Ceramides and pro-inflammatory cytokines for the prediction of acute coronary syndrome: a multi-marker approach.

BACKGROUND: There is a growing body of evidence supporting the significant involvement of both ceramides and pro-inflammatory cytokines in the occurrence and progression of acute coronary syndrome (ACS). METHODS: This study encompassed 216 participants whose laboratory variables were analysed using standardised procedures. Parameters included baseline serum lipid markers, comprising total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides (TGs), lipoprotein(a) (LPa), fasting blood glucose, B-natriuretic peptide and hypersensitive C-reactive protein. Liquid chromatography-tandem mass spectrometry measured the concentrations of plasma ceramides. Enzyme-linked immunosorbent assay quantified tumour necrosis factor-α (TNF-α), interleukin 6 (IL6) and IL8. The correlation between ceramides and inflammatory factors was determined through Pearson's correlation coefficient. Receiver operating characteristic (ROC) curve analysis and multivariate logistic regression evaluated the diagnostic potential of models incorporating traditional risk factors, ceramides and pro-inflammatory cytokines in ACS detection. RESULTS: Among the 216 participants, 138 (63.89%) were diagnosed with ACS. Univariate logistic regression analysis identified significant independent predictors of ACS, including age, gender, history of diabetes, smoking history, TGs, TNF-α, IL-6, ceramide (d18:1/16:0), ceramide (d18:1/18:0), ceramide (d18:1/24:0), ceramide (d18:1/20:0) and ceramide (d18:1/22:0). Multivariate logistic regression analysis revealed significant associations between gender, diabetes mellitus history, smoking history, LPa, IL-6, ceramide (d18:1/16:0) and ACS. Receiver operating characteristic analysis indicated that model 4, which integrated traditional risk factors, IL-6 and ceramide (d18:1/16:0), achieved the highest area under the curve (AUC) of 0.827 (95% CI 0.770-0.884), compared with model 3 (traditional risk factors and ceramide [d18:1/16:0]) with an AUC of 0.782 (95% CI 0.720-0.845) and model 2 (traditional risk factors and IL-6), with an AUC of 0.785 (95% CI 0.723-0.846) in ACS detection. CONCLUSIONS: In summary, incorporating the simultaneous measurement of traditional risk factors, pro-inflammatory cytokine IL-6 and ceramide (d18:1/16:0) can improve the diagnostic accuracy of ACS.

Correlation Between Intracoronary Vascular Ultrasound Indexes in Patients with Coronary Heart Disease.

