载脂蛋白E基因多态性及血脂与心肌梗死的关系

为了研究载脂蛋白Ｅ基因多态性及血脂与老年心肌梗死的关系,本文采用聚合酶链反应－限制片长多态性对９７例对照者和４９例心肌梗死患者载脂蛋白Ｅ基因型进行分析,同时检测血脂指标。结果发现,两组的Ｅ３／３基因型所占百分比最大,其次是Ｅ３／４基因型;对照组和心肌梗死组的ｅ２,ｅ３,ｅ４等位基因频率为０．０３０９、０．８９１８、０．０７７３和０．０３０６、０．８１６３、０．１５３１。心肌梗死组ｅ４携带者百分比大     

急性心肌梗死患者载脂蛋白E基因多态性及其与血脂代谢的关系

为探讨载脂蛋白Ｅ基因性与心肌梗死的相关性，以及载脂蛋白Ｅ基因多态性对心肌梗死患者血脂代谢的影响，选取１００例正常人及５０例急性心肌梗死患者，采用聚合酶链反应－限制片长多态性法来分析载脂蛋白Ｅ的基因型，并按常规酶法及免疫法测定血脂和载脂蛋白。结果发现Ｅ３／３基因型及ε３等位基因频率均多见于正常人及病例组中，但两组间Ｅ３／３基因型频率存在明显差异（Ｐ〈０．０５）；ε４等位基因及Ｅ４／３基因型频率在病例     

反义寡脱氧核苷酸抑制大鼠肝细胞载脂蛋白B的表达

为研究载脂蛋白Ｅ基因多态性在冠心病发生发展中的作用及其对血脂水平的影响，应用聚合酶链反应－ 限制片长多态性检测法，测定２２０ 例冠心病患者和１８０ 例正常对照者的载脂蛋白Ｅ基因型；并按常规方法测定血脂水平。结果发现中国汉族人群中存在５ 种载脂蛋白Ｅ基因型，分别为Ｅ３３、Ｅ３２、Ｅ４３ 、Ｅ４２ 及Ｅ４４。冠心病组载脂蛋白Ｅ４３ 基因型和ε４ 等位基因频率（ 分别为２５．０％ 和１４．３％ ） 均显著高于对照组（１３ ．３％ 和８．１％ ）（ Ｐ＜ ０．０１）， 载脂蛋白Ｅ３３ 基因型频率（５９．５ ％） 则低于对照组（７０ ．０ ％）（Ｐ＜０．０５）；冠心病组总胆固醇、低密度脂蛋白胆固醇水平显著高于对照组（ Ｐ＜ ０．０１）；在冠心病组的各亚型之间，总胆固醇和低密度脂蛋白胆固醇水平之间存在统计学差异（ Ｐ＜０ ．０５） 。上述实验结果说明，载脂蛋白Ｅ基因多态性与冠心病的发生发展密切相关并影响血脂的代谢水平；ε４ 等位基因可能是冠心病重要的遗传易患因素之一。     

两型脑卒中患者载脂蛋白E基因型的分布比较

为了解载脂蛋白Ｅ基因型与两型脑卒中的关系，采用聚合酶链反应技术对９０例脑出血和９０例脑梗死患者及其１０７例性别、年龄配对的对照者进行载脂蛋白Ｅ基因型检测。结果发现脑血患者载脂蛋白Ｅε２／ε３基因频率高于对照组（Ｐ〈０．０５），而载脂蛋白Ｅε３／ε３基因频率在对照组较高（Ｐ〈０．０５）。脑梗死患者中载脂蛋白Ｅε４携带频率较对照组显著增高（Ｐ〈０．０５）。研究结果表明载脂蛋白Ｅε２可能与出血性脑卒中有     

