Early Acute Myocardial Infarction Research Articles

Identification of a lactylation-related gene signature as the novel biomarkers for early diagnosis of acute myocardial infarction

Cardiovascular disease, particularly acute myocardial infarction (AMI), is a major global health concern. Current diagnostic methods for AMI lack sensitivity and specificity, necessitating novel biomarkers for early detection. In this study, we analyzed AMI gene expression datasets from the GEO database, employing Differential Gene Expression Analysis and WGCNA to identify key genes and co-expression modules. Lactylation-related genes (LRGs) from the MSigDB database were examined to identify those linked to AMI. Unsupervised consensus clustering classified AMI into subtypes, and machine learning models were developed for diagnosis. Immune cell infiltration was assessed using CIBERSORT, xCell, and MCPcounter, focusing on monocyte activation-related LRGs. We identified four LRGs (AMPD2, PYGL, SLC7A7, SAT1) significantly expressed in AMI, validated through in vitro experiments with primary cardiomyocytes from Sprague-Dawley rats. Our findings highlight LRGs as potential early AMI biomarkers and provide insights into myocardial repair mechanisms mediated by histone lactylation and monocytes.

Towards real-time myocardial infarction diagnosis: a convergence of machine learning and ion-exchange membrane technologies leveraging miRNA signatures.

Rapid diagnosis of acute myocardial infarction (AMI) is crucial for optimal patient management. Accurate diagnosis and time of onset of an acute event can influence treatment plans, such as percutaneous coronary intervention (PCI). PCI is most beneficial within 3 hours of AMI onset. MicroRNAs (miRNAs) are promising biomarkers, with potential of early AMI diagnosis, since they are released before cell death and subsequent release of larger molecules [e.g., cardiac troponins (cTn)], and have greater sensitivity and stability in plasma versus cTn regardless of timing of AMI onset. However, miRNA-based AMI diagnosis can result in false positives due to miRNA content overlap between AMI and stable coronary artery disease (CAD). Accordingly, we explored the possibility of using a miRNA profile, rather than a single miRNA, to distinguish between CAD and AMI, as well as different stages following AMI onset. First we screened a library of 800 miRNA using plasma samples from 4 patient cohorts; no known CAD, CAD, ST-segment elevation myocardial infarction (STEMI) and STEMI followed by PCI, using Nanostring miRNA profiling technology. From this screening, based on machine learning SCAD and Lasso algorithms, we identified 9 biomarkers (miR-200b, miR-543, miR-331, miR-3605, miR-301a, miR-18a, miR-423, miR-142, and miR-132) that were differentially expressed in CAD, STEMI and STEMI-PCI and explored them to identify a miRNA profile for rapid and accurate AMI diagnosis. These 9 miRNAs were selected as the most frequently identified targets by SCAD and Lasso, as indicated in the "drum-plot" model in the machine learning approach. We used age-matched patient samples to validate selected 9 miRNA biomarkers using a multiplexed ion-exchange membrane-based miRNA sensor platform, which measures specific miRNAs, and cTn as a control, simultaneously as a point-of-care device. Findings from this study will inform timely and accurate diagnosis of AMI and its stages, which are essential for effective management and optimal patient outcomes.

Target-promoted activation of DNAzyme walker for in situ assembly of hemin/G-quadruplex nanowires enable ultrasensitive and label-free electrochemical myocardial microRNA assay

The concentration elevation of myocardial microRNA (miRNA) biomarker is associated with the pathogenic process of acute myocardial infarction (AMI), and sensitive quantification of myocardial miRNA biomarker plays an important role for early AMI diagnosis and its treatment. In response, this work describes an ultrasensitive and non-label electrochemical biosensor for the assay of myocardial miRNA based on cascade signal amplifications integrated by DNAzyme walker and hemin/G-quadruplex nanowires. The DNAzyme walker is activated by presence of target miRNAs to move along the electrode surface to cyclically cleave the substrate hairpins to release G-quadruplex segments, which further trigger the in situ formation of many hemin/G-quadruplex nanowires. The large amounts of hemin intercalated into the DNA nanowires subsequently generate drastically magnified electrochemical current signals for highly sensitive label-free assay of myocardial miRNAs down to 15.7 fM within dynamic range of 100 fM to 10 nM. Such a biosensor also has high selectivity and can monitor myocardial miRNAs in diluted serums at low levels, providing a sensitive and reliable platform for diagnosing infarct-associated cardiovascular diseases.

