Inflammation In Acute Coronary Syndromes Research Articles

Plasma levels of bactericidal/permeability-increasing protein correlate with systemic inflammation in acute coronary syndrome

BackgroundNeutrophils play important roles in atherosclerosis and atherothrombosis. Bactericidal/permeability-increasing protein (BPI) is mainly expressed in the granules of human neutrophils in response to inflammatory stress. This observational, cross-sectional study investigated the plasma level of BPI in patients with acute coronary syndrome (ACS) and its correlation with blood neutrophil counts and circulating inflammatory biomarkers. MethodsA total of 367 patients who had acute chest pain and who were admitted to our hospital for coronary angiography (CAG) and/or percutaneous coronary intervention (PCI) from May 1, 2020 to August 31, 2020 were recruited. Among them, 256 had a cardiac troponin value above the 99th percentile upper reference limit and were diagnosed with ACS. The remaining patients (n = 111) were classified as non-ACS. The TIMI and GRACE scores were calculated at admission. The Gensini score based on CAG was used to determine atherosclerotic burden. Plasma levels of interleukin (IL)-1β, myeloperoxidase-DNA (MPO-DNA), high sensitivity C-reactive protein (hs-CRP), S100A8/A9, and BPI were measured using enzyme-linked immunosorbent assays. Correlations of plasma BPI levels with examination scores and levels of circulating inflammatory biomarkers were explored. Receiver operating characteristic (ROC) curve analysis was used to determine the diagnostic efficacy of BPI for ACS and myocardial infarction. ResultsPatients in the ACS group showed significantly higher plasma BPI levels compared to the non-ACS group (46.42 ± 16.61 vs. 16.23 ± 6.19 ng/mL, p < 0.05). Plasma levels of IL-1β, MPO-DNA, hs-CRP, and S100A8/A9 in the ACS group were also significantly higher than those in the non-ACS group (all p < 0.05). In addition, plasma BPI levels were positively correlated with the TIMI, GRACE, and Gensini scores (r = 0.176, p = 0.003; r = 0.320, p < 0.001; r = 0.263, p < 0.001, respectively) in patients with ACS. Plasma BPI levels were also positively correlated with blood neutrophil counts (r = 0.266, p < 0.001) and levels of circulating inflammatory biomarkers (IL-1β, r = 0.512; MPO-DNA, r = 0.452; hs-CRP, r = 0.554; S100A8/A9, r = 0.434; all p < 0.001) in patients with ACS. ROC curve analysis revealed that the diagnostic efficacy of BPI for ACS was not inferior to that of IL-1β, MPO-DNA, hs-CRP, S100A8/A9, or blood neutrophil counts. ROC analysis also showed that the diagnostic efficacy of BPI for myocardial infarction was not inferior to that of creatine kinase (CK)-MB or cardiac troponin I. ConclusionBPI is associated with systemic inflammation in ACS and may be involved in the process of atherosclerosis and atherothrombosis. The potential of BPI as a prognostic and diagnostic biomarker for ACS should be investigated in clinical settings.

No evidence of coronary plaque stabilization by allopurinol in patients with acute coronary syndrome

BackgroundAllopurinol, a xanthine inhibitor that lowers uric acid concentration, has been proven to reduce inflammation and oxidative stress in patients with cardiovascular disease. However, it is unknown whether these beneficial effects translate into favorable plaque modification in acute coronary syndromes (ACS). This study aimed to investigate whether allopurinol could improve coronary plaque stabilization using coronary computed tomography angiography (CCTA). MethodsThis was a prospective, single-center, randomized, double-blind clinical trial began in March 2019. A total of 162 ACS patients aged 18–80 years with a blood level of high-sensitivity C-reactive protein (hsCRP) ​> ​2 ​mg/L were included. The subjects were randomly assigned in a 1:1 ratio to receive either allopurinol sustained-release capsules (at a dose of 0.25 ​g once daily) or placebo for 12 months. The plaque analysis was performed at CCTA. The primary efficacy endpoint was the change in low-attenuation plaque volume (LAPV) from baseline to the 12-month follow-up. ResultsAmong 162 patients, 54 in allopurinol group and 51 in placebo group completed the study. The median follow-up duration was 14 months in both groups. Compared with placebo, allopurinol therapy did not significantly alter LAPV (−13.4 ​± ​3.7 ​% vs. −17.8 ​± ​3.6 ​%, p ​= ​0.390), intermediate attenuation plaque volume (−16.1 ​± ​3.0 ​% vs. −16.2 ​± ​2.9 ​%, p ​= ​0.992), dense calcified plaque volume (12.2 ​± ​13.7 ​% vs. 9.7 ​± ​13.0 ​%, p ​= ​0.894), total atheroma volume (−15.2 ​± ​3.2 ​% vs. −16.4 ​± ​3.1 ​%, p ​= ​0.785), remodeling index (2.0 ​± ​3.9 ​% vs. 5.4 ​± ​3.8 ​%, p ​= ​0.536) or hsCRP levels (−73.6 [−91.6–17.9] % vs. −81.2 [−95.4–47.7] %, p ​= ​0.286). ConclusionsOur findings suggest that allopurinol does not improve atherosclerotic plaque stability or inflammation in ACS.

