Inflammation as a cause of acute myocardial infarction in patients with myeloproliferative neoplasm

Myeloproliferative neoplasms(MPN)are a group of diseases characterized by the clonal proliferation of hematopoietic progenitor or stem cells.They are clinically classifiable into four main diseases:chronic myeloid leukemia,essential thrombocythemia,polycythemia vera,and primary myelofibrosis.These pathologies are closely related to cardio-and cerebrovascular diseases due to the increased risk of arterial thrombosis,the most common underlying cause of acute myocardial infarction.Recent evidence shows that the classical Virchow triad(hypercoagulability,blood stasis,endothelial injury)might offer an explanation for such association.Indeed,patients with MPN might have a higher number and more reactive circulating platelets and leukocytes,a tendency toward blood stasis because of a high number of circulating red blood cells,endothelial injury or overactivation as a consequence of sustained inflammation caused by the neoplastic clonal cell.These abnormal cancer cells,especially when associated with the JAK2V617F mutation,tend to proliferate and secrete several inflammatory cytokines.This sustains a pro-inflammatory state throughout the body.The direct consequence is the induction of a pro-thrombotic state that acts as a determinant in favoring both venous and arterial thrombus formation.Clinically,MPN patients need to be carefully evaluated to be treated not only with cytoreductive treatments but also with cardiovascular protective strategies.

Anti-inflammatory and profibrinolytic effect of tetramethylpyrazine in acute coronary syndromes

Tetramethylpyrazine (TMP) is a herb used widely in Traditional Chinese Medicine (TCM) as an antianginal drug. The exact mechanism whereby TMP treat ischemic heart disease is still not fully understood. The purpose of this study is to examine the anti-inflammatory effect of TMP in patients with acute coronary syndromes (ACS). Methods Thirty-two patients with acute myocardial infarction or unstable angina were randomly assigned to TMP group or control group. All patients received the same standard treatment. Patients in TMP group received TMP 3mg/kg every 12 hours for 5 days. Plasma concentrations of high-sensitivity Creactive protein (CRP), serum amyloid A (SAA) and plasminogen activator inhibitor-1 (PAI-1) were measured at baseline and after 5 days of therapy. Results Both CRP and SAA concentrations increased significantly in control group (P＜0.05) whilst in TMP group, only SAA had a significant increase (P＜0.05); the absolute increase of CRP, SAA, and PAI-1 were significantly less in TMP group than in control group (P＜0.05). Conclusion TMP has an anti-inflammatory and profibrinolytic effect in patients with ACS. These effects may contribute to the clinical benefits of TMP in ischemic heart disease.

CLINICAL SIGNIFICANCE OF SERUM CYTOKINES IL-1β, sIL-2R, IL-6, TNF-α,AND IFN-νIN ACUTE CORONARY SYNDROME

Objectives To explore serum cytokines levels (including IL-1β, sIL-2R, IL-6, TNF-α, and IFN-ν) and their significance in patients with acute coronary syndrome (ACS) and the subsequent follow-ups, with attempt to estimate the role of various serum inflammatory markers in the diagnosis and assessment of ACS. Methods The study population include 40 patients with acute myocardial infarction (AMI), 40 patients with unstable angina pectoris (UAP), and 40 controls. Among the 80 patients, 60 patients attended a follow up 4 months later. Serum inflammatory markers including IL-1β, sIL-2R, IL-6, TNF-α, and IFN-νwere measured by enzyme linked immunosorbent assay. ResultsSerum IL-1β, sIL-2R, IL-6, TNF-αwere significantly higher in AMI group or UAP group compared to the con-trol group and became significantly lower 4 months later in the follow-up patients. Serum levels of IFN-νshows no signifi-cant difference between AMI group or UAP group and controls, also showing no significant change when measured in follow up patients. There was no correlation between serum creatine kinase-MB isoenzyme levels and serum inflammatory markers either in UAP or AMI group. Furthermore, when divided into two subgroups using Wagner’s QRS scoring system in the AMI group, there is no difference of each serum inflammatory marker between ≤6 scores group and > 6 scores group. Conclusion Serum levels of certain inflammatory markers may have some diagnostic value for ACS, and can be a us-eful marker reflecting disease stability.

