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Kawasaki disease (KD), the most common cause of acquired heart disease in children, can be easily missed as it shares clinical findings with other pediatric illnesses, leading to risk of myocardial infarction or death. KD remains a clinical diagnosis for which there is no diagnostic test, yet there are classic findings on exam that can be captured in a photograph. This study aimed to develop a deep convolutional neural network, KD-CNN, to differentiate photographs of KD clinical signs from those of other pediatric illnesses. To create the dataset, we used an innovative combination of crowdsourcing images and downloading from public domains on the Internet. KD-CNN was then pretrained using transfer learning from VGG-16 and fine-tuned on the KD dataset, and methods to compensate for limited data were explored to improve model performance and generalizability. KD-CNN achieved a median AUC of 0.90 (IQR 0.10 from tenfold cross validation), with a sensitivity of 0.80 (IQR 0.18) and specificity of 0.85 (IQR 0.19) to distinguish between children with and without clinical manifestations of KD. KD-CNN is a novel application of CNN in medicine, with the potential to assist clinicians in differentiating KD from other pediatric illnesses and thus reduce KD morbidity and mortality., (© 2022. The Author(s).)

Objectives: More robust attribution methods are necessary to understand physician-level variation in quality of care across risk-adjusted inpatient measures. We address a gap in the literature involving attribution of physicians to inpatient stays using administrative claims data, in which rule-based methods often inadequately attribute physicians., Study Design: Methodology comparison study using a cross-section of inpatient stays., Methods: A novel approach is proposed in which physicians' relative degrees of responsibility for inpatient stays are expressed through physician-specific attribution ratios informed by existing patient characteristics and comorbidities. Attribution results are compared with the rule-based benchmark method for 7 CMS-defined clinical cohorts, including a COVID-19 cohort., Results: Using 6,835,460 unique patient encounters during 2020 (n = 136,339 in out-of-sample cohort), the proposed approach favored specialists generally considered responsible for primary clinical conditions when compared with the benchmark. The most salient shift within the acute myocardial infarction (+17.0%), heart failure (+20.2%), and coronary artery bypass graft (+4.0%) cohorts was toward the cardiovascular diseases specialty, and the chronic obstructive pulmonary disease (+24.0%) and pneumonia (+16.2%) cohorts resulted in a shift toward the pulmonary diseases specialty. The COVID-19 cohort resulted in considerable shifts toward infectious diseases and pulmonary diseases specialties (+17.4% and +14.1%, respectively). The stroke cohort experienced a considerable shift toward the neurology specialty (+42.2%)., Conclusions: We provide a robust method to attribute physicians to patients, which is a necessary tool to understand physician-level variation in quality of care within the inpatient acute care setting. The proposed method provides consistency across facilities and eliminates unattributed patients resulting from unsatisfied business rules.

Evidence from randomized controlled clinical trials and registries suggest that primary percutaneous coronary intervention provides superior clinical outcomes when compared with fibrinolytic therapy for the treatment of ST segment elevation myocardial infarction (STEMI). However, the delivery of expert and timely primary percutaneous coronary intervention to the majority of patients with STEMI is extremely challenging. This objective has fueled the concept of regional centers of excellence for the care of patients with STEMI as well as regional STEMI networks similar to those currently available for trauma or stroke victims. This article reviews the rationale behind, as well as the issues inherent to, the development of systems of care for STEMI patients.

Abstract Myocardial infarction (MI) is a leading cause of heart failure, disability and mortality worldwide. In this study, the effects of intramyocardial injection of human platelet lysate (HPL), bone marrow mesenchymal stem cells pretreated with HPL (PMSCs), and PMSC lysate (lys), alone and in combination were investigated on MI-induced by LAD ligation in male Wistar rats. The experiment was carried out on sham, vehicle (Veh), HPL, PMSCs, PMSC lysate (PMSC lys), HPL + PMSCs, and HPL + PMSC lys groups. SBP, DBP, and ± dp/dt max were monitored by the PowerLab physiograph. The MSC characteristics and CD31, NKX2.5, and cardiac troponin I (cTnI) contents were determined by flow cytometry, immunohistochemistry, and immunofluorescence, respectively. SBP, DBP, and ± dp/dt max that decreased in the MI group were recovered by HPL, PMSC, PMSC lys, HPL + PMSC, and HPL + PMSC lys treatments. CD31 density was higher in all treated groups compared to the Veh group. CD31 density in the HPL + PMSCs and HPL + PMSC lys groups was higher than in the PMSCs group. The number of Dil+/NKX2.5 + and Dil+/cTnI + cells was higher in the HPL + PMSCs group compared to the PMSCs group. The HPL and PMSCs mitigates heart injuries and cardiac dysfunction after MI. HPL provides an appropriate environment for cardiomyocyte differentiation from PMSCs.