痴呆患者载脂蛋白E基因型及表型的研究

目的研究载脂蛋白Ｅ（ＡｐｏＥ）多态性与痴呆疾病的关系。方法对对照组（５３例）和痴呆组［其中包括Ａｌｚｈｅｉｍｅｒ’ｓ病（ＡＤ）１８例，血管性痴呆（ＶＤ）２３例和帕金森病痴呆（ＰＤＤ）１３例］的载脂蛋白Ｅ基因频率和表型多态性的关系进行了比较。结果对照组ＡｐｏＥ基因频率以ε３最为常见，占９２．５％，其表型分布以Ｅ３／３型为主（占８６．８％）；在痴呆组中，ＡＤ组ＡｐｏＥε４和ε２基因频率分别为１９．４％和１３．９％，明显多于对照组（Ｐ＜０．０５～０．０１），而ＶＤ组和ＰＤＤ组ＡｐｏＥε４和ε２基因频率与非痴呆对照组相比差别无显著性（Ｐ＞０．０５）；ＡＤ组ＡｐｏＥ表型中的Ｅ３／４型和Ｅ２／３型明显高于对照组，而ＶＤ组和ＰＤＤ组中其他各型差异均不显著。结论ＡｐｏＥε４和ε２与ＡＤ关系极为密切，与ＶＤ和ＰＤＤ的关系尚需进一步研究     

老年冠心病载脂蛋白E基因多态性相关性分析及其对血脂的影响

目的 研究载脂蛋白Ｅ（ＡｐｏＥ）基因多态性与老年冠心病（ＣＨＤ）的相关关系及其对血脂水平的影响。方法 应用聚合酶链反应－限制性片段长度多态性（ＰＣＲ－ＲＦＬＰ）基因分析方法，测定１６１例老年ＣＨＤ患者和８６例同年龄对照者的ＡｐｏＥ基因型；血脂水平按常规方法测定。结果 本共发现５种ＡｐｏＥ基因型，分别为Ｅ３／３、Ｅ４／４、Ｅ４／３及Ｅ４／２。老年ＣＨＤ组ＡｐｏＥ４／３基因型和ε４等位基因频率均高于对     

心肌梗塞患者载脂蛋白E基因多态性研究及其对临床与血脂代谢的影响

目的：研究载脂蛋白（Ａｐｏ）Ｅ基因多态性对心肌梗塞发生、发展及预后的作用及其对血脂水平的影响。 方法;应用聚合酶链反应－限制性片段长度多态性检测方法,测定１０４例心肌梗塞患者（心肌梗塞组）和１８０例正常对照者（对照组）的Ａｏｐ　Ｅ基因型;并按常规方法测定血脂水平。 结果：共检测出 ５种 Ａｐｏ Ｅ基因型,分别为 Ａｐｏ Ｅ３／３、Ａｐｏ　 Ｅ３／２、Ａｐｏ Ｅ４／３、Ａｐｏ Ｅ４／２及 Ａｐｏ Ｅ４／４。心肌梗塞组Ａｐｏ　Ｅ４／３基因型和ＡｐｏＥε４等位基因频率均显著高于对照组（Ｐ＜０．０１）;心肌梗塞组总胆固醇（ＴＣ）和低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）高于对照组（Ｐ＜０．０５）;心肌梗塞组泵功能Ⅲ～Ⅳ级患者ＡｐｏＥ４／３基因型频率高于泵功能Ⅰ～Ⅱ级患者（Ｐ＜０．０５）;Ａｐｏ　Ｅε４等位基因具有升高ＴＣ、ＬＤＬ－Ｃ的作用,Ａｐｏ　Ｅε２等位基因则有降低ＴＣ、ＬＤＬ－Ｃ的作用。 结论：ＡｐｏＥ基因多态性与心肌梗塞的发生、发展和血脂的代谢水平密切相关;Ａｐｏ　Ｅε４等位基因可能是心肌梗塞重要的遗传标记,Ａｐｏ　Ｅ４／３亦影响心肌梗塞泵功能分级。     