High Serum Resistin Level may be an Indicator of the Severity of Coronary Disease in Acute Coronary Syndrome

Objective To investigate the correlation between serum resistin level, cardiovascular risk factors and severity of coronary disease in acute coronary syndrome (ACS). Methods After evaluated by clinical history, electrocardiography, exercise tolerance tests, laboratory tests, and coronary angiography, 220 consecutive patients with suspected chest pain were divided into normal control group, stable angina pectoris (SAP) group, and ACS group, respectively. Baseline clinical characteristics, including height, weight, waist circumference, hip circumference, white blood cell count, high-sensitive C-reactive protein (hsCRP), total cholesterol, triglyceride, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, were compared among three groups. ELISA was used to detect serum resistin levels. Pearson's correlation coefficient analysis was used to assess association between resistin and other traditional cardiovascular risk factors. Multinomial logistic regression analyses were used to define the relationship between serum resistin level and SAP or ACS. Results Serum resistin level in ACS group (1.18±0.48 μg/L) was significantly higher than that in normal control and SAP groups (0.49±0.40 and 0.66±0.40 μg/L; P<0.01). Only in ACS group, increased serum resistin level was significantly correlated with hsCRP (r=0.262, P=0.004) and white blood cell count (r=0.347, P=0.001). Furthermore, serum resistin levels showed a stepwise increase with the number increase of > 50% stenosed coronary vessels. Multinomial logistic regression test demonstrated that serum resistin was a strong risk factor for ACS (OR=29.132, 95%CI: 10.939-77.581, P<0.001). Conclusion These findings suggested the potential role of resistin in atherosclerosis and especially its involvement in ACS.

Down-regulation and Clinical Implication of Galectin-9 Levels in Patients with Acute Coronary Syndrome and Chronic Kidney Disease

Summary:In various autoimmune diseases,Galecin-9(Gal-9)has been shown to regulate the T-cell balance by decreasing Th1 and Th17,while increasing the number of regulatory T cells(Tregs).However,the role of Gal-9 in the patients with acute coronary syndrome(ACS)and chronic kidney disease(CKD)remains unclear.This study aims to measure the Gal-9 levels in serum and peripheral blood mononuclear cells(PBMCs)in patients with ACS plus CKD and examine their clinical implication.The serum levels of Gal-9 were determined by enzyme linked immunosorbent assay(ELISA),the expression levels of Gal-9,Tim-3,and Foxp3 mRNA in PBMCs were detected by real-time reverse transcription-polymerase chain reaction(RT-PCR),and the expression of Gal-9 on the surface of PBMCs and in PBMCs was analyzed by flow cytometry.Furthermore,the correlation of serum Gal-9 levels with anthropometric and biochemical variables in patients with ACS plus CKD was analyzed.The lowest levels of Gal-9 in serum and PBMCs were found in the only ACS group,followed by the ACS+CKD group,and the normal coronary artery(NCA)group,.respectively.Serum Gal-9 levels were increased along with the progression of glomerular filtration rate(GFR)categories of G1 to G4.Additionally,serum Gal-9 levels were negatively correlated with high-sensitivity C-reactive protein(hs-CRP),estimated GFR(eGFR),and lipoprotein(a),but positively with creatinine,age,osmotic pressure,and blood urea nitrogen(BUN).Notably,serum Gal-9 was independently associated with hs-CRP,osmotic pressure,and lipoprotein(a).Furthermore,serum Gal-9 levels were elevated in patients with type 2 diabetes(T2DM)and impaired glucose tolerance(IGT)in ACS group.It was suggested that the levels of Gal-9 in serum and PBMCs were decreased in patients with simple ACS and those with ACS plus CKD,and hs-CRP,eGFR,osmotic pressure and T2DM may have an influence on serum Gal-9 levels.

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 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 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.