Abstract 11734: Allopurinol &amp; Plaque Stabilization in Patients With Acute Coronary Syndrome: A Randomized Clinical Trial

Background: Allopurinol, a xanthine inhibitor that lowers uric acid (UA) concentration, has been proven to reduce inflammation and oxidative stress in patients with cardiovascular disease. However, it is unknown whether these beneficial effects translate into favorable plaque modification in acute coronary syndromes (ACS). Aims: This study aimed to investigate whether allopurinol therapy could improve plaque stabilization in ACS patients using coronary computed tomography angiography (CCTA). Methods: This was a prospective, single-center, randomized, double-blind clinical trial began in March 2019 (clinical trial.gov identifier NCT03745729). A total of 162 acute coronary syndromes (ACS) patients aged 18-80 years with a blood level of high-sensitivity C-reactive protein (hsCRP) &gt; 2 mg/L were included. The subjects were randomly assigned in a 1:1 ratio to receive either allopurinol sustained-release capsules (at a dose of 0.25 g once daily) or placebo for 12 months. The primary efficacy endpoint was the change in low-attenuation plaque volume (LAPV) from baseline to the 12-month follow-up. Results: Among 162 patients, 54 in allopurinol group and 51 in placebo group completed the study. There were no significant differences between the allopurinol and placebo groups in terms of baseline data for age (58.5±10.2 years vs. 56.8±10.0 years, P=0.392) and sex (male/female, 40/14 vs. 40/11, P=0.600). The median follow-up duration was 14 months in both groups. Compared with placebo, allopurinol therapy did not significantly alter LAPV (-13.4±3.7% vs. -17.8±3.6%, P=0.390), intermediate attenuation plaque volume (-16.1±3.0% vs. -16.2±2.9%, P=0.992), dense calcified plaque volume (12.2±13.7% vs. 9.7±13.0%, P=0.894), total atheroma volume (-15.2±3.2% vs. -16.4±3.1%, P=0.785), remodeling index (2.0±3.9% vs. 5.4±3.8%, P=0.536) or hsCRP levels (-73.6 [17.9-91.6] % vs. -81.2 [47.7-95.4] %, P=0.286). Conclusions: Our findings suggest, for the first time, that allopurinol therapy does not improve atherosclerotic plaque instability or inflammation in ACS.

Oxidative metabolism of neutrophils in acute coronary syndrome.

Inflammation in acute coronary syndrome (ACS) involves neutrophil activation and oxidative stress. Here, we studied the production of reactive oxygen species (ROS) by neutrophils in ACS. The study included 42 patients, men and women aged 46-91 years with ischaemic heart disease (IHD), non-ST-segment elevation ACS and ST-segment elevation ACS. Neutrophil-derived ROS were quantified with double-step stimulated luminol-enhanced chemiluminometry. The specific indices of spontaneous and double-step stimulated chemiluminescence did not differ in the subgroups of IHD, non-ST-segment elevation ACS and ST-segment elevation ACS. The total double-step stimulated ROS production by neutrophils was significantly higher in ST-segment elevation ACS than in non-ST-segment elevation ACS and IHD. In ACS, special activation mechanisms of peripherical neutrophils were not triggered in our study. The significant increase in free radical production by neutrophils in acute myocardial infarction was presumably a consequence of an increase in their number.