Postmortem Immunohistochemical Findings in Early Acute Myocardial Infarction: A Systematic Review.

The diagnosis of early acute myocardial infarction is of particular importance in forensic practice considering the frequency of sudden cardiac death and the difficulty of positively identifying it through classical histological methods if survival is less than 6 h. This article aims to analyze potential immunohistochemical markers that could be useful in diagnosing acute myocardial infarction within the first 6 h of its onset. We conducted an extensive evaluation of the literature according to the PRISMA guidelines for reporting systematic literature reviews. We searched the Web of Science and PubMed databases from their inception to 2023 using the following keywords: "myocardial infarction" and "immunohistochemistry". Fifteen studies met the inclusion criteria. Immunohistochemical markers as complement factors and CD59, myoglobin, fibrinogen, desmin, tumor necrosis factor alpha (TNF-α), P-38, JNK (Jun N Terminal Kinase), transforming growth factor β1 (TGF-β1), cardiac troponins, fibronectin, H-FABP (heart fatty acid binding protein), dityrosine, fibronectin, CD15, IL-1β, IL-6, IL-15, IL-8, MCP-1, ICAM-1, CD18, and tryptase can be used to identify the first six hours of acute myocardial infarction. These markers are mostly studied in experimental animal models. It is necessary to conduct extensive studies on human myocardial tissue fragments, which will involve the analysis of several immunohistochemical markers and careful analysis of the available data on perimortem events, resuscitation, and postmortem intervals in the context of a uniform laboratory methodology.

Efficacy of single-dose evolocumab injection in early-phase acute myocardial infarction: a retrospective single-center study.

Achieving rapid reduction of low-density lipoprotein cholesterol (LDL-C) levels below 55 mg/dL in patients with acute myocardial infarction (AMI) can be challenging with statins alone. This single-center, retrospective study aimed to assess the impact of single-dose injection of evolocumab 140 mg on LDL-C levels during the peri-percutaneous coronary intervention (PCI) period in patients with AMI. A total of 95 patients with AMI who underwent PCI were divided into the evolocumab (n = 50) and non-evolocumab (n = 45) groups. The percentage change of LDL-C level at 1-3 weeks from baseline was 78.4 ± 13.4% reduction in the evolocumab group versus 45.6 ± 22.6% in the non-evolocumab group, with a mean difference of -33.5% between the groups (95% CI: -42.6 to -24.5%; p < 0.001). The achievement rate of LDL-C levels below 55 mg/dL at 1-3 weeks was significantly higher in the evolocumab group than in the non-evolocumab group (97.7% vs. 60.0%, p < 0.001). Patients with AMI who received single-dose injection of evolocumab 140 mg during the peri-PCI period had a significantly greater LDL-C reduction and higher proportion of patients achieved the target LDL-C level in the early phase AMI than those who did not receive evolocumab.

Fouling-Free electrochemical strategy based on vertically-aligned peptide layer for cardiac troponin I sensitive detection in human serum

BackgroundCardiac troponin I (CTnI) is demonstrated as one of the most promising disease biomarkers for early diagnosing acute myocardial infarction (AMI). To date, electrochemical immunosensors have been extensively studied in the field of cTnI determination. But highly accurate and sensitive cTnI detection by this method is still a challenge due to non-specific adsorption on electrode interfaces in complex human serum. As a result, it is necessary to develop an antifouling electrochemical immunosensor with high sensitivity for the detection of cTnI. ResultsIn this work, an antifouling electrochemical immunosensor was constructed based on vertically-aligned peptide layer consisting of Au nanoparticles (AuNPs) and amphiphilic CEAK16 peptide (CEAK16@AuNPs) for sensitive and accurate detection of cTnI in human serum. The vertically-aligned CEAK16@AuNPs interface provided a stable hydration layer originated from attraction of water molecules by amino acids on the hydrophilic side of the CEAK16, which effectively reduced non-specific adsorption and enhanced electron transfer rate. The cTnI immunosensor possessed great analytical performance with a wide range from 1 fg mL−1 to 1 μg mL−1 and a low detection limit of 0.28 fg mL−1 (S/N = 3). Additionally, the proposed CEAK16@AuNPs sensing interface showed excellent long-term antifouling performance and electrochemical activity that preserved 80 % of the initial signal after 20-days exposure in human serum samples. Consequently, the cTnI immunosensor displayed excellent detection accuracy compared to clinical methods and owned good selectivity, stability and reproducibility. SignificanceThe development of this strategy provides a versatile tool for accurate quantitative cTnI analysis in real human serum, thus helping to achieve early AMI diagnosis effectively and holding the promising potentials for other immunosensor in disease diagnosis.