Relationship between coronary artery ectasia, cocaine abuse and acute coronary syndromes

Coronary artery ectasia(CAE)often represents a coronary angiography finding casually detected or following the occurrence of an acute coronary syndrome.The pathogenetic role of cocaine abuse in the genesis of CAE is still little known and very few data are available in literature.We describe a case of a 31-year-old male cocaine user admitted to our department for typical acute chest pain.Coronary angiography showed diffuse coronary ectasia with slow flows and without hemodynamically significant stenosis.An increasing of matrix metalloproteinases values and a reduction of their tissue inhibitors was showed both during hospitalization and at one month after discharge.This case report emphasizes the close relationship between cocaine abuse,CAE and acute coronary syndromes in patients without hemodynamically significant coronary stenosis.As reported by Satran et al,cocaine abuse should be considered an important risk factor for CAE and these patients appear to be at increased risk of angina and acute myocardial infarct.Further studies that can strengthen this hypothesis would be useful to deepen and better analyze this interesting association.

The clinical role of increase of serum matrix metalloproteinase-8 concentration in patients with acute coronary syndrome

Objective To study the clinical role of the variation of serum matrix metalloproteinase-8 (MMP-8) concentration in patients with acute coronary syndrome (ACS). Methods ELISA method was adopted to detect serum MMP-8 concentration and to observe concentration’s differences and features among 80 selected ACS cases (43 acute myocardial infarction and 37 unstable angina pectoris), 43 stable angina pectoris (SAP) cases and 37 control cases. And meanwhile the atherosclerosis risk factors of each case, such as age, sex, hypertension, body mass index, smoking, family history, diabetes, and hyperlipidemia were collected and analyzed as a whole. Results First, serum MMP-8 concentration reached the highest point in ACS, and there was significant difference between SAP and control groups (P<0.01). Second, serum MMP-8 in AMI was much higher than that in UAP with significant difference (P<0.01). There was no difference between UAP and SAP groups (P>0.05). Third, Logistic regression analysis revealed that serum MMP-8 concentration might be the indicator of ACS (B=4.493, P=0.000), particularly, that of AMI (B=9.961, P=0.000). Fourth, linear correlation and linear regression analysis found that only neutrophil was likely to influence serum MMP-8 concentration (r=0.274, P=0.001). Fifth, in the diagnosis of ACS, the area under ROC curve of MMP-8 was 0.785, the sensitivity and specificity were 68.6% and 76.5%, respectively. Conclusion ① Serum MMP-8 concentration has close relationship with the occurrence of ACS, particularly with AMI; ② Serum MMP-8 concentration may be one of the predicting indicators of ACS and particularly of AMI; ③ Neutrophil may be correlated with serum MMP-8 concentration; ④ MMP-8 is of somewhat valuable in diagnosing ACS.

Acute coronary syndrome with severe atherosclerotic and hyperthyroidism: A case report

BACKGROUND Acute coronary syndrome(ACS)encompasses a spectrum of cardiovascular emergencies arising from the obstruction of coronary artery blood flow and acute myocardial ischemia.Recent studies have revealed that thyroid function is closely related to ACS.However,only a few reports of thyrotoxicosis-induced ACS with severe atherosclerosis have been reported.CASE SUMMARY A 33-year-old man,who had a history of hyperthyroidism without taking any antithyroid drugs and no history of coronary heart disease,experienced neck pain with occasional heart palpitations starting 3 mo prior that were aggravated after an activity.As the symptoms worsened at 21 d prior,he went to a hospital for treatment.The electrocardiogram examination showed a multilead ST segment elevation and pathological Q waves.Based on these findings and his symptoms,the patient was diagnosed with a suspected myocardial infarction and transferred to our hospital on July 2,2020.He was diagnosed with a rare case of ACS due to coronary artery atherosclerosis in the anterior descending artery complicated by hyperthyroidism.A paclitaxel-coated drug balloon was used for treatment to avoid the use of metal stents,thus reducing the time of antiplatelet therapy and facilitating the continued treatment of hyperthyroidism.The 9-mo follow-up showed favorable results.CONCLUSION This case highlights that atherosclerosis is a cause of ACS that cannot be ignored even in a patient with hyperthyroidism.

