Systemic bacteria in ST-elevation myocardial infarction
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB24590 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR2264810.fastq.gz | Fastqsanger.gz | |||
| ERR2264810_1.fastq.gz | Fastqsanger.gz | |||
| ERR2264810_2.fastq.gz | Fastqsanger.gz | |||
| ERR2264830.fastq.gz | Fastqsanger.gz |
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Project description:Aims. We sought for peripheral blood gene expression signatures at presentation that distinguish the ST elevation (STEMI) and non-ST elevation myocardial infarction (NSTEMI) conditions, to define a precise map of differentially regulated biological processes, unveil new distinctive traits, and help predict markers of outcome. Methods and results. Total RNA from whole blood of STEMI and NSTEMI patients was used to prepare poly(A)+ enriched libraries for paired-end RNA-Seq. Transcriptomes were reconstructed and, after adjustment for unwanted variation, we performed differential expression analysis. Enrichment analyses was performed to infer differentiating functional networks. We identified 153 differentially expressed genes, which stood correction for TnI levels at admission and included 32 putative novel genes (false discovery rate-adjusted P<0.05). We found a divergent modulation of inflammatory, immune-response, angiogenic, and mitochondrial dynamics pathways. Finally, we showed that specific gene expression patterns at admission predict troponin I (TnI) peak levels and/or GRACE risk score. Conclusions. RNA-Seq allowed identifying novel differentially expressed genes in STEMI vs. NSTEMI, which might uncover unappreciated mechanisms underlying acute MI. Overall, our results depicted a scenario characterizing different pathological traits of these two types of acute MI that could pave the way for the identification of novel, specific biomarkers for early diagnosis, risk stratification, and therapeutic decision-making.
2020-05-27 | GSE103182 | GEO
Project description:We aimed to confirm the different expression profiles of circular RNAs (circRNAs) between ST-elevation myocardial infarction (STEMI) and chronic coronary syndromes (CCS) and identify the role of circRNAs in STEMI.
2022-11-20 | GSE213144 | GEO
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: ST-elevation myocardial infarction (STEMI, n=7), Non-ST-elevation MI (NSTEMI, n=10) and unstable angina (UA, n=9), and normal control (n=7)
2015-05-23 | E-GEOD-60993 | biostudies-arrayexpress
Project description:Affymetrix microarray (GeneChip microRNA 4.0) profilling of circulating miRNAs. We used miRNA arrays to profile miRNAs isolated from plasma of ST-segment elevation acute myocardial infarction (STEMI)-patients with cardiogenic shock (CS) or without cariogenic shock (Non-CS)
2024-03-26 | GSE254068 | GEO
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI)
2015-05-23 | GSE60993 | GEO
Project description:ST segment elevation myocardial infarction remains a significant contributor to morbidity and mortality worldwide, despite a declining incidence and better survival rates. It usually results from thrombotic occlusion of a coronary artery at the site of a ruptured or eroded plaque. Diagnosis is based on characteristic symptoms and electrocardiogram changes, and confirmed subsequently by raised cardiac enzymes. Prognosis is dependent on the size of the infarct, presence of collaterals and speed with which the occluded artery is reopened. Mechanical reperfusion by primary percutaneous coronary intervention is superior to fibrinolytic therapy if delivered by an experienced team in a timely fashion. Post-reperfusion care includes monitoring for complications, evaluation of left ventricular function, secondary preventive therapy and cardiac rehabilitation.