Pyroptosis inhibitors MCC950 and VX-765 mitigate myocardial injury by alleviating oxidative stress, inflammation, and apoptosis in acute myocardial hypoxia

Acute myocardial infarction (AMI) is a prevalent cardiovascular disease with high morbidity and mortality rates worldwide. Pyroptosis is an inflammatory form of programmed cell death that has been linked to various pathological conditions. However, its exact contribution to the onset and progression of heart injury in AMI has not yet fully elucidated. Herein, we established mouse AMI model by ligating the left anterior descending artery and performed transcriptome analysis during the early phase of AMI. Mouse HL-1 and human AC-16 cardiomyocytes were subjected to hypoxia to simulate ischemic injury in vitro. Our results revealed a significant activation of the inflammatory response at 3 h post-ligation, as confirmed by RNA sequencing. We identified the occurrence of NLRP3 inflammasome-mediated pyroptosis in the cardiac tissues of human cases with AMI, as well as in mouse models of AMI and hypoxia-induced cardiomyocytes, using immunohistochemistry staining and Western blotting assays. Concurrently, pharmacological inhibition of NLRP3 inflammasome-mediated pyroptosis with MCC950 and VX-765 effectively decreased hypoxia-induced cardiomyocytes injury, while mitigating myocardial oxidative stress, apoptosis and inflammation caused by hypoxia. Moreover, the circulating levels of gasdermin D (GSDMD), the pyroptosis executor, were remarkably elevated in the plasma of mice with early AMI and in the supernatant of hypoxia-exposed cardiomyocytes in a time-dependent manner using ELISA and Western blotting. Furthermore, the change in circulating GSDMD positively correlated with Creatine Kinase-MB (CK-MB) in the plasma of early-stage AMI mouse. In summary, these findings indicated a critical role for NLRP3 inflammasome-mediated pyroptosis in the progression of AMI, the administration of MCC950 and VX-765 may be attractive candidate therapeutic approaches for cardiac injury caused by acute hypoxia or even AMI. Additionally, the circulating GSDMD exhibits potential as a newly diagnostic biomarker for AMI.

Hollow-microsphere-integrated optofluidic immunochip for myocardial infarction biomarker microanalysis

This work developed an optofluidic immunochip that uses whispering gallery mode with fiber laser enhancement, for the rapid detection of a key biomarker cardiac troponin I for acute myocardial infarction (AMI). The immunochip adopted an innovative design, using perforated hollow glass microspheres (HGMS) as carriers, with antibodies immobilized on the inner surface of the HGMS, thereby achieving ultra-low sample consumption. The performance of the immunochip was improved by fiber laser, including spectral width compression to 0.019 nm, optical signal-to-noise ratio amplification to 63.17 dB, and an enhancement in the limit of detection to 5 pg/mL. Moreover, this immunochip can provide results within 15 minutes, making it highly suitable for early AMI risk management. Compared to the standard electrochemiluminescence detection method, although some differences exist in the results of the immunochip due to the principle of detection and differences in antibody affinity, its positive reference value can be calculated as 0.0754 ng/mL, with a successful recognition rate of 88% for positive patients. The immunosensor is integrated on a polydimethylsiloxane substrate, with a compact size suitable for use in point-of-care devices and AMI self-screening, as well as rapid disease screening and microanalysis of various biomarkers, offering new possibilities for applications in these fields.

The Value of Combined Detection of Serum BNP, Cardiac Troponin-I and Dynamic Electrocardiogram in Early Clinical Diagnosis and Prognosis of Patients with Acute Myocardial Infarction.