炎症在基于冠状动脉粥样硬化的急性冠脉综合征中的作用

炎症在基于冠状动脉粥样硬化的急性冠脉综合征中的作用

Low-dose interleukin 2 for the reduction of vascular inflammation in acute coronary syndromes (IVORY): protocol and study rationale for a randomised, double-blind, placebo-controlled, phase II clinical trial

IntroductionInflammation plays a critical role in the pathogenesis of atherosclerosis, the leading cause of ischaemic heart disease (IHD). Studies in preclinical models have demonstrated that an increase in regulatory T...

Inflammation in acute coronary syndrome: prognostic significance

Abstract Funding Acknowledgements Type of funding sources: None. Background In patients with acute coronary syndrome (ACS) the acute phase reactant, C-reactive protein (CRP), might be significantly elevated. Several reports suggest that CRP may play a direct pathophysiological role on the development and progression of atherosclerosis, and CRP values correlate with infarct size when measured by magnetic resonance imaging. Purpose The aim of the present study was to evaluate the prognostic value of CRP in patients presenting with an ACS. Methods Retrospective analysis of 635 consecutively admitted patients due to ACS in a single coronary intensive care unit. CRP levels were measured at admission. Clinical variables and therapeutic strategies were examined. The primary endpoint analysed during follow-up was all-cause mortality. Possible predictors for all-cause mortality were assessed by Cox regression models. When statistically significant values were found in univariate analysis, multivariate analysis was used to determine whether CRP was an independent predictor of outcome. Results In the studied sample, 75% were male. Median age was 69 [interquartile range (IQR) 57–78]. ST-elevation myocardial infarction (STEMI) occurred in 39.6%, non-ST segment elevation myocardial infarction in 44.9% and unstable angina in 15.5% of the patients. Median left ventricular ejection fraction (LVEF) was 48% (IQR 40–55%) and median CRP level at admission 0.7 mg/dL (IQR 0.5–1.9 mg/dL). Regarding important comorbidities and past medical history, 75.9% had hypertension (HTN), 34.0% diabetes, 20.3% chronic kidney disease (CKD), 68.6% dyslipidaemia and 17.3% heart failure (HF). The median follow-up was 34 months (IQR 22–72). In univariate analysis, CRP was significantly associated with all-cause mortality (HR 1.06 per 1 mg/dL increase, 95% CI 1.04–1.08, p&amp;lt;0.001), as was gender, age, LVEF, STEMI and previous history of diabetes, HTN, CKD or HF. In multivariate analysis, CRP remained significantly associated with the primary endpoint (HR 1.02, 95% CI 1.00–1.05, p=0.033), as did age, LVEF and previous history of HF. Conclusions In our study, CRP at admission was an independent risk factor for all-cause mortality following an ACS. This finding indicates that inflammation associated with the acute event has a significant impact in the long-term prognosis. More evidence is needed to determine if treating inflammation (and when, in the course of the disease) could result in better outcomes.

Relationship of Troponin I with Neutrophil Lymphocyte Ratio and Serum Amyloid A in Acute Coronary Syndrome

Abstract&#x0D; Introduction: Acute coronary syndrome (ACS) is the leading cause of death in the world. Acute myocardial infarction can initiate an acute inflammatory process by inducing pro-inflammatory cytokines at the cellular level measured by NLR, at the biomolecular level characterized by SAA production in liver. The relationship of elevated troponin I levels as a marker of myocardial necrosis with NLR and SAA as inflammatory markers need further discussion. The purpose of this study was to determine the relationship between cardiac necrosis markers and inflammatory parameters in ACS.&#x0D; Methods: An analytic observational study with a cross-sectional approach was conducted from March to May 2019. This study involved 32 patients with ACS at the Emergency Department of Dr.Kariadi Hospital, with the onset of attacks of 4-6 hours which met the inclusion and exclusion criteria. Examination of troponin I level was done using the ELFA method, NLR value was measured using a hematology analyzer, and SAA level was measured using the ELISA method. Statistical test was done using Spearman correlation. Value of p &lt; 0.05 was considered significant.&#x0D; Results: The median (min-max) of troponin I, NLR, and SAA values were 0.617 (0.001-40,000) μg/L, 4.92 (1.38-18.16) and 40.454 (5.879-66.059) μg/ml, respectively. The correlation of troponin I level with NLR and SAA were r=0.180, p=0.243 and r=0.655, p=0.000.&#x0D; Conclusions: There was a significant positive moderate relationship between troponin I level and SAA which could be used as a marker of acute inflammation in ACS, whereas cell inflammation marker of NLR did not provide a significant meaning.&#x0D; Keywords: ACS, NLR, SAA, troponin

Redefining residual inflammatory risk after acute coronary syndrome.

