Apolipoprotein B as a marker of familial hyperlipoproteinemia

AIMS: Families with 10-12-year-old schoolchildren were informed about and asked to participate in a study to identify children with hyperlipoproteinemia. We hypothesised that children and families with familial blood lipid abnormalities, specifically those with familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCHL), could be identified by the child's apolipoprotein B level exceeding the 95th percentile. METHODS: Written information and consent was distributed to the families. Families whose child had an apoB concentration exceeding the 95th percentile were further examined. Children and parents were divided into normal, high and very high low density lipoprotein cholesterol (LDLC) groups. In adults a high LDLC level was defined as > 4.1-4.9, a very high as > 4.9 mmol/l, in children as > 3.4-4.1 and > 4.1 mmol/l, respectively. The triglyceride level was regarded as high when > 3.6 mmol/l. RESULTS: Of 2,855 families, 2,186 agreed to participate. The 95th percentile apoB level was for boys 0.98 and girls 1.07 g/l. Of the 131 children with an apoB level above the 95th percentile, 109 families accepted further examinations. Of 109 hyperapoB children 23 were obese. Normal LDLC was found in 28 hyperapo B children of whom six parents had high/very high LDLC and one high triglyceride concentrations. A high LDLC level was found in 52 children of whom 23 parents had higy/very high LDLC and another five high LDLC and/or high triglyceride concentrations. A very high LDLC level was found in 29 children, in two of them due to hypothyroidism, 17 had a parent with high/very high LDLC and another two parents a high triglyceride concentration. Familial hypercholesterolemia, defined as a LDLC concentration above twice the normal one in the child and a very high level in a parent, was suspected in six families, five having a relative with premature CHD. The families with FCHL should be included in the 20 families with hyperapoB and a child with high-very high LDLC and a parent with very high LDLC or TG levels. CONCLUSION: Of the 109 children examined due to the child's increased apoB concentration, about 20% were obese and 75% had an increased LDLC concentration. A familial occurrence of hyperlipoproteinemia was evident in about 50% of the families with an hyperapoB child. Six families probably suffer from familial hypercholesterolemia. The definite number of FCHL families could not be defined since extended pedigrees were not available. A high suspicion of FCHL was evident in 20 families. ApoB is an important marker of hyperlipoproteinemia of familial occurrence identifying families in need of primary CHD prevention.     

Familial lipoprotein disorders in patients with premature coronary artery disease.

BACKGROUND. Genetic lipoprotein disorders have been associated with premature coronary artery disease (CAD). METHODS AND RESULTS. The prevalence of such disorders was determined in 102 kindreds (n = 603 subjects) in whom the proband had significant CAD documented by angiography before the age of 60 years. Fasting plasma cholesterol, triglyceride, low density lipoprotein (LDL) cholesterol, apolipoprotein (apo) B, and lipoprotein (a) [Lp(a)] values above the 90th percentile and high density lipoprotein (HDL) cholesterol and apo A-I below the 10th percentile of age- and sex-specific norms were defined as abnormal. An abnormality was noted in 73.5% of probands compared with 38.2% in age-matched controls (p less than 0.001), with a low HDL cholesterol level (hypoalphalipoproteinemia) being the most common abnormality (39.2% of cases). In these kindreds, 54% had a defined phenotypic familial lipoprotein or apolipoprotein disorder. The following frequencies were observed: Lp(a) excess, 18.6% (includes 12.7% with no other dyslipidemias); hypertriglyceridemia with hypoalphalipoproteinemia, 14.7%; combined hyperlipidemia, 13.7% (11.7% with and 2.0% without hypoalphalipoproteinemia); hyperapobetalipoproteinemia (elevated apo B only), 5%; hypoalphalipoproteinemia, 4%; hypercholesterolemia (elevated LDL only), 3%; hypertriglyceridemia, 1%; decreased apo A-I only, 1%. Overall, 54% of the probands had a familial dyslipidemia; unclassifiable lipid disorders (spouse also affected) were found in 3%. No identifiable familial dyslipidemia was noted in 43% of kindreds of those; nearly half (45%) had a sporadic lipid disorder. Parent-offspring and proband-spouse correlations for these biochemical variables revealed that lipoprotein and apolipoprotein levels are in part genetically determined, with Lp(a) showing the highest degree of parent-offspring correlation. CONCLUSIONS. Our data indicate that more than half of patients with premature CAD have a familial lipoprotein disorder, with Lp(a) excess, hypertriglyceridemia with hypoalphalipoproteinemia, and combined hyperlipidemia with hypoalphalipoproteinemia being the most common abnormalities.     