Erosion-Induced Inflammation on Coronary Plaque Stress/Strain and Flow Shear Stress Calculations Using OCT-Based FSI Computational Model

Plaque erosion,together with plaque rupture,is a common cause for acute coronary syndrome(ACS).Plaque erosion alone is responsible for about one third of the patients with ACS.Eroded plaque is defined as thrombosed,endothelium-absent and non-ruptured but often-inflamed plaques based on histological findings.Even though there is efficient imaging technologies to detect the eroded plaque in vivo and tailored treatment strategy has also been developed for ACScaused by erosion in clinics,the pathogenesis mechanisms that cause plaque erosion are not fully understood.It is widely postulated that thrombus formation and endothelial apoptosis(the precursors of plaque erosion)have closed association with biomechanical conditions in the coronary vessel.Revealing of the mechanical conditions in the eroded plaque could advance our knowledge in understanding the formation of plaque erosion.To this end,patient-specific OCT-based fluid-structure interaction(FSI)models were developed to investigate the plaque biomechanical conditions and investigate the impact of erosioninduced inflammation on biomechanical conditions.In vivo OCTand Biplane X-ray angiographic data of eroded coronary plaque were acquired from one male patient(age:64). OCT images were segmented manually with external elastic membrane contour and the trailing edge of the lipid-rich necrotic core(lipid)assumed to have positive remodeling ratio 1.1.Locations with luminal surface having direct contact with intraluminal thrombus on OCT images were identified erosion sites.Fusion of OCT and biplane X-ray angiographic data were performed to obtain the 3D coronary geometry.OCT-based FSI models with pre-shrink-stretch process and anisotropic material properties were constructed following previously established procedures.To reflect tissue weakening caused by erosion-induced inflammation,the material stiffness of plaque intima at the erosion site was adjust to one tenth of un-eroded fibrous plaque tissue.Three FSI models were constructed to investigate the impacts of inflammation and lipid component on plaque biomechanics:M1,without erosion(this means plaque intima at the erosion sites were not softened)and without inclusion of lipid component;M2,with erosion but no lipid;M3,with erosion and inclusion of lipid.FSI models were solved by ADINA to obtain the biomechanical conditions at peak blood pressure including plaque wall stress/strain(PWS/PWSn)and flow wall shear stress(WSS).The average values of three biomechanical conditions at the erosion sites and at the fibrous cap overlaying lipid component were calculated from three models for analysis.The results of M1 and M2 were compared to investigate the impact of erosion-induced inflammation on plaque biomechanics.Mean PWS value decreases from 49.98 kPa to 18.83 kPa(62.32%decrease)while Mean PWSn value increases from 0.123 1 to 0.138 4(12%increase)as the material stiffness becomes 10times soft.Comparing M2 and M3 at the cap sites,M3(with inclusion of lipid)will elevates mean PWS and PWSn values by48.59%and 16.09%,respectively.The impacts of erosion and lipid on flow shear stress were limited(<2%).To conclude,erosion-induced inflammation would lead to lower stress distribution but larger strain distribution,while lipid would elevate both stress and strain conditions.This shows the influence of erosion and lipid component has impacts on stress/strain cal-culations which are closely related to plaque assessment.

Clinical Significance of Inflammation Factors in Acute Coronary Syndrome from Pathogenic Toxin

The inflammation factors and roles of them in acute coronary syndrome(ACS)were explored. The similarity between the theory of pathogenic toxin in Chinese Medicine and the inflammation response theory in ACS was discussed.The exploration of new inflammatory factors may be helpful for Chinese Medicine in the research of ACS.

The role of inflammatory stress in acute coronary syndrome

Objective To summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover,markers of inflammation stress and ways to block involved pathways are elucidated. Data sources A literature search (MEDLINE 1997 to 2002) was performed using the key words “inflammation and cardiovascular disease”. Relevant book chapters were also reviewed. Study selection Well-controlled,prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected. Data extraction Data and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research. Data synthesis Inflammation is closely linked to atherosclerosis and acute coronary syndrome. Chronic and long-lasting inflammation stress,present both systemically or in the vascular walls,can trigger acute coronary syndrome. Conclusions Inflammation stress plays an important role in the process of acute coronary syndrome. Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress,such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin Ⅱ receptor blockers,statins,and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein Ⅱb/Ⅲa receptor antagonists,mechanical intervention strategies, etc).