Over the last decades, inflammation proved to play a pivotal role in atherosclerotic plaque formation, progression and destabilization. Several studies showed that the patients presenting with acute coronary syndrome are at increased risk of adverse cardiovascular events at both short- and long-term follow-up. Results from different clinical trials highlighted that a residual inflammatory riskexist and targeting inflammation is a successful strategy in selected cases associated to an increased inflammatory burden. Recently, the optimization of intracoronary and multimodality imaging allowed to also assess the entity of local inflammation, thus encouraging the individuation of plaque characteristics that portend a higher risk of future cardiovascular events. In this short review, we aim to highlight the role of systemic and local inflammation in acute coronary syndromes, to provide a summarized overview of the possible medical strategies applicable in selected cases and to underline the diagnostic and prognostic potential of multimodality imaging.

Association of Platelet Lymphocyte Ratio (PLR) and Neutrophil Lymphocyte Ratio (NLR) with Global Registry of Acute Coronary Events (GRACE) Score in Acute Coronary Syndrome

Introduction: Acute Coronary Syndrome (ACS) has morbidity and mortality significantly increase, it requires risk stratification for the assessment and selection of initial invasive strategies. The Global Registry of Acute Coronary Events (GRACE) scores recommended as risk stratification of ACS. Some of studies found that the combination of GRACE scores with other clinical and laboratory parameters can increase predictive value of ACS. Platelet Lymphocyte Ratio (PLR) and Neutrophil Lymphocyte Ratio (NLR) act as parameter of systemic inflammation in ACS. Aims of the study to determine the association between PLR and NLR with risk stratification GRACE score. Method: This study is analytical with a cross-sectional retrospective design. This study included 70 patients with a diagnosis of ACS based on medical record data. Data analysis was performed using the Statistical Package for the Social Sciences (SPSS) 22.0. P-value &lt;0.05 was considered statistically significant. Results: This study was found a positive correlation between PLR and NLR with the GRACE score of patients ACS (r=0.485, p&lt;0.001; r=0.570, p&lt;0.001). The PLR and NLR were both found the significantly higher in the high risk GRACE score respectively (188 ± 47, p &lt; 0.001; 7.9± 2.7, p&lt;0.001). The ROC curve analysis, cutt-off PLR of 123 and above (sensitivity of 72.7 %; specificity of 70.3), while cutt-off NLR of 4 and above (sensitivity of 78.8%; specificity of 70.3%) to detect high risk GRACE score. Conclusion: There is a significant association between PLR and NLR with GRACE score Keywords: Platelet Lymphocyte Ratio, Neutrophil Lymphocyte Ratio, GRACE score, Acute Coronary Syndrome.

Effect of PCSK9 E670G and R46L Polymorphisms on Major Adverse Cardio-Cerebrovascular Events in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

AbstractMajor adverse cardio-cerebrovascular events (MACCE) in ST-segment elevation myocardial infarction (STEMI) are still high, although there have been advances in pharmacology and interventional procedures. Proprotein convertase subtilisin/Kexin type 9 (PCSK9) is a serine protease regulating lipid metabolism associated with inflammation in acute coronary syndrome. The MACCE is possibly related to polymorphisms in PCSK9. A prospective cohort observational study was designed to confirm the association between polymorphism of E670G and R46L in the PCSK9 gene with MACCE in STEMI. The Cox proportional hazards model and Spearman correlation were utilized in the study. The Genotyping of PCSK9 and ELISA was assayed.Sixty-five of 423 STEMI patients experienced MACCE in 6 months. The E670G polymorphism in PCSK9 was associated with MACCE (hazard ratio = 45.40; 95% confidence interval: 5.30–390.30; p = 0.00). There was a significant difference of PCSK9 plasma levels in patients with previous statin consumption (310 [220–1,220] pg/mL) versus those free of any statins (280 [190–1,520] pg/mL) (p = 0.001).E670G polymorphism of PCSK9 was associated with MACCE in STEMI within a 6-month follow-up. The plasma PCSK9 level was higher in statin users.