武汉地区Ⅱ型糖尿病患者冠心病与载脂蛋白E基因型的关系

应用聚合酶链反应（ＰＣＲ）技术，对随机选择的１２５例ＮＩＤＤＭ患者和５０例非ＤＭ患者进行ＡｐｏＥ基因型检测，以研究ＮＩＤＤＭ患者ＣＨＤ与ＡｐｏＥ基因型间的关系。结果表明，ＮＩＤＤＭ患者心肌梗塞和缺血性心电图改变在Ａｐｏε４／４和ε４／３型组中发生率分别为２１％和４１％，但不同基因型组间差异无显著性。心绞痛在Ａｐｏε４／４和ε４／３型组中为５２％，显著高于ε３／３型组（３１％，Ｐ＜０．０５）。Ａｐｏε４／４和ε４／３型ＮＩＤＤＭ患者，任何证据的ＣＨＤ发生率为７２％，显著高于ε３／３型组（３７％）及ε２／２、ε３／２型组（３３％，Ｐ＜０．０１）。ＮＩＤＤＭ患者中ＣＨＤ组Ａｐｏε３／３和ε４／３基因型频率分别为５２％和３４％，分别低于（ε３／３）、高于（ε４／３）非ＣＨＤ组（７１％，Ｐ＜０．０５；１０％，Ｐ＜０．０１）；ＣＨＤ组ε４等位基因频率为２１％，明显高于非ＣＨＤ组（７％，Ｐ＜０．０１）。提示Ａｐｏε４／４和ε４／３为ＮＩＤＤＭ患者ＣＨＤ的重要危险指标。     

载脂蛋白E基因多态性与冠心病关系的研究

目的：探讨载脂蛋白Ｅ（ａｐｏＥ）基因多态性在冠心病（ＣＨＤ）发生发展中的作用及其对血脂质、脂蛋白水平的影响。方法：应用聚合酶链反应技术和遗传学方法,测定９３ 例ＣＨＤ患者和９４例正常对照者的ａｐｏＥ基因型;按常规方法测定血浆脂质、脂蛋白水平。结果：共发现５ 种ａｐｏＥ基因型,分别为Ｅ３／３、Ｅ３／２、Ｅ４／３、Ｅ４／２和Ｅ４／４。ＣＨＤ组ａｐｏＥ４／３ 基因型和ε４ 等位基因频率及总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）均显著高于对照组（均Ｐ＜ ０．０１）,ａｐｏＡＩ的水平高于对照组（Ｐ＜ ０．０５）,其他血脂指标无显著性差异（ Ｐ＞ ０．０５）。在ＣＨＤ组各亚型之间,ＴＣ、ＬＤＬ－Ｃ和ａｐｏＡＩ水平之间存在显著性差异（Ｐ＜ ０．０５）。结论：ａｐｏＥε４ 等位基因是ＣＨＤ重要的遗传易患因素,ａｐｏＥ基因多态性亦影响血ＴＣ、ＬＤＬ－Ｃ和ａｐｏＡＩ水平。     

载脂蛋白E基因多态性与冠心病关系的研究

目的：探讨载脂蛋白（Ａｐｏ）Ｅ基因多态性与冠心病的相关性，以及ＡｐｏＥ基因多态性对冠心病患者血脂水平的影响。方法：１００例冠心病患者和４３例正常对照者。按常规方法测定血浆脂质和Ａｐｏ水平。ＡｐｏＥ基因型的确定采用聚合酶链反应和ＨｈａＩ酶切的方法。结果：本研究只发现３种常见的ＡｐｏＥ基因型，即Ｅ３／３，Ｅ３／４，Ｅ３／２。在病例组和正常对照组之间，ＡｐｏＥ等位基因频率以及基因型频率分布没有统计学差异（Ｐ＞０．０５）。在冠心病患者不同基因型之间，总胆固醇和ＡｐｏＢ的水平有差异（Ｐ＜０．０５）；其它血脂指标无差异（Ｐ＞０．０５）。结论：本研究证实ＡｐｏＥ基因多态性影响冠心病患者总胆固醇和ＡｐｏＢ的水平；但ＡｐｏＥ基因多态性并不是冠心病发病的直接危险因子。     