Abstract The relationship between the triglyceride-glucose (TyG) index and mortality among survivors of myocardial infarction (MI) remains understudied. This study aims to evaluate the association between the TyG index and mortality among adult MI patients in the US. Our study included 986 MI patients, sourced from the National Health and Nutrition Examination Survey conducted from 1999 to 2018. Employing a multivariate Cox proportional hazards model, we examined the association between the TyG index and mortality. To explore potential nonlinear relationships, we employed restricted cubic splines in our analysis. Additionally, we applied a two-piecewise Cox proportional hazards model for a more nuanced analysis of the data, using key turning points as boundaries. To validate the robustness of our research findings, we also performed subgroup analyses. During a 7,342 person-years follow-up period, 434 MI survivors succumbed to various causes, including 158 cardiovascular disease-related deaths. The study revealed a U-shaped pattern between the TyG index and mortality. At TyG index levels below the thresholds (8.85 for all-cause mortality and 9.02 for cardiovascular mortality), mortality exhibited a negative correlation with the TyG index (HR = 0.56, 95%CI 0.39–0.82; HR = 0.67, 95%CI 0.39–1.14). Conversely, mortality rates increased when the TyG index surpassed these thresholds (HR = 1.38, 95%CI 1.08–1.76; HR = 1.56, 95%CI 1.02–2.38). Furthermore, among diabetic patients, subgroup analyses demonstrated that the U-shaped pattern between the TyG index and cardiovascular mortality was particularly pronounced. Our research indicates that among MI survivors, a U-shaped pattern exists between the TyG index and mortality rates, which is particularly pronounced in the diabetic patient subgroup. The corresponding threshold values for all-cause and cardiovascular mortality are 8.85 and 9.02, respectively.

Abstract Background The effect of milk on the risk of ischemic heart disease (IHD) and acute myocardial infarction (MI) is unclear. We aimed to examine the association between non-fermented and fermented milk consumption on these endpoints and investigate the relationship between milk intake and cardiometabolic-related proteins in plasma. Methods Our study is based on two Swedish prospective cohort studies that included 59,998 women and 40,777 men without IHD or cancer at baseline who provided repeated measures of diet and lifestyle factors and plasma proteomics data in two subcohorts. Through registry linkage, 17,896 cases with IHD were documented during up to 33 years of follow-up, including 10,714 with MI. We used time-updated multivariable Cox regression analysis to examine non-fermented or fermented milk intake with time to IHD or MI. Using high-throughput multiplex immunoassays, 276 cardiometabolic plasma proteins were measured in two subcohorts. We applied multivariable-adjusted regression models using a discovery-replication design to examine protein associations with increasing consumption of non-fermented or fermented milk. Results The results for non-fermented milk differed by sex (p-value for interaction = 0.01). In women, we found a pattern of successively greater risk of IHD and MI at non-fermented milk intake levels higher than 1.5 glasses/day. Compared with an intake of 0.5 glass/day (100 mL/day), non-fermented milk intake of 2 glasses/day in women conferred a multivariable-adjusted hazard ratio (HR) of 1.05 (95% CI 1.01–1.08) for IHD, an intake of 3 glasses/day an HR of 1.12 (95% CI 1.06–1.19), and an intake of 4 glasses/day an HR of 1.21 (95% CI 1.10–1.32). Findings were similar for whole, medium-fat, and low-fat milk. We did not detect higher risks of IHD with increasing milk intakes in men. Fermented milk intake was unrelated to the risk of IHD or MI in either sex. Increasing non-fermented milk intake in women was robustly associated with a higher concentration of plasma ACE2 and a lower concentration of FGF21. Conclusions We show a positive association between high amounts of non-fermented milk intake and IHD in women but not men. We suggest metabolic pathways related to ACE2 and FGF21 potentially underlie the association. Graphical abstract Our analysis of two large cohort studies involving 100,775 participants and 17,896 clinically confirmed IHD events supports a dose–response positive association between non-fermented milk intake higher than 300 mL/day with higher rates of IHD (and acute MI specifically) in women, but not in men. The higher risk of IHD with high milk intake in women was evident, irrespective of the fat content of the milk. Fermented milk intake was unrelated to the risk of IHD in both women and men. Non-fermented milk intake was associated in different directions with circulating levels of ACE2 and FGF21 in women—two essential cardiometabolic proteins, also related to IHD in women in our study.