The Correlation between Neutrophil Lymphocyte Ratio, C-reactive Protein, and Serum Amyloid a with the Degree of Stenosis in Acute Coronary Syndrome

BACKGROUND: Inflammation plays a central role in the pathophysiology of acute coronary syndrome (ACS), involving neutrophils as non-specific markers of inflammation and lymphocytes as regulatory markers, measured in the form of neutrophil lymphocyte ratio (NLR). C-reactive protein (CRP) plays a role in the blockage of heart arteries and serum amyloid A (SAA) plays a role in the pathophysiology of coronary stenosis.&#x0D; AIM: The study aimed to determine the correlation between NLR, CRP, and SAA levels with the degree of coronary artery stenosis in ACS.&#x0D; METHOD: The design of this study was cross-sectional. The target population in this study was patients with ACS in Dr. Kariadi Hospital Semarang. We performed an NLR measurement with a hematologic analyzer, CRP, and SAA levels using the ELISA method, and coronary angiography using the Gensini score. Furthermore, we also performed the Spearman correlation test between variables.&#x0D; RESULTS: The median (min; max) values of NLR, CRP, SAA levels, and Gensini score were 4.39 ± 0.48 (0.36; 18.17); 8.63 ± 2.22 (5; 105.11) mg/dL; 36.859 (3.909–69.724); 65 (6–178), respectively. The correlation between NLR, CRP, and SAA levels with the Gensini scores was r = 0.064, p = 0.595; r = 0.240, p = 0.044; r = −0,164, p = 0.171, respectively.&#x0D; CONCLUSION: CRP measurement could be used as a marker of inflammation in ACS to manage the inflammation process. Furthermore, SAA levels were clinically useful biomolecular parameters in evaluating acute inflammation in ACS, although it did not correlate with the Gensini scores.

Association of Neutrophil Lymphocyte Ratio (NLR) with Global Registry of Acute Coronary Events (GRACE) Scores in Acute Coronary Syndrome

Background. Inflammation plays an important role in the initiation of atherosclerosis from the beginning of plaque to rupture cause Acute Coronary Syndrome (ACS). Neutrophil Lymphocyte Ratio (NLR) indicator of systemic inflammation in ACS. Risk stratification was needed for assessment and selection of initial invasive strategies and find the best strategy in ACS. The Global Registry of Acute Coronary Events (GRACE) scores recommended risk stratification of ACS. Aims of the study to determine the association and cut-off value NLR with risk stratification GRACE score. Method. This study is analytical with a cross-sectional retrospective design. Data were analyzed after distribution test, then mean difference and correlation test was using the SPPS program where p &lt;0.05 was considered statistically significant. Results. This study showed significantly higher NLR value in the high risk stratification and intermediate-risk compared to low risk stratification (7.9 ± 2.7 vs 3.6 ± 1.7; p=0.001) (5.2 ± 2.3 vs 3.6 ± 1.7; p=0.018). Significant correlation between NLR ​​with GRACE scores (r=0.570; p&lt;0.001). Significant AUC values ​​were obtained (0.782, p &lt;0.001, IK95% 0.674-0.89), and cut-off values NLR 4 ​​with sensitivity (78.8%) and specificity (70.3%) on the GRACE score. Conclusion. The significant association between NLR ​​with GRACE risk score in ACS.

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications.

Acute coronary syndrome (ACS) is a major cause of acute death worldwide. Both innate and adaptive immunity regulate atherosclerosis progression, plaque stability, and thrombus formation. Immune and inflammation dysfunction have been indicated in the pathogenesis of ACS. The imbalance in the proatherogenic and antiatherogenic immune networks promotes the transition of plaques from a stable to unstable state and results in the occurrence of acute coronary events. The residual inflammatory risk (RIR) has received increasing attention in recent years, and lowering RIR has been expected to improve the outcomes of ACS patients. The CANTOS, COLCOT, and LoDoCo trials verified the benefits of reducing cardiovascular events using anti-inflammation therapies; however, most of the other studies focusing on lowering RIR produced negative or contradicting results. Therefore, restoring the balance in autoimmune regulation is essential because proatherogenic and antiatherogenic immunomodulatory effects are equally important in the complex human immune network. In this review, we summarized the recent evidence of the roles of proatherogenic and antiatherogenic immune networks in the pathogenesis of ACS and discussed how immune and inflammation contribute to atherosclerosis progression, plaque instability, and adverse cardiovascular events. We also provide a “from bench to bedside” perspective of a novel and promising personalized strategy in RIR intervention and therapeutic approaches for the treatment of ACS.

