Unstable Angina Group Research Articles

Gamma-glutamyl transferase to high-density lipoprotein cholesterol ratio: A valuable predictor of coronary heart disease incidence

Background and AimExisting studies have found that serological markers for predicting coronary heart disease (CHD) have relatively low predictive value for the severity of coronary arteries and the types of CHD. GGT to HDL-C ratio (GHR) has been shown to be associated with T2DM and non-alcoholic fatty liver disease. Therefore, we explore the relationship among GHR, CHD and its subgroups. Methods and ResultsThe study retrospectively analyzed 2703 participants from August 2022 to August 2023. The patients were divided into CHD group (N=1911) and control group (N=792) according to the diagnostic criteria of CHD. Adjustments for all covariates found that the GHR was an independent risk factor for CHD (OR: 1.025, 95% CI 1.016-1.033) and had the highest AUC of 0.767 (95% CI 0.744-0.790) in identifying CHD. Additionally, GHR was significantly associated with multi-vessel CHD (OR: 1.018, 95% CI 1.012-1.023) and showed excellent diagnostic capability for patients with multi-vessel CHD (AUC: 0.638). Moreover, compared with chronic coronary syndromes (CCS) and unstable angina (UA) groups, the level of GHR was significantly increased in acute myocardial infarction (AMI) (ST elevation myocardial infarction and Non-ST elevation myocardial infarction) groups (P<0.05). GHR had the higher AUC in STMETI [0.819 (95% CI 0.796-0.854)] and NASTEMI [0.792 (95% CI 0.766-0.816)] than the CCS and UA groups. ConclusionsOur study analyses found that GHR is an independent risk factor for CHD and can predict the severity of coronary artery stenosis. Moreover, GHR has a high predictive value for AMI than CCS and UA in CHD patients.

Different levels of lipids, Hb1Ac and cytokines among patients with coronary artery disease

BackgroundDifferent risk factors are responsible for the occurrence of coronary artery disease (CAD). Among these, the main factors are dyslipidemia, dysglycaemia, and endothelial inflammation. The aim of the study was to analyze the levels of lipids, glucose, and cytokine in patients with different coronary heart diseases. MethodsA total of 2147 patients diagnosed with coronary atherosclerosis, stable angina, unstable angina, acute non-ST-segment elevation infarction (NSTEMI) and acute ST-segment-elevation myocardial infarction (STEMI) at the Cardiovascular Center of Beijing Tongren Hospital from February 2022 to April 2023. The data were gathered from the medical record system.Nonparametric Wilcoxon test was used for statistical analysis of continuous variables, and chi-square test was used for statistical analysis of categorical variables among multiple groups. ResultsCompared with coronary atherosclerosis group, acute myocardial infarction group showed a significant increase in IL-6 level (p < 0.001). Compared with stable angina group, acute myocardial infarction group showed a significant increase in IL-6 and decrease in INF-γlevels (p < 0.001). Compared with unstable angina group, acute myocardial infarction group showed a significant increase in IL-6 level and decrease in IL-17, as well as INF-γlevels (p < 0.001). Compared with NSTEMI group, the proportion of younger, males, glycemic-lowering drugs, as well as the levels of TC, LDL-C in STEMI group increased significantly, while the proportion of hypertension, IFG/IGT/DM, hyperlipidemia and Hb1Ac level decreased significantly. STEMI group showed a significant increase in IL-2 and IL-6 levels (p < 0.05). ConclusionsThe levels of lipids, Hb1Ac, IL-2 and IL-6 were varying in patients with different stages of coronary heart diseases.The data would contribute to a deeper understanding of the roles of lipids, glucose, and inflammation in the occurrence and development of CAD.

Integrating genomic profiling to clinical data: assessing the impact of CD147 expression on plaque stability.

Acute Coronary Syndrome (ACS) continues to be a leading cause of death and illness worldwide. Differentiating stable from unstable coronary plaques is essential for enhancing patient outcomes. This research investigates the role of CD147 as a biomarker for plaque stability among coronary artery disease patients. The study began with high-throughput sequencing of blood samples from six patients, divided equally between those with Stable Angina (SA) and Unstable Angina (UA), followed by bioinformatics analysis. Expanding upon these findings, the study included 31 SA patients and 30 patients with ACS, using flow cytometry to examine CD147 expression on platelets and monocytes. Additionally, logistic regression was utilized to integrate traditional risk factors and evaluate the predictive value of CD147 expression for plaque stability. Initial sequencing displayed a notable difference in CD147 expression between SA and UA groups, with a significant increase in UA patients. Further analysis confirmed that elevated platelet CD147 expression was strongly associated with unstable plaques (OR = 277.81, P < .001), after adjusting for conventional risk factors, whereas monocyte CD147 levels did not show a significant difference. Elevated CD147 expression on platelets is a crucial biomarker for identifying unstable coronary artery plaques, offering insights into patient risk stratification and the development of targeted treatment strategies. This underscores the pivotal role of molecular research in understanding and managing coronary artery disease, paving the way for improved clinical outcomes.

A comparative study examining the impact of coronary artery bypass grafting surgery with non-extracorporeal circulation on heart function and structure in patients with various forms of coronary heart diseases.

