Prevention Of Acute Myocardial Infarction Research Articles

From Atherosclerosis to Spontaneous Coronary Artery Dissection: Defining a Clinical and Genetic Risk Spectrum for Myocardial Infarction.

Spontaneous coronary artery dissection (SCAD) has been increasingly recognized as a significant cause of acute myocardial infarction (AMI) in young and middle-aged women and arises through mechanisms independent of atherosclerosis. SCAD has a multifactorial etiology that includes environmental, individual, and genetic factors distinct from those typically associated with coronary artery disease. Here, we summarize the current understanding of the genetic factors contributing to the development of SCAD and highlight those factors which differentiate SCAD from atherosclerotic coronary artery disease. Recent studies have revealed several associated variants with varying effect sizes for SCAD, giving rise to a complex genetic architecture. Associated genes highlight an important role for arterial cells and their extracellular matrix in the pathogenesis of SCAD, as well as notable genetic overlap between SCAD and other systemic arteriopathies such as fibromuscular dysplasia and vascular connective tissue diseases. Further investigation of individual variants (including in the associated gene PHACTR1) along with polygenic score analysis have demonstrated an inverse genetic relationship between SCAD and atherosclerosis as distinct causes of AMI. SCAD represents an increasingly recognized cause of AMI with opposing clinical and genetic risk factors from that of AMI due to atherosclerosis, and it is often associated with complex underlying genetic conditions. Genetic study of SCAD on a larger scale and with more diverse cohorts will not only further our evolving understanding of a newly defined genetic spectrum for AMI, but it will also inform the clinical utility of integrating genetic testing in AMI prevention and management moving forward.

Dyslipidemia: A Narrative Review on Pharmacotherapy.

Dyslipidemia plays a fundamental role in the development and progression of atherosclerosis. Current guidelines for treating dyslipidemia focus on low-density lipoprotein-cholesterol (LDL-C). Despite advances in the pharmacotherapy of atherosclerosis, the most successful agents used to treat this disease-statins-remain insufficient in the primary or secondary prevention of acute myocardial infarction. Advancing therapy for hypercholesterolemia with emerging new drugs, either as monotherapy or in combination, is expected to improve cardiovascular outcomes. An emerging field in dyslipidemia pharmacotherapy is research on genetic therapies and genetic modulation. Understanding the genetic mechanisms underlying lipid alterations may lead to the development of personalized treatments that directly target the genetic causes of dyslipidemia. RNA messenger (mRNA)-based therapies are also being explored, offering the ability to modulate gene expression to normalize lipid levels. Furthermore, nanotechnology raises new possibilities in drug delivery for treating dyslipidemia. Controlled-release systems, nanoparticles, and liposomes can enhance the effectiveness and safety of medications by providing more precise and sustained release. This narrative review summarizes current and emerging therapies for the management of patients with dyslipidemia.

Platelet-derived growth factor subunit-B mediating the effect of dickkopf-1 on acute myocardial infarction risk: a two-step Mendelian randomization study.

Previous studies have indicated a potential connection between plasma levels of Dickkopf-1 (DKK1) and platelet-derived growth factor subunit-B (PDGF-B) with the development of atherosclerosis. However, the causal relationship between DKK1, PDGF-B, and the risk of acute myocardial infarction (AMI) is yet to be established. To address this research gap, we conducted Mendelian randomization (MR) and mediation analyses to investigate the potential mediating role of PDGF-B in the association between DKK1 and AMI risk. Summary statistics for DKK1 (n = 3,301) and PDGF-B (n = 21,758) were obtained from the GWAS meta-analyses conducted by Sun et al. and Folkersen et al., respectively. Data on AMI cases (n = 3,927) and controls (n = 333,272) were retrieved from the UK Biobank study. Our findings revealed that genetic predisposition to DKK1 (odds ratio [OR]: 1.00208; 95% confidence interval [CI]: 1.00056-1.00361; P = 0.0072) and PDGF-B (OR: 1.00358; 95% CI: 1.00136-1.00581; P = 0.0015) was associated with an increased risk of AMI. Additionally, genetic predisposition to DKK1 (OR: 1.38389; 95% CI: 1.07066-1.78875; P = 0.0131) was linked to higher PDGF-B levels. Furthermore, our MR mediation analysis revealed that PDGF-B partially mediated the association between DKK1 and AMI risk, with 55.8% of the effect of genetically predicted DKK1 being mediated through genetically predicted PDGF-B. These findings suggest that genetic predisposition to DKK1 is positively correlated with the risk of AMI, and that PDGF-B partially mediates this association. Therefore, DKK1 and PDGF-B may serve as promising targets for the prevention and treatment of AMI.