Acute myocardial infarction (AMI) is a prevalent cardiovascular disease resulting from myocardial ischemia and necrosis due to coronary artery occlusion. AMI is characterized by a sudden onset and high mortality, underscoring the significance of early diagnosis and treatment for improving patient prognosis. This study endeavors to assess the utility of a combined assessment involving serum brain natriuretic peptide (BNP), cardiac troponin-I (cTnI), and dynamic electrocardiogram (ECG) in the early clinical diagnosis and prognosis prediction of AMI. This paper constitutes a retrospective study. All enrolled patients underwent dynamic ECG examination. The study compared the serum levels of BNP and cTnI, along with pertinent dynamic ECG parameters [turbulence slope (TS) and standard deviation (SDNN) of the 24-hour interval between normal atrial depolarization and ventricular depolarization (R-R)], between the observation group (AMI patients) and the control group (patients with unstable angina (UA)). To evaluate the early diagnostic potential of AMI, we utilized receiver operating characteristic (ROC) curves to analyze serum BNP, cTnI, dynamic ECG, and their combined utility. Furthermore, a follow-up period of 6 months was conducted for AMI patients to record major adverse cardiovascular events (MACE). In the observation group, the serum levels of BNP and cTnI were significantly higher than those in the control group (p < 0.001), while dynamic ECG parameters, specifically TS and SDNN, were significantly lower in the observation group compared to the control group (p < 0.001). The results obtained from the ROC curve analysis revealed that the area under the curve (AUC) for BNP, cTnI, dynamic ECG, and their combination in early AMI diagnosis were 0.838, 0.887, 0.874, and 0.974, respectively. The 95% confidence intervals (CI) were 0.781~0.884, 0.836~0.926, 0.822~0.915, and 0.942~0.991, respectively. Sensitivity values were 64.29%, 82.14%, 91.07%, and 88.39%, and specificity values were 91.00%, 88.00%, 70.00%, and 98.00%, respectively. Significantly, the combination of all three markers demonstrated superior efficacy in early AMI diagnosis compared to any single index (p < 0.05). During the 6-month follow-up of 112 AMI patients, 22 experienced MACE. The MACE group exhibited notably higher serum BNP and cTnI levels compared to the non-MACE group. Additionally, dynamic electrocardiogram parameters TS and SDNN demonstrated a significant decrease (p < 0.05) in the MACE group. The combined assessment of serum BNP, cTnI, and dynamic electrocardiogram enhances the early clinical diagnostic potential for AMI and holds value in assessing the prognosis of AMI patients.

Value of Cardiac Troponin, Myoglobin Combined with Heart-type Fatty Acid-binding Protein Detection in Diagnosis of Early Acute Myocardial Infarction.

To evaluate the value of cardiac troponin(cTn), myoglobin(Myo) combined with heart-type fatty acid-binding protein(H-FABP) detection in the diagnosis of early acute myocardial infarction(AMI). This study was a clinical comparative study. Eighty patients with AMI hospitalized in Tangshan Workers' Hospital were selected as study group, and another 80 individuals receiving normal physical examination were selected as control group from September 20, 2021 to September 20, 2022. The concentrations of cTn, Myo and H-FABPP, diagnostic indicators, the sensitivity and specificity of combined diagnosis, as well as the diagnostic efficacy for AMI were compared between the two groups. The levels of cTn, Myo and H-FABPP in the study group were significantly higher than those in the control group(P= 0.00). Multivariate logistic regression analysis showed that cTn, Myo and H-FABP were all relevant indicators for AMI. H-FABP alone has better diagnostic efficacy for AMI. The area under the curve of their combined detection, the specificity, and the sensitivity were higher than those of cTn, Myo and H-FABP alone, indicating that their combined application has the best diagnostic efficiency. cTn, Myo and H-FABP levels were positively correlated with Glu, TC, LDL-C and hs-CRP levels(P< 0.01), while negatively correlated with HDL level(P< 0.01). The combined detection of cardiac markers such as cTn, Myo and H-FABP presents higher sensitivity and specificity in the diagnosis of AMI compared with any single detection, and can provide better data support for the definite diagnosis of AMI, with high clinical application value.

Machine learning-based mRNA signature in early acute myocardial infarction patients: the perspective toward immunological, predictive, and personalized.