Divergent association of apolipoprotein E polymorphism with vascular disease in patients with NIDDM and control subjects

We analysed a well-characterized group of 83 patients (43 men, 40 women; mean age ± SEM: 65.5 ± 0.6 years at the 10-year examination) with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) and in 123 control subjects (56 men, 67 women; mean age ± 0.9 years) retrospectively for the relationship of apolipoprotein E (apo E) genotypes (E2/3, E3/3 vs E3/4, E4/4) to the incidence of clinical macrovascular disease and its risk factors and the incidence of microvascular complications of diabetes during the first 10 years of NIDDM, as well as carotid intima-media thickness measured by B-mode ultrasound at the 10-year examination. In patients with NIDDM, apo E4 genotype showed no relationship to clinical events or carotid intima-media thickness. However, in the control subjects with apo E4, the incidence of non-fatal myocardial infarction during the follow-up was increased (apo E4 positivity: 17.1 %; apo E4 negativity 5.1 %; p = 0.035) and they had higher common carotid intima-media thickness than those with apo E2/3 or apo E3/3 (1.15 ± 0.05 mm vs 1.01 ± 0.03 mm, p = 0.008). Apo E genotype groups showed no relationship to microvascular complications of diabetes, although control subjects with apo E4 positivity showed a higher frequency of microalbuminuria than those lacking apo E4. We conclude that apo E4 was a marker of vascular disease and increased atherosclerosis in non-diabetic subjects, whereas in the diabetic patients these relationships were absent. It is likely that NIDDM per se influences the vascular risk so overwhelmingly that the effects of other risk factors are obscured. © 1997 by John Wiley & Sons, Ltd.     

Association of apolipoprotein E genotype with early onset of coronary heart disease in Greek men

Apolipoprotein (apo) E polymorphism has been associated with coronary heart disease (CHD) although its relation to the age of CHD onset is still not defined. The age of onset of established CHD was obtained from 502 Greek men and compared to 103 healthy men. The age grouping was based on the age of CHD onset (earlier < or =44 years, n = 73, intermediate 45-64 years, n = 321, and later > or =65 years, n = 108). Apo E genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the lipid profile was assessed. No differences in genotype and allele frequencies were found within the CHD groups. The apo epsilon3/4 genotype and the apo epsilon4 allele were less frequent in the earlier-onset group than in healthy men (11.0 % vs 22.3%, Pearson Chi-Square p = 0.028 and 6.8% vs 13.6%, Pearson Chi-Square p = 0.023, respectively). The lipid profile was similar in all genotypes of all groups except for high-density lipoprotein cholesterol levels, which were higher in epsilon2 carriers compared to non-epsilon2 carriers (in mg/dL [+/-SD]; 44 [9] vs 39 [10], in mmol/L [+/-SD]; 1.1 [0.2] vs 1.0 [0.3] p = 0.005). There is an association between apo E genotype and early onset of CHD in Greek men. In the earlier CHD onset group, the apo epsilon3/4 genotype was less frequent compared to healthy men. This supports that the apo epsilon3/4 genotype is associated with decreased risk of premature CHD. Because the results of similar studies are not consistent, it may be that the relationship between apo E genotype and CHD is related to ethnicity rather than a universal phenomenon.     

Effect of apo E phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction: the EARS II study. European Atherosclerosis Research Study.