Abstract Background Hyperuricemia is independently associated with a poor prognosis in patients with myocardial infarction (MI). Furthermore, MI induces activation of the repair response in local fibroblasts, resulting in extracellular matrix accumulation that generates a stable fibrotic scar in the infarcted area. However, researchers have not determined whether hyperuricemia affects fibroblast activation and its involvement in postinfarction cardiac remodeling. Objectives We aimed to trigger hyperuricemia by administering potassium oxonate in a mouse model of MI to evaluate the role of hyperuricemia in MI pathogenesis. Methods Microarray datasets and single-cell sequencing data from gout patients, heart failure patients, and model mice were used to identify the underlying mechanisms responsible for the effect of hyperuricemia on MI progression. A hyperuricemia-related MI mouse model was established. Cardiac function was assessed, followed by sample collection and a uric acid assay. We conducted an enzyme-linked immunosorbent assay, histological detection, immunofluorescence, sequencing data processing, single-cell RNA-seq, and functional enrichment analysis. We then isolated and cultured cardiac fibroblasts and performed Western blotting, quantitative real-time polymerase chain reaction, and shRNA-mediated lumican knockdown assays. Results Hyperuricemia decreased cardiac function, increased mortality, and aggravated adverse fibrosis remodeling in mice after MI. These outcomes were closely related to reduced levels of fibroblast-derived lumican. This reduction activated the TGF-β/SMAD signaling pathway to induce aberrant myofibroblast activation and extracellular matrix deposition in the infarcted area. Furthermore, lumican supplementation or uric acid-lowering therapy with allopurinol alleviated hyperuricemia-mediated abnormal cardiac remodeling. Conclusion Hyperuricemia aggravates postinfarction cardiac remodeling by reducing lumican expression and promoting fibroblast phenotype transition. We highlight the clinical importance of lowering uric acid levels in hyperuricemia-related MI to prevent adverse ventricular remodeling.

Abstract Histological analysis with 2,3,5-triphenyltetrazolium chloride (TTC) staining is the most frequently used tool to detect myocardial ischemia/reperfusion injury. However, its practicality is often challenged by poor image quality in gross histology, leading to an equivocal infarct-boundary delineation and potentially compromised measurement accuracy. Here, we introduce several crucial refinements in staining protocol and sample processing, which enable TTC images to be analyzed with light microscopy. The refined protocol involves a two-step TTC staining process (perfusion and immersion) and subsequent Zamboni fixation to differentiate myocardial viability and necrosis, and use of Coomassie brilliant blue to label area-at-risk. After the duo-staining steps were completed, the heart sample was embedded and sliced transversally by a cryostat into a series of thin sections (50 µm) for microscopic analysis. The refined TTC (redTTC) assay yielded remarkably high-quality images with striking color intensity and sharply defined boundaries, permitting unambiguous and reliable delineation of the infarct and area-at-risk. In the same animals, the redTTC assay showed good agreement with the in-vivo gold standard measurements (LGE and MEMRI). Meanwhile, redTTC imaging allows tracking of viable cardiomyocytes at cellular resolution, and with this enhanced capability, we convincingly demonstrated the pro-survival action of stem cells based-therapy. Therefore, the redTTC assay represents a significant technical advance that permits precise detection of the true extent of cardiac injury and cardiomyocyte viability. This approach is cost-effective and may be adapted for use in diverse applications, making it highly appealing to many laboratories performing ischemia/reperfusion injury experiments.

