Loading…

Association of Lp-PLA2 with digital reactive hyperemia, coronary flow reserve, carotid atherosclerosis and arterial stiffness in coronary artery disease

Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has a powerful inflammatory and atherogenic action in the vascular wall and is an independent marker of poor prognosis in coronary artery disease (CAD). We investigate the association of Lp-PLA2 with markers of vascular dysfuncti...

Full description

Saved in:
Bibliographic Details
Published in:Atherosclerosis 2014-05, Vol.234 (1), p.34-41
Main Authors: Ikonomidis, Ignatios, Kadoglou, Nikolaos N.P, Tritakis, Vlassis, Paraskevaidis, Ioannis, Dimas, Kleanthi, Trivilou, Paraskevi, Papadakis, Ioannis, Tzortzis, Stavros, Triantafyllidi, Helen, Parissis, John, Anastasiou-Nana, Maria, Lekakis, John
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has a powerful inflammatory and atherogenic action in the vascular wall and is an independent marker of poor prognosis in coronary artery disease (CAD). We investigate the association of Lp-PLA2 with markers of vascular dysfunction and atherosclerosis with proven prognostic value in CAD. Methods In 111 patients with angiographically documented chronic CAD, we measured 1) carotid intima-media thickness (CIMT), 2) reactive hyperemia using fingertip peripheral arterial tonometry (RH-PAT), 3) coronary flow reserve (CFR), by Doppler echocardiography 4) pulse wave velocity (PWV) and 5) blood levels of Lp-PLA2. Results Patients with Lp-PLA2 concentration >234.5 ng/ml (50th percentile) had higher CIMT (1.44 ± 0.07 vs. 1.06 ± 0.06 mm), PWV (11.0 ± 2.36 vs. 9.7 ± 2.38 m/s) and lower RH-PAT(1.24 ± 0.25 vs. 1.51 ± 0.53) and CFR (2.39 ± 0.75 vs. 2.9 ± 0.86) compared to those with lower Lp-PLA ( p  
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2014.02.004