Identification of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE61145 | GEO | 2015/05/23
SECONDARY ACCESSION(S): PRJNA260346
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-05-23 | E-GEOD-61145 | biostudies-arrayexpress
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: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:Blood transcriptome reflects the status of diseases, and characteristic molecular signature provides a novel window on gene expression preceding acute coronary events. 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: STEMI (n = 10), Non-ST-segment-elevation MI (NSTEMI, n = 10) and unstable angina (UA, n = 11). Blood transcriptome scans revealed that a characteristic gene expression change exists in STEMI, resulting in 531 outlier genes as STEMI molecular signature (Welch's t test, P < 0.05). Another analysis with a set of blood samples of patients with STEMI (n = 7) before and 7 days after the primary percutaneous coronary intervention (n = 7) and normal control (n = 10) evidenced that STEMI molecular signature directly reflects the onset of STEMI pathogenesis. From the two sets of transcriptome-based STEMI signatures, we identified 10 genes encoding transmembrane or secretory proteins that are highly expressed in STEMI. We validated blood protein expression levels of these 10 putative biomarkers in 40 STEMI and 32 healthy subjects by ELISA. Data suggested that PGLYRP1, IRAK3 and VNN3 are more specific and sensitive diagnostic biomarkers for STEMI than traditional CK-MB or troponin.Blood transcriptome scans of ACS evidenced early stage molecular markers for STEMI. Here, we report novel biomarkers to diagnose STEMI at emergency department in hospitals by a simple ELISA method.
| S-EPMC4536992 | biostudies-literature
Project description:Identification of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction
| PRJNA260346 | ENA
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.
| S-EPMC5922709 | biostudies-other
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.
| S-EPMC10858964 | biostudies-literature
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.
| S-EPMC5501718 | biostudies-other
Project description:The present study explored patterns of circulating metabolites and proteins that can predict future risk for ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). We conducted a prospective nested case-control study in northern Sweden in individuals who developed STEMI (N = 50) and NSTEMI (N = 50) within 5 years and individually matched controls (N = 100). Fasted plasma samples were subjected to multiplatform mass spectrometry-based metabolomics and multiplex protein analyses. Multivariate analyses were used to elucidate infarction-specific metabolite and protein risk profiles associated with future incident STEMI and NSTEMI. We found that altered lysophosphatidylcholine (LPC) to lysophosphatidylethanolamine (LPE) ratio predicted STEMI and NSTEMI events in different ways. In STEMI, lysophospholipids (mainly LPEs) were lower, whereas in NSTEMI, lysophospholipids (mainly LPEs) were higher. We found a similar response for all detected lysophospholipids but significant alterations only for those containing linoleic acid (C18:2, p < 0.05). Patients with STEMI had higher secretoglobin family 3A member 2 and tartrate-resistant acid phosphate type 5 and lower platelet-derived growth factor subunit A, which are proteins associated with atherosclerosis severity and plaque development mediated via altered phospholipid metabolism. In contrast, patients with NSTEMI had higher levels of proteins associated with inflammation and macrophage activation, including interleukin 6, C-reactive protein, chemerin, and cathepsin X and D. The STEMI risk marker profile includes factors closely related to the development of unstable plaque, including a higher LPC:LPE ratio, whereas NSTEMI is characterized by a lower LPC:LPE ratio and increased inflammation.
| S-EPMC7823877 | biostudies-literature
Project description:To assess safety of early discharge following primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI).Retrospective analysis of prospectively collected data of 2448 STEMI patients treated with PPCI surviving to hospital discharge. Post-discharge all-cause mortality was reported at 1, 7, and 30 days and long-term follow up. A total of 1542 patients (63.0%) were discharged within 2 days of admission (early discharge group) and 906 patients (37.0%) after 2 days (late discharge group). In both groups, no deaths were recorded 1 day post discharge. The early and late discharge group mortality figures for 7 days were 0 and 4 patients (0.04%) and between 7 and 30 days were 11 (0.7%) and 11 patients (1.2%), respectively. During a mean follow up of 584 days, 178 patients (7.3%) died: 67 in the early discharge group (4.3%) and 111 in the late discharge group (12.3%).This exploratory, observational study demonstrates that discharging low-risk STEMI patients within 2 days following PPCI is safe. For providers of health care, early discharge can help to allay the cost of providing a 24-hour PPCI service and adds to the recognized benefits arising from PPCI.
| S-EPMC3821814 | biostudies-other