The aim of this study is to assess alterations in heart function and structure in patients diagnosed with non-ST segment elevation acute myocardial infarction (NSTEAMI), unstable angina (UA), and stable angina (SA) 1 year after undergoing off-pump coronary artery bypass grafting (OPCABG) performed without extracorporeal circulation. A total of 182 patients who underwent OPCABG were included and classified into 3 groups based on their preoperative diagnosis: the NSTEAMI group (n = 68), the UA group (n = 64), and the SA group (n = 50). Cardiac ultrasonography data were collected for all groups both preoperatively and 1 year postoperatively. Clinical data were subjected to statistical analysis. In the NSTEAMI group, postoperative observations revealed increases in left ventricular stroke volume and left ventricular end-systolic diameter, along with reductions in left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic diameter (LVEDD) 1-year post-surgery. The UA group demonstrated decreases in LVEDV and LVEDD 1-year post-surgery. Similarly, the SA group exhibited an increase in left ventricular ejection fraction (LVEF) and reductions in LVEDV and LVEDD 1-year post-surgery. Comparative analysis of cardiac ultrasonography data revealed that the NSTEAMI group displayed significantly lower left ventricular stroke volume and notably higher left ventricular end-systolic diameter and volume compared to the UA and SA groups 1-year post-surgery. Furthermore, the SA group exhibited significantly elevated LVEF compared to the UA and NSTEAMI groups 1-year post-surgery. Cardiac ultrasonography findings indicate that all 3 groups exhibited improvements in cardiac function and left ventricular structure 1-year post-surgery. However, the NSTEAMI group demonstrated more substantial improvements in comparison to the UA and SA groups.

Comparison of Immature Platelet Fraction (IPF) Values for ACS Patients with Unstable Angina Pectoris (UAP), Non-ST Elevation Myocardial Infarct (NSTEMI), and ST Elevation Myocardial Infarct (STEMI)

Background: Acute coronary syndrome (ACS) is a medical emergency that requires rapid diagnosis and treatment. Immature platelet fraction (IPF) is a hematological parameter that has the potential to be a biomarker for differentiating types of ACS. This study aims to compare IPF values in ACS patients with unstable angina pectoris (UAP), Non-ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Methods: This research is an analytical observational study with a cross-sectional design. The research subjects were ACS patients treated at Dr. M. Djamil General Hospital, Padang, Indonesia between January 2023 to December 2023. IPF values were measured using the Sysmex XN-1500 tool. Statistical analysis was carried out using the ANOVA test and post-hoc Tukey test. Results: A total of 150 ACS patients (50 UAP, 50 NSTEMI, 50 STEMI) were included in this study. The mean IPF value in the STEMI group (6.8 ± 2.1%) was significantly higher than that in the NSTEMI (4.5 ± 1.8%) and UAP (3.2 ± 1.5%) groups (p &lt; 0.001). ROC analysis showed that the IPF value had an AUC of 0.89 (95% CI: 0.84-0.94) for differentiating STEMI from NSTEMI/UAP. Conclusion: IPF values were higher in STEMI patients compared to NSTEMI and UAP. This parameter has the potential to be a biomarker for differentiating types of ACS, especially in differentiating STEMI from NSTEMI/UAP.

The Relationship Between the Serum NLRP3 and Adiponectin Levels and Coronary Lesions in Patients with Unstable Angina with Type 2 Diabetes.

To investigate the Levels of Nucleotide-binding, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) and Adiponectin (APN) and their relationship with the severity of coronary artery disease in patients with Unstable Angina (UA) and Type 2 Diabetes (T2D). Two hundred and thirty-one patients with UA were diagnosed by CAG in the Department of Cardiology of the Affiliated Hospital of Xuzhou Medical University from July 2022 to May 2023 were included, and 74 healthy subjects were included as the control group. The levels of NLRP3 and APN in each group were detected by ELISA and the Gensini score in each patient according to the results of CAG. The correlations between NLRP3, APN, and Gensini score were analyzed. According to whether complicated with T2D or not, we further analyze the effect of NLRP3 and APN levels of patients with UA and T2D on the severity of coronary artery stenosis. The levels of NLRP3 in UA with T2D group were the highest, followed by simple UA group, and the lowest in the control group, and the level of APN was the opposite. Spearman Correlation analysis showed that the level of NLRP3 was positively correlated with Gensini score (ρ1=0.688, P<0.05) and the level of APN was negatively associated with Gensini score (ρ2= -0.515, P<0.05). There was a negative correlation between NLRP3 and the level of APN (ρ3= -0.366, P<0.05). High NLRP3 and low APN levels are the risk factors for atherosclerosis. The NLRP3 and APN were abnormally expressed in patients with UA complicated with T2D. With the aggravation of atherosclerosis, the level of NLRP3 increased and the level of APN decreased.