A narrative analysis of patients’ experiences of taking medication for secondary prevention of acute myocardial infarction

Abstract Introduction Following an acute myocardial infarction, patients are given a daily regime of five medications to prevent secondary cardiovascular events. However, adherence to these medications has been measured to be 66%1. Sub-optimal adherence leads to increased mortality, morbidity and associated healthcare system costs. There is a lack of qualitative research of this experience for these patients, and current interventions, such as Dossett trays and New Medicines Service interviews are based upon presumed difficulties, such as memory and physical medication issues. Aim The aim of this study was to better understand patient’s experience of taking medication to prevent a further AMI, using a narrative analysis framework to describe their relationship with their medication and healthcare professionals. Methods Following ethical approval (UREC 18/36), participants were recruited with inclusion criteria of adults taking medication following at least one previous episode of AMI. Following signed informed consent, semi-structured interviews were conducted with fifteen people from central and southern England. Interviews were conducted in person, online, or on the telephone and audio recorded. The recordings were transcribed verbatim and organised using NVivo software. A narrative analysis framework was used to organise themes within the whole of each participant’s story and then separated into narrative arcs and organised by theme2. Results The whole story analysis showed the differences between each participant’s story, and that each participant’s story contained varying complicating factors that were personal and specifically important to their lives. The presence of side effects was a complicating factor for most participants. The narrative arc analysis showed that initially, participants felt they began taking medication with little control, feeling compelled to follow their prescriber’s directions and ‘do what they were told’. They understood the benefit to their health, and quickly built routine into their lives. At the next stage, participants worked in collaboration with their prescriber. They had acquired knowledge and social support of non-prescribing professionals, which enabled them to recognise side effects, which they tolerated. Missed doses were viewed as insignificant, happening infrequently and balanced by a history of medication continuity. A crisis point was reached when side effects became unmanageable, where they sought help from their prescriber to change their medication. The desired stage to reach was stability, where participants continued to take medication, and found it simple, unnoticed, fitted into their life and monitored using biometric results. Discussion/Conclusion These participants were non-intentional non-adherers, and described how they successfully added a medication regime into their lives, the details of which could assist patients who find this process more difficult. They described personal and detailed stories, indicating that interventions to assist medication-taking are suited to individual patient work. Themes across all their narratives included the presence of side effects, for which they deferred to their prescriber as decision-maker for their treatment. Non-prescribing healthcare professionals were described as providing social support at later stages, but there is a potential for pharmacists to offer more support at the initial stage where participants felt they lacked control, using services such as the New Medicines Service.

Causal effect of gallstone disease on the risk of coronary heart disease or acute myocardial infarction: a Mendelian randomization study

Gallstone disease (GSD) is thought to be associated with the risk of coronary heart disease (CHD) or acute myocardial infarction (AMI), which may be due to abnormal cholesterol metabolism. We used multiple Mendelian randomization (MR) methods based on publicly available genome-wide association study data to assess whether this association is genetically causal and to search for loci driving causality. Pooled data for GSD were obtained from FinnGen Biobank and Biobank Japan, while CHD and AMI were obtained as pooled data from the CARDIoGRAMplusC4D consortium. In this MR study, we found a significant negative causal effect of genetic susceptibility to GSD on AMI in the Finnish population, but no causal effect was found on CHD. This causal effect was not confounded by reverse causality and the same findings were obtained in the Japanese population. Furthermore, the negative causal effect of GSD on AMI risk may be driven by the rs4245791-regulated ABCG5/8 protein. In conclusion, the results of this MR study support a negative causal effect of GSD on AMI and suggest that rs4245791 is the causal driver locus of this effect, which provides new ideas and evidence for the prevention and etiologic study of AMI in patients with GSD.