Background: Coronary atherosclerosis is a serious and progressive condition characterized by the accumulation of plaques, consisting of fat, cholesterol, and other substances, within the arteries that supply blood to the heart. These plaques can harden and narrow the arteries, leading to reduced blood flow to the heart muscle. Objective: The primary objective of this study is to investigate the correlation between specific cardiovascular parameters and intracoronary vascular ultrasound indexes in patients diagnosed with coronary heart disease. This investigation aims to explore the relationships between intracoronary vascular ultrasound measurements and three key cardiovascular parameters: epicardial fat pad thickness, mono-platelet polymer levels, and small dense low-density lipoprotein cholesterol (sdLDL-C) levels. Methods: In this investigation, we applied a comprehensive method to evaluate atherosclerotic plaque characteristics in patients with diverse stages of coronary heart disease (CHD), contrasting these profiles with those of healthy individuals. Our study included 80 acute myocardial infarction (AMI) patients, 145 with unstable angina pectoris (UAP), 175 with stable angina pectoris (SAP), and 100 controls. We utilized intravascular ultrasound (IVUS), an advanced imaging technique that surpasses traditional angiography by providing detailed, high-resolution images of both the coronary artery lumen and wall, including plaque composition. This approach is pivotal for assessing plaque stability, a key factor in the risk of rupture and subsequent cardiovascular events, indicated by features like lipid-rich cores and thin fibrous caps. During IVUS, we quantified parameters such as plaque area, load, and the remodeling index, the latter offering insights into vascular adaptation to plaque buildup. Additionally, we conducted a correlation analysis between IVUS indices and three cardiovascular markers: epicardial fat pad thickness, monocyte-platelet aggregates, and sdLDL-C levels. The goal was to ascertain the predictive value of these markers in tandem with IVUS for determining the stability of coronary artery atherosclerotic plaques. This integrative approach enhances understanding of plaque formation and destabilization, potentially informing more effective CHD prevention and management strategies. Results: Our study revealed distinct variations in key parameters across patient groups with different forms of CHD and healthy controls. Notably, we observed significant differences in gender distribution, hypertension, and diabetes mellitus prevalence among these groups. In terms of IVUS indexes and cardiovascular parameters, the SAP group exhibited markedly different results compared to the AMI and UAP groups. Specifically, the SAP patients showed the lowest values for EMMA, plaque area, plaque burden, reconstruction index, and positive remodeling. Additionally, they exhibited the thickest fibrous caps. In contrast, the AMI and UAP groups presented similar outcomes in these aspects. Regarding the epicardial fat pad thickness, the positive rate of monocyte-platelet aggregates, and the levels of sdLDL-C, there were no significant differences between the AMI and UAP groups. However, these parameters were notably higher in the AMI and UAP groups compared to the SAP group. Crucially, we established a significant correlation between the thickness of the epicardial fat pad, the positive rate of monocyte-platelet aggregates, and the sdLDL-C levels with plaque loading rate and remodeling index. These correlations underscore the potential utility of these parameters as indicators of plaque stability and cardiovascular risk in patients with CHD. This highlights the complexity of atherosclerotic disease progression and underscores the importance of a multifaceted approach to assessing and managing CHD. Conclusion: Our research delineates the critical role of the remodeling index, epicardial fat pad thickness, monocyte-platelet aggregates, and sdLDL-C levels as key prognostic tools for assessing coronary plaque stability in coronary artery disease (CAD). These biomarkers collectively provide an enhanced perspective on plaque vulnerability, an essential aspect in the genesis of acute coronary events. Clinically, these findings are pivotal. They offer a refined approach to CAD management and risk evaluation, allowing for the precise identification of patients at increased risk of plaque rupture, a precursor to acute coronary syndromes. This precision facilitates the adoption of more individualized treatment strategies, focusing on aggressive interventions for high-risk patients and more conservative management for those with stable plaques.

L-ascorbic acid could ameliorate the damage of myocardial microvascular endothelial cell caused by hypoxia-reoxygenation via targeting HMGB1.

In this study, we intend to explore the potential function of l-ascorbic acid in hypoxia-reoxygenation (H/R)-induced damage of CMECs and its related molecular mechanism. With different concentrations of l-ascorbic acid treatment, the proliferation, migration, inflammation and autophagy of cardiac microvascular endothelial cells (CMECs) were determined by several biological experiments. Si-HMGB1 transfection was used to reduce HMGB1 expression and to detect the function of HMGB1 in H/R-induced damage of CMECs. Under H/R condition, the proliferation and migration abilities of CMECs were reduced, and the inflammation and autophagy of CMECs were increased. Whereas, after l-ascorbic acid treatment, the reduction in the proliferation and migration of CMECs, as well as the increase in the inflammation and autophagy of CMECs induced by H/R were reversely altered. HMGB1 was confirmed as a specific target of l-ascorbic acid, and si-HMGB1 treatment strengthened the beneficial effect of l-ascorbic acid on H/R-induced damage of CMECs, followed by further reduction in the proliferation and migration abilities of CMECs, as well as the increase in the inflammation and autophagy of CMECs. Few studies have reported the function of l-ascorbic acid in myocardial ischemia on CMECs, but our experimental data showed that l-ascorbic acid treatment could ameliorate the H/R-induced damage of CMECs by regulating HMGB1 expression.

Metal-phenolic capsules with ROS scavenging reshape the oxidative microenvironment of atherosclerosis.