Alterations in the gut mycobiome with coronary artery disease severity

BackgroundCoronary artery disease (CAD) is a prevalent cardiovascular condition, and numerous studies have linked gut bacterial imbalance to CAD. However, the relationship of gut fungi, another essential component of the intestinal microbiota, with CAD remains poorly understood. MethodsIn this cross-sectional study, we analyzed fecal samples from 132 participants, split into 31 healthy controls and 101 CAD patients, further categorized into stable CAD (38), unstable angina (41), and acute myocardial infarction (22) groups. We conducted internal transcribed spacer 1 (ITS1) and 16S sequencing to examine gut fungal and bacterial communities. FindingsBased on ITS1 analyses, Ascomycota and Basidiomycota were the dominant fungal phyla in all the groups. The α diversity of gut mycobiome remained unaltered among the control group and CAD subgroups; however, the structure and composition of the mycobiota differed significantly with the progression of CAD. The abundances of 15 taxa gradually changed with the occurrence and progression of the disease and were significantly correlated with major CAD risk factor indicators. The mycobiome changes were closely linked to gut microbiome dysbiosis in patients with CAD. Furthermore, disease classifiers based on gut fungi effectively identified subgroups with different degrees of CAD. Finally, the FUNGuild analysis further categorized these fungi into distinct ecological guilds. InterpretationIn conclusion, the structure and composition of the gut fungal community differed from healthy controls to various subtypes of CAD, revealing key fungi taxa alterations linked to the onset and progression of CAD. Our study highlights the potential role of gut fungi in CAD and may facilitate the development of novel biomarkers and therapeutic targets for CAD. FundingThis work was supported by the grants from the National Natural Science Foundation of China (No. 82170302, 92168117, 82370432), National clinical key specialty construction project- Cardiovascular Surgery, 2024 Reform and Development Program of Beijing Institute of Respiratory Medicine, the Beijing Natural Science Foundation (No. 7222068); the Reform and Development Program of Beijing Institute of Respiratory Medicine (No. Ggyfz202308); and the Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medical University (No. CYFH202209).

A Cross-Sectional Study of Acute Coronary Syndrome and Thyroid Profile: Dissecting the Relationship to Improve Patient Care.

Thyroid-releasing hormones are pivotal in regulating cardiovascular (CVS) function and maintaining its hemodynamics and homeostasis. Even a minor alteration in thyroid function has an enormous implication on CVS morbidity and mortality. Moreover, hypothyroidism was found to be a potential menace for coronary artery disease (CAD).The objective of this study was to determine the role of thyroid-releasing hormones in patients suffering from acute coronary syndrome (ACS). Among a cohort of 100 patients suffering with ACS, a complete history and clinical information followed by physical examinationand electrocardiography were recorded. Blood samples were also collected to record the blood sugar levels i.e., fasting blood sugar (FBS), postprandial blood sugar (PPBS), and thyroid profile, including free thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and reverse triiodothyronine (rT3). The data was analyzed using SPSS version 26 software (IBM Corp., Armonk, NY, USA). The study identified alterations in the thyroid hormone levelsin 27% of patients suffering from ACS. The prevalence of euthyroid sick syndrome was found to be 59.3%, while subclinical hypothyroidism and subclinical hyperthyroidism were reported among 18.5% and 14.8% of patientsrespectively. Therewas no significant difference found between males and females. The study illustrated a greater occurrence of aberrant thyroid hormone profiles among those aged 40-60 years. The ST-elevated myocardial infarction (STEMI) group had a statistically significant higher prevalence of an aberrant thyroid hormone profile compared to the non-ST-elevated myocardial infarction (NSTEMI) and unstable angina (UA)groups (p=0.02). A total of nine patients died with ACS and all of those had statistically significant low fT3 and TSH values while higher rT3 values (p<0.05). An atypical thyroid status has been found to elevate the likelihood of developing CAD and experiencing CVS mortality. This condition can impact ventricular function and serum cholesterol levelsas well as heart rate and rhythm. Therefore, understanding this relationship could potentially lead to improved treatment strategies for individuals with ACS which will further prevent major CVS complications.

Potential biomarkers of acute myocardial infarction based on the composition of the blood microbiome

BackgroundIt is difficult to distinguish between acute myocardial infarction (AMI) and unstable angina (UA) due to their similar clinical features. In recent years, studies have shown that microbiomes have great potential in distinguishing diseases. The purpose of this study is to describe the composition of serum microbiome in the AMI and UA by 16S rDNA sequencing. MethodsBased on the high-throughput detection platform and 16S rDNA amplification sequencing technology, this study detected the blood microbial composition of 55 patients with AMI and 62 patients with UA. Alpha diversity and Beta diversity analysis were used to compare the differences in microbial composition and bacterial colony structure between AMI and UA groups. We perform PCoA (Principal Co-ordinates Analysis) based on Unweighted Unifrac distance. In addition, various statistical methods were employed to examine the significance of differences in microbial composition and genus between the two groups. PICRUSt (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States) was employed to predict KEGG (Kyoto Encyclopedia of Genes and Genomes) function from 16S sequencing data. Random forest was applied to identify biomarkers and construct the diagnostic model. Subsequently, the stability of the model was verified by 10-fold cross and the diagnostic effectiveness was evaluated through ROC (Receiver Operating Characteristic). ResultsIn this study, we found that alpha diversity index of serum microbiome in AMI group was significantly higher than in UA group. T-test analysis demonstrated that the UA group presented a higher abundance of Ralstonia, Faecalibaculum and Gammaproteobacteria, while Bacteroides, Sphingomonas, Faecalibaculum, Haemophilus, Serratia, Bifidobacterium and Chloroplast were more abundant in the AMI group. The LefSe (LDA Effect Size) analysis showed that the Gammaproteobacteria, Proteobacteria, Ralstonia pickettli, Ralstonia, Burkholderiaceae and Burkholderiales were enriched in UA group, and Bacteroidales, Bacteroidia, Bacteroidota, Clostridia and Firmicutes were more abundant in the AMI group. Ten bacterial diagnostic models were constructed in the random forest. The area under the curve (AUC) in the training set was 88.01%, and the AUC value in the test set was 95.04%. ConclusionIn this study, the composition of blood microorganisms in the groups of patients with AMI and UA has been analyzed, providing novel insights for understanding the pathogenesis of AMI; Blood microbiome may serve as novel diagnostic biomarkers of AMI.