Bioinformatics analysis of potential common pathogenic mechanisms for systemic lupus erythematosus and acute myocardial infarction.

Systemic lupus erythematosus (SLE) patients have a higher risk of acute myocardial infarction (AMI) compared to the general population. However, the underlying common mechanism of this association is not fully understood. This study aims to investigate the molecular mechanism of this complication. Gene expression profiles of SLE (GSE50772) and AMI (GSE66360) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) in SLE and AMI were identified, and functional annotation, protein-protein interaction (PPI) network analysis, module construction, and hub gene identification were performed. Additionally, transcription factor (TF)-gene regulatory network and TF-miRNA regulatory network were constructed for the hub genes. 70 common DEGs (7 downregulated genes and 63 upregulated genes) were identified and were mostly enriched in signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, lipid metabolism, and atherosclerosis. Using cytoHubba, 12 significant hub genes were identified, including IL1B, TNF, FOS, CXCL8, JUN, PTGS2, FN1, EGR1, CXCL1, DUSP1, MMP9, and ZFP36. This study reveals a common pathogenesis of SLE and AMI and provides new perspectives for further mechanism research. The identified common pathways and hub genes may have important clinical implications for the prevention and treatment of AMI in SLE patients.

Declining risk of heart failure hospitalization following first acute myocardial infarction in Scotland between 1991-2016.

Mortality from acute myocardial infarction (AMI) has declined, increasing the pool of survivors at risk of later development of heart failure (HF). However, coronary reperfusion limits infarct size and secondary prevention therapies have improved. In light of these competing influences, we examined long-term trends in the risk of HF hospitalization (HFH) following a first AMI occurring in Scotland over 25 years. All patients in Scotland discharged alive after a first AMI between 1991 and 2015 were followed until a first HFH or death until the end of 2016 (minimum follow-up 1 year, maximum 26 years). A total of 175 672 people with no prior history of HF were discharged alive after a first AMI during the period of study. A total of 21 445 (12.2%) patients had a first HFH during a median follow-up of 6.7 years. Incidence of HFH (per 1000 person-years) at 1 year following discharge from a first AMI decreased from 59.3 (95% confidence interval [CI] 54.2-64.7) in 1991 to 31.3 (95% CI 27.3-35.8) in 2015, with consistent trends seen for HF occurring within 5 and 10 years. Accounting for the competing risk of death, the adjusted risk of HFH at 1 year after discharge decreased by 53% (95% CI 45-60%), with similar decreases at 5 and 10 years. The incidence of HFH following AMI in Scotland has decreased since 1991. These trends suggest that better treatment of AMI and secondary prevention are having an impact on the risk of HF at a population level.

KNOCKDOWN OF CIRC_0001379 ATTENUATES HYPOXIA/REOXYGENATION-INDUCED CARDIOMYOCYTE APOPTOSIS AND INFLAMMATORY RESPONSE BY MIR-98-5P/SOX6 AXIS.

Background: Aberrant expression of circular RNAs (circRNAs) has been revealed to have crucial roles in the pathological processes of cardiovascular disease. Here, this study aimed to investigate the role and mechanism of circ_0001379 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury to explore the potential action of circ_0001379 in acute myocardial infarction (AMI). Methods: Levels of genes and proteins were examined by quantitative real-time polymerase chain reaction and western blot. Cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry were used to detect cardiomyocyte proliferation and apoptosis, respectively. The activity of IL-1β, IL-6, and TNF-α was determined by ELISA analysis. The target relationship between miR-98-5p and circ_0001379 or SOX6 (SRY-Box Transcription Factor 6) was verified by dual-luciferase reporter and RNA immunoprecipitation assays. Results: Circ_0001379 was highly expressed in AMI mouse model and H/R-induced cardiomyocytes. Functionally, circ_0001379 silencing attenuated H/R-evoked cardiomyocyte apoptosis and inflammatory response. Mechanistically, circ_0001379 functioned as a sponge for miR-98-5p, which directly targeted SOX6. Moreover, circ_0001379 could regulate SOX6 expression via sponging miR-98-5p. Further rescue experiments showed that inhibition of miR-98-5p reversed the protective effects of circ_0001379 silencing on H/R-induced cardiomyocytes. Besides that, miR-98-5p overexpression abolished H/R-evoked cardiomyocyte apoptosis and inflammatory response, while this condition was abated by SOX6. Conclusion: Circ_0001379 silencing protects cardiomyocytes from H/R-induced apoptosis and inflammatory response by miR-98-5p/SOX6 axis, suggesting a novel therapeutic strategy for AMI prevention.