Acute coronary syndrome remains the leading cause of death in both patients with coronary artery disease and patients with other diseases (such as diabetes mellitus, chronic kidney disease, inflammatory diseases of various etiologies, and others). Early diagnosis of cardiomyocyte damage and necrosis opens up wide opportunities to improve the prognosis of patients with atherosclerotic lesions of the coronary arteries, and also makes it possible to discharge patients without acute cardiovascular pathology from intensive care units with a high degree of probability. The article discusses the evolution of the research and introduction into broad clinical practice of markers of myocardial damage and necrosis, which have largely improved modern clinical practice.

Abstract Background: Histone deacetylase 4 (HDAC4) and histone deacetylase 5 (HDAC5) are two isoforms of class IIa HDACs, and LMK235 is an HDAC inhibitor with higher selectivity for HDAC4/5. This study aimed to explore the expression and subcellular localization of HDAC4/5 and determine the mechanisms underlying the impact of LMK235 on ventricular remodelling post-MI. Methods: The MI model was established by left anterior descending branch (LAD) ligation, and LMK235 or vehicle was intraperitoneally injected daily for 21 days. Cardiac function was determined by echocardiography. Inflammation was evaluated by HE staining and measuring inflammatory cytokine expression, and fibrosis was evaluated by Masson staining and measuring fibrotic biomarker expression. Results: We found that LMK235 ameliorated cardiac dysfunction post-MI by suppressing inflammation and fibrosis, and LMK235 inhibited upregulation of lysine-specific demethylase 1 (LSD1) expression post-MI. In macrophages, LMK235 attenuated lipopolysaccharide (LPS) - induced inflammatory cytokine expression and inhibited LSD1 expression, while overexpression of LSD1 abrogated the anti-inflammatory effect of LMK235. In cardiac fibroblasts, LMK235 attenuated transforming growth factor-β1 (TGF-β1) - induced fibrotic biomarker expression and inhibited LSD1 expression, while overexpression of LSD1 abrogated the antifibrotic effect of LMK235. Conclusion: LMK235 attenuates chronic inflammation and fibrosis post-MI, leading to improved cardiac function. The anti-inflammatory effect of LMK235 may result from inhibition of the LSD1-NF-κB pathway in macrophages. The antifibrotic effect of LMK235 may result from inhibition of the LSD1-Smad2/3 pathway in cardiac fibroblasts.

Aim. To determine the relationships between serum concentrations of growth and differentiation factor 15 (GDF 15) and NTproBNP and features of heart remodeling in patients with heart failure and preserved ejection fraction (HFPEF) depending on the history of Q-myocardial infarction (MI). Materials and methods. The study was performed on the basis of the Cardiology Department of the Municipal non-profit Enterprise “City Hospital of Urgent and Emergency Medical Care” of Zaporizhzhia City Council. 72 patients (mean age 62.1 ± 1.7 years) with HFPEF after MI were enrolled. The patients were divided into two groups depending on the time of previous MI. The patients were examined using two-dimensional echocardiography on a MyLab50 device (Esaote, Italy) according to the recommendations of the American Society of Echocardiography. Serum concentrations of GDF 15 and NTproBNP were measured by enzyme immunoassay using Elabscience reagent kits (USA). Results. In the 1st and 2nd groups of patients who suffered MI within a year, a significant increase in GDF 15 has been found (by 66.1 % and 74.7 %, respectively; p < 0.05) compared to the control group. The level of GDF 15 was significantly higher (by 41.8 %, p < 0.05) in the group of patients who had MI over a one-to-two-year period as compared to those who had MI within one year. The serum concentration of NTproBNP was also significantly higher in HFPEF groups compared to the control group (by 84.7 % and 87.2 %, respectively, p < 0.05). In the 2nd group of patients with the history of MI between 1 and 2 years, a significant increase in end-systolic volume (by 11.8 %, p < 0.05), end-diastolic volume (by 22.3 %, p < 0.05), left ventricular myocardial mass index (by 19.1 %, p < 0.05) and the E/e’ ratio (by 20.9 %, p < 0.05) has been revealed as compared to the 1st patient group. A strong direct correlation has been shown between the time of MI occurrence and the concentration of GDF 15 (r = 0.58, p < 0.05), the interventricular septum thickness at diastole (r = 0.61, p < 0.05) and the left ventricular myocardial mass index (r = 0.63, p < 0.05), GDF 15 and E/e’ (r = 0.37, p < 0.05), GDF 15 and the left atrial volume index (r = 0.41, p < 0.05), GDF 15 and NTproBNP (r = 0.56, p < 0.05). Conclusions. Progression of left ventricular myocardial hypertrophy and diastolic dysfunction with dilatation of the heart chambers has been observed in HFPEF patients with a longer history of MI. The time period of MI in patients with HFPEF was associated with the serum concentration of GDF 15, the interventricular septum thickness and the mass index of the left ventricular myocardium. The serum concentration of GDF 15 was significantly correlated with the deterioration of the left ventricular diastolic function, such as an increase in the E/e’ ratio and the left atrial volume index.

