Marker For Acute Myocardial Infarction Research Articles

Plasma desmosine for prediction of outcomes after acute myocardial infarction.

Elastin degradation is implicated in the pathology of vulnerable plaque. Recent studies show promising results for plasma desmosine (pDES), an elastin-specific degradation product, as a marker of cardiovascular disease (CVD) outcomes. The aim of this study was to investigate the potential role of pDES as a marker of clinical outcome in patients with acute myocardial infarction (AMI). In this case-control study, we studied 236 AMI patients: 79 patients who had death and/or myocardial infarction (MI) at 2 years, and 157 patients who did not have an event at 2 years. pDES was measured using a validated liquid chromatography-tandem mass spectrometry method. Association of pDES with adverse outcomes, and the incremental value of pDES to global registry of acute coronary events (GRACE) score for risk stratification was assessed. pDES levels were elevated in patients with the composite outcome of death/MI at 2 years (p = 0.002). Logistic regression analyses showed pDES to be associated with death/MI at 2 years [Odds ratio (OR) 5.99 (95% CI 1.81-19.86) p = 0.003]. pDES remained a significant predictor of death/MI at 2 years even after adjustment for age, sex, history of CVD, revascularisation, blood pressure, medications on discharge, Troponin I, and NT-proBNP levels.[OR 5.60 (95% CI 1.04-30.04) p = 0.044]. In another multivariable model including adjustment for eGFR, pDES was significantly associated with the composite outcome at 6 months, but not at 2 years follow up. DES was also able to reclassify risk stratification for death/MI at 6 months, when added to the GRACE risk model [Net Reclassification Index (NRI) 41.2 (95% CI 12.0-70.4) p = 0.006]. pDES concentrations predict clinical outcomes in patients with AMI, demonstrating its potential role as a prognostic marker in AMI.

Robust prognostic prediction model developed with integrated biological markers for acute myocardial infarction

Commonly used prediction methods for acute myocardial infarction (AMI) were created before contemporary percutaneous coronary intervention was recognized as the primary therapy. Although several studies have used machine learning techniques for prognostic prediction of patients with AMI, its clinical application has not been achieved. Here, we developed an online application tool using a machine learning model to predict in-hospital mortality in patients with AMI. A total of 2,553 cases of ST-elevation AMI were assigned to 80% training subset for cross validation and 20% test subset for model performance evaluation. We implemented random forest classifier for the binary classification of in-hospital mortality. The selected best feature set consisted of ten clinical and biological markers including max creatine phosphokinase, hemoglobin, heart rate, creatinine, systolic blood pressure, blood sugar, age, Killip class, white blood cells, and c-reactive protein. Our model achieved high performance: the area under the curve of the receiver operating characteristic curve for the test subset, 0.95: sensitivity, 0.89: specificity, 0.91: precision, 0.43: accuracy, 0.91 respectively, which outperformed common scoring methods. The freely available application tool for prognostic prediction can contribute to risk triage and decision-making in patient-centered modern clinical practice for AMI.

Cardiac troponin T as a postmortem biomarker for acute myocardial infarction

The diagnosis of acute myocardial infarction (AMI), especially within the first hours after onset of ischemia, poses a challenge to the forensic pathologist. During this time, the infarction is generally not visible macroscopically nor with routine histology. Whilst cardiac Troponin T (cTnT) is a well-established biomarker for AMI clinically, its use as a postmortem diagnostic tool is less conclusive, warranting further investigation. The aim of this study was to investigate the sensitivity and specificity of cTnT as a postmortem diagnostic marker of AMI and the impact of postmortem interval (PMI) and cardiopulmonary resuscitation (CPR) on cTnT-concentrations. Samples from 64 subjects, 15 AMI cases and 49 controls, were collected at the Department of Forensic Medicine in Stockholm and analyzed for cTnT: one femoral blood sample was taken at arrival of the body to the morgue, and again during autopsy. Pericardial fluid (PCF) was only collected during autopsy. Sensitivity and specificity for serum cTnT were calculated to be 86.7 %/67.3 % and for pericardial fluid 86.7 %/44.9 %. cTnT samples taken during autopsy were generally higher than samples taken upon arrival to the morgue. A CPR-dependent elevation in serum cTnT was noted (P = .005). With a cut off at 56 n/L, serum cTnT can be used to rule out AMI. The postmortem interval and CPR must be taken into consideration when interpreting postmortem cTnT.

