but not with risk of IS. Further studies are needed to evaluate the predictive value of plasma resistin levels for cardiovascular disease.     

Urinary excretion of apolipoprotein(a) fragments in type 1 diabetes mellitus patients

High levels of plasma lipoprotein(a) [Lp(a)] represent an independent risk factor for cardiovascular morbidity; however, Lp(a) has not yet been identified as a risk factor for type 1 diabetic patients. Results from the limited number of available studies on plasma Lp(a) levels in relation to renal function in type 1 diabetes mellitus are inconclusive. We hypothesized that only type 1 diabetes mellitus patients with impaired renal function show increased plasma Lp(a) levels, due to decreased urinary apolipoprotein(a) [apo(a)] excretion. We therefore measured urinary apo(a) levels in 52 type 1 diabetes mellitus patients and 52 matched controls, and related the urinary apo(a) concentration to the plasma Lp(a) level, kidney function, and metabolic control. Our findings indicate that patients with incipient diabetic nephropathy as evidenced by microalbuminuria (20 to 200 microg/min) exhibit significantly higher plasma Lp(a) levels (median, 15.6 mg/dL) in comparison to normoalbuminuric patients (median, 10.3 mg/dL) and healthy controls (median, 12.0 mg/dL). Urinary apo(a) normalized to creatinine excretion was significantly elevated in both normoalbuminuric (median, 22.3 microg/dL) and microalbuminuric type 1 diabetic patients (median, 29.1 microg/dL) compared with healthy subjects (median, 16.0 microg/dL) and correlated significantly with Lp(a) plasma levels in both patient and control groups (P < .003). No correlation existed between the Lp(a) plasma level or urinary apo(a) concentration and metabolic control in type 1 diabetes mellitus patients. From these studies, we conclude that urinary apo(a) excretion is significantly increased in type 1 diabetic patients and correlates with plasma Lp(a) levels, and only type 1 diabetic patients with microalbuminuria have higher plasma levels of Lp(a) compared with patients with normoalbuminuria and healthy controls.     

High VWF, low ADAMTS13, and oral contraceptives increase the risk of ischemic stroke and myocardial infarction in young women

VWF and ADAMTS13 are major determinants of platelet adhesion after vessel injury. In the present study, we aimed to determine whether VWF or ADAMTS13 plasma antigen levels influence the risks of ischemic stroke (IS) or myocardial infarction (MI) in young women and how these risks are affected by oral contraceptive (OC) use. VWF and ADAMTS13 plasma antigen levels were measured in a frequency-matched case-control study of 1018 young (18-49 years) women including 175 IS patients and 205 MI patients. Increasing levels of VWF and decreasing levels of ADAMTS13 were associated with the risk of IS and MI in a dose-dependent manner. Having both high VWF and low ADAMTS13 resulted in an odds ratio (OR) of 6.9 (95% confidence interval [95% CI], 2.0-23.0) for IS and 11.3 (95% CI, 3.6-35.2) for MI. Use of OCs increased the risk of IS and MI associated with high VWF (OR = 12; 95% CI, 5.5-26.2 and OR = 7.5, 95% CI, 3.6-15.7, respectively) and the risk of IS associated with low ADAMTS13 (OR = 5.8, 95% CI, 2.7-12.4). We conclude that high VWF and low ADAMTS13 plasma levels both increase the risk of IS and MI. The risks associated with high VWF or low ADAMTS13 levels are further increased by the use of OCs.     

Plasma lipoprotein (a) levels in Turkish NIDDM patients with and without vascular diabetic complications.