Arterial injury makes the tissue in a state of high oxidative stress. At the same time, abnormal lipid metabolism can further lead to bleeding and thrombosis. Therefore, the anti-inflammatory and anti-oxidant polyphenol, EGCG was organically complexed with Fe3+ to form a metal-phenolic framework carrier. And the antihyperlipidemic drug, atorvastatin (ATV) was loaded into the carrier to enhance the bioavailability, and simultaneously alleviate the oxidative stress of the inflammatory site and abnormal lipid metabolism. The results confirmed that the obtained material EGCG-Fe-ATV had good biocompatibility and biosafety effect. In addition, EGCG-Fe-ATV showed outstanding anti-inflammatory, anti-oxidant and lipid-lowering properties. These therapeutic outcomes of EGCG-Fe-ATV were achieved by reducing systemic and local oxidative stress and inflammation, alleviating inflammatory cell infiltration in plaques, and modulating lipid synthesis and transferase to alter cholesterol transport. In conclusion, the combination of metal-phenolic capsules with ATV provides a new strategy for reshaping the oxidative microenvironment of atherosclerosis.

Association between T-tau protein and Aß42 in plasma neuronal-derived exosomes and cognitive impairment in patients with permanent atrial fibrillation and the role of anticoagulant therapy and inflammatory mechanisms.

BACKGROUND: This study explores whether the differences in cognitive performance among individuals with permanent atrial fibrillation (AF) are attributable to the duration of AF and anticoagulant therapy and explores the possible inflammatory mechanism of cognitive dysfunction related to AF. METHODS: A total of 260 patients aged 50-75 years without previous cerebrovascular events were enrolled in this study. These 260 patients had been divided into the AF group (140 patients) and sinus rhythm group (120 patients). In the AF group, we divided participants into cognitive impairment (CI) group (90 patients) and cognitive normal (CN) group (50 patients). In the sinus rhythm group, we also divided participants into CI group (61 patients) and CN group (59 patients). The Mini-Mental State Examination (MMSE) was used to assess the cognitive function of all participants. Neuronal-derived exosomes were enriched in peripheral blood by immunoprecipitation and were confirmed by a transmission electron microscope, nanoparticle tracking analysis, and western blot. Alzheimer's disease-pathogenic exosomal proteins and inflammatory cytokines were quantified. The association between AF and cognitive function was estimated by logistic regression analysis. ANOVA or Welch's t-test compared the difference in protein concentrations between groups. RESULTS: Non-anticoagulant therapy in patients with AF was significantly associated with CI (OR = 13.99, 95% CI: 2.67-73.36, p < .01). The incidence of dementia in patients with AF > 3 years was significantly higher than in patients with AF ≤ 3 years, but there was no significant difference in total cognitive dysfunction (mild cognitive impairment [MCI] + dementia) (p = .126). The adjusted exosome concentrations of T-tau and amyloid-ß protein 42 (Aß42) in the CI group were significantly higher than in the CN group (p < .001). The serum concentrations of IL-6 and matrix metalloproteinase-9 (MMP-9) in patients with AF were higher than those in patients with sinus rhythm (p < .001). CONCLUSION: Aß42 and T-tau in peripheral blood neuronal-derived exosomes maybe be associated with the early diagnosis of CI in patients with permanent AF. However, the value of Aß42 and T-tau for CI in patients with permanent AF still needs to be confirmed in future randomized control trials.

Overexpression of lncRNA HULC Attenuates Myocardial Ischemia/reperfusion Injury in Rat Models and Apoptosis of Hypoxia/reoxygenation Cardiomyocytes via Targeting miR-377-5p through NLRP3/Caspase­1/IL­1ß Signaling Pathway Inhibition.