Relation of combined non-high density lipoprotein cholesterol and apolipoprotein B with Gensini Score of coronary atherosclerosis in non-diabetic acute coronary syndrome

Background Non-high-density lipoprotein cholesterol （non-HDL-C） and Apolipoprotein B （apoB） increase car- diovascular disease （CVD） risk, but few studies have explored the correlations of non-HDL-C and apoB with cor- onary atherosclerosis in non-diabetes acute coronary syndrome （ACS）. Methods The study enrolled 443 sub- jects with non-diabetic ACS, and all subject check coronary angiography, and coronary atherosclerosis were eval- uated using Gensini Score （GS） scale including small （GS 1-15）, middle （GS16-43）, and severe （GS≥44）. All sub- jects were classified into 4 groups： High apoB （≥90 mg/dL） and High non-HDL-C （≥130 mg/dL）, High non-HDL -C alone, High apoB alone, and normal apoB and non-HDL-C. Results After adjusted for risk factors, non-HDL -C and apoB were positively correlated with GS （ r = 0.075, P = 0.002 and r = 0.092, P 〈 0.001）. In the GS 0-15, high non-HDL-C ＋ high apoB group 29.3% and high apoB alone group 28.2% were significantly lower than nor- mal non-HDL-C＋ normal apoB group 48% （p = 0.010）. In the GS 16-43, high non-HDL-C alone group 50.4% and high apoB alone group 47.6% were significantly more than high non-HDL-C＋ high apoB group 34.1% （P = 0.036）. In the GS ≥44, high non-HDL-C＋ high apoB group 36.6% was significantly higher than high non-HDL- C alone group 16% and normal non-HDL-C＋ normal apoB 14.2%（P 〈 0.001）. Conclusions The high non-HDL- C and apoB are the risk factors for coronary artery atherosclerosis in non-diabetic ACS.

EFFECT OF ASPIRIN PLUS CLOPIDOGREL ON INFLAMMATORY MARKERS IN PATIENTS WITH NON-ST-SEGMENT ELEVATION ACUTE CORONARY SYNDROME

Background Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome （NSTEACS）. Methods One hundred and fifteen patients with NSTEACS were randomized into two groups： group A （aspirin alone, n=58） and group B （aspirin plus clopidogrel, n=57）. Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein （hs-CRP） and tumor necrosis factor-α （TNF-α ） were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls （group C）. Results Baseline levels of hs-CRP and TNF-α in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A： （6.15 ± 1.39） mg/L vs （9.18 ± 1.62） rag/L, P 〈0.01; Group B：（4.99 ± 1.62） mg/L vs （10.29 ± 1.47） rag/L, P〈0.01]. Similarly, levels of TNF-α in both groups decreased at 7 days compared to baseline [Group A： （90.99 ± 28.91） pg/ml vs （117.20 ± 37.13） pg/ml, P 〈0.01; Group B： （74.32± 21.83） pg/ml vs （115.27 ± 32.11） pg/ml, P 〈0.01]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to （3.49 ± 1.53） rag/L, and （2.40 ± 1.17） mg/L respectively （P 〈0.01 for both comparisons）. Levels of TNF-α in groups A and B also decreased significantly between 7 and 30 days, to 63.28 ± 29.01 pg/ml （group A） and （43.95 ± 17.10） pg/ml （group B; P 〈0.01 for both comparisons）. Significantly lower levels of hs-CRP and TNF-α were observed in group B compared to Group A at thirty days after initiating drug treatment （P 〈0.05）. Conclusions Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-α in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.

钙化结节与急性冠脉综合征

动脉粥样硬化病变钙化结节(ACN)是引起冠状动脉血栓形成与急性冠脉综合征(ACS)的少见但重要的原因。爆裂型钙化结节(ECN)是引起心源性猝死的一种病因,其典型表现为突入管腔的成簇的爆裂样钙化碎片伴有纤维帽破裂,表面附着有血栓。ACN相关的ACS预后较差,围手术期心肌梗死、心源性死亡、靶病变再次血运重建等的发生率较高。本文就ACN的研究进展作一综述。

Effect of high-dose rosuvastatin loading before percutaneous coronary intervention in female patients with non-ST-segment elevation acute coronary syndrome