Patients diagnosed with stable coronary artery disease (CAD) are at continued risk of experiencing acute myocardial infarction (AMI). This study aims to unravel the pivotal biomarkers and dynamic immune cell changes, from an immunological, predictive, and personalized viewpoint, by implementing a machine-learning approach and a composite bioinformatics strategy. Peripheral blood mRNA data from different datasets were analyzed, and CIBERSORT was used for deconvoluting human immune cell subtype expression matrices. Weighted gene co-expression network analysis (WGCNA) in single-cell and bulk transcriptome levels was conducted to explore possible biomarkers for AMI, with a particular emphasis on examining monocytes and their involvement in cell-cell communication. Unsupervised cluster analysis was performed to categorize AMI patients into different subtypes, and machine learning methods were employed to construct a comprehensive diagnostic model to predict the occurrence of early AMI. Finally, RT-qPCR on peripheral blood samples collected from patients validated the clinical utility of the machine learning-based mRNA signature and hub biomarkers. The study identified potential biomarkers for early AMI, including CLEC2D, TCN2, and CCR1, and found that monocytes may play a vital role in AMI samples. Differential analysis revealed that CCR1 and TCN2 exhibited elevated expression levels in early AMI compared to stable CAD. Machine learning methods showed that the glmBoost+Enet [alpha=0.9] model achieved high predictive accuracy in the training set, external validation sets, and clinical samples in our hospital. The study provided comprehensive insights into potential biomarkers and immune cell populations involved in the pathogenesis of early AMI. The identified biomarkers and the constructed comprehensive diagnostic model hold great promise for predicting the occurrence of early AMI and can serve as auxiliary diagnostic or predictive biomarkers.

FRET cascade miRNA addition probe from non-crosstalk DNA photonic wire assisted with clustering algorithm for early diagnosis of acute myocardial infarction

Early and accurate diagnosis of acute myocardial infarction (AMI) can significantly reduce patient mortality. A variety of miRNAs are found to dysregulate in AMI patients, but the up- or down-regulation of a specific miRNA may not be evident in the early stage, making it difficult to achieve accurate diagnosis. Here, proposing the design that DNA photonic wire (PW) with no spectral crosstalk would make an excellent template for miRNA conjoint analysis, we report the construction of a miRNA addition probe for the additive analysis of two up-regulated miRNAs (miR-133a and miR-208a) for early diagnosis of AMI in clinical serum samples. A three-dye non-crosstalk DNA PW is built to form the two-step fluorescence resonance energy transfer (FRET) cascade system, in which three paths can blocking the FRET cascade for separate or additive analysis of the two miRNAs. K-Means clustering algorithm is further utilized to classify the output signals of the miRNA addition probe, achieving a 100% accurate diagnosis of early AMI in both the training (n = 40) and validation (n = 19) cohorts of clinical serum samples.

5mC modification patterns provide novel direction for early acute myocardial infarction detection and personalized therapy.

Most deaths from coronary artery disease (CAD) are due to acute myocardial infarction (AMI). There is an urgent need for early AMI detection, particularly in patients with stable CAD. 5-methylcytosine (5mC) regulatory genes have been demonstrated to involve in the progression and prognosis of cardiovascular diseases, while little research examined 5mC regulators in CAD to AMI progression. Two datasets (GSE59867 and GSE62646) were downloaded from Gene Expression Omnibus (GEO) database, and 21 m5C regulators were extracted from previous literature. Dysregulated 5mC regulators were screened out by "limma." The least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE) algorithm were employed to identify hub 5mC regulators in CAD to AMI progression, and 43 clinical samples (Quantitative real-time PCR) were performed for expression validation. Then a logistic model was built to construct 5mC regulator signatures, and a series of bioinformatics algorithms were performed for model validation. Besides, 5mC-associated molecular clusters were studied via unsupervised clustering analysis, and correlation analysis between immunocyte and 5mC regulators in each cluster was conducted. Nine hub 5mC regulators were identified. A robust model was constructed, and its prominent classification accuracy was verified via ROC curve analysis (area under the curve [AUC] = 0.936 in the training cohort and AUC = 0.888 in the external validation cohort). Besides, the clinical effect of the model was validated by decision curve analysis. Then, 5mC modification clusters in AMI patients were identified, along with the immunocyte infiltration levels of each cluster. The correlation analysis found the strongest correlations were TET3-Mast cell in cluster-1 and TET3-MDSC in cluster-2. Nine hub 5mC regulators (DNMT3B, MBD3, UHRF1, UHRF2, NTHL1, SMUG1, ZBTB33, TET1, and TET3) formed a diagnostic model, and concomitant results unraveled the critical impact of 5mC regulators, providing interesting epigenetics findings in AMI population vs. stable CAD.

