IRAK-4 Variants in acute coronary syndrome patients.
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ABSTRACT:
SUBMITTER: Ergen A
PROVIDER: S-EPMC5469098 | biostudies-literature | 2017 May
REPOSITORIES: biostudies-literature
Publications
IRAK-4 Variants in acute coronary syndrome patients.
Ergen Arzu A Fazlıoğulları Osman O Başaran Cem C Çelik Faruk F Candan Gonca G Timirci Kahraman Özlem Ö Zeybek Ümit Ü
Anatolian journal of cardiology 20170501 5
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Project description:IntroductionWe aimed to compare the outcomes of acute coronary syndrome (ACS) patients undergoing in-hospital percutaneous coronary intervention treated with prasugrel versus ticagrelor.MethodsAmong 7,233 patients enrolled to the Acute Coronary Syndrome Israeli Survey (ACSIS) between 2010 and 2018, we identified 1,126 eligible patients treated with prasugrel and 817 with ticagrelor. Comparison between the groups was performed separately in ST-elevation myocardial infarction (STEMI) patients, propensity score matched (PSM) STEMI patients, and non-ST-elevation ACS (NSTE-ACS) patients.ResultsIn-hospital complication rates, including rates of stent thrombosis, were not significantly different between groups. In PSM STEMI patients, 30-day re-hospitalization rate (p < 0.05), 30-day MACE (the composite of death, MI, stroke, and urgent revascularization, p = 0.006), and 1-year mortality rates (p = 0.08) were higher in the ticagrelor group compared to the prasugrel group; in NSTE-ACS patients, outcomes were not associated with drug choice. In Cox regression analysis applied on the entire cohort, prasugrel was associated with lower 1-year mortality in STEMI patients but not in NSTE-ACS patients (p for interaction 0.03).ConclusionsCompared to ticagrelor, prasugrel was associated with superior clinical outcomes in STEMI patients, but not in NSTE-ACS patients.
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Project description:IntroductionHigh residual platelet reactivity (RPR) in patients after percutaneous coronary intervention (PCI) receiving antiplatelet agents has been associated with a high risk of developing acute kidney injury (AKI).Study aimThis study aimed at identification of independent prognostic predictors of AKI risk in patients with acute coronary syndrome (ACS) after PCI.Study design, setting and patientsThis was a prospective single-center clinical trial that included 155 patients (n = 119 without AKI, n = 36 with AKI, mean age 64.0±10.6 years, of whom 74.2% were males), who underwent PCI with stenting. We prospectively evaluated RPR using optical aggregometry. Development of AKI was the primary endpoint.ResultsAcute renal dysfunction was observed in 36 patients (23.2%) after PCI, the risk factors of which according to univariate regression analysis were: age (p = 0.040), low diastolic blood pressure (DBP) (p = 0.001), having severe heart failure (HF) according to Killip (p<0.001), low level of hemoglobin (p = 0.026) and erythrocytes (p = 0.005), increased creatinine (p<0.001), low baseline glomerular filtration rate (GFR) (p<0.001), low left ventricular ejection fraction (LV EF) (p = 0.003), high residual platelet reactivity (RPR) (p<0.001) and platelet aggregation area under the curve (AUC) with 10 μg/mL ADP (p<0.001), as well as dose of X-ray contrast medium (XCM) (p = 0.008). As a result of multivariate regression analysis the following independent predictors of AKI were established with the inclusion of the above factors: baseline creatinine level [OR 1.033 at 95% CI from 1.017 to 1.049; p<0.001], RPR with 10 μg/mL ADP [OR 1.060 at 95% CI from 1.027 to 1.094; p = 0.001], dose of an XCM [ОR 1.005 at 95% CI from 1.001 to 1.008; р = 0.014], diastolic blood pressure (DBP) [OR 0.926 at 95% CI from 0.888 to 0.965; p<0.001].ConclusionADP-induced high residual platelet reactivity, baseline creatinine level, X-ray contrast medium, low diastolic blood pressure were independent predictors of AKI in patients with ACS after PCI.