Background Early loading statin therapy before percutaneous coronary intervention （PCI） is associated with reduced mortality and periprocedural myocardial injury. The aim of this study was to study the effect of rosuvastatin loading therapy before PCI in female patients with non-ST-segment elevation acute coronary syndrome （NSTEACS）. Methods Consecutive 117 female patients with NSTEACS were randomly assigned to either the group of rosuvastatin loading before PCI （20 mg 12 hours before angioplasty procedure, with a further 10 mg dose 2 hours before procedure, the loading dose group, n=59） or the no rosuvastatin treatment group before PCI （control group, n=58）. Periprocedural myocardial injury, periprocedural changes of high sensitivity C-reactive protein （hs-CRP）, interleukin （IL）-l, IL-6, and tumor necrosis factor （TNF）-a in serum and the incidence of major adverse cardiac events （MACE） 3 months and 6 months later were assessed. Results The incidence of periprocedural myocardia~ injury was higher in control group than loading dose group （CKMB： 10.17% vs. 25.86%, P=0.027; Troponin I： 11.86% vs. 29.31%, P=-0.019）. MACE occurred in 1.69% of patients in loading dose group and 12.07% of those in control group 3 months after procedure （P=-0.026）, 3.39% vs. 17.24% at 6 months （P=-0.014）. The levels of hs-CRP, IL-1, IL-6, and TNF-c（ in serum were not significantly different between the two groups before PCI, but after PCI they were significantly higher in control group.Conclusions High-dose rosuvastatin loading before PCI significantly reduced periprocedural myocardial injury and periprocedural inflammation cytokines release and improved 3-month and 6-month clinical outcomes in female patients with NSTEACS who underwent PCI.

Soluble CD40 ligand is associated with angiographic severity of coronary artery disease in patients with acute coronary syndrome

Background Recently,studies have disclosed soluble CD40 ligand （sCD40L） during atherosclerosis development and plaque destabilization.The objective of the present study was to test the hypothesis that sCD40L levels are higher in acute coronary syndrome （ACS） patients with a greater extent of angiographic coronary involvement.Methods This cross-sectional study examined ACS patients who underwent coronary angiography by measuring their sCD40L levels.In order to estimate the serum levels of sCD40L,10 ml of peripheral venous blood was drawn within 24 hours of admission.sCD40L levels were measured using an enzyme-linked immunosorbent assay （ELISA,RapidBio,West Hills,CA,USA）.Demographic data,presence of concomitant diseases,ACS characteristics,and angiographic findings were evaluated.A review of medical records and patient interviews were conducted to assess coronary risk factors.And the severity of coronary artery disease was evaluated using the Gensini score index.Results Two hundred and eighty-nine patients were included in the study,of whom 186 were male,with an average age of 64.1±10.0 years.Median sCD40L levels were 1.7 ng/ml （0.3-7.3 ng/ml） and Gensini scores were 50 （0-228）.After adjusting for demographic variables and cardiovascular risk factors,the Gensini score was associated with the natural logarithm of the sCD40L level （Coefficient b=0.002,95％ CI 0.000-0.003,P=0.029）.Conclusion sCD40L levels were independently associated with angiographic severity of coronary artery disease in patients with ACS.