Lipoprotein and apolipoprotein abnormalities in familial combined hyperlipidemia: a 20-year prospective study.

In order to characterize the lipoprotein abnormalities in familial combined hyperlipidemia (FCHL) and to describe factors associated with the stability of the FCHL phenotype during 20-year follow-up, 287 individuals from 48 families with FCHL originally identified in the early 1970s (baseline) were studied. Hyperlipidemia was defined as lipid-lowering medication use, or > or =age- and sex-specific 90th percentile for triglycerides or cholesterol. Triglyceride, cholesterol and medical history data were obtained at baseline and 20-year follow-up. Additional follow-up measures included HDL-C, LDL-C, LDL particle size, lipoprotein(a), apolipoprotein (apo) A-I, apoB, and apoE polymorphism. Longitudinally, two-thirds of relatives were consistently normolipidemic or hyperlipidemic, and one third were discordant for hyperlipidemic status at baseline and 20-year follow-up. Individuals with hyperlipidemia at baseline and/or follow-up had higher apoB levels than those with consistently normal lipids (P<0.05), whereas small LDL size was associated with concurrent hyperlipidemia. Among individuals who were normolipidemic at baseline, the following variables were independently associated with development of hyperlipidemia over 20 years: older age at baseline, male sex, greater increase in BMI during follow-up, and apoE alleles epsilon 2 or epsilon 4. In conclusion, apoB is associated with hyperlipidemia and apoE polymorphism is associated with later onset of hyperlipidemia in FCHL.     

Familial dyslipidemic hypertension syndrome: familial combined hyperlipidemia,and the role of abdominal fat mass

Familial combined hyperlipidemia (FCHL) is the most frequent genetic lipid abnormality in humans, with a 5- to 10-fold increased risk of early myocardial infarction. Familial combined hyperlipidemia has been proposed as the leading cause of dyslipidemia in familial dyslipidemic hypertension (FDH). It was the objective of this study to quantify and analyze the simultaneous occurrence of hypertension and hyperlipidemia in FCHL families. We assessed blood pressure (BP) and hyperlipidemia in 27 families with FCHL (235 relatives and 140 spouses, aged 30 to 60 years). Hypertension was defined as a BP more than 140/90 mm Hg, or the use of antihypertensive medication. Multiple backward linear regression analysis was used to derive a biological formula describing BP in FCHL families. One-third of 27 FCHL families were diagnosed with FDH. Sixty-four of 235 (27.2%) relatives had dyslipidemic hypertension (DH), compared to 20 of 140 (14.3%) spouses (P = .005); odds ratio = 2.25 (95% confidence interval 1.29–3.91). Multiple linear regression analysis showed that age, FCHL status, and waist circumference significantly contributed to systolic blood pressure (SBP) in female FCHL relatives. In conclusion, in FCHL we defined age, waist circumference, and hyperlipidemia as predictors of SBP. This study indicates that visceral adipose tissue strongly contributes to the high prevalence of DH in FCHL families. Reduction of visceral fat should be tested as a potential therapeutic intervention for hyperlipidemia and hypertension in FCHL individuals.     

