The Role of Inflammation in Myocardial Infarction

Daskalopoulos, Evangelos P.; Hermans, Kevin C.M.; Delft, L. van; Altara, Raffaele; Blankesteijn, Matthijs

doi:10.1016/b978-0-12-800039-7.00003-7

Cited by 7 publications

(7 citation statements)

References 321 publications

(329 reference statements)

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“…3), suggesting that inflammation might play a critical role in AMI. These results corroborated a great deal of previous work indicating that inflammation is an essential part of pre-infarction atherosclerosis and post-infarction myocardial repair (Frangogiannis et al, 2002;Melamed and Goldhaber, 2014;Daskalopoulos et al, 2014;Ong et al, 2018).…”

Section: Discussionsupporting

confidence: 90%

“…(1) Elevated numbers of monocytes, epithelial cells and neutrophils, which were positively correlated with the immune score. In accordance with our present results, previous studies have demonstrated pivotal roles for these cells in plaque formation, inflammation regulation and post-infarction adverse cardiac events (Daskalopoulos et al, 2014). ( 2) Elevated CD8 + T cells, which reflected the findings of Zhang et al (2018) that the frequency of CD8 + CD28 + T cells was independently associated with AMI, positively correlated with cardiac troponin I concentration, and negatively associated with left ventricular ejection factor.…”

Section: H 36 H 24 H 12 H 2 H Admissionsupporting

confidence: 92%

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S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration

et al. 2022

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Acute myocardial infarction (AMI) is one of the leading causes of death globally, with a mortality rate of over 20%. However, the diagnostic biomarkers frequently used in current clinical practice have limitations in both sensitivity and specificity, likely resulting in delayed diagnosis. This study aimed to identify potential diagnostic biomarkers for AMI and explored the possible mechanisms involved. Datasets were retrieved from the Gene Expression Omnibus. First, we identified differentially expressed genes (DEGs) and preserved modules, from which we identified candidate genes by LASSO (least absolute shrinkage and selection operator) regression and the SVM-RFE (support vector machine-recursive feature elimination) algorithm. Subsequently, we used ROC (receiver operating characteristic) analysis to evaluate the diagnostic accuracy of the candidate genes. Thereafter, functional enrichment analysis and an analysis of immune infiltration were implemented. Finally, we assessed the association between biomarkers and biological processes, infiltrated cells, clinical traits, tissues and time points. We identified nine preserved modules containing 1,016 DEGs and managed to construct a diagnostic model with high accuracy (GSE48060: AUC = 0.923; GSE66360: AUC = 0.973) incorporating two genes named S100A9 and SOCS3. Functional analysis revealed the pivotal role of inflammation; immune infiltration analysis indicated that eight cell types (monocytes, epithelial cells, neutrophils, CD8 + T cells, Th2 cells, NK cells, NKT cells and platelets) were likely involved in AMI. Furthermore, we observed that S100A9 and SOCS3 were correlated with inflammation, variably infiltrated cells, clinical traits of patients, sampling tissues and sampling time points. In conclusion, we suggested S100A9 and SOCS3 as diagnostic biomarkers of AMI and discovered their association with inflammation, infiltrated immune cells and other factors.

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Section: Discussionsupporting

confidence: 90%

Section: H 36 H 24 H 12 H 2 H Admissionsupporting

confidence: 92%

S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration

et al. 2022

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“…The production of pro-inflammatory cytokines will further cause the secretion of chemokines and adhesion molecules that are vital for the recruitment of inflammatory cells in the infarcted area. The first cells to arrive within hours following MI are neutrophils, which phago-cytize the necrotic cardiomyocytes and degrade the extracellular matrix (ECM) [44,45]. In addition, by secreting chemotactic factors, neutrophils regulate the inflammatory response and modulate the recruitment of monocytes that will differentiate into inflammatory macrophages [46,47].…”

Section: Inflammationmentioning

confidence: 99%

Cardiac Reverse Remodeling in Ischemic Heart Disease with Novel Therapies for Heart Failure with Reduced Ejection Fraction

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et al. 2023

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Despite the improvements in the treatment of coronary artery disease (CAD) and acute myocardial infarction (MI) over the past 20 years, ischemic heart disease (IHD) continues to be the most common cause of heart failure (HF). In clinical trials, over 70% of patients diagnosed with HF had IHD as the underlying cause. Furthermore, IHD predicts a worse outcome for patients with HF, leading to a substantial increase in late morbidity, mortality, and healthcare costs. In recent years, new pharmacological therapies have emerged for the treatment of HF, such as sodium-glucose cotransporter-2 inhibitors, angiotensin receptor-neprilysin inhibitors, selective cardiac myosin activators, and oral soluble guanylate cyclase stimulators, demonstrating clear or potential benefits in patients with HF with reduced ejection fraction. Interventional strategies such as cardiac resynchronization therapy, cardiac contractility modulation, or baroreflex activation therapy might provide additional therapeutic benefits by improving symptoms and promoting reverse remodeling. Furthermore, cardiac regenerative therapies such as stem cell transplantation could become a new therapeutic resource in the management of HF. By analyzing the existing data from the literature, this review aims to evaluate the impact of new HF therapies in patients with IHD in order to gain further insight into the best form of therapeutic management for this large proportion of HF patients.

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“…Cardiac fibrosis, the extracellular matrix (ECM) accumulation in the myocardium, is classified as either reactive interstitial fibrosis or reparative fibrosis, defined by the pathophysiological status ( Travers et al, 2016 ). The inflammatory responses will start quickly after MI and trigger fibrogenesis, leading to the clearance and replacement of damaged cardiac fibroblasts in the injured necrotic part by a solid fibrotic scar ( Weber et al, 2013 ; Daskalopoulos et al, 2014 ). This is vital and protective for wound healing and viability via preserving myocardial integrity and prevent cardiac rupture development.…”

Section: Role Of Ampk Signaling In Cardiovascular Diseasesmentioning

confidence: 99%

Natural AMPK Activators in Cardiovascular Disease Prevention

et al. 2022

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Cardiovascular diseases (CVD), as a life-threatening global disease, is receiving worldwide attention. Seeking novel therapeutic strategies and agents is of utmost importance to curb CVD. AMP-activated protein kinase (AMPK) activators derived from natural products are promising agents for cardiovascular drug development owning to regulatory effects on physiological processes and diverse cardiometabolic disorders. In the past decade, different therapeutic agents from natural products and herbal medicines have been explored as good templates of AMPK activators. Hereby, we overviewed the role of AMPK signaling in the cardiovascular system, as well as evidence implicating AMPK activators as potential therapeutic tools. In the present review, efforts have been made to compile and update relevant information from both preclinical and clinical studies, which investigated the role of natural products as AMPK activators in cardiovascular therapeutics.

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The Role of Inflammation in Myocardial Infarction

Cited by 7 publications

References 321 publications

S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration

S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration

Cardiac Reverse Remodeling in Ischemic Heart Disease with Novel Therapies for Heart Failure with Reduced Ejection Fraction

Natural AMPK Activators in Cardiovascular Disease Prevention

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