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The early lesions of atherosclerosis in youth are strongly related to antemortem levels of total and low-density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglyceride to ponderal index and to blood pressure. The major apolipoproteins of LDL and high-density lipoprotein (HDL), apoB and apoA1 respectively, and levels of Lp(a) lipoprotein are often abnormal in children born in a family with premature coronary artery disease (CAD). Other risk factors for CAD include obesity, high blood pressure, cigarette smoking, diabetes mellitus, positive family history of CAD, and physical inactivity. Children from families with premature CAD, dyslipidemia, or hypertension, and/or two other risk factors should have a lipoprotein profile determined. Treatment begins with a diet low in total fat, saturated fat, and cholesterol, combined with treatment of overnutrition and obesity, if necessary, and regular habits of aerobic physical activity. Children with inherited disorders of LDL metabolism may require the addition of lipid-lowering therapy. The early detection and treatment of youth at risk for premature CAD offer the greatest promise to decrease morbidity and mortality.
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PMID:Detection and treatment of elevated blood lipids and other risk factors for coronary artery disease in youth. 769 75

The early lesions of atherosclerosis in youth are strongly related to antemortem levels of total and low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglyceride, to ponderal index and to systolic and diastolic blood pressure. The major apolipoproteins of LDL and high density lipoprotein (HDL), apo B and apo A1, respectively, as well as levels of Lp(a) lipoprotein are often abnormal in children born to a parent with coronary artery disease (CAD). Other risk factors for CAD include obesity, high blood pressure, cigarette smoking, diabetes mellitus, positive family history of CAD and physical inactivity. Children from families with premature CAD, familial dyslipidemia or hypertension, and/or two other risk factors should have a lipoprotein profile determined. The first form of treatment is a diet low in total fat, saturated fat and cholesterol, combined with treatment of overnutrition and obesity, if necessary, and regular habits of aerobic physical activity. Children with inherited disorders of LDL metabolism may require the addition of lipid lowering therapy. The early detection and treatment of youth at risk for premature CAD offers the greatest promise to decrease morbidity and mortality.
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PMID:Dyslipoproteinemia and other risk factors for atherosclerosis in children and adolescents. 780 29

The purpose of this report is to compare the distribution of total lipoprotein(a) [Lp(a)] mass in a population-based sample of blacks and whites, and to investigate the association of Lp(a) with other cardiovascular risk factors. A cross-sectional study design was used. Black and white men and women (n = 4125), aged 23-35 from the Coronary Artery Risk Development in Young Adults Study had the following data collected: Lp(a), lipids and lipoproteins, other metabolic parameters, anthropometry, physical activity, dietary intake, cigarette use, and alcohol use. Blacks had concentrations of Lp(a) approximately three-fold higher than whites. Medians were: black men 21.5 mg/dL, black women 23.9 mg/dL, white men 6.1 mg/dL, and white women 6.4 mg/dL. Lp(a) concentrations were higher in women than in men. Lp(a) was not consistently associated with smoking, alcohol consumption, physical activity, dietary fat, or obesity. In stepwise regression analyses in both blacks and whites, Lp(a) was consistently associated with low-density lipoprotein (LDL) cholesterol, fibrinogen, and apoB; regression models explained about 7% of the variance in Lp(a). In whites, Lp(a) tended to be higher in those with a positive family history of myocardial infarction. The large differences in Lp(a) between blacks and whites, and the absence of association with many other variables are consistent with previous suggestions that Lp(a) concentration is in large part genetically determined. The association of Lp(a) with LDL and fibrinogen, two strong risk factors for cardiovascular disease (CVD), could represent part of the mechanism of the CVD risk associated with Lp(a) in other studies. Longitudinal data are needed to determine the extent to which Lp(a) will independently predict disease, especially in diverse ethnic groups.
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PMID:Concentrations of Lp(a) in black and white young adults: relations to risk factors for cardiovascular disease. 798 40

In order to elucidate the influence of the risk factors of coronary heart disease on the fibrinolytic activity, relationships between blood pressure, body mass index (BMI), plasma lipoprotein (a) (Lp(a)) level and the plasma levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) were analyzed in the subjects with mild hypertension. Systolic blood pressure showed a positive correlation with total PAI-1 and free PAI-1. Diastolic blood pressure showed no correlation with these proteins involved in the fibrinolytic system. BMI had a positive correlation with total PAI-1, free PAI-1 and euglobulin clot lysis time (ECLT). Plasma Lp(a) level showed correlation with neither blood pressure nor fibrinolytic parameters, but it showed weak negative correlation with body mass index (BMI). These results suggest that high blood pressure and obesity tend to increase free PAI-1 which reduces fibrinolytic activity. Lp(a), however, seems not to influence directly the fibrinolytic system but may work to decrease fibrinolytic activity only in conjunction with other risk factors. The effects of daily drinking of alcohol and smoking on the fibrinolytic system were also investigated in the present study and we obtained the results that habitual drinking increased plasma levels of both tPA and PAI-1 whereas smoking did not affect fibrinolytic activity. These results suggest that risk factors for coronary heart disease such as hypertension and obesity are closely related to the impaired fibrinolysis.
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PMID:Impaired fibrinolysis in hypertension and obesity due to high plasminogen activator inhibitor-1 level in plasma. 835 19