The goal of the present study was to assess whether the effect of the apolipoprotein E polymorphism on postprandial lipemia explained part of the risk attributable to familial history of coronary heart disease. Cases (n = 407) were students, aged between 18 and 28 years, whose fathers had a proven myocardial infarction before the age of 55 years. Age-matched controls (n = 415) were recruited from the corresponding student registers. Blood was obtained after an overnight fast and at 2, 3, 4 and 6 h after ingestion of a fatty meal for triglyceride measurements. Apolipoprotein E phenotype was associated with postprandial triglyceride variability in both cases and controls. However, the apolipoprotein E-dependent triglyceride response was not significantly heterogeneous between cases and controls. In the pooled data, postprandial triglyceride levels were higher in carriers of the E2 and, to a lesser extent, of the E4 isoform, than in E3/3 homozygotes, independently of fasting triglyceride levels. At 6 h, triglyceride levels were increased by 21.2% (P < 0.01) in E2 carriers and 11.5% (P = 0.053) in E4 carriers by comparison to E3/3 subjects. These effects were not significantly different between regions. In conclusion, the effects of the apolipoprotein E polymorphism on postprandial triglyceridemia are similar across regions of Europe, and homogeneous in healthy young subjects with and without a family history of early myocardial infarction. This suggests that the influence of apolipoprotein E on myocardial infarction risk may be acting through mechanisms other than through effects on postprandial triglyceridemia.     

Myocardial infarction in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an angiopathy caused by mutations in the NOTCH3 gene. Typical microvascular changes are found throughout the arterial tree, but the documented disease expression is confined to the central nervous system. In an ongoing CADASIL study, we noted a number of patients with early acute myocardial infarction (before the age of 50 years), as well as patients with electrocardiogram (ECG) abnormalities. We analyzed these data to determine whether myocardial ischemia is associated with NOTCH3 mutations. ECGs were recorded in mutated (n = 41) and nonmutated (n = 22) individuals from 15 genetically confirmed CADASIL families, and blindly classified according to the Minnesota code. Cardiologic history was assessed and cardiovascular disease risk factors were determined. Evidence for myocardial infarction was defined as a positive history for acute myocardial infarction and/or a Minnesota Code 1 (Q-waves) on ECG. We examined CADASIL myocardial tissue ultrastructurally and immunohistochemically for evidence of microangiopathy.We found that almost 25% (10/41) of mutation carriers had evidence of myocardial infarction, versus none of the 22 nonmutation carriers (p = 0.011). Five had a medical history of acute myocardial infarction, and 5 had current pathologic Q-waves on ECG. Acute myocardial infarction occurred at a mean age of 39.6 +/- 5.22 years, and predated major neurologic symptoms of CADASIL in all cases. Pathologic examination of myocardial tissue revealed typical CADASIL arteriopathic changes of the coronary microvasculature. To our knowledge, this is the first study showing that NOTCH3 mutation carriers may be at increased risk of early acute myocardial infarction, expanding CADASIL disease expression beyond the central nervous system to include the heart.     

Elevated Lp(a) is the most frequent familial lipoprotein disorder leading to premature myocardial infarction in a country with low cholesterol levels

Disorders of the lipoprotein metabolism are an important cause of premature coronary artery disease and myocardial infarction. Of the genetic lipoprotein disorders, elevation of apoprotein (apo) B containing lipoproteins is the most frequent one in the western population. We aimed to define the prevalence of genetic lipoprotein disorders and other risk factors in a population from a country with a low average cholesterol levels. We examined 48 consecutive patients with premature myocardial infarction below age 55, their 78 siblings and age and body mass index matched controls for familial lipoprotein disorders. The patients with premature myocardial infarction had higher triglyceride, low-density lipoprotein, apo B, lipoprotein (Lp) (a) and lower apo A1 levels then controls (p<0.05). Of the nonlipid risk factors, 67% smoked, 8% had diabetes mellitus, 17% had hypertension and 58% a family history of premature coronary artery disease. Fifty percent of these patients with premature myocardial infarction had a familial lipoprotein disorder. Familial excess of Lp(a) was the most frequent lipoprotein abnormality present in 16% of the patients followed by familial combined hyperlipidemia. We conclude that, Lp(a) increase was the most frequent familial lipoprotein abnormality in this population. The frequency of familial lipoprotein disorders in this population emphasises the need to screen siblings of patients with premature myocardial infarction.     