Association of Increased Pulse Wave Velocity With Long-Term Clinical Outcomes in Patients With Preserved Ankle-Brachial Index After Acute Myocardial Infarction

Low ankle-brachial index (ABI) is an established risk factor for long-term cardiovascular outcomes in patients with acute myocardial infarction (AMI), and brachial-ankle pulse wave velocity (ba-PWV) may also be a risk factor. However, there is a significant overlap between low ABI and high ba-PWV. The purpose of this retrospective study was to examine whether increased ba-PWV was associated with long-term clinical outcomes in AMI patients with normal ABI. We included 932 AMI patients with normal ABI and divided them into the high PWV group (≥1,400 cm/s; n=646) and the low PWV group (<1400 cm/s; n=286) according to the ba-PWV values measured during the AMI hospitalisation. The primary endpoint was the major adverse cardiovascular events (MACE) defined as the composite of all-cause death, nonfatal myocardial infarction, and hospitalisation for heart failure. During the median follow-up duration of 541 days (Q1: 215 days-Q3: 1,022 days), a total of 154 MACE were observed. The Kaplan-Meier curves showed that MACE was more frequently observed in the high PWV group than in the low PWV group (p<0.001). The multivariate Cox hazard analysis revealed that high ba-PWV was significantly associated with MACE (hazard ratio [HR] 1.587; 95% CI 1.002-2.513; p=0.049) after controlling multiple confounding factors. High ba-PWV was significantly associated with long-term adverse events in AMI patients with normal ABI. Our results suggest the usefulness of PWV as a prognostic marker in AMI with normal ABI.

Expression of ATP-binding cassette subfamily B member 1 gene in peripheral blood of patients with acute myocardial infarction

ABSTRACT This study aimed to determine the amount of expression of the ATP-binding cassette subfamily B member 1 (ABCB1) gene chip as a prospective diagnostic marker for acute myocardial infarction (AMI) in a wide population . In the AMI and control groups, 113 patients with AMI and 83 persons with non-coronary artery disease were selected for peripheral venous leukocyte collection. Western blot and real-time polymerase chain reaction (RT-PCR) were employed to detect relative ABCB1 expression in both groups. The results showed that the ABCB1 transcription and protein levels in the AMI group were higher than in the control. The relative mRNA expression of ABCB1 was 0.26 (0.03–0.79) in the AMI group and 0.13 (0.01–0.52) in the control group (P < 0.05). The expression of the ABCB1 gene at the protein level in the AMI group was 1.65 times that in the control (P < 0.05). Further, the subjects in the AMI group were older (P < 0.001), had lower levels of high-density lipoprotein cholesterol (P = 0.038), and had higher incidence of type II diabetes mellitus (P = 0.003) compared with the control. Logistic regression analysis showed that the expression of ABCB1 in peripheral blood was correlated with the occurrence of AMI (P = 0.003). High ABCB1 expression, type II diabetes, and advanced age were found to serve as potential independent risk factors for AMI, with a 4.88-fold, 2.99-fold, and 2.63-fold increased risk of AMI. Overall, the high expression of ABCB1 in peripheral blood might be related to the occurrence of AMI.

Integrated RNA gene expression analysis identified potential immune-related biomarkers and RNA regulatory pathways of acute myocardial infarction.

