Abstract
Alterations in lipid metabolism mediated by oxidative stress play a key role in the process of atherosclerosis and superimposed thrombosis; these can lead to acute coronary syndrome (ACS) and acute ischemic stroke (AIS). Multiple studies have shown that the formation of atheromatous lesions is initiated by oxidation of low-density lipoproteins incorporated into the intima of the vessel wall. Here, we studied lipids in plasma samples from three cohorts: 61 patients with ACS (group A), 49 patients with AIS (group D), and 82 controls (group K). Untargeted lipidomics based on high-performance liquid chromatography coupled to mass spectrometry (UHPLC-HRMS) was employed to obtain comprehensive information on whether relationships exist between these patient categories based on lipid patterns. In addition, malondialdehyde (MDA) as a standard marker of oxidative stress was monitored. The most characteristic lipids in group K were fatty acyls of hydroxyfatty acids (FAHFAs). As expected, MDA concentrations were the lowest in group K. Our findings can better explain ongoing pathologies, both acute and chronic, with the potential for future diagnosis and treatment.
Highlights
Lipids are involved in many metabolic processes of living organisms and represent a heterogenous biochemical group
Low-density lipoproteins (LDL) can be modified by metabolites of oxidative stress and penetrate through this dysfunctional endothelium from plasma to the vessel wall; the LDL are internalized by macrophages to form foam cells
Statistical evaluation of generated data must be carried out carefully, especially with regard to the type of administered heparin, because the extent of neutral lipid hydrolysis largely differs between LMWH and UFH
Summary
Lipids are involved in many metabolic processes of living organisms and represent a heterogenous biochemical group. Low-density lipoproteins (LDL) can be modified by metabolites of oxidative stress and penetrate through this dysfunctional endothelium from plasma to the vessel wall; the LDL are internalized by macrophages to form foam cells. Together with immunologically active cells, are the cornerstones of the formation and growth of atherosclerotic lesions. The growth of these plaques, their rupture, and subsequent superimposed thrombosis lead to abrupt closure of the vessel, resulting in acute coronary syndrome (ACS), acute ischemic stroke (AIS), or acute limb ischemia. These are leading causes of morbidity and mortality in high-income countries [6]
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