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Rivista di Angiologia

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899

Periodicità: Bimestrale

ISSN 0392-9590

Online ISSN 1827-1839


International Angiology 2000 Dicembre;19(4):331-6


The independent correlation of the impact of lipoprotein(a) levels and apolipoprotein E polymorphism on carotid artery intima thickness

Horejsí B., Spacil J., Ceska R., Vrablík M., Haas T., Horíneck A.

III Depart­ment of Inter­nal Med­i­cine of The ­Charles Uni­ver­sity ­Prague, Praha Czech Repub­lic

Back­ground. Apo­lip­o­pro­tein E (apoE) plays a key role in lip­o­pro­tein metab­olism. It ­occurs in three iso­forms E2, E3 and E4. These iso­forms have dif­fer­ent ­impacts on plas­ma lip­o­pro­tein lev­els. The ­allele, or gene, cod­ing apoE4 is con­sid­ered a can­di­date for pre­ma­ture ath­ero­scler­o­sis devel­op­ment while the apoE2 gene is ­assumed to be pro­tec­tive. Lip­o­pro­tein(a) is also ather­o­gen­ic and its ­increased plas­ma con­cen­tra­tion is pre­sumed to be an inde­pen­dent risk fac­tor for pre­ma­ture ath­ero­scler­o­sis. Lip­o­pro­tein(a) is a pro­tein depos­it­ing direct­ly into the ath­e­rom­a­tous ­plaques, enhanc­ing cho­les­te­rol oxi­da­tion, com­pet­i­tive­ly inhib­it­ing plas­mi­no­gen for­ma­tion and thus hav­ing a pro­throm­bo­gen­ic ­effect. The aim of our study was to estab­lish a rela­tion­ship ­between com­mon carot­id ­artery inti­ma thick­ness and two inde­pen­dent risk fac­tors, apoE poly­mor­phism and ele­va­tion of plas­ma lip­o­pro­tein(a) lev­els.
Meth­ods. A cross-sec­tion­al study was per­formed on 114 ­patients who were ­referred to the lipid clin­ic for pri­mary hyper­li­pop­ro­tei­nae­mia. The ­patients ­received no treat­ment prior to exam­ina­tion. Plas­ma lev­els of total cho­les­te­rol, tri­gly­ce­rides, HDL-cho­les­te­rol, LDL-cho­les­te­rol, apoA, apoB, lip­o­pro­tein(a) and the apoE gen­o­type were deter­mined and the carot­id ­artery inti­ma thick­ness was meas­ured using ultra­so­nog­ra­phy.
­Results. The rel­a­tive fre­quen­cies of apoE2, E3 and E4 were 0.049, 0.830 and 0.121. The equal­ity of carot­id inti­ma thick­ness was test­ed using the Krusk­al-Wal­lis test. ­Medians of inti­ma thick­ness in a sub­group with the ­allele E2 were 0.72 mm, in a sub­group with the E3/E3 gen­o­type 0.70 mm and in a sub­group with the E4 ­allele 0.80 mm. The rela­tion­ship ­between carot­id inti­ma thick­ness and lip­o­pro­tein(a) lev­els was test­ed using ­Spearman’s cor­re­la­tion coef­fi­cient.
Con­clu­sions. No sta­tis­ti­cal­ly sig­nif­i­cant dif­fer­enc­es of carot­id inti­ma thick­ness among sub­groups divid­ed accord­ing to their apoE gen­o­type were found. No rela­tion­ship ­between carot­id inti­ma thick­ness and lip­o­pro­tein(a) lev­els was found. On the con­trary a close rela­tion­ship ­between carot­id inti­ma thick­ness and age and also some of the plas­ma lipid var­i­ables was record­ed using the meth­od of mul­ti­var­i­ate lin­e­ar regres­sion.

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