OBJECTIVE: Acute myocardial infarction (AMI) is characterized by myocardial tissue necrosis and activation of inflammatory response. This study aims to elucidate the potential mechanism underlying the protective effects of long non-coding RNA (lncRNA) highly up-regulated in liver cancer (HULC) against myocardial ischemia/reperfusion (I/R) injury in rat models and apoptosis of cardiomyocytes. METHODS: We firstly established rat models of myocardial I/R injury and rat cardiomyocyte (H9c2 cells) models of hypoxia/reoxygenation (H/R) injury. Sprague-Dawley (SD) neonatal rats were randomized into four groups: sham, I/R, I/R+ microRNA (miR) -377-5p mimic, and I/R+ miR-377-5p antagomir, respectively. Then, histopathological examination was applied. Apoptosis was evaluated by transferase-mediated dUTP nick end labeling (TUNEL) staining. Cell vitality was measured using MTT assay. The concentrations of creatine kinase MB (CK-MB), cardiac troponin I (cTnI), interleukin (IL) -6 (IL-6), and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). The expression of Cleaved-Caspase-3, Caspase-3, NOD-like receptor P3 (NLRP3), Caspase-1, and IL-1ß was analyzed by immunohistochemical (IHC) or Western blot analysis. RESULTS: We found that HULC was downregulated and miR-377-5p was upregulated in IR-injured myocardial tissue and the H/R-induced H9c2 cell. Overexpression of miR-377-5p increased myocardial dysfunction and apoptosis and activated formation and secretion of IL-6 and TNF-α. The preprocessing of miR-377-5p silencing emerged opposite results. Strikingly, dual luciferase reporter assay showed that HULC was a sponge of miR-377-5p. Subsequently, mechanism experiments revealed that NLRP3/Caspase­1/IL­1ß was a target axis of miR-377-5p. In vitro, the protective effect of HULC overexpression on H9c2 cell viability and inflammation was offset by miR-377-5p silencing. Finally, rescue assay suggested that HULC-miR-377-5p -NLRP3/Caspase­1/IL­1ß axis regulated the apoptosis and inflammation of H/R-induced H9c2 cells. CONCLUSIONS: Overall, these results indicate that the protective effect of HULC against myocardial I/R injury and H/R cardiomyocyte apoptosis partially relies on the inhibition of NLRP3/Caspase­1/IL­1ß signaling pathway.

Amiodarone Advances the Apoptosis of Cardiomyocytes by Repressing Sigmar1 Expression and Blocking KCNH2-related Potassium Channels.

BACKGROUND: Heart failure (HF) is the ultimate transformation result of various cardiovascular diseases. Mitochondria-mediated cardiomyocyte apoptosis has been uncovered to be associated with this disorder. OBJECTIVE: This study mainly delves into the mechanism of the anti-arrhythmic drug amiodarone on mitochondrial toxicity of cardiomyocytes. METHODS: The viability of H9c2 cells treated with amiodarone at 0.5, 1, 2, 3, and 4 µM was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and Sigmar1 expression was examined by quantitative real-time PCR (qRTPCR). After transfection, the viability, apoptosis, reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP), and potassium voltage-gated channel subfamily H member 2 (KCNH2) expression in H9c2 cells were assessed by MTT, flow cytometry, ROS assay kit, mitochondria staining kit, and Western blot. RESULTS: Amiodarone at 1-4 µM notably weakened H9c2 cell viability with IC50 value of 2.62 ± 0.43 µM. Amiodarone at 0.5-4 µM also evidently suppressed the Sigmar1 level in H9c2 cells. Amiodarone repressed H9c2 cell viability and KCNH2 level and triggered apoptosis, ROS production and mitochondrial depolarization, while Sigmar1 upregulation reversed its effects. Moreover, KCNH2 silencing neutralized the combined modulation of amiodarone and Sigmar1 up-regulation on H9c2 cell viability, apoptosis, and ROS production. CONCLUSION: Amiodarone facilitates the apoptosis of H9c2 cells by restraining Sigmar1 expression and blocking KCNH2-related potassium channels.

The effect of dapagliflozin on anemia in elderly patients with heart failure by bioinformatics analysis.