Proteomic analysis revealed the pharmacological mechanism of Xueshuantong injection in preventing early acute myocardial infarction injury.

Background: Acute myocardial infarction (AMI) is a common and life-threatening cardiovascular disease. However, there is a lack of pathology and drug studies on AMI within 20min. Xueshuantong injection (XST) is mainly composed of Panax notoginseng saponins, which can dilate blood vessels and improve blood circulation, and is clinically used in the treatment of cardiovascular and cerebrovascular diseases. Purpose: The study aimed to investigate the protective mechanism of Xueshuantong injection against acute myocardial infarction within 20min in rats by proteomic methods and molecular docking. Method: The male Sprague-Dawley rat acute myocardial infarction model was established by LAD ligation, and Xueshuantong injection (38mg/kg) was injected into the caudal vein 15min before surgery. Cardiac function evaluation, morphological observation, label-free quantitative proteomics, Western blotting analysis, molecular docking, and affinity measurement were applied in this study. Results: In a span of 20min after acute myocardial infarction, the model group showed significant cardiac function impairment. Xueshuantong injection can significantly improve cardiac function and prevent pathological injury of myocardial tissue. A total of 117 vital differentially expressed proteins were identified by proteomic analysis, including 80 differentially expressed proteins (DEPs) in the sham group compared with model rats (Sham: model) and 43 DEPs in model rats compared with the Xueshuantong injection group (Model: XST). The treatment of Xueshuantong injection mainly involves "poly(A) RNA binding" and "cadherin binding involved in cell-cell adhesion." The differentially expressed levels of the pathways related to proteins Echdc2, Gcdh, Dlst, and Nampt, as well as 14-3-3 family proteins Ywhaz and Ywhab, could be quantitatively confirmed by WB. Molecular docking analysis and SPR analysis revealed that Ywhaz has a generally stable binding with five Xueshuantong injection components. Conclusion: Xueshuantong injection (XST) could protect rat myocardial function injury against AMI in 20min. Echdc2, Ywhaz, Gcdh, Ywhab, Nampt, and Dlst play an essential role in this protective effect. In particular, Ywhaz might be the core target of Xueshuantong injection when treating acute myocardial infarction in the early stage. This study promoted the understanding of the protective mechanism of Xueshuantong injection in 20min injury of acute myocardial infarction and contributed to the identification of possible targets of Xueshuantong injection.

CircSMARCC1 and CircLRBA are potential biomarkers in forensic postmortem diagnosis of acute myocardial infarction

Postmortem diagnosis of acute myocardial infarction (AMI), especially early AMI, is a challenge for forensic scientists. Circular RNAs (circRNA) are a unique type of RNA with a closed loop structure and more stability, compared with linear RNA. We aimed at evaluating whether circRNAs are ideal postmortem diagnostic markers for AMI. We employed bioinformatics methods to screen for target circRNAs. Divergent and convergent primers were used to confirm the loop structure. Ribonuclease R (RNaseR) digestion and artificial simulated room temperature test were performed to evaluate the stability of circRNAs. Furthermore, RT-PCR analysis was performed to assess the expressions of target circRNAs in a mouse model of AMI and in autopsy cases, while the diagnostic significance of circRNAs was evaluated by the receiver-operator characteristic (ROC) curve. The bioinformatics analysis screened out circSMARCC1 and circLRBA as target circRNAs. Agarose gel electrophoresis revealed the loop structure of target circRNAs. RNaseR digestion and the artificial simulated room temperature test showed that the stability of circRNAs was good. In mouse AMI model, circSMARCC1 levels were elevated while circLRBA levels were suppressed. Finally, in forensic autopsy cases, circSMARCC1 levels were significantly elevated, while circLRBA levels were significantly suppressed in the MI and early-MI group, relative to the normal control group. The ROC curve analysis showed that both circSMARCC1 and circLRBA can distinguish between AMI and normal control cases. Futher, a combination of the two circRNAs can increase the diagnostic efficacy of AMI. Thus, circSMARCC1 and circLRBA are potential biomarkers for postmortem diagnosis of AMI.

