Inflammatory Response During Myocardial Infarction

Introduction. The outcome of patients with ST-elevation myocardial infarction (STEMI) strongly depends on a successful reperfusion. In some patients receiving an effective treatment myocardial infarction can be aborted.Aim. The aim of the study was to estimate the incidence, clinical outcome, prognosis and inflammatory response in patients with aborted MI.Material and methods. 119 consecutive patients with STEMI treated with a primary percutaneous coronary intervention (pPCI) were enrolled in the study. Aborted MI was diagnosed when the maximal increase in cardiac enzymes (CK-MB) was up to twice the upper limit of normal (CK-MB ? 50 U/I) and at least 50% reduction of ST-segment deviation was observed within 90 min of pPCI.Results. Aborted MI was diagnosed in 16 subjects (13.4%). Patients with the aborted MI had lower serum troponin I levels (p < 0.0001). The time to treatment was significantly shorter in the aborted MI group (101 min vs. 220 min, p < 0.00001). Patients with aborted MI had a lower corrected TIMI frame count (p < 0.05) and a lower wall motion score index (p < 0.005), less pronounced inflammatory response (lower serum levels of IL-6, p < 0.01, and MCP-1, p < 0.05), higher ejection fraction six months after MI (72% vs. 64%, p < 0.05). None of the aborted MI patients died during the 3-year follow-up, while there were 13 deaths among patients with non-aborted MI.Conclusions. The abortion of myocardial infarction results in a better outcome and more favorable prognosis. An inflammatory response is less pronounced in the aborted MI.

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Screening and bioinformatics analysis of key biomarkers in acute myocardial infarction

Pteridines ◽

10.1515/pteridines-2020-0031 ◽

2021 ◽

Vol 32 (1) ◽

pp. 79-92

Author(s):

Dongmei Wei ◽

Rui Li ◽

Tao Si ◽

Hankang He ◽

Wei Wu

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Immune Response ◽

Inflammatory Response ◽

Receptor Binding ◽

Decisive Role ◽

Enrichment Analysis ◽

Neutrophil Chemotaxis ◽

Ppi Network ◽

Extracellular Region

Abstract Acute myocardial infarction (AMI) is the most severe manifestation of coronary artery disease. Considerable efforts have been made to elucidate its etiology and pathology, but the genetic factors that play a decisive role in the occurrence of AMI are still unclear. To determine the molecular mechanism of the occurrence and development of AMI, four microarray datasets, namely, GSE29111, GSE48060, GSE66360, and GSE97320, were downloaded from the Gene Expression Omnibus (GEO) database. We analyzed the four GEO datasets to obtain the differential expression genes (DEGs) of patients with AMI and patients with non-AMI and then performed gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and Protein-protein interaction (PPI) network analysis. A total of 41 DEGs were identified, including 39 upregulated genes and 2 downregulated genes. The enriched functions and pathways of the DEGs included the inflammatory response, neutrophil chemotaxis, immune response, extracellular space, positive regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcription factor activity, response to lipopolysaccharide, receptor for advanced glycation end products (RAGE) receptor binding, innate immune response, defense response to bacterium, and receptor activity. The cytoHubba plug-in in Cytoscape was used to select the most significant hub gene from the PPI network. Ten hub genes were identified, and GO enrichment analysis revealed that these genes were mainly enriched in inflammatory response, neutrophil chemotaxis, immune response, RAGE receptor binding, and extracellular region. In conclusion, this study integrated four datasets and used bioinformatics methods to analyze the gene chips of AMI samples and control samples and identified DEGs that may be involved in the occurrence and development of AMI. The study provides reliable molecular biomarkers for AMI screening, diagnosis, and prognosis.

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Abstract 81: B Lymphocytes Trigger MCP3-Dependent Mobilization of Monocytes and Promote Adverse Ventricular Remodeling After Myocardial Infarction

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.32.suppl_1.a81 ◽

2012 ◽

Vol 32 (suppl_1) ◽

Author(s):

Yasmine Zouggari ◽

Hafid Ait-Oufella ◽

Philippe Bonnin ◽

José Vilar ◽

Coralie Guerin ◽

...

Keyword(s):

Myocardial Infarction ◽

Bone Marrow ◽

Inflammatory Response ◽

Cardiac Function ◽

B Cell ◽

B Lymphocytes ◽

Cardiac Remodeling ◽

Ventricular Remodeling ◽

Cell Depletion ◽

B Cell Depletion

Leukocyte infiltration in ischemic areas is a hallmark of myocardial infarction, and persistent infiltration of innate immune cells, such as neutrophils and Ly6Chi monocytes, has been shown to promote adverse cardiac tissue remodeling. However, little is known regarding the role of mature B lymphocytes, which play a crucial role in the activation of the inflammatory response in several immune-mediated diseases. Here, we hypothesized that B lymphocytes might modulate the inflammatory response and affect the immune-dependent adverse cardiac remodeling. In a mouse model of myocardial infarction, cardiac B lymphocytes levels peaked at day 5 after the onset of infarction. Of interest, treatment with a CD20-specific monoclonal antibody decreased circulating and infiltrating B cell numbers (p=0.0008 and p=0.0002 vs control), reduced infarct size and post-ischemic immunoinflammatory response, and improved cardiac function (p=0.02 vs control) assessed by echocardiography. Intriguingly, B cell depletion was associated with an impairment of Ly6Chi monocytes mobilization from bone marrow (p=0.02 vs control), leading to reduced levels of circulating and infiltrating cardiac monocytes. The acute infarction led to transient increase of both MCP-1 and MCP-3 levels. Interestingly, B cell depletion was associated with a significant and selective reduction of MCP-3 (p=0.03 vs control) but did not alter MCP-1 levels (p=0.11). Cultured activated B cells released MCP-3 and treatment with a neutralizing MCP-3 antibody abrogated B lymphocytes-induced migration of cultured monocytes. Finally, transfer of B cell-depleted splenocytes into Rag1 -/- mice improved cardiac function after myocardial infarction compared to the transfer of non-depleted splenocytes (p=0.005). This effect was abrogated after re-supplementation with B lymphocytes isolated from wild-type mice (p=0.0007) but not from MCP-3-deficient animals (p=0.7008). In conclusion, we show that following acute myocardial infarction, B lymphocytes, trigger an MCP-3-dependent mobilization of Ly6Chi monocytes from the bone marrow to the blood, leading to their recruitment into the injured myocardium and to exacerbation of tissue inflammation, thereby promoting adverse cardiac remodeling.

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