IFN regulatory Factor-1 induced macrophage pyroptosis by modulating m6A modification of circ_0029589 in patients with acute coronary syndrome

BackgroundPyroptosis is identified as a novel form of inflammatory programmed cell death and has been recently found to be closely related to atherosclerosis (AS). We found that IFN regulatory factor-1(IRF-1) effectively promotes macrophage pyroptosis in patients with acute coronary syndrome (ACS). Subsequent studies have demonstrated that circRNAs are implicated in AS. However, the underlying mechanisms of circRNAs in macrophage pyroptosis remain elusive. MethodsWe detected the RNA expression of hsa_circ_0002984, hsa_circ_0010283 and hsa_circ_0029589 in human PBMC-derived macrophages from patients with coronary artery disease (CAD). The lentiviral recombinant vector for hsa_circ_0029589 overexpression (pLC5-GFP-circ_0029589) and small interference RNAs targeting hsa_circ_0029589 and METTL3 were constructed. Then, macrophages were transfected with pLC5-GFP-circ_0029589, si-circ_0029589 or si-METTL3 after IRF-1 was overexpressed and to explore the potential mechanism of hsa_circ_0029589 involved in IRF-1 induced macrophage pyroptosis. ResultsThe relative RNA expression level of hsa_circ_0029589 in macrophages was decreased, whereas the N6-methyladenosine (m6A) level of hsa_circ_0029589 and the expression of m6A methyltransferase METTL3 were validated to be significantly elevated in macrophages in patients with ACS. Furthermore, overexpression of IRF-1 suppressed the expression of hsa_circ_0029589, but induced its m6A level along with the expression of METTL3 in macrophages. Additionally, either overexpression of hsa_circ_0029589 or inhibition of METTL3 significantly increased the expression of hsa_circ_0029589 and attenuated macrophage pyroptosis. ConclusionOur observations suggest a novel mechanism by which IRF-1 facilitates macrophage pyroptosis and inflammation in ACS and AS by inhibiting circ_0029589 through promoting its m6A modification.

Is There a Role for Colchicine in Acute Coronary Syndromes? A Literature Review

Inflammation is identified as a keystone of atherosclerosis. This review of the literature explores the unique anti-inflammatory effects of colchicine and summarizes the mechanisms of inflammation in acute coronary syndrome. It outlines other therapeutic strategies employed until now to target coronary inflammation and analyzes the role of colchicine in improving the outcomes of acute coronary syndrome. Despite the existence of guideline-directed medical therapy, there still remains a higher risk for recurrence due to continuous inflammation at remaining vascular sites. Several anti-inflammatory strategies have been employed, but they have not been shown to be beneficial. However, colchicine is becoming increasingly popular in tackling this problem. For this review, databases were searched for trials on the role of colchicine as an anti-inflammatory therapy in acute coronary syndrome.

Low-dose Interleukin-2 for the Reduction of Vascular Inflammation in Acute Coronary Syndromes - IVORY

Low-dose Interleukin-2 for the Reduction of Vascular Inflammation in Acute Coronary Syndromes - IVORY

Predictive Value of Neutrophil-to-Lymphocyte Ratio in Outcomes of Patients with Acute Coronary syndrome.

Objectives: Previous studies have demonstrated the role of inflammation in acute coronary syndrome (ACS). The neutrophil-to-lymphocyte ratio (NLR) was found to be a useful inflammatory marker for predicting adverse outcomes. We hypothesized that an elevated neutrophil-to-lymphocyte ratio would be associated with increased mortality in patients with acute coronary syndrome. Methods: The study consisted of 40 patients with acute coronary syndrome who were admitted to Cardiology Department—Menoufia University Hospitals. The primary endpoint was all-cause in-hospital as well as 30-day mortality, and the patients were divided into three tertiles according to their admission NLR results. Results: All-cause 30-day mortality in the three groups based on NLR was 0.0%, 7.7% and 28.6%, in the low-, middle- and high-NLR groups, respectively (P < 0.05; χ2 test). In a logistic regression analysis, including baseline demographic, clinical, and biochemical covariates, the neutrophil-to-lymphocyte ratio was an independent predictor of mortality (OR = 2.44, 95% CI = 1.185 - 5.007, P < 0.05). Conclusion: An elevated neutrophil-to-lymphocyte ratio (NLR), a simple, relatively inexpensive and universally available inflammatory marker, seems to be a predictor of 30-day mortality in patients with acute coronary syndrome.

