Decreased phosphatidylcholine plasmalogens--A putative novel lipid signature in patients with stable coronary artery disease and acute myocardial infarction

Iryna Sutter; Roland Klingenberg; Alaa Othman; Lucia Rohrer; Ulf Landmesser; Dierik Heg; Nicolas Rodondi; Francois Mach; Stephan Windecker; Christian M Matter; Thomas F Lüscher; Arnold von Eckardstein; Thorsten Hornemann

doi:10.1016/j.atherosclerosis.2016.01.003

Decreased phosphatidylcholine plasmalogens--A putative novel lipid signature in patients with stable coronary artery disease and acute myocardial infarction

Atherosclerosis. 2016 Mar:246:130-40. doi: 10.1016/j.atherosclerosis.2016.01.003. Epub 2016 Jan 6.

Authors

Affiliations

¹ Institute of Clinical Chemistry, University and University Hospital of Zurich, Zurich, Switzerland; Competence Center for Integrated Human Physiology, University of Zurich, Zurich, Switzerland.
² Department of Cardiology and Cardiovascular Research, University Heart Center, University Hospital Zurich, Zurich, University of Zurich, Switzerland.
³ Institute of Clinical Chemistry, University and University Hospital of Zurich, Zurich, Switzerland; Institute of Social and Preventive Medicine, Clinical Trials Unit, University of Bern, Bern, Switzerland.
⁴ Institute of Clinical Chemistry, University and University Hospital of Zurich, Zurich, Switzerland.
⁵ Competence Center for Integrated Human Physiology, University of Zurich, Zurich, Switzerland; Department of Cardiology and Cardiovascular Research, University Heart Center, University Hospital Zurich, Zurich, University of Zurich, Switzerland; Department of Cardiology, Charité Universitätsmedizin Berlin, Berlin, Germany.
⁶ Institute of Social and Preventive Medicine, Clinical Trials Unit, University of Bern, Bern, Switzerland.
⁷ Department of Internal Medicine, University Hospital Bern, Bern, Switzerland.
⁸ Cardiology, University Hospital Geneva, Switzerland.
⁹ Cardiovascular Center, University Hospital Bern, Switzerland.
¹⁰ Competence Center for Integrated Human Physiology, University of Zurich, Zurich, Switzerland; Department of Cardiology and Cardiovascular Research, University Heart Center, University Hospital Zurich, Zurich, University of Zurich, Switzerland.
¹¹ Institute of Clinical Chemistry, University and University Hospital of Zurich, Zurich, Switzerland; Competence Center for Integrated Human Physiology, University of Zurich, Zurich, Switzerland; Competence Center for Systems Physiology and Metabolic Diseases, ETH Zurich and University of Zurich, Zurich, Switzerland.
¹² Institute of Clinical Chemistry, University and University Hospital of Zurich, Zurich, Switzerland; Competence Center for Integrated Human Physiology, University of Zurich, Zurich, Switzerland; Competence Center for Systems Physiology and Metabolic Diseases, ETH Zurich and University of Zurich, Zurich, Switzerland. Electronic address: thorsten.hornemann@usz.ch.

PMID: 26773473
DOI: 10.1016/j.atherosclerosis.2016.01.003

Abstract

Objective: Glycerophospholipids and sphingolipids are structurally heterogeneous due to differences in the O- and N-linked fatty acids and head groups. Sphingolipids also show a heterogeneity in their sphingoid base composition which up to now has been little appreciated. The aim of this study was to investigate the association of certain glycerophospholipid and sphingolipid species with stable coronary artery disease (CAD) and acute myocardial infarction (AMI).

Methods: The lipid profile in plasma from patients with stable CAD (n = 18) or AMI (n = 17) was compared to healthy subjects (n = 14). Sixty five glycerophospholipid and sphingolipid species were quantified by LC-MS. The relative distribution of these lipids into lipoprotein fractions was analyzed.

Results: In the CAD cohort, 45 glycerophospholipid and sphingolipid species were significantly lower compared to healthy controls. In the AMI group, 42 glycerophospholipid and sphingolipid species were reduced. Four PC plasmalogens (PC33:1, PC33:2, PC33:3 and PC35:3) showed the most significant difference. Out of eleven analyzed sphingoid bases, four were lower in the CAD and six in the AMI group. Sphingosine-1-phosphate (S1P) levels were reduced in the AMI group whereas an atypical C16:1 S1P was lower in both groups. Phosphatidylcholine and sphingomyelin species were exclusively present in lipoprotein particles, whereas lysophosphatidylcholines were mainly found in the lipoprotein-free fraction. The observed differences were not explained by the use of statins as confirmed in a second, independent cohort.

Conclusions: Reduced levels of four PC plasmalogens (PC33:1, PC33:2, PC33:3 and PC35:3) were identified as a putatively novel lipid signature for CAD and AMI.

Keywords: Acute myocardial infarction; Coronary artery disease; Glycerophospholipids; Sphingolipids.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Aged
Biomarkers / blood
Case-Control Studies
Chromatography, Liquid
Coronary Artery Disease / blood*
Coronary Artery Disease / diagnosis
Female
Humans
Male
Mass Spectrometry
Middle Aged
Myocardial Infarction / blood*
Myocardial Infarction / diagnosis
Phosphatidylcholines / blood*
Plasmalogens / blood*
Predictive Value of Tests

Substances

Biomarkers
Phosphatidylcholines
Plasmalogens