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Project description:Rationale: Pro-angiogenic effects of mobilised bone-marrow-derived stem/progenitor cells are essential for cardiac repair after myocardial infarction. MicroRNAs (miRNA/miR) are key regulators of angiogenesis. Objective: To determine the differential regulation of angiomiRs, i.e microRNAs regulating neovascularisation, in mobilised CD34+ progenitor cells obtained from patients with an acute ST-segment elevation myocardial infarction (STEMI) as compared to those with stable coronary artery disease (sCAD) or healthy subjects. Methods and Results: CD34+ progenitor cells were isolated from patients with STEMI (on day 0 and day 5), sCAD and healthy subjects (n=27). CD34+ progenitor cells of patients with STEMI exhibited increased pro-angiogenic activity as compared to CD34+ cells from the other groups. Using a PCR-based miRNA-array and Real-Time PCR validation we identified a profound up-regulation of two known angio-miRs, i.e. miR-378 and let-7b, in CD34+ cells of patients with STEMI. Especially, we demonstrate that miR-378 is a critical regulator of the pro-angiogenic capacity of CD34+ progenitor cells and its stimulatory effects on endothelial cells in-vitro and in-vivo, whereas let-7b up-regulation in CD34+ cells failed to proof its effect on endothelial cells in-vivo. Conclusion: The present study demonstrates for the first time a significant upregulation of the angiomiRs miR-378 and let-7b in mobilised CD34+ progenitor cells of patients with STEMI. The increased pro-angiogenic activity of these cells in patients with STEMI and the observation that in particular miR-378 regulates the angiogenic capacity of CD34+ progenitor cells in-vivo suggest that this unique microRNA expression pattern represents a novel endogenous repair mechanism activated in acute myocardial infarction.
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Project description:The ST-elevation Myocardial Infarction (STEMI) and Non-ST-elevation Myocardial Infarction (NSTEMI) might occur because of coronary artery stenosis. The gene biomarkers apply to the clinical diagnosis and therapeutic decisions in Myocardial Infarction. The aim of this study was to introduce, enrich and estimate timely the blood gene profiles based on the high-throughput data for the molecular distinction of STEMI and NSTEMI. The text mining data (50 genes) annotated with DisGeNET data (144 genes) were merged with the GEO gene expression data (5 datasets) using R software. Then, the STEMI and NSTEMI networks were primarily created using the STRING server, and improved using the Cytoscape software. The high-score genes were enriched using the KEGG signaling pathways and Gene Ontology (GO). Furthermore, the genes were categorized to determine the NSTEMI and STEMI gene profiles. The time cut-off points were identified statistically by monitoring the gene profiles up to 30 days after Myocardial Infarction (MI). The gene heatmaps were clearly created for the STEMI (high-fold genes 69, low-fold genes 45) and NSTEMI (high-fold genes 68, low-fold genes 36). The STEMI and NSTEMI networks suggested the high-score gene profiles. Furthermore, the gene enrichment suggested the different biological conditions for STEMI and NSTEMI. The time cut-off points for the NSTEMI (4 genes) and STEMI (13 genes) gene profiles were established up to three days after Myocardial Infarction. The study showed the different pathophysiologic conditions for STEMI and NSTEMI. Furthermore, the high-score gene profiles are suggested to measure up to 3 days after MI to distinguish the STEMI and NSTEMI.
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Project description:Hyperthyroidism is well known to be associated with cardiac disease. Delay in making the diagnosis and occurrence of complications are common and are associated with a worse outcome. A 54-year-old male, non-smoker, with no past medical history and no significant family history presented to our hospital with severe left sided chest pain, "crushing" in nature. Electrocardiogram showed ST-segment elevations in the inferior leads. Troponin I level was 0.32 ng/mL (normal range 0-0.05 ng/mL) on presentation. The patient underwent an emergent coronary angiography which showed no evidence of occlusive coronary artery disease. The patient's symptoms and signs prompted a high suspicion of thyrotoxicosis which was subsequently confirmed by a low thyroid stimulating hormone and high free thyroxine levels. The patient was given Methimazole and atenolol and his symptoms resolved. Awareness of coronary vasospasm due to thyrotoxicosis should be raised in patients presenting with typical angina pectoris with subsequent normal coronary angiographic results. History and physical examination may suggest underlying hyperthyroidism, but the absence of typical findings does not rule out the diagnosis.
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