The predictive value of serum Dickkopf-1, Dickkopf-3 level to coronary artery disease and acute coronary syndrome

BackgroundPrevious studies have already confirmed the association between Dickkopf (Dkk) protein and the occurrence and progression of atherosclerosis. However, there is limited clinical evidence regarding the serum levels of Dickkopf-1 (Dkk1) and Dickkopf-3 (Dkk3) in relation to atherosclerotic cardiovascular disease (ASCVD), particularly acute coronary syndrome (ACS). Materials and methodsA total of 88 healthy volunteers and 280 patients with coronary artery disease (CAD) undergoing coronary angiography for angina between October 2021 and October 2022, including 96 cases of stable angina (SA), 96 of unstable angina (UA) and 88 of acute myocardial infarction (AMI) were included finally. The serum concentrations of Dkk1 and Dkk3 were measured using electrochemiluminescence of Meso Scale Discovery. The predictive value of single or combined application of serum Dkk1 and Dkk3 in CAD and ACS were evaluated. ResultsThe serum levels of Dkk1 were significantly higher in the SA group, UA group, and AMI group compared to the control group. Multivariable logistic regression analysis demonstrated that elevated serum Dkk1 levels were independent predictive factors for increased risk of CAD and ACS (OR = 1.027, 95%CI = 1.019–1.034, p < 0.001; OR = 1.045, 95%CI = 1.028–1.053, p < 0.001, respectively). Receiver operating characteristic curve (ROC) analysis showed that the optimal cutoff value of serum Dkk1 for predicting ACS was 205 ng/dl, with a sensitivity of 82.6% and specificity of 96.6%. The area under the curve (AUC) was 0.930 (95%CI: 0.899–0.961, p < 0.001). Regarding Dkk3, serum Dkk3 levels were elevated in CAD patients compared to the healthy control group, and significantly higher in ACS patients compared to SA patients. Serum Dkk3 was significantly associated with increased risk of CAD and ACS (OR = 1.131, 95%CI = 1.091–1.173, p < 0.001; OR = 1.201, 95%CI = 1.134–1.271, p < 0.001, respectively). ROC curve analysis showed that the optimal cutoff value of serum Dkk3 for predicting ACS was 50.82 ng/ml, with a sensitivity of 85.9% and specificity of 87.5%. The AUC was 0.925 (95%CI: 0.894–0.956, p < 0.001). When serum Dkk1 and Dkk3 are combined as predictive factors for ACS, the AUC was 0.975. ConclusionSerum levels of Dkk1 and Dkk3 are significantly associated with an increased risk of CAD and ACS, and they possess predictive value for CAD and ACS. The combination of serum Dkk1 and Dkk3 is a superior predictive factor for CAD and ACS.

The role of computed tomography angiography in assessing the correlation between properties of coronary atherosclerotic plaque and blood lipids.

Coronary atherosclerotic heart disease (CAHD) is the leading cause of death in developed countries. This study aimed to explore the correlation between the properties of coronary atherosclerotic plaque and blood lipids using computed tomography angiography (CTA). A total of 83 patients with coronary heart disease were included in this study (males: 50; females: 33; average age: [59 ± 8] years old). They were classified into the stable angina group and unstable angina group. Atherosclerotic plaques were classified as fatty plaques (soft plaques), fibrous plaques, and calcified plaques based on the computed tomography (CT) values. SPSS 17.0 statistical software was used to analyze the correlation between the properties of angina and the CT values of atherosclerotic plaques, blood lipids, and plaque properties, and then compared between the stable and unstable angina groups. There were statistically significant differences in plaque properties between the stable and unstable angina groups (P< 0.001). During CTA examination, we found statistically significant differences in the CT density values of atherosclerotic plaques between the stable and unstable angina groups (P< 0.001). There were statistically significant differences between the properties of angina and the level of blood lipids (P< 0.05). Anginal properties negatively correlated with calcified plaques and positively correlated with non-calcified plaques. Calcified plaques negatively correlated with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and positively correlated with high-density lipoprotein cholesterol (HDL-C). Non-calcified plaques negatively correlated with HDL-C and positively correlated with TC, LDL-C, and TG.

Association of GAL-8 promoter methylation levels with coronary plaque inflammation