Rapid simultaneous SERS detection of dual myocardial biomarkers on single-track finger-pump microfluidic chip

Acute myocardial infarction (AMI) is a serious disease with high mortality that afflicts many people around the world. The main cause of death from AMI was the inaccurate early diagnosis, which resulted from the medical treatment might be a delay. Therefore, it is crucial to achieve the rapid detection of AMI. The cardiac troponin I (cTnI) level in human serum may significantly increase as the myocardial membrane ruptured, and the creatine kinase-MB (CK-MB) was also associated with the AMI recurrence and the infarct size of myocardial infarction. Both of them are regarded as important cardiac biomarkers for the early diagnosis of AMI. Therefore, we chose these two cardiac biomarkers as indicators for simultaneous detection. We proposed a single-track finger-pump microfluidic chip for simultaneous surface-enhanced Raman scattering (SERS) detection of cTnI and CK-MB. The entire detection process takes only 5 min without the cumbersome syringe pump. Meanwhile, it enables multiple reagent additions and removals of the unbonded reactants. This microfluidic sensor employed "sandwich" immunoassays based on SERS nanoprobes, AMI biomarkers, and magnetic beads. It is possible to detect two cardiac biomarkers simultaneously in a single measurement, greatly simplifying the detection process and reducing the detection time. Magnetic beads with SERS nanoprobes were separated and captured in the microchamber by a round magnet integrated into the chip. Our results showed that the detection limits of cTnI and CK-MB could reach to 0.01 ng mL−1, respectively. The limit of detections (LODs) match with the clinical threshold values for AMI biomarkers. It is believed that the proposed single-track finger-pump microfluidic chip can be used as an effective tool for determining early AMI.

Abstract 14384: A Decade Trend, Sex, Racial and Economic Disparities in Hospitalization for Premature Acute Myocardial Infarction Among Patients With Obesity and Morbid Obesity: A Decade Trend From the National Inpatient Sample

Introduction: Epidemiological evidence suggests that obesity is associated with Acute myocardial infarction (AMI). Studies on the incidence and outcomes of patients with premature AMI who are obese are limited with attention to disparities are scarce. Hypothesis: Obesity and Morbid Obesity is associated with increasing premature AMI Methods: This was a trend study of the National Inpatient database from 2010 to 2019. We searched for AMI as primary reason for hospitalization with obesity or morbid obesity as a comorbidity using the ICD codes. We estimated trends, inpatient mortality, mean length of hospital stays (LOS) and mean total hospital charges (THC) over the period. We performed a stratified analysis in categories: sex (male and female), race (Caucasians, Blacks, Hispanics), and median household income for patient's zip code (low-income quartile [LIQ] vs high-income quartile [HIQ]) to assess disparities in outcomes. Multivariable regression analysis adjusted for age and sex was used to obtain trend statistics on outcomes. Results: There was a total of 173,106 hospitalizations for obesity with early AMI with the proportion of females (63.7%). There was an increase in early MI by 60.9% among obese patients, with mean in-hospital mortality of 1.3%. Female obese patients had a 33% increase in inpatient mortality with premature AMI, with the highest increase among black women compared to white women (78.7% vs. 35.0%). Hospitalization for adult premature AMI in patients with morbid obesity was 64,926 with proportion of female 66.1% from 2010 to 2019. The incidence of hospitalization for premature AMI among morbidly obese patients increased by 120% from 2010 to 2019. The average mortality from 2010 to 2019 among morbidly obese patient with premature AMI was 2.0% in the decade studied. There was a trend toward decreased mortality over the years; however, on subgroup analysis, the decrease in mortality was significant among whites but not among blacks, LIQ, or HIQ in early MI with morbid obesity. Conclusions: Our study shows a significant increase in hospitalization for premature AMI in obese and morbidly obese patients. The female obese patient has higher inpatient mortality with highest among blacks compared to whites.

Flexible and High-Throughput Photothermal Biosensors for Rapid Screening of Acute Myocardial Infarction Using Thermochromic Paper-Based Image Analysis.