BackgroundAcute lesions are among the most important causes of death due to vascular lesions worldwide. However, there are no accurate genetic markers for Acute myocardial infarction (AMI). This project will use microarray integration analysis in bioinformatics analysis to find and validate relevant AMI gene markers.MethodsFive microarray gene expression datasets were downloaded through the GEO database. We identified 50 significant DEGs by comparing and analyzing gene expression between 92 AMI and 57 standard samples. The BioGPS database screened differentially expressed genes specific to the immune system. DEGs were mainly involved in immune-related biological processes based on Enrichment analysis. Eight hub genes and three-gene cluster modules were subsequently screened using Cytoscape and validated using Box plot’s grouping comparison and ROC curves. Combined group comparison results and ROC curves analysis concluded that AQP9, IL1B, and IL1RN might be potential gene markers for the AMI process. We used the StarBase database to predict target miRNAs for eight essential genes. The expected results were used to screen and obtain target lncRNAs. Then Cytoscape was used to create CeRNA networks. By searching the literature in PubMed, we concluded that AQP9, IL1B, and IL1RN could be used as gene markers for AMI, while FSTL3-miR3303p-IL1B/IL1RN and ACSL4-miR5905p-IL1B could be used as RNA regulatory pathways affecting AMI disease progression.ConclusionsOur study identified three genes that may be potential genetic markers for AMI’s early diagnosis and treatment. In addition, we suggest that FSTL3-miR-330-3p-IL1B/IL1RN and ACSL4-miR-590-5p-IL1B may be possible RNA regulatory pathways to control AMI disease progression.

Iron and Ferritin as novel screening markers of Acute Myocardial Infarction

Introduction: Cardiovascular disease is a public health problem globally. In India, the prevalence of Acute Myocardial Infarction (AMI) was 6.43%. Several causes lead to AMI, among which excess serum Iron and Ferritin is responsible for an increase in the generation of free radicals, thus accelerate atherogenesis through oxidation of Low-density lipoprotein – cholesterol (LDL-C). Assess serum Iron and Ferritin status and compare them with the cardic marker (CK-MB) among patients with AMI. Methods: The study was performed in a tertiary care centre in TamilNadu, India. This casecontrol study was conducted on 25 patients diagnosed with AMI and 25 age and sex-matched healthy participants as control group. Iron, Ferritin, CK-MB and lipid profile parameters were analyzed in serum samples of the participants. Result: The mean levels of serum Iron, Ferritin, CK-MB and lipid profile parameters were increased significantly among the cases when compared to the control group. CK-MB had a strong positive correlation with serum Iron and Ferritin. Serum Iron and Ferritin also had a positive correlation with total cholesterol and LDL-C, and a negative correlation with Highdensity lipoprotein – cholesterol. The odds of developing AMI in those with serum Iron &gt;51.5µg/dl and Ferritin &gt;137ng/dl were 36 and 61.7 times at higher risk respectively. Conclusion: Higher levels of serum Iron and Ferritin seem to be stronger risk factors for AMI, and shall be considered as early screening cardiac markers for AMI.

Role of Physio Biochemical Markers of Acute Myocardial Infarction in Young Adults

Introduction: Background: Universally, cardiovascular problems remains a major cause of unfavorable results in young individuals, unlike its decrease in other age bunches. This group isn't well studied and includes an interesting hazard profile with less conventional cardiovascular risk components compared with more seasoned populations. Objective: To highlight the prevalence and risk factors of myocardial infarction in young individuals Material and Methods Study design: quantitative cross sectional Settings: Punjab Institute of Cardiology (PIC) Duration: Six months i.e. 1st July2021 to 31st December 2021 Data Collection procedure: A cross sectional study was conducted with the duration of six months in a tertiary care hospital Lahore. Young hospitalized patients were selected with the age limit of 40 years and admitted to hospital with acute myocardial infarction. Total number of patients was 100 placed in the group one and same numbers of individuals with same age group were also selected without history of any cardiovascular diseases from the population as control. Validated Hamilton anxiety rating scale was used to access the anxiety levels of an individual. BMI, cardiac serum markers and liver enzymes were calculated. For this purpose venous blood was obtained from each individual and test was performed. Results: The average age of the participant in this study was in between 20-40 years of age. In group one 77 were males and 23 females. Group two consist of 82 males and 18 females. As we see in the table 1 findings the levels of LDH, trop I, CKMB and SGOT are significantly high in group 1 which showing myocardial injury as the release of these markers in blood. Anxiety levels and cigarette smoking also noticed high in group 1 as compared to group 2. Conclusion: This study illustrated uneasiness as a possibly driving hazard figure of AMI in young individuals, requiring the need for superior administration of psychosocial wellbeing in youthful age for relieving the hazard of AMI. Preventive intercessions are more likely to abdicate useful results in young individuals and future work on such preventive procedures may empower definition of worldwide arrangements and community campaigns to decrease the health-economic burden of AMI in young grown-ups and make strides results of wellbeing and quality of life Keywords: Depression, Anxiety, Smoking, Acute Myocardial Infarction, Blood pressure