In subjects with insulin-dependent diabetes mellitus, microalbuminuria has been associated with increased triglyceride and lipoprotein (a) (Lp[a]) concentrations and increased blood pressure. However, few studies have examined whether this association is present in subjects with non-insulin-dependent diabetes mellitus (NIDDM). We measured lipids, lipoproteins, Lp(a), blood pressure, and albumin excretion in 234 subjects with NIDDM from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Seventy-two subjects had microalbuminuria (> or = 30 mg/dl). These subjects had increased systolic and diastolic blood pressures and higher fasting glucose concentrations relative to subjects without microalbuminuria. However, there were no significant differences between subjects with and without microalbuminuria with respect to lipids, lipoproteins, Lp(a), self-reported myocardial infarction, obesity, or body fat distribution. Subjects with diabetic retinopathy had increased microalbuminuria. In multivariate analysis both glycemia and blood pressure continued to be significantly related to the presence of microalbuminuria. We conclude that NIDDM subjects with microalbuminuria have elevated blood pressure and more severe glycemia but do not have a significantly more atherogenic pattern of lipids, lipoproteins, or Lp(a) than subjects without microalbuminuria.
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PMID:Cardiovascular risk factors in non-insulin-dependent diabetic subjects with microalbuminuria. 842 56

Lipoprotein(a) (Lp[a]) is generally considered to be a risk factor for the development of cardiovascular disease, but little is known about the possible influence of obesity on the circulating levels of this lipoprotein. The present study was undertaken to examine this aspect in 136 menstrually active women by comparing the serum concentrations of Lp(a) between 72 obese and 64 age-matched nonobese women. Since an adverse effect of androgens and a protective effect of estrogens have been described for plasma lipoprotein profiles in obese women, the relation between the circulating levels of Lp(a) and those of these other hormones was also investigated in obese patients. In addition, other lipoproteins, anthropometric parameters (body mass index and waist-to-hip ratio), and insulin were evaluated. The levels of Lp(a) were not significantly different (Mann-Whitney U test chi 2, 3.59; p = 0.0582 [NS]) between obese (rank sum, 5,367) and control (rank sum, 3,949) women; in addition, the percentage of patients with high Lp(a) levels (cutoff defined at 30 mg/dL) did not differ between the two groups (obese women, 30%; control, 21.8%; chi 2, 0.90; two-sided p = 0.341 [NS]). Moreover, no correlation was found between Lp(a) and body mass index. Lastly, when the Lp(a) prevalence odds ratio for obesity was examined by adjusting the levels of this lipoprotein for age, triglycerides, total cholesterol, and high density lipoprotein cholesterol, the probability value (0.88) was far from significant. In obese women, no correlation was found between the logarithmically transformed Lp(a) concentrations and all the other variables evaluated in the study. In conclusion, the present study shows that the circulating levels of Lp(a) are not influenced by body weight and cardiovascular risk factors commonly associated with obesity, such as enhanced androgenic activity, hyperinsulinemia, adverse lipoprotein profile, and abdominal fat accumulation.
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PMID:Relation between sex hormones and serum lipoprotein and lipoprotein(a) concentrations in premenopausal obese women. 848 18

The present report is a description of the characteristics of a studied population and of the methodology used in a study performed to investigate high blood pressure prevalence and cardiovascular risk factors among the adult population of Mexico City. A cross-sectional study was conducted from January 1991 to March 1992. Random samplings of multiple stages was used and 825 adult subjects were studied in Mexico City. The following measurements were registered: blood pressure, body mass index (BMI), waist-hip ratio (WHR), total cholesterol (TC), triglycerides (TG), high density lipoproteins (HDL-C) and low density lipoproteins (LDL-C), lipoprotein (a) (Lp(a)), glucose and insulin. Personal and family history of cardiovascular illness were investigated, as well as exposure to some risk factors such as smoking, alcohol consumption and sedentarism. The response rate was 86.6%. The prevalence of high blood pressure was 21.1%, and of non-insulin dependent diabetes mellitus was 8.7%. Frequency of dyslipidemia in the studied sample was 24.4% for high TG, 23.6% for low HDL-C, 23.6% for high LDL-C, 14.9% for Lp(a) excess (Lp(a) > or = 30 mg/dl; overweight and obesity were more prevalent among women. The diversity of living conditions among the population of Mexico City was included in the sampling strategy design, not only to register the high blood pressure (HBP) frequency in each stratum but to identify other cardiovascular risk factors which could be decisive in the development of HBP. Regarding the features of the studied population, BMI did not reveal differences among men, but their TG levels were higher and HDL levels lower than those of other populations. In women, the results obtained for BMI, WHR, lipids and lipoproteins were also higher compared with the mean reported for other populations.
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PMID:High blood pressure and cardiovascular risk factors in an adult population of Mexico City. Characteristics of the studied population. 869 67