Background and aimsCoronary heart disease (CHD) is a condition that carries a high risk of mortality and is associated with aging. CHD is characterized by the chronic inflammatory response of the coronary intima. Recent studies have shown that the methylation level of blood mononuclear cell DNA is closely associated with adverse events in CHD, but the roles and mechanisms of DNA methylation in CHD remain elusive. Methods and resultsIn this study, the DNA methylation status within the epigenome of human coronary tissue in the sudden coronary death (SCD) group and control (CON) group of coronary heart disease was analyzed using the Illumina® Infinium Methylation EPIC BeadChip (850 K chip), resulting in the identification of a total of 2553 differentially methylated genes (DMGs). The differentially methylated genes were then subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and significant differential DNA methylation was found. Among the differentially hypomethylated genes were GAL-8, LTF, and RFPL3, while the highly methylated genes were TMEM9B, ANK3, and C6orF48. These genes were mainly enriched in 10 significantly enriched pathways, such as cell adhesion junctions, among which the differentially methylated gene GAL-8 was involved in inflammatory pathway signaling. For functional analysis of GAL-8, we first examined the differences in GAL-8 promoter methylation levels among different subgroups of human coronary tissue in the CON, CHD, and SCD groups using pyrophosphate sequencing. The results revealed reduced GAL-8 promoter methylation levels in the SCD group, while the difference between the CHD and CON groups was not statistically significant (P > 0.05). The reduced GAL-8 promoter methylation level was associated with upregulated GAL-8 expression, which led to increased expression of the inflammatory markers TNF-α, IL-1β, MCP-1, MIP-2, MMP-2, and MMP-9. This enhanced inflammatory response contributed to the accumulation of foam cells, thickening of the intima of human coronary arteries, and increased luminal stenosis, which promoted the occurrence of sudden coronary death. Next, we found that GAL-8 promoter methylation levels in PBMC were consistent with human coronary tissue. The unstable angina group (UAP) had significantly lower GAL-8 promoter methylation levels than stable angina (SAP) and healthy controls (CON) (P < 0.05), and there was a significant correlation between reduced GAL-8 promoter methylation levels and risk factors for coronary heart disease. These findings highlight the association between decreased GAL-8 promoter methylation and the presence of coronary heart disease risk factors. ROC curve analysis suggests that methylation of the GAL 8 promoter region is an independent risk factor for CHD. In conclusion, our study confirmed differential expression of GAL-8, LTF, MUC4D, TMEM9B, MYOM2, and ANK3 genes due to DNA methylation in the SCD group. We also established the consistency of GAL-8 promoter methylation alterations between human coronary tissue and patient peripheral blood monocytes. The decreased methylation level of the GAL-8 promoter may be related to the increased expression of GAL-8 and the coronary risk factors. ConclusionsAccordingly, we hypothesized that reduced levels of GAL-8 promoter methylation may be an independent risk factor for adverse events in coronary heart disease.

Improved heart function and cardiac remodelling following sacubitril/valsartan in acute coronary syndrome with HF.

This study sought to assess the effect of treatment of sacubitril/valsartan (S/V) on improving cardiac function and reversing cardiac remodelling in patients with acute coronary syndrome (ACS) complicated with heart failure with reduced ejection fraction after percutaneous coronary intervention (PCI). We enrolled 275 ACS patients with reduced left ventricular ejection fraction after PCI. The patients were divided into the routine and S/V groups according to the treatment drugs. The symptoms, N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations, echocardiographic parameters [left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI)], major adverse cardiac events (MACEs), and adverse reactions were recorded at baseline and 6months after treatment when a clinical follow-up was performed. The S/V group was further divided into prespecified subgroups including unstable angina (UA) group, non-ST-elevation myocardial infarction (NSTEMI) group, and ST-elevation myocardial infarction (STEMI) group according to the type of ACS. We analysed the changes in LVEF, LVMI, LVEDVI, LVESVI, and NT-proBNP in both groups and evaluated the correlation between the changes in the above variables (ΔLVEF, ΔLVMI, ΔLVEDVI, ΔLVESVI, and ΔNT-proBNP). Cox regression model was used to assess the independent risk factors of MACE. Prespecified subgroup analyses were also conducted. Compared with baseline, LVEF increased significantly (P<0.05), NT-proBNP, LVMI, and LVESVI decreased significantly in both groups after 6months (P<0.05), and LVEDVI decreased significantly in the S/V group (P=0.001). In the S/V group, ΔLVEF (t=-2.745, P=0.006), ΔNT-proBNP (P=0.009), ΔLVEDVI (t=4.203, P=0.001), and ΔLVESVI (t=3.907, P=0.001) were significantly improved than those in the routine group. In the S/V group, ΔLVEF was negatively correlated with ΔNT-proBNP (r=-0.244, P=0.004), ΔLVMI (r=-0.190, P=0.028), ΔLVEDVI (r=-0.173, P=0.045), and ΔLVESVI (r=-0.261, P=0.002). In Cox regression model analysis,ΔLVEF {hazard ratio [HR]=0.87 [95% confidence interval (CI) 0.80-0.95], P=0.003}, ΔLVEDVI [HR=1.04 (95% CI 1.01-1.06), P=0.013], and ΔLVESVI [HR=1.04 (95% CI 1.01-1.08), P=0.026] were independent risk factors for MACE. Subgroup analysis showed that ΔLVEF (t=6.290, P=0.001), ΔLVEDVI (t=2.581, P=0.011), and ΔNT-proBNP (P=0.019) in the NSTEMI group were significantly improved than those in the UA group, ΔLVEDVI in the NSTEMI group was significantly better than that in the STEMI group (t=-3.365, P=0.001), and ΔLVEF in the STEMI group was significantly better than that in the UA group (t=-3.928, P=0.001). There was a significant difference in the survival probability without MACE among the three groups in the analysis of the Kaplan-Meier curve (P=0.042). The incidence of MACE in the UA group was significantly higher than that in the NSTEMI group (32.4% vs. 6.3%, P=0.004). The cardiac function is improved and cardiac remodelling is reversed significantly after treatment of S/V in ACS patients with reduced left ventricular ejection fraction after PCI, and the improvement is more obvious than the routine group. There is a significant negative correlation between the change in LVEF and the changes in NT-proBNP, LVMI, LVEDVI, and LVESVI. The increase of LVEF and the decrease of LVEDVI and LVESVI are protective factors to improve the prognosis. Patients with myocardial infarction and reduced left ventricular ejection fraction might benefit more from the initiation of S/V as first-line heart failure treatment after PCI.