Abstract Unlike adult mammals, the hearts of neonatal mice possess the ability to completely regenerate from myocardial infarction (MI). This observation has sparked vast interest in deciphering the potentially lifesaving and morbidity-reducing mechanisms involved in neonatal cardiac regeneration. In mice, the regenerative potential is lost within the first week of life and coincides with a reduction of Insulin-like growth factor 1 receptor (Igf1r) expression in the heart. Igf1r is a well-known regulator of cardiomyocyte maturation and proliferation in neonatal mice. To test the role of Igf1r as a pivotal factor in cardiac regeneration, we knocked down (KD) Igf1r specifically in cardiomyocytes using recombinant adeno-associated virus (rAAV) delivery and troponin T promotor driven shRNAmirs. Cardiomyocyte specific Igf1r KD versus control mice were subjected to experimental MI by permanent ligation of the left anterior descending artery (LAD). Cardiac functional and morphological data were analyzed over a 21-day period. Neonatal Igf1r KD mice showed reduced systolic cardiac function and increased fibrotic cardiac remodeling 21 days post injury. This cardiac phenotype was associated with reduced cardiomyocyte nuclei mitosis and decreased AKT and ERK phosphorylation in Igf1r KD, compared to control neonatal mouse hearts. Our in vivo murine data show that Igf1r KD shifts neonatal cardiac regeneration to a more adult-like scarring phenotype, identifying cardiomyocyte-specific Igf1r signaling as a crucial component of neonatal cardiac regeneration.

Several previous research studies have shown that air pollution has broad impacts on human health, particularly in the cardiovascular field. Exposure to air pollution entering the respiratory system can trigger inflammatory responses and increase the risk of cardiovascular diseases such as coronary artery disease. This systematic review aim to determine the relationship between air pollution and the occurrence of Coronary Artery Disease (CAD). Journal searches were conducted on five electronic databases, namely Pubmed, Science Direct, Europe PMC, Wiley Online Library, and Cochrane, following the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) method. The search results get six original articles that meet the inclusion and exclusion criteria for analysis. Based on the results of the analysis shows that there is a significant relationship between air pollution in the form of gas components or particulate matter with the incidence of coronary artery disease. High levels of air pollution in an area can also increase the risk of CAD higher than areas with lower levels of air pollution.

Aim: The occlusion myocardial infarction (OMI) and non-OMI (NOMI) paradigms aim to improve the quality to ensure effective diagnosis and treatment. Due to the lack of universally accepted diagnostic criteria, the study aimed to investigate the correlation between laboratory parameters commonly analyzed in the emergency department in patients with and non-segment elevation myocardial infarction and OMI/NOMI definitions. Materials and Methods: Demographic characteristics, mortality status, laboratory parameters and thrombolysis in MI (TIMI) scores of patients were recorded. Patients with TIMI scores of 0-2 and 3 were considered OMI and NOMI. Findings were considered significant when p

Abstract Background Elevated susceptibility to acute myocardial infarction and various cardiovascular diseases has been observed in individuals infected with the human immunodeficiency virus compared with the uninfected population, as demonstrated in numerous studies. The precise mechanism by which human immunodeficiency virus infection heightens the risk of acute myocardial infarction remains elusive. The manifestation of acute coronary syndrome in young patients with human immunodeficiency virus may deviate from the typical, displaying distinct pathophysiological and clinical characteristics. The occurrence of myocardial infarction with non-obstructive coronary arteries in young patients with human immunodeficiency virus poses diagnostic and treatment challenges. Case presentation We present the case of a 46-year-old African woman with no traditional atherosclerotic risk factors. She was diagnosed with human immunodeficiency virus-1 infection 2 years prior to her current admission for chest pain. Her troponin levels were elevated, suggestive of acute coronary syndrome. Although coronary angiography ruled out coronary artery stenosis, it revealed mild myocardial bridging in the left anterior descending artery. Cardiac magnetic resonance imaging confirmed myocardial infarction, indicating a myocardial infarction with non-obstructive coronary arteries with an apical thrombus in the left ventricle. Following medical treatment, the patient experienced resolution of chest pain and improvement in ST-segment elevation. Conclusions In young female patients without traditional risk factors, human immunodeficiency virus infection is a possible etiological factor for myocardial infarction with non-obstructive coronary arteries. The likely pathophysiological pathway is superficial endothelial cell denudation as a result of chronic inflammation and immune activation.