泛免疫炎症值、全身免疫炎症指数与急性冠脉综合征患者易损斑块的相关性研究

背景泛免疫炎症值(PIV)、全身免疫炎症指数(SII)被认为是评估动脉粥样硬化性心血管疾病风险的新型炎症指标,然而较少有研究探讨PIV、SII对动脉粥样硬化斑块的影响。目的通过光学相干断层成像技术(OCT)探讨急性冠脉综合征(ACS)患者PIV、SII与冠状动脉粥样硬化易损斑块的关系。方法回顾性纳入2020年12月—2023年6月就诊于郑州大学第二附属医院心内科的ACS患者525例为研究对象,患者均接受冠状动脉造影及OCT检查,根据薄纤维帽粥样硬化斑块(TFCA)诊断标准分为非TCFA组(112例)和TCFA组(106例)。收集资料并进行分析。采用多因素有序Logistic回归分析探究TCFA的影响因素。绘制PIV、SII诊断TCFA的受试者工作特征曲线(ROC曲线),计算ROC曲线下面积(AUC)。基于PIV的最佳截断值将患者分为低PIV组(PIV<337.86,79例)和高PIV组(PIV≥337.86,139例),同时基于SII的最佳截断值将患者分为低SII组(SII<775.63,74例)和高SII组(SII≥775.63,144例)。结果TCFA组高血压、糖尿病比例、泛PIV、SII、C反应蛋白(CRP)、有吸烟史比例、术前收缩压高于非TCFA组(P<0.05)。多因素Logistic回归分析结果显示PIV(OR=1.015,95%CI=1.010~1.020,P<0.001)、SII(OR=1.005,95%CI=1.003~1.007,P<0.001)为发生TCFA的危险因素。ROC曲线结果显示PIV、SII诊断TCFA的AUC分别为0.785(95%CI=0.725~0.845,P<0.001)、0.707(95%CI=0.639~0.776,P<0.001)。高PIV组巨噬细胞浸润、点状钙化、易损斑块比例高于低PIV组(P<0.05);高SII组巨噬细胞浸润、微通道、易损斑块比例高于低SII组(P<0.05)。高PIV组纤维帽厚度低于低PIV组,最大脂质斑块角、平均脂质斑块角度、脂质斑块长度、脂质指数高于低PIV组(P<0.05),高SII组纤维帽厚度低于低SII组,最大脂质斑块角、平均脂质斑块角度、脂质斑块长度、脂质指数高于低SII组(P<0.05)。结论高水平PIV、SII可能与ACS患者易损斑块的发生率相关。PIV、SII水平在评估ACS患者冠状动脉粥样硬化易损斑块特征及易损性方面具有一定价值。

膳食炎症潜能与急性冠脉综合征患者冠状动脉病变严重程度的关系研究

背景急性冠脉综合征(ACS)的发生、发展与炎症反应密切相关,但膳食炎症潜能与ACS患者冠状动脉病变严重程度之间的关系尚不清楚。目的采用膳食炎症指数(DII)评估ACS患者膳食炎症潜能,并探讨其与ACS患者冠状动脉病变严重程度之间的关系。方法采用方便抽样法,选取2022年4月—2023年3月在哈尔滨医科大学第二附属医院心内科经冠状动脉造影首次确诊为ACS的患者309例,依据DII四分位数分为4组:DII-1组(-8.35~-4.56)、DII-2组(-4.55~-0.77)、DII-3组(-0.76~3.02)、DII-4组(3.03~6.81),依据Gensini评分四分位数分为4组:Q1组(4~32分)、Q2组(34~52分)、Q3组(54~84分)、Q4组(86~192分)。比较不同冠状动脉病变严重程度ACS患者人口学特征、临床特征、总体DII、营养素DII,并采用多因素Logistic回归分析探究DII与ACS患者冠状动脉病变严重程度之间的关系。结果不同冠状动脉病变严重程度ACS患者文化程度、低密度脂蛋白胆固醇(LDL-C)水平、脂蛋白a(LP-a)水平、总体DII及总脂肪、饱和脂肪酸、维生素E、胡萝卜素DII比较,差异有统计学意义(P≤0.05)。多因素Logistic回归分析结果显示,校正混杂因素文化程度及LDL-C、LP-a水平后,DII-4组是Q2组(OR=15.389,95%CI=1.595~148.432)、Q3组(OR=15.102,95%CI=1.620~140.788)、Q4组(OR=17.319,95%CI=1.901~157.807)的影响因素(P<0.05);总脂肪(OR=3.831,95%CI=1.195~9.094)、饱和脂肪酸(OR=8.562,95%CI=1.519~48.258)、维生素E(OR=0.640,95%CI=0.460~0.890)DII是Q4组的影响因素(P<0.05)。结论膳食炎症潜能及营养素总脂肪、饱和脂肪酸、维生素E炎症潜能是ACS患者冠状动脉病变严重程度的影响因素,临床工作者应进一步加强ACS患者的合理抗炎膳食指导。

脂蛋白相关磷脂酶A2在急性冠状动脉综合征中作用的研究进展

脂蛋白相关磷脂酶A2(Lp-PLA2)是一种由441个氨基酸组成的蛋白。Lp-PLA2能够促进炎细胞向炎性反应部位聚集及炎性因子的释放,促进基质金属蛋白酶的合成,使动脉粥样硬化斑块内泡沫细胞及细胞外基质增多,并且使斑块纤维帽变薄而易于破裂,进而促进急性冠脉综合征(ACS)的发病。因此在急性冠脉综合征患者中测定和调节Lp-PLA2水平具有重要的临床意义。