Clinical particulars of acute coronary syndrome course in patients with COVID-19

Background: Cardiovascular complications of COVID-19 result in challenges for differential diagnosis, patients referral and treatment, which negatively affect the outcomes.&#x0D; Aim: To identify clinical particulars of various types acute coronary syndrome course in patients with COVID-19.&#x0D; Materials and methods: This retrospective cross-sectional study included 202 patients with COVID-19 and acute coronary syndrome (ACS) admitted to a primary vascular medicine center from September to December 2020. Their medical records were used for the analysis of ACS and COVID-19 clinical course, including physical and history data, laboratory and instrumental work-up. For the analysis, the patient sampling was divided into three study groups: 50 patients with unstable angina (UA), 107 patients with acute myocardial infarction with ST segment elevation (STEMI), and 45 patients with acute myocardial infarction without ST segment elevation (non-STEMI).&#x0D; Results: There were no differences in clinical manifestations of ACS in the study groups. As far as clinical manifestations of coronavirus infections are concerned, the patients differed significantly as per prevalence of fever and dry cough. Fever was present in 22 (44%) UA patients, 18 (17%) of STEMI patients and in 10 (22%) of non-STEMI patients (p 0.001 for comparison of 3 groups, Kruskall-Wallis test), whereas dry cough was present in 18 (36%), 19 (18%), and 14 (31%) patients, respectively (p = 0.029). Paired comparison (Mann-Whitney test with Bonferroni adjustment) showed significant differences between US and STEMI groups for both symptoms. The number of involved vessels (median [25%; 75%]) in UA patients was 0 [0; 2], in STEMI and non-STEMI patients 2 [1; 3] (p 0.001). A left coronary artery stenosis was detected in 2 (6%) of the UA patients, 13 (14%) of the STEMI and 4 (13%) of the non-STEMI patients (p = 0.452); left anterior descending artery stenosis, in 12 (36%), 67 (72%) and 23 (72%) patients, respectively (p 0.001). In the pairwise comparison, there were differences between UA and STEMI groups and between UA and non-STEMI groups. A left circumflex artery stenosis was found in 7 (21%) of the UA patients, 45 (48%) of the STEMI and 18 (56%) of the non-STEMI patients (p = 0.008); the pairwise comparisons showed the difference between UA and non-STEMI study groups. A right coronary artery stenosis was identified in 9 (27%), 64 (69%) and 18 (56%) of the study patients, respectively (p 0.001); in the pairwise comparison the difference was found between the UA and STEMI group. There were significant differences in the percentage of the right descendent and right coronary artery stenosis: the right descending artery stenosis was 70% [45; 80] in the UA patients, 90% [70; 100] in the STEMI and 95% [70; 100] in the non-STEMI patients (p = 0.013), whereas the right coronary artery stenosis was 50% [45; 80], 90% [70; 100], 90% [60; 100], respectively (p = 0.018). In the pairwise comparison, the differences were found between the UA and STEMI patients in both arteries. The STEMI patients had higher TIMI thrombus grade scores than those with non-STEMI: 3 [0; 5] vs 0 [0; 4] (p = 0.023). The rates of successful percutaneous coronary intervention and achievement of TIMI flow grade 3 between them was not significantly different (p = 0.170).&#x0D; Conclusion: The ACS patients with ACS and COVID-19 have high thrombotic load according to coronary angiography and TIMI score in the case of STEMI and more frequent absence of hemodynamically significant stenosis in those with UA and non-STEMI. The absence of any difference in clinical manifestations of ACS and viral infection between the study groups (except fever and dry cough difference between the UA and STEMI patients) indicates that specific characteristics of the ACS course in COVID-19 patients can be identified only by coronaroangiography.

Role of Neutrophil to Lymphocyte Ratio in Risk Stratifying Patients with Unstable Angina and NSTEMI