Characteristics and outcomes of 795 patients with renal cell cancer following hospitalization for acute myocardial infarction.

e16516 Background: Renal cell cancer (RCC), as with many cancers, is associated with a hypercoagulable state as well as the potential risk of anemia that can lead to various cardio/cerebrovascular complications. Some of the treatments used in RCC like vascular endothelial growth factor (VEGF) inhibitors increase the thrombotic risk. Thus, the management of RCC patients following an episode of Acute Myocardial Infarction (AMI) can be more complex than that of the general population. We, therefore, conducted an in-depth analysis to study the characteristics and outcomes of AMI among RCC patients in the United States. Methods: We used the 2019 National Inpatient Sample (NIS), a yearly set of hospitalization records from the United States. Patients with a primary diagnosis of AMI and a diagnosis of RCC were identified. We excluded all patients below the age of 18 and those with other malignancies. Multiple patient characteristics were compared via Chi-Square tests. We also compared the odds of requiring Coronary artery bypass graft surgery (CABG) and Percutaneous coronary intervention (PCI) among the two groups. The overall mortality rate and adjusted odds ratios were estimated. Results: Our study found 633410 cases of AMI among adults in the United States in 2019. Among them, 795 (0.1%) had a diagnosis of RCC. A higher number of RCC patients were Male (75.5% vs. 62.7%, p < 0.01), racially classified as White (77.1% vs. 73.0%, p < 0.01), aged 60 or more (88.7% vs. 69.8%, p < 0.01), covered by Medicare (72.3% vs. 56.1%, p < 0.01), had hypertension (66.7% vs. 82.7%, p < 0.01), were diabetics (45.9% vs. 41.4%, p < 0.01) or had anemia (42.1% vs. 22.1%, p < 0.01). A lower percentage of RCC patients underwent various procedures following their AMI, as only 6.3% underwent CABG (vs. 7.5% in the non-RCC group), and 27.6% (vs. 45.8% in the non-RCC group) underwent PCI. Patients with RCC were also older (71.62 years vs. 66.64 years, p < 0.01), had a longer hospitalization (5.51 days vs.4.34 days, p < 0.01), which was also associated with a more expensive mean hospital charge ($114572.98 vs. $106241.24). Unfortunately, we also found that the presence of RCC among AMI patients was also linked with a higher odds ratio of mortality (7.5% vs. 4.4%, aOR 1.643, 95% CI 1.249- 2.160, p < 0.01). Conclusions: Our study confirms various differences in patient characteristics among AMI cases with and without RCC. While fewer RCC patients underwent procedures such as CABG or PCI, they experienced a less favorable outcome, including a longer and more costly stay and higher odds of in-hospital death. It is thus vital to screen RCC patients for potential risk factors for AMI, promote primary and secondary prevention measures, and improve hospitalization protocols to identify potential complications.