Confirmed locus on chromosome 11p and candidate loci on 6q and 8p for the triglyceride and cholesterol traits of combined hyperlipidemia

Background- Combined hyperlipidemia is a common disorder characterized by a highly atherogenic lipoprotein profile and increased risk of coronary heart disease. The etiology of the lipid abnormalities (increased serum cholesterol and triglyceride or either lipid alone) is unknown. METHODS AND RESULTS: We assembled 2 large cohorts of families with familial combined hyperlipidemia (FCHL) and performed disease and quantitative trait linkage analyses to evaluate the inheritance of the lipid abnormalities. Chromosomal regions 6q16.1-q16.3, 8p23.3-p22, and 11p14.1-q12.1 produced evidence for linkage to FCHL. Chromosomes 6 and 8 are newly identified candidate loci that may respectively contribute to the triglyceride (logarithm of odds [LOD], 1.43; P=0.005) and cholesterol (LOD, 2.2; P=0.0007) components of this condition. The data for chromosome 11 readily fulfil the guidelines required for a confirmed linkage. The causative alleles may contribute to the inheritance of the cholesterol (LOD, 2.04 at 35.2 cM; P=0.0011) component of FCHL as well as the triglyceride trait (LOD, 2.7 at 48.7 cM; P=0.0002). CONCLUSIONS: Genetic analyses identify 2 potentially new loci for FCHL and provide important positional information for cloning the genes within the chromosome 11p14.1-q12.1 interval that contributes to the lipid abnormalities of this highly atherogenic disorder.     

Aggregation of plasma lipids and lipoproteins in families with and without coronary heart disease

Familial aggregation of total plasma cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) was analyzed in 37 families with incidence cases of first myocardial infarction (MI), in 154 families of coronary heart disease (CHD) prevalence cases and in control families. Fasting plasma lipid levels were adjusted for age, sex, country of origin and season of year. Mean TC, LDL-C and TG levels were higher among cases, their spouses and among 17-year-old children of incidence cases than among control families. HDL-C was lower among cases and among wives of incidence cases than in their controls. No differences in HDL-C were noted among children. Mid parent-child correlations for TC and LDL-C were higher in 32 families of men who had a MI (r = 0.43 and r = 0.49) than for control families (r = 0.32 and r = 0.29, respectively). When the 5 families of mothers who had a first MI were included in the analysis, the case-child correlations for TC and LDL-C were 0.60 and 0.68, respectively. Father-child correlation for HDL-C was significantly lower (r = -0.17) among the MI incidence case families than among the control families (r = 0.22; P less than 0.05). No substantial differences in familial correlations for lipid variables were noted in the CHD prevalence families and their controls. These findings suggest that total cholesterol and LDL-C levels, but not HDL-C levels, may be a risk marker in adolescents. The associations evident in adolescent children of families with MI incidence cases were not apparent in children whose parents had CHD on entering the study. This could be due to the probably greater misclassification of CHD prevalence cases than MI incidence cases, the awareness in patients with CHD and subsequent behavioural changes, to possible differences in patterns of survival in the two categories, or may reflect a chance finding.     

Distribution of lipid phenotypes in community-living men with coronary heart disease. High prevalence of isolated low levels of high-density lipoprotein cholesterol.

BACKGROUND--Risk factor modification, including treatment of dyslipidemias, has been recommended for the prevention of future coronary events in patients with coronary heart disease (CHD). Since the prevalence of various dyslipidemias among outpatients with CHD has not been well documented, the purpose of this study was to determine the frequency of specific lipid phenotypes among ambulatory men with CHD. METHODS--Lipid profiles were obtained in 255 men (mean age, 65.5 +/- 9.1 years) with CHD in three Veterans Affairs medical centers. Desirable levels of lipids were defined according to National Cholesterol Education Program guidelines as follows: low-density lipoprotein cholesterol (LDL-C) levels less than 3.36 mmol/L (130 mg/dL); high-density lipoprotein cholesterol (HDL-C) levels equal to or greater than 0.90 mmol/L (35 mg/dL); and triglyceride levels less than 2.83 mmol/L. RESULTS--Seventy-six percent of the group had one or more abnormalities on lipid profile: 51% had high LDL-C levels with or without abnormalities of HDL-C and/or triglyceride levels; 22% had low HDL-C levels with desirable levels of LDL-C; and 3% had hypertriglyceridemia without any cholesterol abnormalities. Normal lipid profiles were significantly more prevalent in subjects over the age of 65 years than in younger patients (40% vs 14%). CONCLUSIONS--These data suggest that (1) a high proportion of men with CHD have dyslipidemia, including 50% with LDL-C level elevations. For these men, the potential benefits of therapeutic intervention have been documented in clinical trials, although the cost-efficiency of wide-scale treatment has not been determined; (2) isolated hypertriglyceridemia is rare in this population; and (3) low HDL-C levels in association with desirable LDL-C levels are present in more than one fifth of male patients with CHD. Clinical trials focusing on this large group are urgently needed to determine whether efforts to raise HDL-C levels result in reduced cardiac morbidity and/or mortality.     