Abstract Background A well-known fact about acute myocardial infarction is its association with leukocytosis. The differential analysis of white blood cells gives additional benefit of assessing ACS severity by clinical outcomes. Obtaining peripheral leukocyte count is a cheap and widely available mode. Aim of the Work The aim of the study was to test the value of neutrophil to lymphocyte ratio in risk stratifying patients with acute coronary syndromes and its early outcomes. Patients and Methods A total of 100 patients with UAP and NSTEMI were prospectively evaluated at Ain Shams University Hospital (63% UAP and 37% NSTEMI).The patients were followed for clinical outcomes for 48 hours in-hospital and 1 month after discharge. Results The median (IQR) NLR was 8.4 (5.3 to 9.7) in NSTEMI group versus 1.8 (1.2 to 2.8) in unstable angina group, NLR &amp;gt; 3.9 had a sensitivity of 100%, specificity of 92% as a diagnostic value. All patients were divided into “low risk,” “intermediate risk” and “high risk” groups according to TIMI score. In unstable angina group, the quartiles of NLR in “low risk,” “intermediate risk” and “high risk” groups were 3.01 (2.01, 4.33), 3.39 (2.36, 5.10) and 5.49 (3.44, 9.65). In NSTEMI group, the quartiles of NLR in “low risk,” “intermediate risk” and “high risk” groups were 5.08 (3.07, 8.14), 5.17 (2.98, 9.05) and 6.49 (3.86, 11.68). Meaning that there is positive correlation, as NLR were found to be significantly higher in high risk groups. Conclusion Admission NLR is the strong and independent predictor of cardiovascular outcomes in patients with NSTEMI and UAP. Consequently, given the advantages of NLR, it may be the ideal marker for risk stratification in patients with NSTEMI and UAP. Despite the science of inflammatory biomarkers having been described decades ago, NLR appears to be enjoying a renaissance as a cost-effective biomarker with immediate clinical predictability and prognostication. The ease and rapidity of performing these tests make them an independent, simple, inexpensive and accurate early predictor of high-risk TIMI score patients in ACS. Abbreviations ACS: Acute coronary syndrome; AMI: Acute myocardial infarction; CAD: Coronary artery disease CK: Creatine kinase cTnI: Cardiac troponin I cTnT: Cardiac troponin T; EDTA: Ethylene-diamine-tetra-acetic acid; MI: Myocardial infarction; NLR: Neutrophil-to-lymphocyte ratio; NSTEMI: Non-ST-elevation myocardial infarction; SCD: Sudden cardiac death; STEMI: ST-elevation myocardial infarction; TLC: Total leucocyte count; UA: Unstable angina; UAP: Unstable angina pectoris; VF: Ventricular fibrillation; WBC: White blood cell count

Identification of novel candidate biomarkers for acute myocardial infarction by the Olink proteomics platform

BackgroundBoth pathological and normal processes depend on proteins. In this study, plasma protein profiles were analyzed by a novel proximity extension assay (PEA) to identify potential pathogenic mechanisms and diagnostic biomarkers in patients diagnosed with acute myocardial infarction (AMI). MethodsIn this study, we identified a total of 92 plasma proteins using the Olink Target 96 Cardiovascular III panel in a cohort consisting of 30 healthy controls (HC), 28 patients with unstable angina (UA) and 30 patients with AMI. Subsequently, we conducted a differential expression analysis to identify protein molecules that were specifically expressed in patients with AMI. To gain insights into the potential functional mechanisms of these differentially expressed molecules, we performed Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Following that, the utilization of least absolute shrinkage and selection operator (LASSO) regression facilitated the identification of potential protein biomarkers, enabling the differentiation between AMI and UA. A diagnostic model was subsequently developed through logistic regression, and the effectiveness of these markers was assessed using receiver operating characteristic (ROC) analysis. Ultimately, the diagnostic capabilities of these potential biomarkers were validated in an independent validation cohort consisting of 30 UA cases and 30 AMI cases. ResultsIn this study, a comprehensive analysis of plasma proteins identified a total of 92 proteins. Further analysis using analysis of variance revealed that 25 proteins exhibited specific expression in the AMI group compared to the HC and UA groups. Additionally, KEGG enrichment analysis indicated that these differentially expressed proteins were primarily associated with the activation of cytokine-cytokine receptor interaction, PI3K-Akt signaling pathway, and GnRH signaling pathway. AGRP, TGM2, IL6, GH1, and CA5A were identified through LASSO regression as prospective protein biomarkers for distinguishing between UA and AMI. The diagnostic model comprising these five proteins exhibited exceptional performance in both the discovery and validation datasets, surpassing AUC values of 0.9. ConclusionThe findings of our study provide additional insights into the involvement of the inflammatory response and AKT cascade response in the development of AMI. Moreover, we have identified potential protein markers that could be utilized for the accurate diagnosis of AMI. These results offer a fresh perspective for clinical decision-making in the context of AMI.

Interleukin-33/sST2: Dynamic assessment in patients with acute coronary syndrome

PurposeInterleukin (IL)-33 and its soluble receptor ST2 (sST2) play a crucial role in the immune response. sST2 has been approved by the Food and Drug Administration as a prognostic biomarker of mortality in chronic heart failure patients, however, the role of IL-33 and sST2 in atherosclerotic cardiovascular disease remains unclear. The aim of this study was to measure serum level of IL-33 and sST2 of patients at the onset of acute coronary syndrome (ACS) and 3 months after primary percutaneous revascularization. Patients and methodsForty patients were divided into ST segment elevation myocardial infarction (STEMI) group, non-ST segment elevation myocardial infarction (NSTEMI) and unstable angina (UA) group. IL-33 and sST2 level were measured with ELISA. Additionally, IL-33 expression in peripheral blood mononuclear cells (PBMCs), was evaluated. ResultsAll ACS patients had a significantly lower level of sST2 3 months after ACS as compared to the baseline (p ​< ​0.039). The STEMI patients had higher serum levels of IL-33 at the moment of ACS as compared to 3 months after the event, with an average decrease of 17.87 ​pg/ml (p ​< ​0.007). Conversely, sST2 serum levels were still high after 3 months following an ACS in STEMI patients. ROC curve demonstrated that increased IL-33 serum level could be STEMI predictor. ConclusionsThe assessment of the baseline and dynamics of changes in IL-33 and sST2 concentrations in patients with ACS may be important for the diagnostic process and may help in understanding of how the immune mechanisms work at the moment of an ACS event.