Target-responsive DNA hydrogel with microfluidic chip smart readout for quantitative point-of-care testing of creatine kinase MB

Swift and effective diagnosis of acute myocardial infarction (AMI) is critical to patient survival due to its serious life-threatening effects and increasing incidence. Creatine kinase MB (CK-MB) is one of the markers of AMI. In this work, we enabled a portable visual quantitative assay of CK-MB by incorporating target-responsive DNA hydrogel with a microfluidic chip. The CK-MB aptamer and the complementary short DNA strand were grafted onto the polyacrylamide strand separately and formed the hydrogel by base-paired linkage. Upon introduction of CK-MB, the aptamer bound to CK-MB. This led to hydrogel dissociation and subsequent release of pre-trapped gold nanoparticles (AuNPs), which is proportional to the concentration of CK-MB. To achieve portable on-site detection, we further combined the hydrogel with a microfluidic chip and utilized the color change caused by the released AuNPs to take picture and analyze the average gray value. Then, as low as 0.027 nM CK-MB could be detected by cell phone. With good portability, visualization, and simple sample handling, this method has great potential for quantitative point-of-care testing (POCT) of targets in resource-constrained settings.

Serum miR-96-5p is a novel and non-invasive marker of acute myocardial infarction associated with coronary artery disease

ABSTRACT Acute myocardial infarction (AMI) is a severe cardiovascular disease. AMI associated with coronary artery disease (AMI-CAD) is a subtype of AMI, composed of AMI patients caused by CAD. This study aimed to evaluate the diagnostic value of miR-96-5p in AMI induced by coronary artery disease. Expression of miR-96-5p and BCL2L13 was evaluated by serum samples and cells utilizing Western blot and RT-qPCR assays. The diagnostic value of miR-96-5p in AMI-CAD was analyzed with a receiver operating characteristic (ROC) curves. The correlation between miR-96-5p and BCL2L13 was examined by Spearman’s correlation analysis. The level of oxidative stress and apoptosis were estimated via relative commercial kit, flow cytometry apoptosis assay and TUNEL staining assay. Our study discovered that miR-96-5p was down-regulated while BCL2L13 was up-regulated in patients with AMI-CAD. miR-96-5p was a potential diagnostic parameter, which may help distinguish AMI-CAD patients from healthy controls. In vitro experiments, miR-96-5p expression was down regulated while BCL2L13 was up-regulated in hypoxic cardiomyocytes. After confirming the targeted link of miR-96-5p to BCL2L13 using luciferase reporter and RNA pull down assays, we discovered that miR-96-5p overexpression may restore oxidative stress and cell apoptosis induced by hypoxia treatment in H9c2 cells; meanwhile, co-transfection with BCL2L13 overexpressing plasmid might partly countervail the ameliorative effects of miR-96-5p on oxidative stress and apoptosis. Collectively, miR-96-5p may function as a potential diagnostic biomarker for AMI-CAD patients, and the up-regulation of miR-96-5p would ameliorate AMI-associated cardiomyocytes injury by targeting BCL2L13, hence contributing to the clinical treatment of AMI-CAD.