Effects of Flaxseed on Blood Lipids in Healthy and Dyslipidemic Subjects: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

To address hyperlipidemia, flaxseed demonstrates a great impact on experimental and clinical trials. Therefore, the effects of flaxseed on lipid profiles of healthy and dyslipidemic subjects were assayed. The literature search was performed based on English reports of randomized control trials (RCTs) up to April 2021 to seek the effect of flaxseed on lipid profiles of healthy and dyslipidemic subjects. A total of 14 RCTs with 1107 participants were evaluated. Based on results, flaxseed significantly improves the lipid profile in dyslipidemic patients comprising total cholesterol (TC), low-density lipoprotein (LDL-C) and triglyceride (TG) in comparison with the control group. Nevertheless, no significant changes were observed in high-density lipoprotein (HDL-C). Although in healthy individual flaxseed significantly increased HDL-C, LDL-C and TG. Subgroup analysis on healthy subjects showed that flaxseed improved LDL-C on overweight subjects with BMI>25. The evidence suggests that flaxseed significantly improved TC, LDL-C and TG in dyslipidemic subjects and additionally improved the HDL-C on healthy subjects.     

Recognition of familial dyslipidemias in 5-year-old children using the lipid phenotypes of parents. The STRIP project

Adult dyslipidemias may reveal familial and, therefore, offspring dyslipidemias. We evaluated the prevalences of the adult-offspring dyslipidemias in 441 general population families composed of both parents and one 5-year-old child. Family members were classified using the 90th or 10th percentiles for hypercholesterolemia (IIA), hypertriglyceridemia (IV), combined hyperlipidemia (IIB), and low high density lipoprotein cholesterol concentration without hyperlipidemia (hypoHDL). In familial combined hyperlipidemia (FCHL), the IIB-phenotype was in one generation and one of the three hyperlipidemias in the other generation. Finally, the parental dyslipidemia phenotypes and elevated lipids (>80th percentile) that reveal offspring dyslipidemia were selected by stepwise logistic regression. Either the IIA-, IV- or hypoHDL phenotype was found in both generations in 2.8, 2.0 and 1.4% of the families, respectively. FCHL was seen in 1.8% of the families, which confirms the earlier views. The predictive values of the elevated parental cholesterol, type IV or hypoHDL parents to find type IIA, IV and hypoHDL children were low for systematic screening: 16, 13 and 15%, respectively. However, 44% of the children of IIB parents expressed hyperlipidemia (odds ratio 4.7, P=0.006). The IIB phenotype of the parent is a good predictor of the child's hyperlipidemia, and when encountered, it indicates that the lipids of the child should be studied. This would be as important as selective screening of familial hypercholesterolemia.     

Plasma triglycerides and cholesterol in diabetic ketosis

To better characterize the severity and course of hyperlipidemia in diabetic ketosis and ketoacidosis, we measured plasma triglyceride and cholesterol concentrations in 50 episodes in 46 adults hospitalized on a municipal hospital medical service. Moderate hypertriglyceridemia was common: 32 patients (64%) had triglyceride levels above the 95th percentile (adjusted for age and sex), and 18 patients (36%) had cholesterol levels above the 95th percentile. Severe hypertriglyceridemia (levels above 5.65 mmol/L) was found in 14 patients (28%). Plasma high-density lipoprotein (HDL) cholesterol and the HDL2 and HDL3 subclasses were measured in 22 episodes. The initial HDL cholesterol levels were usually subnormal in the patients who had not received insulin previously and normal in those who had. Treatment of the ketoacidosis was usually associated with a rapid decrease in plasma lipid levels. At late follow-up (between 1 1/2 and 14 1/2 months), only 2 of the 14 patients with initial plasma triglyceride levels above 5.65 mmol/L still had such high concentrations.     