Neutrophil extracellular trap is an important connection between hemodialysis and acute myocardial infarction

The incidence of acute myocardial infarction (AMI) in hemodialysis (HD) patients is high and the prognosis is extremely poor. However, the potential connection between HD and AMI, and its regulatory mechanisms remain unclear. In this study, the gene expression profiles of HD (GSE15072) and AMI (GSE66360) were downloaded from the Gene Expression Omnibus database, common differentially expressed genes (DEGs) were obtained using the limma R package, the biological functions were analyzed according to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, machine learning was conducted to identify hub genes. Receiver operating characteristic curves and gene set enrichment analyses were used to explore the characters and biological function of hub genes, networks were used for candidate identification of transcription factor (TF), microRNA (miRNA), and drug. After a total of 255 common DEGs were selected, GO and KEGG analyses indicated that neutrophil extracellular trap (NET) may be a potential connection between HD and AMI, LILRB2, S100A12, CYBB, ITGAM, and PPIF were finally identified as hub genes. The area under curve of LILRB2, S100A12, and PPIF was higher than 0.8 in both datasets. Networks show the relationship between hub genes, TF, and miRNA, also the relationship between potential drugs and protein. In conclusion, NETs may be the potential connection between AMI and HD. The potential hub gene, signaling pathways, and drugs provided by this study may contribute to future AMI prevention and intervention in HD patients.

Smartphone-Aided Fluorescence Detection of Cardiac Biomarker Myoglobin by a Ratiometric Fluorescent AuNCs-QDs Nanohybrids Probe with High Sensitivity.

Simple and sensitive detection of cardiac biomarkers is of great significance for early diagnosis and prevention of acute myocardial infarction (AMI). Here, a ratiometric fluorescent nanohybrids probe (AuNCs-QDs) was synthesized through the coupling of bovine serum albumin-functionalized gold nanoclusters (AuNCs) with CdSe/ZnS quantum dots (QDs) to realize simple and sensitive detection of cardiac biomarker myoglobin (Mb). The AuNCs-QDs probe shows pink fluorescence under UV light, with two emission peaks at 468nm and 630nm belonging to QDs and AuNCs, respectively. Importantly, the presence of Mb caused fluorescence quenching of the blue-emitting QDs, thereby inhibiting the fluorescence resonance energy transfer (FRET) process between QDs and AuNCs, and reducing the fluorescence intensity ratio (F468/F630) of AuNCs-QDs probe effectively. As the concentration of Mb increases, the ratiometric fluorescent probe also exhibits a visible fluorescence color change. The detection limit was as low as 4.99μg/mL, and the response of the probe to Mb showed a good linear relationship up to 0.52mg/mL. Moreover, the probe has excellent specificity for Mb. Besides, the AuNCs-QDs has been applied to detect Mb of urine samples. More importantly, we also developed an AuNCs-QDs probe modified smartphone-aided paper-based strip for on-site monitoring of Mb. As far as we know, this is the first report of a smartphone-aided paper-based strip for on-site quick monitoring of Mb, which provides a useful approach for AMI biomarker monitoring and may can be extended to other medical diagnostics.

Stable isotope labeling differential glycans discovery in the serum of acute myocardial infarction by ultrahigh-performance liquid chromatography-quadrupole-Orbitrap high resolution mass spectrometry

Acute myocardial infarction (AMI) poses a grave threat to human life. However, most clinical biomarkers have limitations of low sensitivity and specificity. Therefore, screening novel glycan biomarkers with high sensitivity and specificity is crucial for the prevention and treatment of AMI. The novel method of ultrahigh-performance liquid chromatography coupled to quadrupole-Orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS) with d0/d5-BOTC probe labeling for relative quantification of glycans based on Pronase E digestion was established to screen novel glycan biomarkers in the serum of 34 AMI patients relative to healthy volunteers. The monosaccharide model D-glucosamine was used to investigate the effectiveness of the derivatization; the limit of detection (S/N = 3) was 10 amol. The accuracy was verified based on the consistency of different theoretical molar ratios (d0/d5 = 1:2, 2:1) and intensity ratios following digestion of glycoprotein ribonuclease B. Expressions of H4N4F3SA, H4N6F2, H4N6SA, H4N6F3 and H5N4FSA in the serum were significantly different (p < 0.0005) between AMI patients and healthy volunteers. The area under the receiver operating characteristic curve (AUC) for H4N6SA, H5N4FSA, and H4N6F2 was greater than 0.9039. Based on the proposed method, H4N6SA, H5N4FSA, and H4N6F2 in human serum showed high accuracy and specificity and may serve as potential glycan biomarkers, crucial for the diagnosis and treatment monitoring of AMI.