Integrating potential-resolved electrochemiluminescence with molecularly imprinting immunoassay for simultaneous detection of dual acute myocardial infarction markers

A novel potential-resolved molecularly imprinted electrochemical luminescence (ECL) immunosensor has been developed for the first time for the dual sensitive detection of markers of acute myocardial infarction (AMI): cardiac troponin I (cTnI) and myoglobin (Mb). In this work, cost-effective and robust molecularly imprinted polymer (MIP) as biomimetic antibody was used to construct the immunosensors through electropolymerization and elution to form polydopamine (PDA)-MIP modified electrode. In the presence of AMI biomarkers, two ECL probes including Ru(bpy)32+@ MOCs and MoS2 QDs functionalized by cTnI antibody and Mb aptamer could be specifically captured respectively. And two potential distinct ECL signals will be generated in one potential scan. The intensity of ECL reflects the concentrations of cTnI and Mb. The two ECL probes were characterized with field emission scanning electron microscopy, X-ray diffraction, FT-IR spectrum and UV–Vis diffuse reflectance spectroscopy. The prepared sensor exhibited a wide linear range (0.05–104 ng/mL) and a low detection limit (0.0184 ng/mL for cTnI and 0.0492 ng/mL for Mb). Additionally, the MIP-ECL sensor displayed excellent anti-interference, sensitivity and stability to detect cTnI and Mb. Therefore, it will be conducive to accelerate more precise and credible early diagnosis for AMI.

Expression of Membrane Bound O-Acyltransferase Domain Containing 7 after Myocardial Infarction and its Role in Lipid Metabolism in vitro.

Background: Previous microarray analysis on peripheral blood leukocytes from three patients with acute myocardial infarction (AMI) showed that elevated expression of membrane bound o-acyltransferase domain containing 7(MBOAT7) relative to control. To further verify these findings, we investigated more patients and explored the possible mechanisms in vitro.Objective: To study alterations in MBOAT7 expression in leukocytes after AMI, and to explore the relationship between MBOAT7 and lipid metabolism pathways in hepatocytes in vitro.Methods: Ninety patients with AMI and 90 controls were recruited from the Han population in Northeast China. RT-fluorescent PCR was used to measure MBOAT7 mRNA levels. MBOAT7 interference and overexpression vectors were constructed and transfected into L-02 hepatocytes and expression was examined by RT-qPCR and western blotting. The expression of SCAP, LDLR, HMGCR, ACAT1, ABCA1, SREBP1, ACC, FAS, SCD, and PPARγ in the lipid metabolism pathway were investigated by RT-qPCR. Triglyceride and cholesterol levels were measured by ELISA.Results: It was found that MBOAT7 mRNA levels were elevated in the leukocytes of patients with AMI. Hepatocytes were successfully transfected, shown by attenuated MBOAT7 mRNA levels in the silenced group (0.41±0.04 vs 1.01±0.07 for control, P=0.0019 <0.01) and raised levels in the overexpressing cells (23.29±0.39 vs 1.00±0.06 for control, P <0.0001). These results were confirmed by western blotting. Expression of the lipid metabolism-related genes was altered in response to MBOAT7 expression. Triglyceride levels increased after MBOAT7 silencing (118.40 ± 2.26 vs 70.54 ± 0.25 for control, P<0.0001), as did those of cholesterol (628.30 ± 8.89 vs 544.70 ± 11.04, P = 0.0041) but were not altered on MBOAT7 overexpression.Conclusion: MBOAT7 did not affect the metabolism of triglycerides in hepatocytes through fatty acid synthesis and decomposition pathways. The MBOAT7 level in the peripheral blood can be used as a marker for acute myocardial infarction but cannot be used as a single therapeutic target to regulate lipid metabolism.

Potential biomarkers of acute myocardial infarction based on co-expression network analysis.