OBJECTIVE: Plasma concentrations of lipoprotein (a) [Lp(a)], an independent risk factor for atherosclerosis, were measured in 59 non-insulin-dependent diabetes mellitus (NIDDM) patients with and without vascular complications, and 21 non-diabetic healthy subjects. RESULTS: The plasma log Lp(a) levels were found to be significantly increased in the NIDDM patients (1.40 +/- 0.36) compared with the healthy subjects (1.02 +/- 0.53; p < 0.05). Plasma Lp(a) levels in NIDDM patients with diabetic vascular complications (1.51 +/- 0.27) were significantly higher than those of the NIDDM patients without diabetic vascular complications (1.23 +/- 0.43) and healthy subjects (p < 0.05). There were significant correlations between plasma log Lp(a) levels and apolipoprotein B (apo B) in all NIDDM patients (r: 0.68, p < 0.05). No correlation was observed between Lp(a) levels and age, sex, duration of diabetes, fasting blood glucose, haemoglobin Alc, the mode of treatment, triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and apolipoprotein Al levels in all patients. CONCLUSIONS: It was concluded that Lp(a) was a risk factor for angiopathy in NIDDM patients and the patients who have a high plasma Lp(a) concentration should be kept under strict glycaemic control.     

Alteration of erythrocyte biophysical properties in patients with ischemic cerebrovascular disorders]

Several erythrocyte biophysical properties (erythrocyte deformability, erythrocyte aggregation and erythrocyte electrophoretic mobility) were investigated in patients with cerebral infarction and in individuals with risk factors of stroke (RFS population; RFSP). Blood viscosity, plasma viscosity, hematocrit, plasma fibrinogen level and yield shear stress (YSS) were also tested. In comparison with the results in a control group, erythrocyte deformability (erythrocyte length under a certain constant shear stress and erythrocyte filterability) was less in both the patient group and the group of RFSP and there is an accompanying increase of erythrocyte aggregation. Blood viscosity and fibrinogen level were higher in the patient groups. There was no correlation between erythrocyte deformability and other hemorheological parameters. Our results suggest that significant alteration of erythrocyte biophysical properties may be implicated in the pathogenesis of ischemic stroke. These abnormalities are associated with some of the risk factors of stroke such as hypertension, atherosclerosis and cardiovascular disorders.     

Associations among serum lipoprotein(a) levels, apolipoprotein(a) phenotypes, and myocardial infarction in patients with extremely low and high levels of serum lipoprotein(a).

A high serum lipoprotein(a) [Lp(a)] level, which is genetically determined by apolipoprotein(a) [apo(a)] size polymorphism, is an independent risk factor for coronary atherosclerosis. However, the associations among Lp(a) levels, apo(a) phenotypes, and myocardial infarction (MI) have not been studied. Patients with MI (cases, n = 101, M/F: 86/15, age: 62+/-10y) and control subjects (n = 92, M/F: 53/39, age: 58+/-14y) were classified into quintile groups (Groups I to V) according to Lp(a) levels. Apo(a) isoform phenotyping was performed by a sensitive, high-resolution technique using sodium dodecyl sulfate-agarose/gradient polyacrylamide gel electrophoresis (3-6%), which identified 26 different apo(a) phenotypes, including a null type. Groups with higher Lp(a) levels (Groups II, III, and V) had higher percentages of MI patients than that with the lowest Lp(a) levels (Group I) (54%, 56%, or 75% vs. 32%, p<0.05). Groups with different Lp(a) levels had different frequency distributions of apo(a) isoprotein phenotypes: Groups II, III, IV, and V, which had increasing Lp(a) levels, had increasingly higher percentages of smaller isoforms (A1-A4, A5-A9) and decreasingly lower percentages of large isoforms (A10-A20, A21-A25) compared to Group I. An apparent inverse relationship existed between Lp(a) and the apo(a) phenotype. Subjects with the highest Lp(a) levels (Group V) had significantly (p<0.05) higher serum levels of total cholesterol, apo B, and Lp(a). Patients with MI and the controls had different distributions of apo(a) phenotypes: i.e., more small isoforms and more large size isoforms, respectively (A1-A4/A5-A9/A10-A20/A21-A25: 35.7%/27.7%/20.8%/15.8% and 22.8%/23.9%/29.4%/23.9%, respectively). Lp(a) (parameter estimate +/- standard error: 0.70+/-0.20, Wald chi2 = 12.4, p = 0.0004), apo(a) phenotype (-0.43+/-0.15, Wald chi2 = 8.17, p = 0.004), High-density lipoprotein-cholesterol, apo A-I, and apo B were significantly associated with MI after adjusting for age, gender, and conventional risk factors, as assessed by a univariate logistic regression analysis. The association between Lp(a) and MI was independent of the apo(a) phenotype, but the association between the apo(a) phenotype and MI was not independent of Lp(a), as assessed by a multivariate logistic regression analysis. This association was not influenced by other MI- or Lp(a)-related lipid variables. These results suggest that apo(a) phenotype contributes to, but does not completely explain, the increased Lp(a) levels in MI. A stepwise logistic regression analysis with and without Lp(a) in the model identified Lp(a) and the apo(a) phenotype as significant predictors for MI, respectively.     

