8-11-14-eicosatrienoic-acid and Acute-Disease

Dietary triglycerides influence fatty acid (FA) serum concentrations and weight percentages (wt %), which may be associated with the age of onset of acute ischemic stroke (AIS). We investigated the correlations between serum FA levels and proportions at admission and the age of onset of AIS. We evaluated patients with AIS admitted between 2016 and 2019 within 24 h of AIS onset and calculated the correlation coefficients between their ages, serum FA concentrations, and FA wt % values. Multiple linear regression analysis was performed to identify independent FAs indicating AIS age of onset. Furthermore, we estimated the threshold values of independent FAs for age of onset <60 years using receiver operating characteristic curves by logistic regression. A total of 525 patients (median age: 75 years) met the inclusion criteria. The concentration of dihomo-gamma-linolenic acid (DGLA) and wt % of docosahexaenoic acid (DHA) were significant independent variables for age of onset of AIS, and receiver operating characteristic curves for age of onset <60 years showed thresholds of ≥117.7 µmol/L for DGLA and ≤3.7% for DHA. An increased DGLA concentration and decreased DHA wt % were significantly associated with onset of AIS at a younger age.

Topics: 8,11,14-Eicosatrienoic Acid; Acute Disease; Age Factors; Age of Onset; Aged; Cross-Sectional Studies; Docosahexaenoic Acids; Fatty Acids; Female; Humans; Ischemic Stroke; Linear Models; Male; Middle Aged; Patient Admission; ROC Curve

Circulating polyunsaturated fatty acid (PUFA) levels are associated with clinical outcomes in cardiovascular diseases including coronary artery disease and chronic heart failure (HF). However, their clinical implications in acute decompensated HF (ADHF) remain unclear. The aim of this study was to investigate the clinical roles of circulating PUFAs in patients with ADHF.. Circulating levels of PUFAs, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA) and dihomo-gamma linoleic acid (DGLA), were measured on admission in 685 consecutive ADHF patients. Adverse events were defined as all-cause death and worsening HF.. During a median follow-up period of 560 days, 262 (38.2%) patients had adverse events. Although patients with adverse events had lower n-6 PUFA (AA + DGLA) level than those without, n-3 PUFA (EPA + DHA) level was comparable between the groups. Kaplan-Meier analyses showed that lower n-6 PUFA level on admission was significantly associated with the composite of all-cause death and worsening HF, all-cause death, cardiovascular death and worsening HF (p < 0.001, p = 0.005, p = 0.021, p = 0.019, respectively). In a multivariate Cox model, lower n-6 PUFA level was independently associated with increased risk of adverse events (HR 0.996, 95% CI: 0.993-0.999, p = 0.027).. Lower n-6 but not n-3 PUFA level on admission was significantly related to worse clinical outcomes in ADHF patients. Measurement of circulating n-6 PUFA levels on admission might provide information for identifying high risk ADHF patients.

Topics: 8,11,14-Eicosatrienoic Acid; Acute Disease; Aged; Arachidonic Acid; Disease Progression; Docosahexaenoic Acids; Eicosapentaenoic Acid; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Female; Heart Failure; Humans; Male; Prospective Studies; Risk Factors

The widespread use of statins for hypercholesterolemia has uncovered pleiotropic anti-inflammatory properties that were unexpected based on the drugs' original design; yet, mechanisms for these protective actions remain uncertain. In this study lovastatin triggered biosynthesis of the anti-inflammatory and pro-resolving mediator 15-epi-lipoxin A(4) (15-epi-LXA(4)). During interactions between human neutrophils and airway epithelial cells, the statin-induced increase in 15-epi-LXA(4) was associated with increased 14,15-epoxyeicosatrienoic acid (14,15-EET) generation. When added to activated neutrophils, 14,15-EET enhanced 15-epi-LXA(4) biosynthesis. In a murine model of airway mucosal injury and inflammation, lovastatin increased 15-epi-LXA(4) formation in vivo and markedly decreased acute lung inflammation. Administration of 15-epi-LXA(4) also inhibited lung inflammation in an additive manner with lovastatin. Together, these results indicate that statin-triggered 15-epi-LXA(4) generation during human leukocyte-airway epithelial cell interactions is an endogenous mechanism for statin-mediated tissue protection at mucosal surfaces that may also be relevant in the statins' ability to stimulate the resolution of inflammation.

Topics: 8,11,14-Eicosatrienoic Acid; Acute Disease; Animals; Anticholesteremic Agents; Cell Line; Disease Models, Animal; Female; Humans; Hypercholesterolemia; Inflammation; Inflammation Mediators; Lipoxins; Lovastatin; Male; Mice; Neutrophils; Pneumonia; Respiratory Mucosa

Topics: 8,11,14-Eicosatrienoic Acid; Acute Disease; Chronic Disease; Eicosanoids; Endothelium, Vascular; Hemorheology; Humans; Myocardial Infarction; Myocardial Ischemia; Platelet Activation; Stress, Mechanical