The Relationship of Various Factors in the Pathogenesis of Atherosclerosis

1998 ◽  
Vol 4 (2) ◽  
pp. 105-110 ◽  
Author(s):  
Hüseyin Sönmez ◽  
Selma Süer ◽  
Turgut Ulutin ◽  
Emine Kökoglu ◽  
Nergiz Uçişik
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Plasminogen Activator ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Tissue Type ◽  
Control Group ◽  
Low Density ◽  
Lipid Parameters ◽  
Pai 1

In this study we investigated the levels of lipid parameters, fibronectin, tissue-type plasminogen activator and plasminogen activator inhibitor (t-PA-PAI-1) complex and si alidase in patients with coronary heart disease and a control group. Total cholesterol, triglyceride, low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) cholesterol and lipoprotein Lp(a), levels in patients with coronary heart disease were found to be significantly higher than in the control group (p < .001). High-density lipoprotein (HDL) cholesterol levels in patient group were significantly lower than control group (p < .001). Plasma fibronectin and t-PA-PAI-1 complex levels in patients with coronary heart disease were found to be significantly higher than control group (p < .05 and p < .001, respectively). In addition, we found that serum sialidase levels in patients with coronary heart disease were significantly higher than in the control group (p < .001). The electrophoretic mobility of lipoproteins from patients with coronary heart dis ease was found to be greater than those from the control group. As a result Lp(a) may play an important role in the pathogen esis of atherosclerosis by causing foam cell formation because of interacting with LDL or fibronectin and by interfering with the fibrinolytic system because of binding to plasminogen re ceptors. In addition, modifications of Lp(a) (including desi alylation) may effect these events. Key words: Coronary heart disease—tPA-PAI-1 complex-Fibronectin-sialidase-Lipid parameters.

Isolation of plasma small-dense low-density lipoprotein using a simple air-driven ultracentrifuge and quantification using immunassay of apolipoprotein B

2004 ◽  
Vol 42 (1) ◽  
Author(s):  
Valentine C. Menys ◽  
Yifen Liu ◽  
Michael I. Mackness ◽  
See Kwok ◽  
Muriel J. Caslake ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Heart Disease Risk ◽  
Apolipoprotein B ◽  
Disease Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Heart Disease Risk

AbstractSmall-dense low-density lipoprotein (SD-LDL) is associated with coronary heart disease risk. Current methods for its quantification are expensive, complex and time-consuming. Plasma was adjusted to a density (D) of 1.044 g/ml in a volume of 0.18 ml and centrifuged in a Beckman Airfuge at 160 000×

Familial hypercholesterolaemia

2020 ◽  
pp. 343-348
Author(s):  
Perry Elliott ◽  
Pier D. Lambiase ◽  
Dhavendra Kumar
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Inborn Error ◽  
Familial Hypercholesterolaemia ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Clinical Criteria ◽  
Premature Coronary Heart Disease ◽  
Coronary Artery Atherosclerosis

Familial hypercholesterolaemia (FH) is an inborn error of metabolism that leads to accumulation of low-density lipoprotein cholesterol (LDL-C) particles in the blood and premature coronary artery atherosclerosis. This chapter covers the clinical criteria for the diagnosis of FH, the genetics that underpins the condition, cascade testing, premature coronary heart disease, and treatment methods.

Association of apolipoprotein E polymorphism, low-density lipoprotein cholesterol, and coronary artery disease.

1986 ◽  
Vol 32 (5) ◽  
pp. 778-781 ◽  
Author(s):  
H J Lenzen ◽  
G Assmann ◽  
R Buchwalsky ◽  
H Schulte
Keyword(s):  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Apolipoprotein E ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Apolipoprotein E Polymorphism ◽  
Artery Disease

Abstract We determined the frequencies of genetic apolipoprotein E isoforms in 570 survivors of myocardial infarction, all with demonstrable coronary heart disease, as compared with 624 healthy persons. In controls, E-4/E-3 heterozygosity was associated with total cholesterol concentrations of 1985 (SD 364) mg/L and low-density lipoprotein (LDL)-cholesterol concentrations of 1306 (SD 332) mg/L. Significantly lower values, 1811 (SD 312) mg/L and 1121 (SD 274) mg/L, respectively, were observed for E-3/E-2 heterozygous persons. In survivors of myocardial infarction, the respective values were significantly higher than in controls, differing between E-4/E-3 and E-3/E-2 heterozygous patients by 233 and 220 mg/L, respectively. Moreover, E-4/E-3 heterozygosity was accompanied by earlier age of myocardial infarction (48.8 +/- 7.4 years) as compared with E-3/E-2 heterozygosity (53.4 +/- 6.9 years) and E-3/E-3 homozygosity (51.2 +/- 7.7 years). Evidently, apolipoprotein E polymorphism can contribute to total and LDL-cholesterol concentrations in serum, thereby affecting risk of coronary heart disease and myocardial infarction.

scholarly journals A Prospective Study of Trans Fatty Acids in Erythrocytes and Risk of Coronary Heart Disease

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1858-1865 ◽  
Author(s):  
Qi Sun ◽  
Jing Ma ◽  
Hannia Campos ◽  
Susan E. Hankinson ◽  
JoAnn E. Manson ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Fatty Acid ◽  
Acid Content ◽  
Low Density Lipoprotein ◽  
Fatty Acid Content ◽  
Density Lipoprotein ◽  
Elevated Risk ◽  
Low Density ◽  
Relative Risks

Background— High consumption of trans fat has been linked to the risk of coronary heart disease (CHD). We assessed the hypothesis that higher trans fatty acid contents in erythrocytes were associated with an elevated risk of CHD in a nested case-control study among US women. Methods and Results— Blood samples were collected from 32 826 participants of the Nurses’ Health Study from 1989 to 1990. During 6 years of follow-up, 166 incident cases of CHD were ascertained and matched with 327 controls. Total trans fatty acid content in erythrocytes was significantly correlated with dietary intake of trans fat (correlation coefficient=0.44, P <0.01) and was associated with increased plasma low-density lipoprotein cholesterol ( P for trend =0.06), decreased plasma high-density lipoprotein cholesterol concentrations ( P for trend <0.01), and increased plasma low-density lipoprotein to high-density lipoprotein ratio ( P for trend <0.01). After adjustment for age, smoking status, and other dietary and lifestyle cardiovascular risk factors, higher total trans fatty acid content in erythrocytes was associated with an elevated risk of CHD. The multivariable relative risks (95% confidence intervals) of CHD from the lowest to highest quartiles of total trans fatty acid content in erythrocytes were 1.0 (reference), 1.6 (0.7 to 3.6), 1.6 (0.7 to 3.4), and 3.3 (1.5 to 7.2) ( P for trend <0.01). The corresponding relative risks were 1.0, 1.1, 1.3, and 3.1 ( P for trend <0.01) for a total of 18:1 trans isomers and 1.0, 1.5, 2.5, and 2.8 ( P for trend <0.01) for a total of 18:2 trans isomers. Conclusions— These biomarker data provide further evidence that high trans fat consumption remains a significant risk factor for CHD after adjustment for covariates.

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