Herein, we developed a flexible, low-cost thermosensitive fiber paper for the visual display in photothermal biosensing systems for early acute myocardial infarction. The thermal signal visualization device was encapsulated with rewritable thermal fibers, which exhibited excellent stability and reversibility. The mechanism of color change in thermal paper was based on a temperature-driven reversible transformation of the structure of the dye molecule (crystalline violet lactone, CVL). It exhibits a gradation from blue to colorless at higher temperatures and gradually returns to blue when the temperature drops. Immobilization and cascade enzymatic reactions of target molecules occurred in an integrated 3D-printed detection device, a photothermal conversion process occurred under near-infrared light excitation, and the colorimetric change values of the encapsulated thermal paper were recorded and evaluated for possible pathogenicity using a smartphone. It was worth noting that the effect of the thermogenic ring-opening behavior of CVL on the macroscopic phenomenon of color change was obtained by density functional theory calculations. Under optimized conditions, the naked-eye-recognizable range of the thermal paper-based photothermal immunoassay sensor was 0.2-20 ng mL-1, This work creatively presents theoretical studies of promising thermal paper-based photothermal biosensors and provides new insights for the development of low-cost, instrument-free portable photothermal biosensors.

Frequency of In-Hospital Outcomes in patients with Acute MI who have had a Premature Coronary Artery Disease

Background: In underdeveloped nations like Pakistan, a recent estimate showed that the CVD deaths ratio is about 80%. This increasing prevalence of heart disease is partly due to industrial and technical advancements, which are linked to economic and social revolutions that have resulted in lifestyle changes and sedentary behavior. Aim: To determine frequency of in-hospital outcomes in patients with AMI who have had a premature coronary artery disease. Methodology; Study design; Descriptive case series. Setting; Department of Cardiology, D.G. Khan Medical College and teaching hospital, D.G.Khan.Duration; Six months.Results: The findings revealed that male patients made up 96 (66.2%) of the 145 research cases, while female patients made up 49 (33.8%). Our study participants were 47.67± 7.59 years old on average (minimum age 35 years and maximum 63 years). Before arriving at the hospital, the average time was 113.79 ± 54.36 minutes. In our research, 19(13.1%) of the individuals died, 36(24.8%) experienced post-MI angina, and 29(20%) had a cardiogenic shock. Conclusion: According to our findings, patients with early coronary artery disease and acute myocardial infarction had a significantly higher likelihood of poor clinical outcomes. Keywords: Acute myocardial infarction, mortality, and premature coronary artery disease.

DYNAMICS OF ADROPIN AND IRISIN BIOMARKERS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AND TYPE 2 DIABETES MELLITUS

summary. A pressing concern of modern medicine is the search for new biomarkers that can influence the development and course of acute myocardial infarction (AMI) in patents with type 2 diabetes mellitus (DM). The aim – To examine the dynamics of adropin and irisin serum levels in diabetic patients with or without AMI complications. Materials and Methods. In total, 134 AMI patients were enrolled. Among 60 examined AMI patients (group I), 41 patients were identified without early cardiovascular (CV) complications of AMI and 19 patients – with complicated AMI. Among 74 AMI patients with type 2 DM (group II), there were 48 patients without early AMI complications and 26 patients with early AMI complications. The control group consisted of 20 otherwise healthy persons. Serum levels of adropin and irisin were measured by enzyme-linked immunosorbent assay. Results. The adropin and irisin serum levels on day 1 of treatment was low in both nondiabetic (I) and diabetic patients (II) compared with those in the control group (p&lt;0.05). On the 10th day of treatment, the levels of adropin in group II patients without early AMI complications were reduced by 13.91 % compared with those in group I (p&lt;0.05). Group II with the presence of early AMI complications showed a reduction of 17.34 % in adropin levels on day 10 compared with group II (p&lt;0.05). On day 10 of treatment, the irisin levels in group II without early AMI complications were reduced by 18.94 % compared with those in group I (p&lt;0.05). In group II with the presence of early AMI complications on the 10th day, the irisin levels were reduced by 23.87 % compared with those in group I (p&lt;0.05). Conclusions. The concentrations of adropin and irisin were significantly low in group II on day 1 and 10 of hospital stay. In the dynamics of treatment on day 10, the levels of adropin and irisin remained low in group II with early CV complications of AMI.