Apolipoprotein C-III glycoforms correlate heterogeneously with plasma lipid profile in subjects with coronary artery disease

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Abstracts / Atherosclerosis 252 (2016) e1ee196

HTG

Controls

P

N(femme/homme)

26(21/5)

20(11/9)

NS

Age. Year

42 ± 10

52 ± 17

NS

LPL mass T0. Ng/L

25.2 ± 11.6

49.0 ± 20.8

<0.001

LPL mass T10 Ng/L

259.0 ± 102.1

268.6 ± 54.3

NS

LPL activity T10 mmol/L/min

35.0 ± 12.2

34.8 ± 12.8

NS

LPL Specific activity Mmol/g/min

138.3 ± 38.3

128.1 ± 34.1

NS

Pearson correlation Preheparin mass

p

Specific activity

p

Preheparin mass

p

Specific activity

p

TG mmol/L

0.088

NS

0.248

NS

0.263

NS

0.069

NS

HDLc mmol/L

0.558

<0.005

0.037

NS

0.364

NS

0.059

NS

LDLc mmol/L

0.346

NS

0.064

NS

0.22

NS

0.036

NS

LDL mass T10 Ng/L

0.394

0.05

0.35

NS

0.539

0.01

0.269

NS

LPL activity T10 mmol/L/min

0.33

NS

0.285

NS

0.261

NS

0.831

<0.0001

DTG. %

0.06

NS

0.245

NS

0.253

NS

0.14

NS

DTG mmol/L

0.246

NS

0.212

NS

0.335

NS

0.127

NS

Conclusions: In patients with TVHTG, simultaneous determination of LPL mass and activity (especially preheparinLPL concentration) is valuable to elucidate the type V hyperlipidemia complex heterogeneity. EAS16-0865, LIPOPROTEINS AND LIPID METABOLISM: APOB CONTAINING LIPOPROTEINS. APOLIPOPROTEIN C-III GLYCOFORMS CORRELATE HETEROGENEOUSLY WITH PLASMA LIPID PROFILE IN SUBJECTS WITH CORONARY ARTERY DISEASE C. Chiariello 1, A. Castagna 1, N. Martinelli 1, P. Guarini 1, M. Manfredi 2, E. S. Martinotti 3, E. Marengo 3, D. Cecconi 4, O. Ranzato 3, Olivieri 1. 1 University of Verona, Medicine, Verona, Italy; 2 ISALIT S.r.l.-, Sciences and Technological Innovation, Alessandria, Italy; 3 University of Piemonte Orientale, Sciences and Technological Innovation, Alessandria, Italy; 4 University of Verona, Biotechnology, Verona, Italy Objectives: Apolipoprotein C-III (ApoC-III) is well recognized as a main determinant of triglyceride (TG) plasma concentration and plays a crucial role in coronary artery disease (CAD). However, data on ApoC-III glycoforms are only sparse so far. The aim of this study was to quantify ApoC-III glycoforms in CAD patients and to assess their correlations with plasma lipids. Methods: ApoC-III glycoforms were analyzed by mass spectrometry in 55 subjects with clinically stable CAD (90.9% males, mean age 70.2 ± 7.9 years) within the framework of the Verona Heart Study. Results: Three different ApoC-III glycoforms were identified: non-sialylated (ApoC-III0), monosialylated (ApoC-III1), and disialylated isoforms (ApoC-III2). The analyses were performed on the relative proportion of ApoC-III glycoforms. ApoC-III0 correlated negatively with total ApoC-III concentration (R ¼ 0.351; P ¼ 0.009), ApoC-III1 had a positive correlation (R ¼ 0.382; P ¼ 0.004), while ApoC-III2 did not have significant correlation. The different glycoforms showed different pattern of correlations with the other parameters of plasma lipid profile. ApoC-III0 was inversely correlated with TG (R ¼ 0.421; P ¼ 0.001), total cholesterol (R ¼ 0.314; P ¼ 0.020), LDL cholesterol (R ¼ 0.317; P ¼ 0.018), ApoE (R ¼ 0.434; P ¼ 0.001), and Apo B (R ¼ 0.292; P ¼ 0.030), while ApoC-III1 was directly correlated with TG (R ¼ 0.438; P ¼ 0.001)), total cholesterol (R ¼ 0.280; P ¼ 0.038), LDL cholesterol (R ¼ 0.337; P ¼ 0.012), ApoE (R ¼ 0.457; P ¼ 0.001), and ApoB (R ¼ 0.288; P ¼ 0.033). On the other hand, no significant correlation was found for ApoC-III2. The ApoC-III1/ApoC-III0 ratio was a significant

predictor of both TG (b ¼ 0.201; P ¼ 0.025) and ApoE levels (b ¼ 0.270; P ¼ 0.016) in linear regression models adjusted for sex, age, and total ApoC-III concentration. Conclusions: ApoC-III glycoforms have heterogeneous correlations with plasma lipids in CAD patients, suggesting that they could have different metabolic properties and biological activities. EAS16-0962, LIPOPROTEINS AND LIPID METABOLISM: APOB CONTAINING LIPOPROTEINS. PLASMA APOLIPOPROTEIN CIII LEVELS AND INCIDENT CORONARY ARTERY DISEASE RISK: THE EPIC-NORFOLK PROSPECTIVE POPULATION STUDY J. van Capelleveen 1, S.J. Bernelot Moens 1, X. Yang 2, N.T. Wareham 3, K.T. Khaw 4, E.S.G. Stroes 1, J.L. Witztum 2, G.K. Hovingh 1, S.M. Boekholdt 5, S. Tsimikas 2. 1 Academic Medical Center, Vascular Medicine, Amsterdam, Netherlands; 2 University of California- San Diego, Department of Medicine, La Jolla- Ca, USA; 3 Addenbrooke's Hospital, Epidemiology Unit- Institute of Metabolic Science-, Cambridge, United Kingdom; 4 University of Cambridge, Institute of Public Health and Primary Care-, Cambridge, United Kingdom; 5 Academic Medical Center, Cardiology, Amsterdam, Netherlands Background. Apolipoprotein C-III (apoC-III) is a key regulator of triglyceride (TG) metabolism. Elevated TG and apoC-III levels are causally linked to coronary artery disease (CAD) risk. The mechanisms linking apoC-III to CAD risk remain largely unknown. Objectives. To test the association between apoC-III plasma levels and CAD risk in a large prospective cohort and explore which lipoprotein subfractions contribute to the association of apoC-III with CAD risk. Methods: Plasma apoC-III levels were measured at baseline in 2711 apparently healthy participants in a nested case-control study in the prospective EPIC-Norfolk study. During follow-up, 832 participants developed CAD. We assessed the association with incident CAD risk and lipoprotein subfractions, measured by nuclear magnetic resonance spectroscopy (NMR) and inflammatory markers. Results: ApoC-III levels were significantly associated with incident CAD risk in univariate analysis (odds ratio 1.90, 95% CI 1.47e2.45, for highest compared to lowest quintile), retaining significance after adjustment for traditional CAD risk factors (odds ratio 1.51, 95% CI 1.14e1.99). ApoC-III levels were positively associated with levels of very-low density lipoprotein (VLDL; r ¼ 0.25), intermediate-density lipoprotein (IDL; r ¼ 0.23) and