A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

In vivo low density lipoprotein oxidation relates to coronary reactivity in young men




TekijätRaitakari OT, Pitkanen OP, Lehtimaki T, Lahdenpera S, Iida H, YlaHerttuala S, Luoma J, Mattila K, Nikkari T, Taskinen MR, Viikari JSA, Knuuti J

KustantajaELSEVIER SCIENCE INC

Julkaisuvuosi1997

JournalJournal of the American College of Cardiology

Tietokannassa oleva lehden nimiJOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

Lehden akronyymiJ AM COLL CARDIOL

Vuosikerta30

Numero1

Aloitussivu97

Lopetussivu102

Sivujen määrä6

ISSN0735-1097

DOIhttps://doi.org/10.1016/S0735-1097(97)00103-4


Tiivistelmä
Objectives. This study was undertaken to examine the relation of in vivo low density lipoprotein (LDL) oxidation and other lipid risk factors to coronary reactivity in normal subjects.Background. Experimental studies have shown that oxidized LDL (ox-LDL) particles are injurious to the vascular wall by impairing its normal vasodilator function.Methods. We used noninvasive positron emission tomographic (PET) imaging with intravenous dipyridamole to measure coronary flow reserve, a marker of coronary endothelial and smooth muscle function, in 30 healthy men (mean [+/-SD] age 34.4 +/- 3.2 years). As a marker of in vivo LDL oxidation, the autoantibody titer against ox-LDL was measured by the enzyme-linked immunosorbent assay method.Results. Plasma levels of autoantibody titer against ox-LDL were inversely associated with coronary flow reserve (r = -0.42, p = 0.023). High LDL cholesterol levels (above median >3.0 mmol/liter) were associated with a low coronary how reserve only in subjects expressing simultaneously high levels of ox-LDL titer (above median). Subjects with simultaneously high levels of LDL cholesterol and ox-LDL titer had lower coronary how reserve values than subjects in other groups (3.89 vs. >5.0 in Other groups, p = 0.066).Conclusions. These data provide evidence for the role of ox-LDL in affecting the coronary reactivity in vivo and support the concept that oxidative modification of LDL particles provides a mechanism by which high LDL concentrations exhibit injurious effects on the coronary vascular bed. (C) 1997 by the American College of Cardiology.



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