The Relationship between the Serum NLRP1 Level and Coronary Lesions in Patients with Coronary Artery Disease.

The pathogenesis of coronary artery disease is complex, and inflammation is one of the regulatory factors. The nucleotide-binding oligomerization domain (NOD)-like receptor protein 1 (NLRP1) plays an important role in the cellular inflammatory response, cell apoptosis, cell death, and autoimmune diseases. Whether the level of NLRP1 is related to the severity of coronary artery stenosis in patients with coronary artery disease (CAD) has not been reported. To test the serum level of NLRP1 in unstable angina (UA) patients and investigate the effect of NLRP1 on coronary stenosis severity of the coronary artery disease (CAD). 307 patients hospitalized in the Department of Cardiology of the Affiliated Hospital of Xuzhou Medical University for coronary angiography from January 1, 2021, to December 31, 2022 were included. We detect the level of NLRP1 in the serum of the included patients. Patients were divided into UA group and control group according to coronary angiography results and other clinical data. We use logistic regression to screen the influencing factors of UA. Then, subgroups were divided according to the Gensini score and the number of coronary artery lesions, and the difference of serum NLRP1 level between the groups was compared. Spearman correlation analysis was used to explore the correlation between the serum NLRP1 level and Gensini score. We analyze the diagnostic value of NLRP1 for UA by drawing ROC curve. The median level of serum NLRP1 in patients with UA (n = 257) was 49.71 pg/ml, IQR 30.15, 80.21, and that in patients without UA (n = 50) was 24.75 pg/ml, IQR 13.49, 41.95. Serum NLRP1 levels were significantly different among different subgroups. The patient's Gensini score was correlated with the patient's serum NLRP1 level. The serum NLRP1 level is increased in patients with UA, which is increased with the increasing severity of coronary lesions.

Prevalence, hematological parameters, and coagulation profiles: Cardiovascular diseases statistics in the Asir region, Saudi Arabia.

To determine the prevalence of cardiovascular disease (CVD) types in the Asir region of Saudi Arabia and the importance of hematological testing for CVD patients in the context of disease management. This retrospective study comprised 416 CVD patients, and samples were divided based the type of CVD. The Mann Whitney U test was used to compare patients' hematological markers and coagulation profiles to those of healthy controls. The rate of ischemic heart disease (IHD) was 80.7% that of other CVDs, and the rate of ST-elevation myocardial infarction (STEMI) was 37.3% the rate of CVD. Significant differences were observed in the hematological and coagulation parameters of CVD patients compared to the control group. White blood cells (WBC) were significantly higher in STEMI, non-ST-elevation myocardial infarction (NSTEMI), unstable angina (UA), and heart failure (HF) groups. Red blood cells (RBC) were significantly lower in STEMI, NSTEMI, UA, chronic coronary syndrome (CCS), HF, dilated cardiomyopathy (DCM), and ischemic cardiomyopathy (ICM). Red distribution width (RDW) was significantly greater in the HF, DCM, and ICM groups. Prothrombin time (PT) was significantly higher in the STEMI, HF, and DCM groups. ST-elevation myocardial infarction has a higher prevalence rate among CVD patients in the Asir region. Both coagulation and hematological indicators have high potential utility as CVD diagnostic and prognostic markers.

Declined plasma microfibrillar-associated protein 4 levels in acute coronary syndrome

BackgroundMicrofibrillar-associated protein (MFAP4), initially identified as an extracellular matrix protein, has been demonstrated in multiple human disorders, but it is yet to be discovered following acute coronary syndrome (ACS) in clinical practice. Therefore, this study aimed to investigate the relationship between circulating MFAP4 levels and coronary stenosis in ACS.MethodsWe performed the study in 148 ACS subjects, including 75 ST-segment elevation myocardial infarction (STEMI), 27 non-ST-segment elevation myocardial infarction (non-STEMI) and 46 unstable angina (UA). Clinical variables were collected and Gensini and Syntax stenosis scoring systems were applied to assess the severity of coronary stenosis. Kaplan–Meier and logistic regression analysis were used to analyze the relationship between MFAP4 and the severity of coronary stenosis or ACS outcomes. Spearman analysis was used to describe the correlation between MFAP4 and clinical parameters.ResultsCirculating MFAP4 levels were significantly decreased in the STEMI group (0.008 ng/ml) compared with the non-STEMI group (0.014 ng/ml) and UA group (0.019 ng/ml) (p < 0.001). After adjusting for confounding factors, we found that MFAP4 was an independent risk factor for STEMI (odds ratio = 0.395, 95% CI 0.174–0.895, p = 0.026). MFAP4 level was negatively correlated with Gensini score and Syntax score (r = − 0.311 and − 0.211, p < 0.001 and 0.01, respectively). Based on the MFAP4 level of 0.117 ng/ml, ACS patients were divided into two groups: the low-MFAP4 group (< 0.117 ng/ml, n = 60) and the high-MFAP4 group (≥ 0.117 ng/ml, n = 88). After the median follow-up of 165 days, Kaplan–Meier survival analysis revealed that the MACE-free rate was significantly lower in ACS patients with lower MFAP4 levels (p = 0.009).ConclusionsMFAP4 has a potential as a biomarker for the degree of coronary stenosis in ACS. Confirmation of observations in larger cohorts and longer follow-up periods is warranted.