Diabetes mellitus has been shown to be associated with lipid abnormalities. Prior studies have indicated that women with diabetes have a risk of coronary heart disease similar to that of men. We compared lipid parameters in diabetic and nondiabetic participants in cycle 3 of the Framingham Offspring Study. Values for plasma total cholesterol (TC), triglyceride, lipoprotein, cholesterol, apolipoprotein (apo) A1, B, apo and lipoprotein(a) [Lp(a)] and low-density lipoprotein (LDL) particle size were analyzed in 174 diabetic and 3,757 nondiabetic subjects. Data from a total of 2,025 men and 2,042 women participating in the third examination (1983 to 1987) of the Framingham Offspring Study were subjected to statistical analysis. Male and female diabetics showed lower high-density lipoprotein (HDL) cholesterol, higher triglycerides, higher very-low-density lipoprotein (VLDL) cholesterol, lower apo A1, and higher LDL particle scores, indicating smaller size, than nondiabetics. Female diabetics also showed significantly higher TC and apo B values than nondiabetics. The results remained statistically significant after controlling for obesity and menopausal status. The presence of small dense LDL particles (pattern B) was highly associated with diabetes and hypertriglyceridemia in both sexes, and the relative odds for pattern B remained significant in women but not in men after adjustment for age and hypertriglyceridemia. No differences in apo E isoform distribution were found for diabetics and nondiabetics. Diabetes was not associated with elevated LDL cholesterol levels. In conclusion, diabetics have lower HDL cholesterol and higher triglyceride levels and are more likely to have small dense LDL particles. Diabetes is not a secondary cause of elevated LDL cholesterol. Lipid screening of diabetics should include full quantification of lipids for proper assessment of potential atherosclerotic risk.
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PMID:Lipoproteins, apolipoproteins, and low-density lipoprotein size among diabetics in the Framingham offspring study. 884 83

Patients with diabetes mellitus have a higher rate of mortality than the general population. This higher mortality may be attributed mainly to cardiovascular disease. A high prevalence of dyslipidemia in diabetics can be one of the reasons for this. The most commonly recognized lipid abnormality in non-insulin-dependent diabetics (NIDDM) is hypertriglyceridemia, which is known to be an independent risk factor for coronary heart disease in diabetics. Hypertriglyceridemia can be produced by two mechanisms, increased synthesis of very-low-density lipoprotein (VLDL) triglyceride and removal defect of plasma triglyceride. It has been a matter of debate whether insulin always stimulates hepatic VLDL secretion but it is generally accepted that insulin deficiency results in an impairment of plasma triglyceride clearance. Considerable attention has recently been focused on the atherogenecity of postprandial hyperlipidemia, remnant lipoproteins, small, dense LDL, lipoprotein (a) [Lp(a)] and isolated hypo-alphalipoproteinemia in NIDDM subjects. Several reports suggested that these atherogenic lipoprotein abnormalities are present in NIDDMs even if they are apparently normolipidemic. Association of visceral fat obesity, insulin resistance and nephropathy may aggravate the atherogenic lipoprotein profile. Therefore, we propose here that plasma lipid levels of diabetic subjects must be more strictly controlled than for the non-diabetic population in order to avoid an increased risk for coronary heart disease. If they are obese or associated with insulin resistance or nephropathy, these conditions should be carefully controlled.
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PMID:Dyslipidemia in diabetes mellitus. 887 70

One of the characteristics of peripheral vascular disease in diabetic patients is that it occurs at the time of detection of diabetes mellitus. As one of the possible pathogenic mechanisms, in non-smokers, is the sol-called metabolic syndrome (obesity, disorders in regard to metabolism of lipids and carbohydrates and hypertension). Lipoprotein Lp(a) is the most atherogenic among lipoproteins. While data on coronary arterial disease exist, although contradictory, there is a small number of those which document the same for peripheral vascular occlusive disease in diabetics. Two patients, non-smokers, with characteristic constellation of risk factors, are described as possible models for further epidemiologic examinations.
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PMID:[The metabolic syndrome and hyper-Lp(a)-lipoproteinemia in peripheral obliterative atherosclerosis: 2 case reports]. 892 51


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