Evidence of reduced coronary artery disease risk for apolipoprotein epsilon2/3 heterozygotes

BACKGROUND: Polymorphism in the gene for apolipoprotein E (apo E) influences lipid metabolism. Relative to the epsilon3 allele, the epsilon4 allele tends to increase and the epsilon2 allele tends to decrease total and serum cholesterol, but uncertainty remains concerning an influence on the risk of coronary artery disease (CAD). It is possible that the influence of apo E alleles on CAD risk is influenced by the age of subjects studied. In this study, we examine the influence of the epsilon2 and epsilon4 alleles on the risk of CAD in relatively young subjects. METHODS: We determined the apo E genotype of 564 Caucasian CAD subjects below 50 years of age presenting with symptomatic CAD, either with or without prior myocardial infarction, and documented by angiography, and 639 similarly aged Caucasian control subjects without symptomatic CAD randomly selected from the community. RESULTS: The frequency of subjects with the epsilon2/3 genotype was significantly lower in CAD subjects than controls (6 vs. 11%, P<0.01) and, relative to epsilon3/3, the epsilon2/3 genotype was associated with a significant reduction in total and LDL-cholesterol in male and female control subjects. In contrast, there was no difference in the frequency of epsilon4/4 or epsilon4/3 genotypes in CAD cases and controls (30 vs. 26%, NS), and the latter genotypes had little influence on total or LDL-cholesterol. CONCLUSION: The results indicate a beneficial effect of the epsilon2/3 genotype not only on LDL cholesterol but in decreasing the risk of CAD in Caucasians at a young age.     

The effect of age,body mass index,and fasting triglyceride level on postprandial lipemia is dependent on apolipoprotein E polymorphism in subjects with non-insulin-dependent diabetes mellitus

The aim of this study was to evaluate in non-insulin-dependent diabetes mellitus (NIDDM) subjects the respective influence of apolipoprotein (apo) E polymorphism, age, gender, weight, fasting triglyceride (TG) status, and glycemic status on postprandial lipemia. Apo E genotyping was performed in consecutive NIDDM hospitalized patients in order to recruite size-adjusted groups of each apo E genotype. In 57 NIDDM including 22 E3/3 (E3), 18 E2/3 (E2), and 17 E4/3 (E4) subjects, an 8-hour vitamin A-fat loading test was performed and TG and retinyl palmitate (RP) measured. Fasting TG level correlated with the TG area under the incremental curve (AUIC) (r = 0.512, P <.001) but not with RP AUIC. Despite not different fasting and postprandial TG concentrations, E2 and E4 carriers exhibited a 2- to 3-fold higher RP AUIC than E3 carriers (P =.01). Multivariate analysis indicated an age x apo E interaction on postprandial TG (P <.01), since the unfavorable effect of E2 and E4 allele on TG AUIC was unmasked by aging. In addition, a fasting TG x apo E interaction on postprandial TG was shown (P <.01), and the correlation between fasting TG and TG AUIC was actually restricted to E2 or E4 carriers. Finally, the negative correlation between BMI and postprandial TG observed in the experimental group was actually restricted to E4 carriers (r = -0.77, P <.001). Our results indicate interactions between apo E polymorphism and aging, fasting TG level and BMI that may be important for analyzing postprandial TG clearance in NIDDM.     

