Lipoprotein‐associated phospholipase A2 and cardiovascular disease risk in HIV infection. Issue 9 (20th March 2014)

• Record Type: Journal Article
• Authors: Ross Eckard, A; Longenecker, CT; Jiang, Y; Debanne, SM; Labbato, D; Storer, N; McComsey, GA
• Is Part Of: HIV medicine. Volume 15:Issue 9(2014:Oct.)
• Page Start: 537
• Page End: 546
• Publication Date: 2014-03-20
• Subjects: HIV infections -- Treatment -- Periodicals; HIV-positive persons -- Periodicals; HIV infections -- Treatment -- Decision making -- Periodicals; 616.9792
• DOI: 10.1111/hiv.12143
• Languages: English
• ISSNs: 1464-2662

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="hiv12143-sec-0001" sec-type="section"> <title>Objectives</title> <p>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<sub>2</sub> (Lp‐PLA<sub>2</sub>) predicts CVD events in the general population. This study investigated the relationship between Lp‐PLA<sub>2</sub> and markers of CVD risk, systemic inflammation, immune activation, and coagulation in HIV infection.</p> </sec> <sec id="hiv12143-sec-0002" sec-type="section"> <title>Methods</title> <p>One hundred subjects on stable ART with normal fasting low‐density lipoprotein (LDL) cholesterol were enrolled in the study. Plasma Lp‐PLA<sub>2</sub> 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.</p> </sec> <sec id="hiv12143-sec-0003" sec-type="section"> <title>Results</title> <p>The median age of the patients was 47 years and 77% were male. Median (range) Lp‐PLA<sub>2</sub> was 209 (71–402) ng/mL. Fifty‐seven per cent of patients had Lp‐PLA<sub>2</sub> concentrations > 200 ng/mL. Lp‐PLA<sub>2</sub> was positively correlated with soluble markers of inflammation or immune activation (tumour necrosis factor receptor‐II, intercellular and vascular cellular adhesion molecules, and CD14; all <italic>R</italic> = 0.3; <italic>P</italic> < 0.01), and negatively correlated with coagulation markers (D‐dimer and fibrinogen; both <italic>R</italic> = −0.2; <italic>P</italic> < 0.04). Lp‐PLA<sub>2</sub> was not correlated with lipids, coronary artery calcium score, or flow‐mediated vasodilation, but trended towards a significant correlation with carotid intima‐media thickness (<italic>R</italic> = 0.2; <italic>P</italic> = 0.05).</p> </sec> <sec id="hiv12143-sec-0004" sec-type="section"> <title>Conclusions</title> <p>In this population with stable ART and normal LDL cholesterol, Lp‐PLA<sub>2</sub> was in the high CVD risk category in the majority of subjects. Lp‐PLA<sub>2</sub> appears to be associated with inflammation/immune activation, but also with anti‐thrombotic effects. Lp‐PLA<sub>2</sub> may represent a valuable early biomarker of CVD risk in HIV infection before subclinical atherosclerosis can be detected.</p> </sec> </abstract>