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Lipoprotein‐associated phospholipase A 2 and cardiovascular disease risk in HIV infection
Author(s) -
Ross Eckard A,
Longenecker CT,
Jiang Y,
Debanne SM,
Labbato D,
Storer N,
McComsey GA
Publication year - 2014
Publication title -
hiv medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.53
H-Index - 79
eISSN - 1468-1293
pISSN - 1464-2662
DOI - 10.1111/hiv.12143
Subject(s) - medicine , lipoprotein associated phospholipase a2 , inflammation , population , fibrinogen , lipoprotein , immunology , immune system , endocrinology , cholesterol , environmental health
Objectives HIV ‐infected patients on antiretroviral therapy ( ART ) have an increased cardiovascular disease ( CVD ) risk as a result of heightened inflammation and immune activation, despite at times having normal lipids and few traditional risk factors. Biomarkers are needed to identify such patients before a clinical event. Lipoprotein‐associated phospholipase A 2 ( Lp‐PLA 2 ) predicts CVD events in the general population. This study investigated the relationship between Lp‐PLA 2 and markers of CVD risk, systemic inflammation, immune activation, and coagulation in HIV infection. Methods One hundred subjects on stable ART with normal fasting low‐density lipoprotein ( LDL ) cholesterol were enrolled in the study. Plasma Lp‐PLA 2 concentrations were measured by enzyme‐linked immunosorbent assay ( ELISA ; > 200 ng/mL was considered high CVD risk). Subclinical atherosclerosis, endothelial function, inflammation, immune activation and fasting lipids were also evaluated. Results The median age of the patients was 47 years and 77% were male. Median (range) Lp‐PLA 2 was 209 (71–402) ng/mL. Fifty‐seven per cent of patients had Lp‐PLA 2 concentrations > 200 ng/mL. Lp‐PLA 2 was positively correlated with soluble markers of inflammation or immune activation (tumour necrosis factor receptor‐ II , intercellular and vascular cellular adhesion molecules, and CD 14; all R = 0.3; P < 0.01), and negatively correlated with coagulation markers ( D ‐dimer and fibrinogen; both R = −0.2; P < 0.04). Lp‐PLA 2 was not correlated with lipids, coronary artery calcium score, or flow‐mediated vasodilation, but trended towards a significant correlation with carotid intima‐media thickness ( R = 0.2; P = 0.05). Conclusions In this population with stable ART and normal LDL cholesterol, Lp‐PLA 2 was in the high CVD risk category in the majority of subjects. Lp‐PLA 2 appears to be associated with inflammation/immune activation, but also with anti‐thrombotic effects. Lp‐PLA 2 may represent a valuable early biomarker of CVD risk in HIV infection before subclinical atherosclerosis can be detected.