The influence of thrombolytic therapy on selected parameters of left ventricular function in acute myocardial infarction

Our study aimed to evaluate the influence of thrombolytic therapy on some left ventricle (LV) function parameters in patients with acute myocardial infarction. The study was performed on 44 pts admitted to hospital due to acute myocardial infarction. The patients were divided into two groups: I group--30 pts (26 male, 4 female) at average age 57 +/- 10 who were treated with tissue plasminogen activator (t-PA) routinely and II group--14 pts (9 male, 5 female) at average age 62 +/- 10 in whom thrombolytic therapy was contraindicated for various reasons. Transthoracic echocardiography was performed just before treatment (0), 3.5 hours after the onset of drug administration (2 hours after the end of t-PA injection) (1) and on the 10th day of hospitalization (2). Control group consisted of 16 clinically healthy individuals (12 male, 4 female) at average age 54 +/- 9. The following parameters were evaluated: DT-E--wave of early diastolic transmitral flow deceleration time, IVRT--isovolumic relaxation time, E/A--early/atrial peak flow velocity ratio of transmitral flow, LATEF%--left atrial total emptying fraction, EF--left ventricle ejection fraction. In patients with acute myocardial infarction shortening of DT, prolongation of IVRT, lower E/A ratio and decrease of LATEF% compared to controls were observed. In group I EF was less than in clinically healthy individuals. E/A ratio was higher in pts from group I than from group II. In patients treated with t-PA 2 hours after treatment as well as on the 10th day significant prolongation of DT, shortening of IVRT and increase of LATEF% were observed. These changes were accompanied by the increase of EF. In patients with acute myocardial infarction not treated with t-PA significant increase in E/A ratio and EF on 10th day were observed. On the basis of the results were conclude: In patients with acute myocardial infarction LV diastolic function and with unproper relaxation as well as unproper compliance of LV myocardium is present. In patients with thrombolytic therapy LV filling pattern improves just two hours after t-PA administration (DT prolongation, IVRT shortening, LATEF% increase). Such tendency remains on the 10th day after treatment. In patients without thrombolytic therapy slight improvement occurs no sooner than on the 10th day of the MI.     

Total plasma apo E and high density lipoprotein apo E in survivors of myocardial infarction

Total apo E in plasma and the amount of apo E-HDL were measured in 40 normolipidemic male survivors of myocardial infarction and in 40 controls. LDL-C, Lp(a) and apo B were significantly higher and HDL-C and apo A-I were significantly lower in survivors than in controls. Total plasma apo E did not differ between patients and controls, but HDL-E and the ratio HDL-E/apo A-I were lower in survivors. The data support the view that atherosclerotic patients are often characterized by abnormalities in the concentration and distribution of lipoproteins as well as of apoproteins, even in the presence of normal total plasma lipids.     

载脂蛋白E基因多态性对血脂水平的影响及与冠状动脉狭窄的关系

为探讨载脂蛋白E基因多态性对血脂水平的影响及与冠状动脉狭窄程度的关系 ,采用聚合酶链反应—限制片段长度多态性对 95例冠心病患者和 46例正常对照者载脂者蛋白E基因型进行分析 ,同时测定血脂及载脂蛋白B水平。并根据冠状动脉受累支数不同将冠心病患者分为冠状动脉多支病变组和单支病变组。结果显示 ,5 5例冠状动脉病变多支组和 40例冠状动脉单支病变组E3/ 4基因型和ε4等位基因频率均高于对照组 (P <0 .0 1) ,且多支病变组E3/ 4基因型和ε4等位基因频率高于单支病变组 (P <0 .0 5 )。与E3/ 3及E2 / 3基因型比较 ,E3/ 4基因型者有较高的总胆固醇、低密度脂蛋白胆固醇和载脂蛋白B水平及较低的高密度脂蛋白胆固醇水平。与对照组比较 ,冠心病组E3/ 4基因型升高总胆固醇、低密度脂蛋白胆固醇和载脂蛋白B的作用及降低高密度脂蛋白胆固醇的作用更明显。表明载脂蛋白E基因多态性影响血胆固醇代谢 ,ε4等位基因与冠心病危险性增加有关 ,ε4等位基因频率升高的冠心病者冠状动脉受累支数加重 ,推测ε4等位基因可能与冠状动脉狭窄程度存在内在联系。