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Project description:BackgroundAcute coronary syndrome (ACS) is closely related to unstable plaques and secondary thrombosis. The inflammatory cells in plaques and their inflammatory products may be the cause for plaque instability and ruptures. The study aimed to disclose the changes of inflammatory factors including serum intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40), and lipoprotein-associated phospholipase A2 (Lp-PLA2) in patients with ACS and its clinical significance.MethodsA total of 120 patients with coronary heart disease (CHD) were categorized into 2 groups: 69 with ACS and 51 with stable angina pectoris (SAP); 20 patients with chest pain and normal angiography served as a control group. The 120 patients with CHD were categorized into single-vessel disease group, double-vessel disease group, and three-vessel disease group based on the number of coronary artery stenosis. The severity of coronary artery stenosis was quantified based on coronary angiography using Gensini score. They were further divided into mild CHD group with its Gensini score <26 (n = 36), moderate CHD group with its Gensini score being 26-54 (n = 48) and severe CHD group with its Gensini score >54 (n = 36). Serum levels of ICAM-1, YKL-40, and Lp-PLA2 of different groups were determined by enzyme-linked immunosorbent assay. Correlation between ICAM-1, YKL-40, Lp-PLA2, and Gensini score was analyzed.ResultsThe levels of serum inflammatory factors ICAM-1, YKL-40, and Lp-PLA2 were significantly higher in the ACS group than those in control group and SAP group (all P < 0.05); and compared with control group, no significant difference was observed in terms of the serum ICAM-1, YKL-40, and Lp-PLA2 levels in the SAP group (P > 0.05).The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, single-vessel disease group, double-vessel disease group, and three-vessel disease group (all P > 0.05). The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, mild CHD group (Gensini score <26), moderate CHD group (Gensini score 26-54), and severe CHD group (Gensini score >54) (all P > 0.05). Nonparametric Spearman correlation analysis showed that the levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not correlated with the Gensini score in CHD patients (r = 0.093, r = -0.149, and r = -0.085, all P > 0.05; respectively).ConclusionsThe serum levels of ICAM-1, YKL-40, and Lp-PLA2 were correlated with different clinical types of CHD, but not well correlated the severity and extent of artery stenosis, suggesting that ICAM-1, YKL-40, and Lp-PLA2 might be involved in occurrence of instability of atherosclerotic plaque, and might reflect the severity of CHD mostly through reflecting the plaque stability.
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Project description:Long non-coding RNAs (lncRNAs) and dendritic cells (DC) play crucial roles in the development of acute coronary syndrome (ACS); however, the mechanisms remain unclear. To investigate this, we analysed the differentially expressed lncRNAs in monocyte-derived DCs (moDCs) from patients with ACS. Peripheral blood mononuclear cells were transformed into moDCs. Cellular morphology and expression levels of moDC-specific markers (CD80, CD86, CD11c, CD14 and HLA-DR) were analysed using electron microscopy (EM) and flow cytometry (FCM), respectively. Differentially expressed lncRNAs and their functions were predicted using gene sequencing, gene ontology and the Kyoto Encyclopedia of Genes and Genomes. The expression levels of markers, signalling pathway molecules (p-PI3K and p-AKT), inflammatory cytokines (IL-6 and IL-12p70) and target gene (C-C motif chemokine ligand (CCL) 15 and CCL14) were analysed by overexpression or silencing of candidate lncRNAs. EM revealed the cells to be suspended in dendritic pseudopodia. CD11c and HLA-DR were upregulated, while CD80 and CD86 were downregulated. Comparison between the UA versus ST group showed the highest number of differentially expressed lncRNAs (n = 113), followed by UA versus NST (n = 115), CON versus NST (n = 49) and CON versus ST (n = 35); however, the number was low for CON versus UA and ST versus NST groups. moDC-specific marker expression, signalling pathway molecules, inflammatory cytokines and CCL14 were upregulated following lentiviral overexpression of smart silencer-CCL15-CCL14; however, expression levels decreased following transfection with siRNA. The morphology, function and lncRNA expression of moDCs differ depending on the type of ACS. The differentially expressed lncRNAs, particularly CCL15-CCL14, regulate the function of moDCs. Thus, our study provides new insights regarding the role of lncRNAs in ACS and indicates the potential use of CCL15-CCL14 as a novel diagnostic marker and therapeutic target.
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