Acute myocardial infarction (AMI) is a common cause of death in numerous countries. Understanding the molecular mechanisms of the disease and analyzing potential biomarkers of AMI is crucial. However, specific diagnostic biomarkers have thus far not been fully established and candidate regulatory targets for AMI remain to be determined. In the present study, the AMI gene chip dataset GSE48060 comprising blood samples from control subjects with normal cardiac function (n=21) and patients with AMI (n=26) was downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) between the AMI and control groups were identified with the online tool GEO2R. The co-expression network of DEGs was analyzed by calculating the Pearson correlation coefficient of all gene pairs, mutual rank screening and cutoff threshold screening. Subsequently, the Gene Ontology (GO) database was used to analyze the genes' functions and pathway enrichment of genes in the most important modules was performed. Kyoto Encyclopedia of Genes and Genomes (KEGG) Disease and BioCyc were used to analyze the hub genes in the module to determine important sub-pathways. In addition, the expression of hub genes was confirmed by reverse transcription-quantitative PCR in AMI and control specimens. In the present study, 52 DEGs, including 26 upregulated and 26 downregulated genes, were identified. As key hub genes, three upregulated genes (AKR1C3, RPS24 and P2RY12) and three downregulated genes (ACSL1, B3GNT5 and MGAM) were identified from the co-expression network. Furthermore, GO enrichment analysis of all AMI co-expression network genes revealed functional enrichment mainly in ‘RAGE receptor binding’ and ‘negative regulation of T cell cytokine production’. In addition, KEGG Disease and BioCyc analysis indicated functional enrichment of the genes RPS24 and P2RY12 in ‘cardiovascular diseases’, of AKR1C3 in ‘cardenolide biosynthesis’, of MGAM in ‘glycogenolysis’, of B3GNT5 in ‘glycosphingolipid biosynthesis’ and of ACSL1 in ‘icosapentaenoate biosynthesis II’. In conclusion, the hub genes AKR1C3, RPS24, P2RY12, ACSL1, B3GNT5 and MGAM are potential markers of AMI, and have potential application value in the diagnosis of AMI.

Role of Biochemical Markers in Detection of Myocardial Infarction

Introduction: Acute myocardial infarction causes significant mortality and morbidity. Timely conclusion permits clinicians to risk stratify their patients and select suitable treatment. Biomarkers have been utilized to help with timely decision, whereas an expanding number of novel markers have been recognized to predict result taking after an acute myocardial infarction or acute coronary disorder. This may encourage tailoring of appropriate treatment to high-risk patients. This survey focuses on an assortment of promising biomarkers which give symptomatic and prognostic data. Objective: To compare the early demonstrative efficiency of the cardiac troponin I (cTn-I) level with that of the cardiac troponin T (cTn-T) level, as well as the creatine kinase (CK), CK-MB, and myoglobin levels, for acute myocardial infarction (AMI) in patients without an initially diagnostic ECG presenting to the Emergency department within 24 hours of the onset of their symptoms. Material and Methods Study design: Prospective Observational Cohort Settings: Punjab Institute of Cardiology Duration: Six months i.e. 1st January 2020 to 30th June 2020 Data Collection procedure: A planned, observational, cohort study was performed including chest pain patients admitted to territory care hospital. Members were sequential consenting through Emergency department with chest pain and age more than 30 years. Exclusion included having symptoms &gt;24 hours, failure to total information collection, receipt of CPR, and ST-segment elevation on the starting ECG. Estimations included levels of Trop-I, Trop- T, CK, CK-MB, and myoglobin at the time of introduction and 1, 2, 6, and 12-24 hours after presentation as well as showing ECG and clinical follow-up. The collected data was analyzed by using SPSS version 23. Results: 140 included for study out of the 200 patients, 21 (14%) were analyzed as having acute myocardial infarction after diagnostic ECG testing. The sensitivities of all 5 biochemical markers for acute myocardial infarction were poor at the time of emergency department induction. The sensitivity of Trop-T was essentially superior to that of Trop-I over the starting 2 hours (3.2-33.1), but both markers' sensitivities were low (&lt;60%) during this time outline. The Trop-I was significantly more particular for acute myocardial infarction than was the Trop-T, but not essentially better than CK-MB or myoglobin. Likelihood proportion analysis appeared that the biochemical markers with the most elevated positive ratios for acute myocardial infarction amid the primary 2 hours taking after emergency department admission were myoglobin and CK-MB. From 6 through 24 hours, the positive probability proportions for Trop I, CK-MB, and myoglobin were predominant to those of CK and Trop-T. Conclusion: Trop-I, CK-MB, and myoglobin are essentially more particular for acute myocardial infarction than are CK and Trop-T. Myoglobin is the biochemical marker having the most elevated combination of sensitivity, specificity, and negative predictive value for acute myocardial infarction inside 2 hours of emergency department induction. Not one or the other Trop-I nor Trop-T offers significant advantages over myoglobin and CK-MB within the early less than 2 hours starting screening for acute myocardial infarction. The cardiac troponins are of advantage in recognizing acute myocardial infarction greater than 6 hours after presentation. Key words: Myocardial Infarction, CKMB, Trop t, Trop I, Myoglobin

Visfatin as a Promising Marker of Cardiometabolic Risk.