Abstract Interleukin-6 (IL-6) plays a crucial role in the pathogenesis of cardiovascular disease (CVD), and IL-6 receptor (IL-6R) blockade has emerged as a promising therapeutic option. However, their specific therapeutic effects in different types of CVDs remain unclear. This study aimed to assess the efficacy of IL-6R blockade in the management of various CVDs, including hypertension (HTN), coronary heart disease (CHD), myocardial infarction (MI), atrial fibrillation (AF), and heart failure (HF). The Mendelian randomization (MR) approach was utilized to investigate the therapeutic impact of IL-6R blockade on HTN, CHD, MI, AF, and HF based on the genome-wide association study (GWAS) summary statistics. MR-Egger intercept test, Cochran's Q test, and leave-one-out analysis were used for sensitivity analysis to verify the reliability of the MR results. The Bonferroni method was used to correct for bias caused by multiple comparisons. Inverse variance weighted (IVW) results demonstrated that IL-6R blockade significantly influenced CHD (odds ratio (OR) = 0.757, 95% confidence interval (CI): 0.690 - 0.832, P = 5.804 × 10–9) and MI (OR = 0.840, 95% CI: 0.744 - 0.949, P = 0.005). However, IL-6R blockade had no significant effect on HTN (OR = 1.015, 95% CI: 0.950 - 1.084, P = 0.663), AF (OR = 0.905, 95% CI: 0.800 - 1.025, P = 0.116) and HF (OR = 1.012, 95% CI: 0.921 - 1.113, P = 0.805). Genetically predicted IL-6R blockade was associated with a protective effect on CHD and MI, but not HTN, AF and HF. This study's findings offer valuable insights for tailoring IL-6R blockade treatment for different types of CVD, and serve as a reference for future research.

Abstract Background Myocardial fibrosis, a hallmark of heart disease, is closely associated with macrophages, yet the genetic pathophysiology remains incompletely understood. In this study, we utilized integrated single-cell transcriptomics and bulk RNA-seq analysis to investigate the relationship between macrophages and myocardial fibrosis across omics integration. Methods We examined and curated existing single-cell data from dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), myocardial infarction (MI), and heart failure (HF), and analyzed the integrated data using cell communication, transcription factor identification, high dimensional weighted gene co-expression network analysis (hdWGCNA), and functional enrichment to elucidate the drivers of macrophage polarization and the macrophage-to-myofibroblast transition (MMT). Additionally, we assessed the accuracy of single-cell data from the perspective of driving factors, cell typing, anti-fibrosis performance of left ventricular assist device (LVAD). Candidate drugs were screened using L1000FWD. Results All four heart diseases exhibit myocardial fibrosis, with only MI showing an increase in macrophage proportions. Macrophages participate in myocardial fibrosis through various fibrogenic molecules, especially evident in DCM and MI. Abnormal RNA metabolism and dysregulated transcription are significant drivers of macrophage-mediated fibrosis. Furthermore, profibrotic macrophages exhibit M1 polarization and increased MMT. In HF patients, those responding to LVAD therapy showed a significant decrease in driver gene expression, M1 polarization, and MMT. Drug repurposing identified cinobufagin as a potential therapeutic agent. Conclusion Using integrated single-cell transcriptomics, we identified the drivers of macrophage-mediated myocardial fibrosis in four heart diseases and confirmed the therapeutic effect of LVAD on improving HF with single-cell accuracy, providing novel insights into the diagnosis and treatment of myocardial fibrosis.