A STUDY OF SERUM LEVELS OF RANKL AND OPG INPATIENTS WITH ACUTE CORONARY SYNDROME WITH AND WITHOUT PSORIATIC ARTHRITIS

Receptor Activator of Nuclear Factor Kappa B Ligand (RANKL) is a member of the tumor necrosis factor alpha(TNFa) family.It signals by its RANK receptor on monocyte/macrophage progenitors and stimulates the formation of bone-resorbing osteoclasts [1]. In psoriatic arthritis (PsA) RANKL is produced by activated Th17 cells, synovial fibroblasts, macrophages, dendritic cells and activated lymphocytes [2,3]. These are cells involved in systemic and local inflammation and atherogenesis.Osteoprotegerin (OPG) is a glycoprotein first described in 1997 by Simonet et al. [1]who refer to it as a bone-protecting protein. OPG is a new member of theTNFa superfamily,a soluble receptor which acts as a decoy for RANKL and other ligands. It is also synthesized in many other tissues such as kidney, placenta, bones, vessels, lungs, and vascular structures. It circulates in serum and in plasma, although the concentration is much lower than locally in the bone and arterial tissue[4,5,6]. It has been found that vascular smooth muscle cellssynthesize it as a result of various stimuli. OPG also protects large blood vessels from medialcalcification[7].The biological effect of OPG is to oppose RANKL and thus prevent subsequent stimulation of the receptor, therefore the level of OPG increases and acts as a mechanism of self-defense.The role of RANKL and OPG in cardiovascular disease is still insufficiently defined and remains contradictory[8]. Also, the relationship between high serum levels of OPG in acute coronary syndrome( ACS) and their relation to inflammatory joint disease (IJD) is still discussed [9]. Evidence has been collected demonstrating the active involvement of RANKL and OPG in vascular pathology, including atherogenesis, arterial calcification and plaque instability.Epidemiological studies show that elevated OPG levels in the circulation have a prognostic function in cardiovascular mortality and morbidity and may be a serum prognostic marker for future vascular events. On the other hand, the involvement ofRANKL and OPG in the pathogenesis of local and systemic inflammation in ACS and IJD could link them to the amplification of cardiovascular risk and the severity of acute coronary syndromes, especially in patients with PsA. It is possible that the serum OPG level is increased in response to vascular wall damage and ongoing inflammation process within the atherosclerotic plaque lesion as a component of a complex compensatory mechanism in which RANKL plays a central role [11]. Serum OPG levels may be indicative of persistent damage of endothelial cells as well as the activation of VSMCs in advanced atherosclerotic plaque lesion.Together with other inflammatory mediators, RANKL and OPG can play a crucial role in the formation of the atherosclerotic plaque, its maturation and calcification[12, 13]. The present study aimed to examine and compare levels of sRANKL and sOPG in patients with ACS, divided into two groups, with and without PsA.Associations with cardiovascular mortality risk measured by the Global Registry of Acute Coronary Events (GRACE) were sought.ACS patients with and without PsA were compared in relation to sRANKL (24 and 48hrs) and sOPG (24 and 48hrs) to explore the effect of ACS.

Predictive Value of Neutrophil-to-Lymphocyte Ratio in Outcomes of Patients with Acute Coronary Syndrome

Objectives: Previous studies have demonstrated the role of inflammation in acute coronary syndrome (ACS). The neutrophil-to-lymphocyte ratio (NLR) was found to be a useful inflammatory marker for predicting adverse outcomes. We hypothesized that an elevated neutrophil-to-lymphocyte ratio would be associated with increased mortality in patients with acute coronary syndrome. Methods: The study consisted of 40 patients with acute coronary syndrome who were admitted to Cardiology Department—Menoufia University Hospitals. The primary endpoint was all-cause in-hospital as well as 30-day mortality, and the patients were divided into three tertiles according to their admission NLR results. Results: All-cause 30-day mortality in the three groups based on NLR was 0.0%, 7.7% and 28.6%, in the low-, middle- and high-NLR groups, respectively (P < 0.05; χ2 test). In a logistic regression analysis, including baseline demographic, clinical, and biochemical covariates, the neutrophil-to-lymphocyte ratio was an independent predictor of mortality (OR = 2.44, 95% CI = 1.185 - 5.007, P < 0.05). Conclusion: An elevated neutrophil-to-lymphocyte ratio (NLR), a simple, relatively inexpensive and universally available inflammatory marker, seems to be a predictor of 30-day mortality in patients with acute coronary syndrome.