Adipose tissue is an endocrine organ that produces molecules with important functions in the human body called adipokines. Visfatin can be secreted from various sources, such as macrophages, chondrocytes and amniotic epithelial cells other than adipose tissue. The main effect of visfatin is to promote inflammatory processes. In addition, visfatin has pivotal effects on the entire cardiovascular system, such as endothelial dysfunction, atherosclerosis, plaque rupture and mobilization, myocardial damage, fibrosis and new vessel formation. Vascular pathologies in other tissues also mediate its effects. Visfatin changes in a similar manner to cardiac markers in acute myocardial infarction, and the most cited feature in research studies is that it may be a cardiovascular risk marker. Visfatin is therefore expected to be widely used in cardiovascular pathology in the near future. Visfatin has many target tissues and various effects that occur in relatively complex biological pathways, making it difficult to understand visfatin adequately. In this review, we provide comprehensive information about this promising molecule.

Rapid detection of human heart-type fatty acid-binding protein in human plasma and blood using a colloidal gold-based lateral flow immunoassay.

The incidence of acute myocardial infarction (AMI) is currently increasing. Early detection is important for the treatment and prognosis of patients with AMI. Heart-type fatty acid-binding protein (H-FABP) may be used as an early marker of AMI due to its high sensitivity, specificity and prognostic value. Therefore, in the present study, H-FABP was used as a biomarker in a double-antibody sandwich method and colloidal gold-based lateral flow immunoassay to develop a rapid detection kit for H-FABP with a processing time of only 5 min. The sensitivity of the kit in plasma and whole blood was 1 ng/ml and this method had good specificity, exhibiting no cross-reaction with cardiac troponin I, myoglobin or creatine kinase-Mb. The kits had good shelf life and stability, as they were able to be stored at 40˚C for 30 days. A total of 12 clinical samples were collected for detection and the coincidence rate with the ELISA method was up to 91.67%. Therefore, the present study provided a simple, rapid and economical early-detection in-home testing kit.

Silencing long non-coding RNA MIAT ameliorates myocardial dysfunction induced by myocardial infarction via MIAT/miR-10a-5p/EGR2 axis.

Long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) has been widely-demonstrated to function as diagnostic markers for acute myocardial infarction (MI). This study was designed to explore the modulatory role of MIAT and its underlying molecular mechanism in MI. Firstly, MI mouse model was developed via ligation of the descending branch of the left coronary artery, and cell model was established through exposure to hypoxic conditions. Online prediction indicated that MIAT could bind to microRNA-10a-5p (miR-10a-5p), while miR-10a-5p was highlighted to bind to early growth response gene-2 (EGR2). MIAT and EGR2 were subsequently determined to be highly-expressed, whereas miR-10a-5p was found to be poorly-expressed in cardiomyocytes exposed to hypoxia as well as in MI mice using RT-qPCR and Western blot assay. The binding relationships between MIAT and miR-10a-5p, and between miR-10a-5p and EGR2 were further confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. The results of in vitro and in vivo experimentation also suggested that overexpression of miR-10a-5p or silencing of MIAT and EGR2 reduced cardiomyocyte apoptosis and increased ATP content, thus alleviating the impairment of cardiac function following MI. In a word, inhibition of MIAT protects against cardiac dysfunction induced by MI through the crosstalk with miR-10a-5p/EGR2.