Abstract Local inflammatory microenvironment in the early stage of myocardial infarction (MI) severely impaired cardiac recovery post-MI. Macrophages play a pivotal role in this process. A classical glycolytic inhibitor, 2-Deoxy-Glucose (2-DG), has been found to regulate the excessive pro-inflammatory macrophage polarization in the infarcted myocardium. This study investigated the effect of 2-DG-loaded chitosan/gelatin composite patch on the infarct microenvironment post-MI and its impact on cardiac repair. The results showed that the 2-DG patch significantly inhibited the expression of inflammatory cytokines, alleviated reactive oxygen species (ROS) accumulation, repressed the proinflammatory polarization of macrophages, attenuated local inflammatory microenvironment in the ischemic hearts, as well as improved cardiac function, reduced scar size, and promoted angiogenesis post-MI. In terms of mechanism, 2-DG exerts anti-inflammatory effects through inhibiting the NF-κB signaling pathway and reducing the assembly and activation of the NLRP3 inflammasome. These findings suggest that 2-DG composite patch may represent a promising therapeutic strategy for cardiac repair after MI.

Abstract The correlation between diabetes and coronary artery disease (CAD) is well established. Insulin resistance (IR) is considered a primary contributor to elevated CAD risk in diabetic individuals. The triglyceride-glucose (TyG) index serves as a straightforward surrogate marker for insulin resistance. However, few studies have explored their correlations with myocardial infarction and CAD severity. Therefore, our study aimed to investigate the association between the TyG index and the occurrence of myocardial infarction, as well as the severity of coronary artery disease. We conducted a retrospective study involving 3865 consecutive patients who underwent coronary angiography at the First Affiliated Hospital of Zhejiang University, School of Medicine. Of these, 1724 patients were diagnosed with coronary artery disease. Demographic, biochemical, clinical, and angiographic data were gathered. A robust correlation exists between the TyG index and CAD subtypes, suggesting its potential as an independent clinical diagnostic marker. Moreover, the TyG index exhibited a significant positive correlation with disease severity, as assessed by the Gensini score. Elevated TyG index was associated with an increased predisposition to severe CAD, as indicated by the Gensini score, and myocardial infarction, even after adjusting for well-established cardiovascular risk factors.

Abstract We provide an update regarding the differences between men and women in short-term postoperative mortality after coronary artery bypass grafting (CABG) and highlight the differences in postoperative risk of stroke, myocardial infarction, and new onset atrial fibrillation. We included 23 studies, with a total of 3,971,267 patients (70.7% men, 29.3% women), and provided results for groups of unbalanced studies and propensity matched studies. For short-term mortality, the pooled odds ratio (OR) from unbalanced studies was 1.71 (with 95% CI 1.69–1.74, I2 = 0%, p = 0.7), and from propensity matched studies was 1.32 (95% CI 1.14–1.52, I2 = 76%, p

Background/Aims 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. Methods A total of 95 patients with AMI who underwent PCI were divided into the evolocumab (n = 50) and non-evolocumab (n = 45) groups. Results 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). Conclusions 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.

Background: Cardiovascular diseases are the leading cause of mortality in India. Ischemic heart disease is a result of an inadequate supply of blood to a portion of the myocardium caused by atherosclerotic disease of an epicardial coronary artery. The increasing incidence of myocardial infarction (MI) and associated mortality is a concern. Aims and Objectives: The aims and objectives of the study were to evaluate the clinical profile and determine the association of risk factors in patients presenting with acute MI. The study highlights the trend of occurrence of acute MI so as appropriate measures can be taken to mitigate the incidence of coronary artery disease (CAD). Materials and Methods: A cross-sectional study was conducted among 100 patients with acute MI admitted to the intensive coronary care unit and medicine wards of a tertiary center in North-East India. The study was carried out for a period of 2 years from September 2019 to August 2021. Results: The mean age of the study population was 63.13±10.47 years, with an age range from 41 to 90 years. The study population had 75% males and 25% females. The most common presenting symptom was chest pain in 96% of patients. Hypertension in 75% of patients was the most common risk factor studied. About 97% of patients had at least one cardinal risk factor for MI. Inferior wall MI in 47% of patients was the most common site of MI. The highest mortality was seen in those who presented with Killip Class IV. Conclusions: Increasing age and male gender predisposed to MI. The association of risk factors such as hypertension, diabetes, obesity, and family history was higher in females. To bring about a reduction in the risk of CAD, emphasis should be laid on the adoption of a healthy lifestyle particularly for those at risk of CAD.