Contemporary Trends in Acute Myocardial Infarction in the American Indian/Alaska Native U.S. Population, 2000 to 2018

Coronary heart disease is disproportionately prevalent in the American Indian/Alaska Native (AI/AN) population. As care for acute myocardial infarction (AMI) continues to advance, equitable distribution and access for the AI/AN population is essential. Primary AMI hospitalizations for adults ≥18years of age were identified from the Healthcare Cost and Utilization Project National Inpatient Sample from 2000 to 2018. Related co-morbidities, procedures of interest, and in-hospital mortality were also identified. These rates were stratified by race then trended over years using Poisson regression. Overall, 9,904,714 weighted hospitalizations for primary AMI were identified. From 2000 to 2018, AI/AN adults had relatively high rates of primary AMI hospitalization, second only to non-Hispanic (NH) White adults. The AMI rate increased from 14.0/1,000 to 16.1/1,000 among AI/AN adults, remaining higher than NH Black adults (12.1/1,000 to 13.0/1,000) and Hispanic adults (10.3/1,000 and 12.7/1,000) and becoming increasingly closer to NH White adults (25.1/1,000 to 20.0/1,000) (p <0.001 for each). AI/AN adults presented 5years earlier than their NH White counterparts (64 vs 69 years old; p <0.001). In-hospital mortality was approximately 5% for all race categories and decreased in all groups but decreased at a much greater rate for NH White, NH Black and Hispanic adults (0.2% per year) compared with AI/AN adults (0.08% per year; p <0.001 for each comparison). Rates of coronary angiography and percutaneous coronary intervention increased in all groups, but coronary artery bypass graft utilization increased only in AI/AN adults (from 7% to 10%, p <0.001). In conclusion, from 2000 to 2018, AI/AN adults had a high rate of AMI hospitalizations (second only to NH White adults) that increased significantly over time. AI/AN adults were 5years younger than their NH White counterparts at index AMI hospitalization. Care during these hospitalizations was similar among all racial groups, and in-hospital mortality decreased for all groups, albeit to a lesser degree among AI/AN adults. This study highlights the need for improved access to outpatient primary AMI prevention in the AI/AN population.

Progress in the Study of Coronary Atherosclerosis and Prevention of Acute Myocardial Infarction

Cardiovascular disease stands as the leading cause of global mortality, with coronary atherosclerosis emerging as the prevailing pathological alteration within this condition. This lesion is distinguished by a notable escalation in oxidative stress. The prevalence of coronary atherosclerosis has exhibited a steady rise over time, leading to a consequential escalation in fatalities resulting from acute myocardial infarction caused by this condition. This alarming trend poses a significant threat to the well-being of our population. To address the imperative issue of preventing acute myocardial infarction caused by coronary atherosclerosis, this study offers a novel theoretical framework elucidating the pathogenesis and progression of acute myocardial infarction. By presenting and consolidating the findings of our research, this project aims to contribute to the prevention of acute myocardial infarction in recent years. The prevention of atherosclerotic plaque formation, narrowing of blood vessel lumen, obstruction, and myocardial ischemic infarction resulting from heightened oxidative stress in the human body, diminished vitamin C levels, impaired collagen formation, and unregulated cardiac wall repair system necessitates the reduction of oxidative intake, elimination of oxidative accumulation within the body, or augmentation of antioxidant intake. Furthermore, a substantial body of epidemiological evidence indicates that aberrant lipid metabolism serves as the primary predisposing factor for acute myocardial infarction. Additionally, both intermittent fasting and fat reduction therapy have demonstrated efficacy in preventing acute myocardial infarction. Moreover, it is worth noting that reducing non-high-density lipoprotein cholesterol (nHDL-C) is considered a secondary objective of fat reduction therapy. Moreover, magnesium is a significant dietary component that is frequently disregarded, yet numerous scientific investigations have substantiated the inverse relationship between the presence of magnesium ions in potable water and the prevalence of mortality due to coronary heart disease. However, iron, as an additional constituent, significantly contributes to the susceptibility of individuals to coronary artery disease and myocardial infarction.

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion.