BACKGROUND: Anemia associated with heart failure is frequent and can exacerbate the symptoms of heart failure. Dapagliflozin is the first SGLT-2 inhibitor with significant cardiovascular protection. However, the effect of dapagliflozin on anemia in elderly patients with heart failure is unknown. OBJECTIVE: We aimed to study the effect of dapagliflozin on anemia in elderly patients with heart failure by bioinformatics analysis. METHODS: The target genes were determined, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The protein-protein interaction (PPI) network and modules were constructed. The dapagliflozin-targets network in anemia and heart failure was constructed. Molecular docking experiments between dapagliflozin and its key target AKT1 were performed. RESULTS: We found 1 dapagliflozin related target gene and 2 disease related genes. Totally, 134 target genes of dapagliflozin on anemia in elderly patients with heart failure were determined. The pathways may involve lipid and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, hepatitis B, insulin signaling pathway, fluid shear stress and atherosclerosis, neurotrophin signaling pathway, insulin resistance, toxoplasmosis, colorectal cancer, and EGFR tyrosine kinase inhibitor resistance. The hub genes in network were AKT1, TP53, GAPDH, TNF, CASP3, EGFR, and MAPK3. The structure of dapagliflozin and AKT1 molecular docking was exhibited. CONCLUSIONS: The hub genes in network were AKT1, TP53, GAPDH, TNF, CASP3, EGFR, and MAPK3. The structure of dapagliflozin and AKT1 molecular docking was exhibited.

Comparison of intravascular ultrasound-guided with optical coherence tomography-guided percutaneous coronary intervention for left main distal bifurcation lesions: Rationale and design of the ISOLEDS trial.

BACKGROUND: Percutaneous coronary intervention (PCI) can provide benefits for anatomically suitable left main coronary artery (LMCA) lesions. When compared to traditional coronary angiography (CAG) -guided PCI, the use of intravascular ultrasound (IVUS) guidance has shown significant long-term prognostic improvements in LMCA PCI. Optical coherence tomography (OCT) offers a higher axial resolution than IVUS. However, there is currently a lack of relevant randomized controlled trials investigating the use of OCT specifically for left main distal bifurcation lesions. METHODS: The ISOLEDS trial is an ongoing multicenter study that aims to compare IVUS-guided PCI with OCT-guided PCI for patients with true LMCA distal bifurcation lesions. This prospective, randomized, controlled, non-inferiority trial will enroll a total of 664 patients with visually-defined Medina 1,1,1 or 0,1,1 classification of left main distal bifurcation lesions. The patients will be randomly assigned in a 1:1 ratio to either IVUS-guided or OCT-guided PCI. The primary endpoint is to assess the occurrence of target lesion failure (TLF) within 12 months after the procedure. After undergoing PCI, patients are required to visit the hospital for a 12-month clinical follow-up. During this clinical assessment, CAG can be performed to evaluate the status of target lesions. DISCUSSION: The ISOLEDS trial represents the first attempt to compare two distinct intracoronary imaging techniques for guiding PCI in patients with true LMCA distal bifurcation lesions. By evaluating and comparing the outcomes of these two imaging techniques, the trial results will aid operators in selection of the most effective approach for guiding PCI in these patients.

Circ_0003575 knockdown alleviates ox-LDL-induced human aortic endothelial cell dysfunction in atherosclerosis by miR-637/TRAF6 axis.

BACKGROUND: Circular RNAs (circRNAs) are involved in the progression of atherosclerosis (AS). The present study aimed to determine the functions and mechanism of circ_0003575 in AS. METHODS: Oxidized low-density lipoprotein (ox-LDL) was used to induce human aortic endothelial cells (HAECs) to establish an AS cell model. Cell Counting Kit-8 (CCK-8) assay and 5'-ethynyl-2'-deoxyuridine (EdU) assay were conducted to assess cell proliferation. Flow cytometry analysis was utilized to quantify cell apoptosis. Tube formation assay was performed to analyze angiogenesis ability. Enzyme linked immunosorbent assay (ELISA) was used to examine the concentrations of inflammatory factors. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were manipulated for the expression of circ_0003575, microRNA-637 (miR-637) and TNF receptor associated factor 6 (TRAF6). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were adopted to estimate the downstream targets of circ_0003575. RESULTS: Ox-LDL treatment repressed the proliferation and angiogenesis and promoted the apoptosis and inflammation in HAECs. Circ_0003575 knockdown ameliorated ox-LDL-induced injury of HAECs. Circ_0003575 interacted with mi-R-637, which directly targeted TRAF6. Inhibition of miR-637 reversed the impacts of circ_0003575 knockdown on HAEC injury. Moreover, miR-637 overexpression promoted cell proliferation and angiogenesis and inhibited cell apoptosis and inflammation by targeting TRAF6 in ox-LDL-treated HAECs. Further, circ_0003575 silencing inhibited the activation of NF-κB pathway. CONCLUSION: Circ_0003575 knockdown alleviated ox-LDL-induced HAEC damage by regulating miR-637/TRAF6 and NF-κB pathways.