虾青素对高脂血症大鼠脂代谢的影响

目的研究虾青素对高脂饲料喂养下大鼠诱发高脂血症过程中血脂代谢的干预作用。方法将60只SD雄性大鼠,随机分为正常对照组、高血脂模型组、辛伐他汀阳性药组(200 mg/kg)、虾青素高、中、低剂量组(415、210、110 mg/kg),分别饲喂标准、高脂、高脂+辛伐他汀、高脂+虾青素,于实验开始前1 d和开始后第4、8、12周末取空腹血,检测血清甘油三酯(TG)、总胆固醇(TC)和高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)。结果与高血脂模型组比较,虾青素组的TC、TG、LDL-C在8、12 w时降低,差异显著(P<0.01),而HDL-C升高,差异显著(P<0.01)。结论虾青素可以对高脂饲料喂养大鼠诱发高脂血症过程中的血脂代谢产生影响,改善血脂变化。     

Predictors of lipid abnormalities in children with new-onset systemic lupus erythematosus

OBJECTIVE: Lipid abnormalities in patients with systemic lupus erythematosus (SLE) are common and likely are one of the causes of premature atherosclerosis in these patients. Our aims were to determine the frequency and pattern of dyslipoproteinemia at presentation of pediatric SLE; and to determine the association between dyslipoproteinemia and markers of disease activity and inflammatory markers at presentation of pediatric SLE. METHODS: Serum lipid measurements were obtained at diagnosis before corticosteroid treatment for an inception cohort of 54 patients. Total cholesterol, triglyceride, LDL-C, and HDL-C levels were regressed on measures of inflammation, disease activity, and disease symptoms. RESULTS: At least one lipid abnormality was present in the majority of patients (63%), an elevated triglyceride level being the most common lipid abnormality (62%). Triglycerides were best predicted by fibrinogen, nephritis, and pleuritis (model R2 = 0.6). Albumin, C4, and white blood cell count were found to predict HDL-C (model R2 = 0.6). Erythrocyte sedimentation rate, central nervous system involvement, nasal ulcers, and nephritis were found as predictors for LDL-C:HDL-C (model R2 = 0.5). No significant predictors were found for total cholesterol or LDL-C. The European Consensus Lupus Activity Measure disease activity score best predicted abnormal triglyceride and HDL-C levels (OR 1.7, 95% CI 1.2-2.3). CONCLUSION: Children with newly diagnosed SLE exhibited the distinct pattern of dyslipoprotein of increased triglycerides and depressed HDL-C that was twice as common in the presence of kidney disease. This lipid profile puts them at risk for premature atherosclerosis. Good disease control and individualized use of lipid-lowering agents based on the observed pattern of lipid abnormalities may lower the risk of premature atherosclerosis in these patients.     

Use of statins for secondary prevention

Opinion statement The causal role of hyperlipidemia in the pathogenesis of atherosclerosis is beyond dispute. The principal lipid abnormality responsible for coronary heart disease (CHD) is considered to be the elevation of the low-density lipoprotein cholesterol (LDL-C), although reduced levels of high-density lipoprotein cholesterol, and most recently elevated triglyceride levels, have also been associated with increased risk for CHD. The risk with these lipid abnormalities exists both in the asymptomatic population as well as in individuals with clinical evidence of atherosclerosis. Most patients with established CHD, and noncoronary atherosclerosis, will need drug therapy to achieve their National Cholesterol Education Program Adult Treatment Panel LDL-C goal of less than 100 mg/dL; the most efficacious, safe, and well-tolerated drugs for this purpose are the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or statins. The role of statins for secondary cardiovascular disease prevention has been well established in several large randomized clinical trials. New data now suggest that statins offer significant benefits to a broad range of patients at high global CHD risk, and should be regarded as an integral part of the management of acute coronary syndromes.     

Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment.