Application of machine learning and laser optical-acoustic spectroscopy to study the profile of exhaled air volatile markers of acute myocardial infarction

Conventional acute myocardial infarction (AMI) diagnosis is quite accurate and has proved its effectiveness. However, despite this, discovering more operative methods of this disease detection is underway. From this point of view, the application of exhaled air analysis for a similar diagnosis is valuable. The aim of the paper is to research effective machine learning algorithms for the predictive model for AMI diagnosis constructing, using exhaled air spectral data. The target group included 30 patients with primary myocardial infarction. The control group included 42 healthy volunteers. The ‘LaserBreeze’ laser gas analyzer (Special Technologies Ltd, Russia), based on the dual-channel resonant photoacoustic detector cell and optical parametric oscillator as the laser source, had been used. The pattern recognition approach was applied in the same manner for the set of extracted concentrations of AMI volatile markers and the set of absorption coefficients in a most informative spectral range 2.900 ± 0.125 µm. The created predictive model based on the set of absorption coefficients provided 0.86 of the mean values of both the sensitivity and specificity when linear support vector machine (SVM) combined with principal component analysis was used. The created predictive model based on using six volatile AMI markers (C5H12, N2O, NO2, C2H4, CO, CO2) provided 0.82 and 0.93 of the mean values of the sensitivity and specificity, respectively, when linear SVM was used.

Low G0S2 gene expression levels in peripheral blood may be a genetic marker of acute myocardial infarction in patients with stable coronary atherosclerotic disease: A retrospective clinical study.

Background:The G0/G1 switch 2 (G0S2) gene is closely related to lipolysis, cell proliferation, apoptosis, oxidative phosphorylation, and the development of a variety of tumors. The aim of the present study was to expand the sample size to confirm the relationship between the expression of the G0S2 gene in peripheral blood and acute myocardial infarction (AMI) based on previous gene chip results.Methods:Three hundred patients were initially selected, of which 133 were excluded in accordance with the exclusion criteria. Peripheral blood leukocytes were collected from 92 patients with AMI and 75 patients with stable coronary atherosclerotic disease (CAD). mRNA expression levels of G0S2 in peripheral blood leukocytes was measured by RT-PCR, and protein expression levels by Western blot analysis. The results of these assays in the 2 groups were compared.Results:mRNA expression levels of GOS2 in the peripheral blood leukocytes of patients with AMI were 0.41-fold lower than those of patients with stable CAD (P < .05), and GOS2 protein expression levels were 0.45-fold lower. Multivariate logistic regression analysis indicated that low expression levels of the G0S2 gene increased the risk of AMI by 2.08-fold in stable CAD patients.Conclusions:G0S2 gene expression in the peripheral blood leukocytes of AMI patients was lower than that of stable CAD patients. Low G0S2 gene expression in peripheral blood leukocytes is an independent risk factor for AMI in stable CAD patients.

Inflammatory markers in acute myocardial infarction and the correlation with the severity of coronary heart disease

Introduction The inflammatory hypothesis of atherosclerosis is appealing in acute coronary syndromes, but the dynamics and precise role are not established. Objectives The study investigates the levels of C reactive protein (CRP), interleukin 1β (IL-1β) and stromal-derived factor 1α (SDF-1α) at the time of acute myocardial infarction (AMI) and at 1 and 6 months afterwards, compared with a control group. Results In the acute phase of AMI, CRP and SDF-1α were significantly higher, while IL-1β showed lower levels compared with controls. CRP positively correlated with coronary stenosis severity (rho = 0.3, p=.05) and negatively related with left ventricle ejection fraction (LVEF) at 1 month (rho= −0.43, p=.05). IL-1β weakly correlated with the severity of coronary lesions (rho =0.29, p=.02) and strongly with LVEF (rho= −0.8, p=.05). SDF-1α, slightly correlated with LVEF at 1 month (rho = 0.22, p=.01) and with the severity of coronary atherosclerosis (rho= −0.41, p=.003). Conclusions CRP, IL-1β and SDF-1α have important dynamic in the first 6 months after AMI and CRP and SDF-1α levels correlated with the severity of coronary lesions and LVEF at 1 month after the acute ischaemic event.