Clinical Observation of Helicobacter pylori Infection and Risk Factors and Cytotoxin-Associated Protein A in Patients with Coronary Heart Disease.

The aim was to analyze the infection, influencing factors, and clinical manifestations of Helicobacter pylori infection, coronary heart disease, and cytotoxin-associated protein A infection, so as to provide reference for the improvement of clinical diagnosis and treatment level of in-depth treatment. This paper presents a clinical observation method based on Helicobacter pylori infection, risk factors, and cytotoxin-associated protein A in patients with coronary heart disease. Methods. 237 patients with CHD diagnosed and tested by 14C breath test were selected from inpatients of cardiovascular diseases in a hospital for retrospective analysis. The clinical data, serum deepening indicators, Hcy, and other factors were analyzed through general condition investigation, previous history investigation, and physical examination. The patients were observed by the SPSS22.0 statistical data processing method. The results showed that among the respondents, 175 cases were HP-positive, the infection rate was 73.8%, 77 patients with stable angina pectoris were 64.9%, and 160 patients with acute coronary heart disease were 78.1%. The difference between the groups was statistically significant (P < 0.05). Conclusion. Helicobacter pylori cytotoxic-associated protein A can increase the risk of gastric cancer, and Helicobacter pylori eradication treatment is more conducive to reduce the incidence of gastric cancer and ensure the safety of patients.

Evaluation of ABC Bleeding Score and SAMe-TT2R2 Score on the Risk of Bleeding after Anticoagulation in Patients with Nonvalvular Atrial Fibrillation Complicated with Coronary Heart Disease.

Objective: To explore the predictive value of ABC bleeding score and SAMe-TT2R2 score on the risk of bleeding in patients with nonvalvular atrial fibrillation (NVAF) complicated with coronary heart disease (CHD) after anticoagulation. Methods: 149 patients with NVAF complicated with CHD were followed up in our hospital for one year. The bleeding events during the follow-up period were observed, the ABC bleeding score and SAMe-TT2R2 score were calculated, the predictive value of the two scoring methods for the main bleeding risk was analyzed by the ROC curve, and the AUC area under the ROC curve of the two scoring methods was compared by the Delong test. Results: There were 32 bleeding events during the follow-up period. The AUC of ABC bleeding score and SAMe-TT2R2 score were 0.775 (P < 0.01) and 0.624 (P < 0.05), respectively. The Delong test showed that the AUC of ABC bleeding score was significantly higher than that of SAMe-TT2R2 score (d = 2.177, P < 0.05). Conclusion: Both the ABC bleeding score and SAMe-TT2R2 score can predict the risk of bleeding after anticoagulation in patients with NVAF and CHD. The critical value of the SAMe-TT2R2 score for predicting bleeding events in patients with NVAF and CHD may need to be increased to 4 or 5, and the prediction ability of ABC bleeding score is significantly better than that of the SAMe-TT2R2 score.

Correlation of plasma galectin-3 and plasma lipoprotein-associated phospholipase A2 with the severity and prognosis of coronary artery disease.