BACKGROUND. We studied the joint effect of baseline triglyceride and lipoprotein cholesterol levels on the incidence of cardiac end points in the trial group (n = 4,081) of the Helsinki Heart Study, a 5-year randomized coronary primary prevention trial among dyslipidemic middle-aged men. The relative risks (RR) were calculated using Cox proportional hazards models with a dummy variable technique that allows simultaneous study of subgroup combinations from the placebo and treatment groups. METHODS AND RESULTS. In the placebo group (n = 2,045), the low density lipoprotein cholesterol (LDL-C)/high density lipoprotein cholesterol (HDL-C) ratio was the best single predictor of cardiac events. This ratio in combination with the serum triglyceride level revealed a high-risk subgroup: subjects with LDL-C/HDL-C ratio greater than 5 and triglycerides greater than 2.3 mmol/l had a RR of 3.8 (95% CI, 2.2-6.6) compared with those with LDL-C/HDL-C ratio less than or equal to 5 and triglyceride concentration less than or equal to 2.3 mmol/l. In subjects with triglyceride concentration greater than 2.3 mmol/l and LDL-C/HDL-C ratio less than or equal to 5, RR was close to unity (1.1), whereas in those with triglyceride level less than or equal to 2.3 mmol/l and LDL-C/HDL-C ratio greater than 5, RR was 1.2. The high-risk group with LDL-C/HDL-C ratio greater than 5 and triglyceride level greater than 2.3 mmol/l profited most from treatment with gemfibrozil, with a 71% lower incidence of coronary heart disease events than the corresponding placebo subgroup. In all other subgroups, the reduction in CHD incidence was substantially smaller. CONCLUSIONS. Serum triglyceride concentration has prognostic value, both for assessing coronary heart disease risk and in predicting the effect of gemfibrozil treatment, especially when used in combination with HDL-C and LDL-C.     

Coronary risk factors and the severity of angiographic coronary artery disease in members of high-risk pedigrees.

Affected members of early coronary pedigrees in Utah are at markedly increased risk for the development of clinical coronary heart disease (CHD). The relationship between the presence of coronary risk factors and the severity of angiographic coronary artery disease (CAD) in 53 members of high-risk Utah pedigrees was examined. Mean angiographic severity scores were higher in familial hypercholesterolemia or familial low high-density lipoprotein cholesterol (HDL-C) pedigrees than in type III hyperlipidemia or familial combined hyperlipidemia pedigrees. One sibling pair with hyperhomocyst(e)inemia had the highest mean angiographic severity scores. Clinical CHD (p less than 0.0001), increasing low-density lipoprotein cholesterol (LDL-C) (p = 0.0107), and decreasing HDL-C (p = 0.0068) were significant predictors of angiographic CAD severity. There appeared to be an interaction between gender and body mass index but not between gender and serum lipids in the prediction of angiographic CAD severity. Results of the present study in members of high-risk Utah pedigrees are consistent with results from other angiographic studies in non-high-risk persons. Of particular interest is the suggested independent predictive value of low HDL-C for angiographic CAD severity in members of high-risk pedigrees.     

Impact of obesity in primary hyperlipidemias

Obesity is frequently associated with high plasma triglyceride and reduced plasma high-density lipoprotein (HDL)-cholesterol (HDL-C) levels, and an increased concentration of apoB-carrying lipoproteins. The effects of obesity on lipid metabolism are mainly mediated by insulin resistance and, as central (visceral) obesity significantly increases insulin resistance, it aggravates these lipid changes. We have reviewed the impact of obesity on lipid metabolism in different types of primary hyperlipidemias. Obesity is not common in primary (familial and polygenic) hypercholesterolemias, and insulin resistance is infrequent; various investigators have found no or only a weak association between plasma cholesterol concentrations and insulin levels. On the other hand, in familial hypertriglyceridemia (type IV) and familial combined hyperlipidemia (FCH), obesity and insulin resistance are common and, when present, contribute to a further deterioration in the lipid profile. Weight loss in most of these patients is accompanied by a significant decrease in plasma triglyceride levels and an increase in HDL-C. Reviewing the data published by our group, we show that insulin resistance is an important component of the metabolic derangement in FCH subjects; high fasting plasma free fatty acids and triglycerides levels correlate to insulin resistance, thus linking this abnormality to lipid metabolism. A high waist/hip ratio (indicating visceral fat deposits) exacerbates insulin resistance, but this is also present in lean FCH subjects. Furthermore, insulin resistance is associated with a higher prevalence of coronary heart disease in this group of subjects.     

