lysophosphatidylcholine/infarction

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Defective functionality of small, dense HDL3 subpopulations in ST segment elevation myocardial infarction: Relevance of enrichment in lysophosphatidylcholine, phosphatidic acid and serum amyloid A.

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BACKGROUND Low plasma levels of high-density lipoprotein-cholesterol (HDL-C) are typical of acute myocardial infarction (MI) and predict risk of recurrent cardiovascular events. The potential relationships between modifications in the molecular composition and the functionality of HDL subpopulations

Improvement of myocardial infarction risk prediction via inflammation-associated metabolite biomarkers.

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The comprehensive assaying of low-molecular-weight compounds, for example, metabolomics, provides a unique tool to uncover novel biomarkers and understand pathways underlying myocardial infarction (MI). We used a targeted metabolomics approach to identify biomarkers for MI and evaluate their

Metabolomic profiling of rat serum associated with isoproterenol-induced myocardial infarction using ultra-performance liquid chromatography/time-of-flight mass spectrometry and multivariate analysis.

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An ultra-performance liquid chromatography/time-of-flight mass spectrometry (UPLC/TOF-MS)-based metabolomic approach was developed to characterize the metabolic profile associated with isoproterenol (ISO)-induced myocardial infarction (MI). Analysis of the serum samples revealed distinct changes in

Electrophysiological effects of lysophosphatidylcholine on HL-1 cardiomyocytes assessed with a microelectrode array system.

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BACKGROUND Sudden death due to malignant ventricular arrhythmias is the most important cause of death in acute myocardial infarction. Improved knowledge about the pathophysiology underlying these arrhythmias is essential in the search for new anti-arrhythmic strategies. Lysophosphatidylcholine

Common lipid features of lethal ventricular tarchyarrhythmias (LVTAs) induced by myocardial infarction and myocardial ion channel diseases.

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Lethal ventricular tachyarrhythmia (LVTA) is the most prevalent electrophysiological underpinning of sudden cardiac death (SCD), a condition that occurs in response to multiple pathophysiological abnormalities. The aim of this study was to identify common lipid features of LVTA that were induced by

The mechanism of liposome accumulation in infarction.

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This paper explores the mechanism(s) whereby liposomes accumulate in chronically ischaemic myocardium and intestine. Plasma prepared from venous blood obtained at sites of myocardial and intestinal infarction does not promote the lysis of positively and negatively charged liposomes in vitro.

Lipidomic analysis of plasma lipoprotein fractions in myocardial infarction-prone rabbits.

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Lipids play important roles in the body and are transported to various tissues via lipoproteins. It is commonly assumed that alteration of lipid levels in lipoproteins leads to dyslipidemia and serious diseases such as coronary artery disease (CAD). However, lipid compositions in each lipoprotein

Metabolic Profiles Distinguish Non-Dampness-Phlegm and Dampness-Phlegm Patterns among Korean Patients with Acute Cerebral Infarction.

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TRADITIONAL KOREAN MEDICINE CLASSIFIES STROKE INTO FOUR SUBTYPE PATTERNS ACCORDING TO SYMPTOMATIC PATTERN IDENTIFICATION: Qi deficiency (QD), Yin deficiency (YD), Dampness-phlegm (DP), and Fire and Heat (FH). This study investigated the difference in metabolic profiles of plasma comparing subjects

Lysophosphatidylcholine induces cytotoxicity/apoptosis and IL-8 production of human endothelial cells: Related mechanisms.

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Increased levels of oxidized low-density lipoprotein oxLDL) are shown to elevate the risk of cardiovascular diseases such as atherosclerosis, thrombosis, stroke, and myocardial infarction. This is possibly due to the toxic effects of oxLDLs on vascular cells. Various oxLDLs including

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

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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

Circulating microparticles generate and transport monomeric C-reactive protein in patients with myocardial infarction.

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OBJECTIVE Elevated serum C-reactive protein (CRP) following myocardial infarction (MI) is associated with poor outcomes. Although animal studies have indicated a direct pathogenic role of CRP, the mechanism underlying this remains elusive. Dissociation of pentameric CRP (pCRP) into pro-inflammatory

Human Plasma Metabolomics Implicates Modified 9-cis-Retinoic Acid in the Phenotype of Left Main Artery Lesions in Acute ST-Segment Elevated Myocardial Infarction.

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The detection of left main coronary artery disease (LMCAD) is crucial before ST-segment elevated myocardial infarction (STEMI) or sudden cardiac death. The aim of this study was to identify characteristic metabolite modifications in the LMCAD phenotype, using the metabolomics technique. Metabolic

Metabolic Disturbances Identified in Plasma Samples from ST-Segment Elevation Myocardial Infarction Patients.

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ST-segment elevation myocardial infarction (STEMI) is the most severe form of myocardial infarction (MI) and the main contributor to morbidity and mortality caused by MI worldwide. Frequently, STEMI is caused by complete and persistent occlusion of a coronary artery by a blood clot, which promotes

Activated microglia in ischemic stroke penumbra upregulate MCP-1 and CCR2 expression in response to lysophosphatidylcholine derived from adjacent neurons and astrocytes.

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In acute stage of ischemic stroke, the surrounding zone of fresh infarcts is termed penumbra, where microglia are activated in response to damaged cell-derived proinflammatory mediators. Rescuing penumbra by regulating inflammatory activity would minimize infarct volume, which positively correlates

Alteration in metabolic signature and lipid metabolism in patients with angina pectoris and myocardial infarction.

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Lipid metabolites are indispensable regulators of physiological and pathological processes, including atherosclerosis and coronary artery disease (CAD). However, the complex changes in lipid metabolites and metabolism that occur in patients with these conditions are incompletely understood. We

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