The acute myocardial infarction (AMI) and sudden cardiac death (SCD), both associated with acute cardiac ischemia, are one of the leading causes of adult death in economically developed countries. The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine. A study on the cardiovascular effects of chronic hypoxia (CH) may contribute to the development of these methods. Chronic hypoxia exerts both positive and adverse effects. The positive effects are the infarct-reducing, vasoprotective, and antiarrhythmic effects, which can lead to the improvement of cardiac contractility in reperfusion. The adverse effects are pulmonary hypertension and right ventricular hypertrophy. This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion. It is an in-depth analysis of the published data on the underlying mechanisms, which can lead to future development of the cardioprotective effect of CH. A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.

A Case of Colon Cancer Surgery Complicated with Acute Myocardial Infarction

Objective: To investigate the treatment and prevention of acute myocardial infarction after colon cancer surgery. Methods: A patient with acute anterior myocardial infarction who underwent stent implantation in the Seventh Affiliated Hospital, Sun Yat-sen University in 2017 was selected as the subject. The patient was admitted to the emergency department for stent implantation and took antiplatelet and lipid regulating drugs orally on time after the operation. The patient also had a history of colon cancer. The lesion was resected, and the complication after operation was acute myocardial infarction. After active and effective treatment and intervention, the treatment effect of the patient was analyzed. Results: Urgent PTCA was performed, and 0.5 mg Tirofiban was injected into the coronary artery. The results of angiography showed that the blood flow of anterior descending branch recovered to grade 2. Conclusion: The condition of patients with myocardial infarction after colon cancer surgery changes rapidly. Surgery combined with drug treatment can achieve a good prognosis, reduce mortality, and improve patients’ cardiac function.

Generating Practice-Based Evidence in the Use of Guideline-Recommended Combination Therapy for Secondary Prevention of Acute Myocardial Infarction.

Background: Clinical guidelines recommend beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers, and statins for the secondary prevention of acute myocardial infarction (AMI). It is not clear whether variation in real-world practice reflects poor quality-of-care or a balance of outcome tradeoffs across patients. Methods: The study cohort included Medicare fee-for-service beneficiaries hospitalized 2007-2008 for AMI. Treatment within 30-days post-discharge was grouped into one of eight possible combinations for the three drug classes. Outcomes included one-year overall survival, one-year cardiovascular-event-free survival, and 90-day adverse events. Treatment effects were estimated using an Instrumental Variables (IV) approach with instruments based on measures of local-area practice style. Pre-specified data elements were abstracted from hospital medical records for a stratified, random sample to create "unmeasured confounders" (per claims data) and assess model assumptions. Results: Each drug combination was observed in the final sample (N = 124,695), with 35.7% having all three, and 13.5% having none. Higher rates of guideline-recommended treatment were associated with both better survival and more adverse events. Unmeasured confounders were not associated with instrumental variable values. Conclusions: The results from this study suggest that providers consider both treatment benefits and harms in patients with AMIs. The investigation of estimator assumptions support the validity of the estimates.

Clinical Presentation and In-Hospital Outcomes of Acute Myocardial Infarction in Young Patients: Japanese Nationwide Registry.

Acute myocardial infarction (AMI) in young patients is a concerning issue because of its adverse health and social impacts. Nevertheless, risk factors and prognosis of AMI in young patients are yet to be characterized. This study aimed to characterize AMI in young patients who underwent primary percutaneous coronary intervention (PCI) using large-scale nationwide all-comer registry data in Japan, the Japanese Percutaneous Coronary Intervention (J-PCI). This retrospective cohort study evaluated the J-PCI registry data of patients with AMI aged 20 to 79 years who underwent primary PCI between January 2014 and December 2018. Data on risk factor profiles, clinical features, post-procedural complications, and in-hospital outcomes were reviewed. Among 213,297 patients with AMI who underwent primary PCI, 23,985 (11.2%) were young (ages 20 to 49 years). Compared with the older group (ages 50 to 79 years; n=189,312), the younger group included a higher number of men, smokers, patients with dyslipidemia, and patients with single-vessel disease, and a lower number of patients with hypertension and diabetes. Despite favorable clinical profiles, younger age was associated with a higher rate of presentation with cardiopulmonary arrest (CPA). Further, concomitant CPA was strongly associated with in-hospital mortality in young patients (odds ratio: 14.2; 95%CI: 9.2 - 21.9). Younger patients with AMI presented a higher risk of CPA, which was strongly associated with in-hospital mortality. The results of this study highlight the importance of primary AMI prevention strategies in young individuals.