冠心病患者年龄与血脂异常的关系

目的:探讨不同年龄冠心病病人血脂水平的差异,为临床更合理地调脂治疗提供依据。方法:采用回顾性方法对120例70～86岁(A组)和 162例 35～60岁(B组)的冠心病病人的血脂水平进行对比分析。结果:老年冠心病病人的血清总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)水平略高于中年组,但无统计学意义;高密度脂蛋白胆固醇(HDL-C)老年组高于中年组(P<0.05);而血清甘油三酯(TG)水平则中年组非常显著高于老年组(P<0.01)。结论:在各年龄组都要严格控制TC和LDL-C水平以预防冠心病,对于中年人群还需注意降低过高的TG水平,提高HDL-C水平。     

Total cholesterol and lipoproteins in school children: prediction of coronary heart disease in adult relatives

The distribution of risk factors and the prevalence of coronary heart disease (CHD) were studied in 850 first- and second-degree relatives of 98 healthy index cases selected from 3666 school children surveyed for lipid levels in Rochester, Minnesota. Three groups of families were based on an index child's total plasma cholesterol level: 18 families with a child in less than the fifth percentile (low-cholesterol group), 47 with a child in the fifth to ninety-fifth percentiles (middle-cholesterol group) and 33 with a child in greater than the ninety-fifth percentile (high-cholesterol group). The children's cholesterol levels clustered with those of their relatives; mortality due to CHD before age 65 was increased by 2.5 times in grandfathers of index cases in the high-cholesterol group compared with those of the middle-cholesterol group (p less than 0.016). The prevalence of CHD in all the grandfathers was associated with an index child's total cholesterol, more strongly associated with an index child's low-density lipoprotein cholesterol level and most strongly associated with an index child's high-density lipoprotein cholesterol level as a fraction of total cholesterol. This study establishes that childhood lipid and lipoprotein levels from a single cross-sectional survey identify families at elevated risk for CHD.     

SERUM LIPID AND APOLIPOPROTEIN A AND B LEVELS IN FAMILIAL HYPERCHOLESTEROLEMIA

Serum lipid and apolipoprotein A (apo A) and B (apo B) levels were studied in a family with familial hypercholesterolemia (FH), which comprised two heterozygous parents, five heterozygous children, one homozygote and one normal child. Lipid levels were compared with those of age- and sex-matched normal controls. All subjects with FH had total serum cholesterol and low density lipoprotein-cholesterol (LDL-C) levels greater than the 90th percentile value for the reference range. High density lipoprotein-cholesterol (HDL-C) levels were less than the corresponding 13th percentile in heterozygous subjects. The homozygous child had grossly elevated levels of LDL-C and apo B, and very low levels of HDL-C and apo A. The most powerful discriminating variable between normal, heterozygous and homozygous family members was the LDL-C/HDL-C ratio.     

冠状动脉病变与血脂代谢异常的相关性

目的　探讨冠状动脉病变与血脂代谢紊乱的关系。方法　将2 6 7例疑似冠心病的患者依据冠状动脉造影结果分为对照组(非冠心病组) 1 0 1例,冠心病组1 6 6例,其中单支病变组54例,双支病变组6 8例,三支病变组4 4例,同时测定并统计分析血脂各成分及其比值与冠状动脉病变之间的关系。结果　冠心病(CHD)组总胆固醇(TC)、低密度脂蛋白胆固醇(LDL- C)、甘油三脂(TG)水平明显高于对照组,高密度脂蛋白胆固醇(HDL C)水平明显低于对照组,差异有统计学意义。随着冠状动脉病变范围的增加,TC、LDL C、载脂蛋白B(ApoB)、TC HDL- C、LDL- C HDL- C升高,HDL- C降低,与对照组比较,差异有统计学意义。冠心病组血脂各组分和其比值与冠状动脉积分的相关分析表明,TC HDL- C、LDL -C HDL -C与冠状动脉病变的相关性最强。结论　血脂代谢紊乱的严重程度与冠状动脉病变的严重程度是一致的,通过异常的血脂代谢有可能初步预测冠状动脉病变,其中LDL- C HDL- C、TC- HDL C比值优于其他血脂指标。