Literature DB >> 179743

Lp(a) lipoprotein/pre-beta1-lipoprotein, serum lipids and atherosclerotic disease.

G Dahlén, K Berg, M H Frick.   

Abstract

With appropriate electrophoretic techniques and fresh serum samples, the Lp(a) lipoprotein/pre-beta1-lipoprotein is demonstrable as a distinct zone in the area between beta-lipoprotein and ordinary pre-beta-lipoprotein, when sera which are strongly positive with respect to the Lp(a) antigen are analyzed. The Lp(a) lipoprotein is a genetically determined normal serum component. The phenotype Lp(a+) was found significantly more frequently in two series of patients with coronary heart disease (CHD) than in appropriate controls. The frequency difference between patients and controls was particularly pronounced for the Finnish samples studied, 55% of the patients having the phenotype Lp(a+), as opposed to only 31% of the healthy controls. As judged from electrophoresis strips, hibh concentrations of Lp(a) lipoprotein/pre-beta1-lipoprotein were positively correlated with coronary score as determined by angiography. This correlation was highly significant. Total serum cholesterol value was slightly higher in Lp(a+) than in Lp(a-) persons from two of the four population samples studied, but no statistically significant difference was found. Serum triglyceride levels exhibited a statistically insignificant trend towards higher values in Lp(a-) than in Lp(a+) individuals, in three of the four samples tested. The strong association between the phenotype Lp(a+) and CHD, as well as the correlation between high amounts of Lp(a) lipoprotein/pre-beta1-lipoprotein and coronary score on one hand, and the weak correlation between presence of Lp(a) lipoprotein/pre-beta1-lipoprotein and lipid values on the other, make it highly unlikely that the increased frequency of the Lp(a+) phenotype in CHD patients merely reflects an over-all increase of the intravascular pool of LDL and/or VLDL reflected in increased serum levels of cholesterol and/or triglycerides. By the same token, it is unlikely that the insignificant effect on lipid values can, on its own, explain the correlation between Lp(a) phenotype and CHD.

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Year:  1976        PMID: 179743     DOI: 10.1111/j.1399-0004.1976.tb01613.x

Source DB:  PubMed          Journal:  Clin Genet        ISSN: 0009-9163            Impact factor:   4.438


  6 in total

1.  Reduction of Lp(a) by different methods of plasma exchange.

Authors:  I Schenck; C Keller; S Hailer; G Wolfram; N Zöllner
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2.  Nicotinic acid inhibits hepatic APOA gene expression: studies in humans and in transgenic mice.

Authors:  Indumathi Chennamsetty; Karam M Kostner; Thierry Claudel; Manjula Vinod; Sasa Frank; Thomas S Weiss; Michael Trauner; Gerhard M Kostner
Journal:  J Lipid Res       Date:  2012-08-28       Impact factor: 5.922

3.  Lipoprotein(a) is related to the extent of lesions in the coronary vasculature and to unstable coronary syndromes.

Authors:  J D Zampoulakis; A A Kyriakousi; K A Poralis; N T Karaminas; I D Palermos; E T Chimonas; D V Cokkinos
Journal:  Clin Cardiol       Date:  2000-12       Impact factor: 2.882

4.  Plasma lipoprotein levels and the prevalence of hyperlipoproteinemia in a Canadian working population.

Authors:  G J Jones; D Hewitt; G J Godin; W C Breckenridge; J Bird; M A Mishkel; G Steiner; J A Little
Journal:  Can Med Assoc J       Date:  1980-01-12       Impact factor: 8.262

5.  Genetic variation in lipoprotein (a) levels in families enriched for coronary artery disease is determined almost entirely by the apolipoprotein (a) gene locus.

Authors:  C A DeMeester; X Bu; R J Gray; A J Lusis; J I Rotter
Journal:  Am J Hum Genet       Date:  1995-01       Impact factor: 11.025

6.  Apolipoprotein(a) deposition in atherosclerotic plaques of cerebral vessels. A potential role for endothelial cells in lesion formation.

Authors:  D G Jamieson; D C Usher; D J Rader; E Lavi
Journal:  Am J Pathol       Date:  1995-12       Impact factor: 4.307

  6 in total

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