Lack of association between plasma lipoprotein(a) concentrations and the presence or absence of coronary atherosclerosis

BACKGROUND: Findings from previous studies relating lipoprotein(a) [Lp(a)] as an independent risk factor for coronary atherosclerosis and the presence of angiographically detectable coronary atherosclerotic lesions are not consistent. This study was performed to determine whether the plasma concentration of Lp(a) is associated with coronary atherosclerosis asessed by coronary angiography. METHODS: We studied a total of 100 men and women (41 women, 59 men, age 63.7 +/- 11.0 years) who were referred for coronary angiography. Base-line data collection comprised conventional risk factors for coronary artery disease, lipids, fasting total homocysteine, and clinical characteristics. The relation between plasma Lp(a) levels and the presence or absence of coronary lesions was studied. The coronary angiograms were evaluated in a blinded manner. Any coronary stenosis was considered as coronary artery disease (CAD). RESULTS: From the 100 patients, 40 were found to have no CAD and 60 had CAD assessed by coronary angiography. Estimates of the relative risk of coronary heart disease for the fifth quintile of plasma Lp(a) as compared with the first quintile were 0.87 (95 percent confidence interval, 0.66 to 1.34). After adjustment for age, sex, lipoproteins, and homocysteine levels, estimates of the relative risk of coronary heart disease for the fifth quintile of plasma Lp(a) as compared with the first quintile were 1.06 (95 percent confidence interval, 0.81 to 1.39). The presence of angiographic CAD was associated with patient age (p=0.048), male sex (p<0.01), high LDL-cholesterol levels (p=0.02), low HDL-cholesterol levels (p=0.02), high plasma fibrinogen levels (p<0.01) and high fasting total homocysteine levels (p=0.04). CONCLUSION: These results suggest that the plasma concentration of Lp(a) is not associated with the presence of coronary artery disease in patients referred for coronary angiography.     

The relationship between lipoprotein(a) and the complications of diabetes mellitus

The risk of cardiovascular disease is increased approximately two- to four-fold in patients with diabetes mellitus compared with non-diabetic controls. The nature of this increased risk cannot be completely explained by the contribution of traditional risk factors. As such, there has been a great deal of interest in assessing the role of lipoprotein(a) (Lp(a)), an LDL-like lipoprotein, in the vascular complications of diabetes. Although numerous studies in the non-diabetic population have demonstrated an association between elevated plasma Lp(a) concentration and risk for atherosclerotic disorders, the contribution of Lp(a) to the enhanced risk of vascular disease in the diabetic population is not clearly defined. Herein we review the structure and potential functions of Lp(a), the determination of Lp(a) levels, and the epidemiological evidence supporting its role in coronary heart disease and address the following controversial questions regarding the role of Lp(a) in diabetes mellitus: (1) are plasma Lp(a) levels and phenotype distributions altered in type 1 (insulin-dependent) diabetes mellitus and type 2 (non-insulin-dependent) diabetes mellitus and does the degree of metabolic control influence Lp(a) levels in these patients; (2) what is the relationship between Lp(a) and renal disease in patients with diabetes mellitus; (3) do increased plasma Lp(a) concentrations in patients with diabetes contribute to the vascular complications of this disease; and (4) can the atherogenicity of Lp(a) in diabetes be enhanced in the absence of elevated levels of this lipoprotein due to biochemical modifications. Received: 11 January 2002 / Accepted in revised form: 9 December 2002 Correspondence to S.M. Marcovina     