Transplantation of mesenchymal stem cells for prevention of acute myocardial infarction induced heart failure: study protocol of a phase III randomized clinical trial (Prevent-TAHA8)

BackgroundResults from recent clinical trials on bone marrow mononuclear cell (BM-MNC) transplantation show that this intervention can help reduce the incidence of heart failure (HF) after acute myocardial infarction (AMI). However, no study has evaluated the effect of the transplantation of mesenchymal stem cells (MSCs) on a clinical endpoint such as HF.MethodsThis single-blinded, randomized, multicenter trial aims to establish whether the intracoronary infusion of umbilical cord-derived Wharton’s jelly MSCs (WJ-MSCs) helps prevent HF development after AMI. The study will enroll 390 patients 3 to 7 days following AMI. Only patients aged below 65 years with impaired LV function (LVEF < 40%) will be included. They will be randomized (2:1 ratio) to either receive standard care or a single intracoronary infusion of 107 WJ-MSCs. The primary outcome of this study is the assessment of HF development during long-term follow-up (3 years).DiscussionData will be collected until Nov 2024. Thereafter, the analysis will be conducted. Results are expected to be ready by Dec 2024. We will prepare and submit the related manuscript following the CONSORT guidelines. This study will help determine whether or not the infusion of intracoronary WJ-MSCs in patients with AMI will reduce the incidence of AMI-induced HF.Trial registrationClinicalTrials.gov NCT05043610, Registered on 14 September 2021 - retrospectively registered.

Identifying patterns of immune related cells and genes in the peripheral blood of acute myocardial infarction patients using a small cohort

BackgroundThe immune system plays a vital role in the pathophysiology of acute myocardial infarction (AMI). However, the exact immune related mechanism is still unclear. This research study aimed to identify key immune-related genes involved in AMI.MethodsCIBERSORT, a deconvolution algorithm, was used to determine the proportions of 22 subsets of immune cells in blood samples. The weighted gene co-expression network analysis (WGCNA) was used to identify key modules that are significantly associated with AMI. Then, CIBERSORT combined with WGCNA were used to identify key immune-modules. The protein–protein interaction (PPI) network was constructed and Molecular Complex Detection (MCODE) combined with cytoHubba plugins were used to identify key immune-related genes that may play an important role in the occurrence and progression of AMI.ResultsThe CIBERSORT results suggested that there was a decrease in the infiltration of CD8 + T cells, gamma delta (γδ) T cells, and resting mast cells, along with an increase in the infiltration of neutrophils and M0 macrophages in AMI patients. Then, two modules (midnightblue and lightyellow) that were significantly correlated with AMI were identified, and the salmon module was found to be significantly associated with memory B cells. Gene enrichment analysis indicated that the 1,171 genes included in the salmon module are mainly involved in immune-related biological processes. MCODE analysis was used to identify four different MCODE complexes in the salmon module, while four hub genes (EEF1B2, RAC2, SPI1, and ITGAM) were found to be significantly correlated with AMI. The correlation analysis between the key genes and infiltrating immune cells showed that SPI1 and ITGAM were positively associated with neutrophils and M0 macrophages, while they were negatively associated with CD8 + T cells, γδ T cells, regulatory T cells (Tregs), and resting mast cells. The RT-qPCR validation results found that the expression of the ITGAM and SPI1 genes were significantly elevated in the AMI samples compared with the samples from healthy individuals, and the ROC curve analysis showed that ITGAM and SPI1 had a high diagnostic efficiency for the recognition of AMI.ConclusionsImmune cell infiltration plays a crucial role in the occurrence and development of AMI. ITGAM and SPI1 are key immune-related genes that are potential novel targets for the prevention and treatment of AMI.