OBJECTIVE: To evaluate the correlation of galectin-3 (Gal-3) and lipoprotein-associated phospholipase A2 (Lp-PLA2) with the severity of coronary artery disease and major adverse cardiovascular events (MACE). METHODS: 130 patients diagnosed with coronary heart disease (CHD) by coronary angiography from October 2018 to August 2019 in the Department of Cardiology, the First Affiliated Hospital of Hebei North University, were matched into the CHD group, with 68 cases in the mild stenosis (MS) group (degree of stenosis 50%~75%), and 62 cases in the severe stenosis (SS) group (degree of stenosis ≥75%). For comparison, patients with negative results of angiography during the same period (stenosis degree <50%) were assigned to the normal group. Indicators for detection included plasma Gal-3, Lp-PLA2 concentrations, Gensini scores, and MACE events in a 30-day follow-up visit. RESULTS: Remarkably higher plasma Gal-3 and Lp-PLA2 concentrations in the CHD group were observed in comparison with the normal group. The SS group obtained a more positive result regarding plasma Gal-3 and Lp-PLA2 concentrations and Gensini scores than the MS group (P<0.05). The highest concentration of plasma Gal-3 and Lp-PLA2 was detected in the multi-vessel disease (MVD) group, followed by the double-vessel disease (DVD) group, and finally the single-vessel disease (SVD) group. Pearson correlation analysis revealed a positive correlation of plasma Gal-3 and Lp-PLA2 concentrations with Gensini scores (P<0.05). Results of the follow-up visit presented strong relevance between noticeably higher concentrations of the plasma Gal-3 and Lp-PLA2 and MACE events (P<0.05). Increased Gal-3 and Lp-PLA2 are risk factors for the prognosis of coronary artery disease. CONCLUSION: Plasma Gal-3 and Lp-PLA2 concentrations in patients with CHD are strongly related to the severity of coronary artery disease and MACE events, which is valuable for assessing the risk of patients in clinical practice.

IVUS plus multivariate analysis for evaluating the stability of coronary artery plaque in coronary heart disease.

OBJECTIVE: To investigate the effect of intravascular ultrasound (IVUS) plus multivariate analysis in evaluating the stability of coronary artery plaque in coronary heart disease (CHD). METHODS: A retrospective analysis was conducted on ninety-five patients with CHD admitted to our hospital from February 2020 to February 2021. Patients with CHD were examined by IVUS and assigned to a stable plaque group (n=60) and an unstable plaque group (n=35) according to their characteristics. Multivariate logistic regression analysis was performed to evaluate the risk factors affecting the stability of coronary artery plaque. RESULTS: Of 95 patients, 35 cases with unstable plaque were determined by IVUS, with a detection rate of 36.84%; notable differences were found in HDL-C, hs-CRP, and homocysteine (Hcy) between the two groups (P<0.05). The eccentricity index and reconstruction index of the two groups were statistically different (P<0.05). Moreover, 17 cases were diagnosed by IVUS as mild coronary stenosis, 28 cases as moderate stenosis, and 50 cases as severe stenosis. In addition, compared with the stable plaque group, the unstable plaque group yielded a much higher stenosis rate (P<0.05) and a higher level of plaque thickness and plaque area (P<0.05). Multivariate logistic regression analysis showed eccentricity index, remodeling index, plaque thickness, and plaque area, stenosis rate, HDL-C, Hcy, and hs-CRP were independent risk factors for unstable plaque (P<0.05). CONCLUSION: IVUS plus multivariate analysis can accurately assess plaque stability.

Plasma miR-22-5p, miR-132-5p, and miR-150-3p Are Associated with Acute Myocardial Infarction.

Circulating microRNAs (miRNAs) are potential biomarkers for cardiovascular diseases. Our study aimed to determine whether miR-22-5p, miR-132-5p, and miR-150-3p represent novel biomarkers for acute myocardial infarction (AMI). Plasma samples were isolated from 35 AMI patients and 55 matched controls. Total RNA was extracted, and quantitative real-time PCR and ELISA were performed to investigate the expressions of miRNAs and cardiac troponin I (cTnI), respectively. We found that plasma levels of miR-22-5p and miR-150-3p were significantly higher during the early stage of AMI and their expression levels peaked earlier than cTnI. Conversely, circulating miR-132-5p was sustained at a low level during the early phase of AMI. All three circulating miRNAs were correlated with plasma cTnI levels. A receiver operating characteristic (ROC) analysis suggested that each single miRNA had considerable diagnostic efficacy for AMI. Moreover, combining the three miRNAs improved their diagnostic efficacy. Furthermore, neither heparin nor medications for coronary heart disease (CHD) affected plasma levels of miR-22-5p and miR-132-5p, but circulating miR-150-3p was downregulated by medications for CHD. We concluded that plasma miR-22-5p, miR-132-5p, and miR-150-3p may serve as candidate diagnostic biomarkers for early diagnosis of AMI. Moreover, a panel consisting of these three miRNAs may achieve a higher diagnostic value.