Temporal increases in plasma markers of oxidized low-density lipoprotein strongly reflect the presence of acute coronary syndromes

OBJECTIVES: This study was conducted to test the hypothesis that plasma markers of oxidized low-density lipoprotein (OxLDL) reflect acute coronary syndromes (ACS). BACKGROUND: Oxidized LDL contributes to the pathogenesis of atherosclerosis, but its role in ACS is not established. METHODS: Serial plasma samples were prospectively obtained from patients with an acute myocardial infarction (MI) (n = 8), unstable angina (UA) (n = 15), stable coronary artery disease (CAD) (n = 17), angiographically normal coronary arteries (n = 8), and from healthy subjects (n = 18), at entry into the study, hospital discharge (MI group only), and at 30, 120, and 210 days. Chemiluminescent enzyme-linked immunosorbent assay was used to quantitate plasma levels of: 1) immunoglobulin (Ig)M and IgG OxLDL autoantibody titers (presented as a mean OxLDL autoantibody titer by averaging the results of four distinct epitopes); 2) LDL-autoantibody immune complexes (LDL-IC); and 3) minimally OxLDL measured by antibody E06 (OxLDL-E06), as determined by the content of oxidized phospholipids (OxPL) per apolipoprotein B-100. RESULTS: Baseline OxLDL IgG autoantibody levels were higher in the MI group (p < 0.0001). At 30-day follow-up, the mean IgM OxLDL titers increased by 48% (p < 0.001) and 20% (p < 0.001), and IgM LDL-IC increased by 60% (p < 0.01) and 26% (p < 0.01) in the MI and UA groups, respectively. The OxLDL-E06 levels increased by 54% (p < 0.01) in the MI group at hospital discharge and by 36% at 30 days. No significant changes in any OxLDL markers were noted in the other groups. The OxLDL-E06 levels strongly paralleled the acute rise in lipoprotein(a), or Lp(a), in the MI group, suggesting that toxic OxPL are preferentially bound to Lp(a). Oxidized LDL-E06 also correlated extremely well with Lp(a) in the entire cohort of patients (r = 0.91, p < 0.0001). CONCLUSIONS: Circulating OxLDL-specific markers strongly reflect the presence of ACS, implying immune awareness to newly exposed oxidation-specific epitopes and possible release of OxLDL in the circulation. The OxLDL-E06 measurements provide novel insights into plaque rupture and the potential atherogenicity of Lp(a).     

Effect of cardiopulmonary bypass on plasma levels of lipoprotein (a) in hypercholesterolemic patients.

Increments of lipoprotein (a) (Lp (a)) concentration during cardiopulmonary bypass (CPB) have not been justified in the literature yet. We have investigated whether Lp (a) levels remain constant or increase during CPB and if high plasma levels of low density lipoprotein (LDL; containing apolipoprotein (apo) B) in hypercholesterolemic patients affect the assembly of Lp (a) (containing apoB: Apo (a)). In this study, the change in plasma lipid and lipoprotein levels of 40 patients with hypercholesterolemia and 40 patients who have normal cholesterol values were determined and compared during CPB, and in the postoperative early stage. In our study, lipid and lipoproteins, except Lp (a), showed a falling trend and paradoxically, Lp (a) statistically showed a significant rising trend, like the acute phase reactant in two groups (p=0.011 for LDL, p=0.016 for high density lipoprotein (HDL) and p<0.001 for the others, in 80 patients). Concentrations of Lp (a) in plasma increased more sharply in the hypercholesterolemic group than the normocholesterolemic group during CPB. This difference was significant at the 60th minute of cardiopulmonary bypass with a nonparametric test (p<0.05 Mann-Whitney U test). High density lipoprotein values showed more decline in the hypercholesterolemic group patients than in the normocholesterolemic group patients (p<0.05). In conclusion, lipoprotein (a) levels increased more pronounced in patients with hypercholesterolemia during CPB. On the other hand, high LDL levels in hypercholesterolemic patients accelerated Lp(a)formation in the acute phase.