Document Detail


Reduction of arteriosclerotic nanoplaque formation and size by n-3 fatty acids in patients after valvular defect operation.
MedLine Citation:
PMID:  19729934     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND/METHODS: Coating a silica surface with the isolated lipoprotein receptor heparan sulfate proteoglycan (HS-PG) from arterial endothelium and vascular matrices, we could observe the very earliest stages of arteriosclerotic plaque development by ellipsometric techniques in vitro (patent EP 0 946 876). This so-called nanoplaque formation is represented by the ternary aggregational complex of the HS-PG receptor, lipoprotein particles and calcium ions. The model was validated in several clinical studies on statins in cardiovascular high-risk patients applying their native blood lipoprotein fractions. RESULTS: In 7 patients who had undergone a valvular defect operation, the reduction of arteriosclerotic nanoplaque formation in normal Krebs solution amounted to 6.1 +/- 2.3% (p < 0.0156) and of nanoplaque size to 37.5 +/- 13.2% (p < 0.0312), respectively, after a 3-month therapy with n-3 fatty acids (3 ..3 g daily, Ameu 500 mg). Additionally, the quotient oxLDL/LDL was lowered by 6.8 +/- 2.1% (p < 0.0166), the MDA concentration remained unchanged and the lipoprotein(a) concentration decreased by 15.8 +/- 5.6% (p < 0.0469) in the patients' blood. The concentration of the nanoplaque promoting particles VLDL and total triglycerides was diminished by 34.1 +/- 11.6% (p < 0.0469) and 26.7 +/- 10.8% (p < 0.0156), respectively. Furthermore, the ratio of the strongly atherogenic small dense to the total LDL cholesterol (LDL5+LDL6)/LDLtot decreased by 9.9 +/- 3.0% (p < 0.0174). CONCLUSIONS: A combinatorial regression analysis revealed a basis for a mechanistic explanation of nanoplaque reduction under n-3 fatty acid treatment. This effect was possibly due to the beneficial changes in lipid concentrations and an attenuation of the risk factors oxLDL/LDL and (LDL5+LDL6)/LDLtot.
Authors:
Cordelia Koppe; Miguel Rodr?guez; Karl Winkler; Jens Pietzsch; Konrad Neumann; Nicola E Hiemann; Roland Hetzer; Martin Malmsten; G?nter Siegel
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Publication Detail:
Type:  Journal Article     Date:  2009-08-13
Journal Detail:
Title:  Forschende Komplement?rmedizin (2006)     Volume:  16     ISSN:  1661-4127     ISO Abbreviation:  Forsch Komplementmed     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-09-04     Completed Date:  2010-02-01     Revised Date:  2010-05-13    
Medline Journal Info:
Nlm Unique ID:  101269884     Medline TA:  Forsch Komplementmed     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  237-45     Citation Subset:  IM    
Copyright Information:
Copyright 2009 S. Karger AG, Basel.
Affiliation:
Institute of Physiology, Charit?, Campus Benjamin Franklin, Berlin, Germany.
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MeSH Terms
Descriptor/Qualifier:
Aged
Arteriosclerosis / pathology*,  prevention & control*
Calcium / blood
Endothelium, Vascular / pathology
Fatty Acids, Omega-3 / administration & dosage*
Female
Heart Valve Diseases / pathology,  surgery*
Heart Valves / pathology
Humans
Lipids / blood
Lipoproteins / blood
Male
Middle Aged
Models, Cardiovascular
Nanotechnology
Chemical
Reg. No./Substance:
0/Fatty Acids, Omega-3; 0/Lipids; 0/Lipoproteins; 7440-70-2/Calcium
Comments/Corrections
Erratum In:
Forsch Komplementmed. 2009 Oct;16(5):312

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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