Browse
Submit Data
Databases
API
Help

Dataset Information

27 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mild Therapeutic Hypothermia Alters Hemostasis in ST Elevation Myocardial Infarction Patients.

ABSTRACT: Background and Rationale: Mild therapeutic hypothermia (MTH) is a concept to reduce infarct size and improve outcome after ST-segment elevation myocardial infarction (STEMI). In the STATIM trial, we investigated MTH as an additional therapy for STEMI patients. In the intention-to-treat set, 101 patients were included. No difference in primary and secondary endpoints measured by cardiac magnetic resonance imaging was found. Platelet activation and plasmatic coagulation are key in the pathophysiology of STEMI. In the present study, we investigated the effect of MTH on primary and secondary hemostasis in STEMI patients. Methods and Results: Platelet function and morphology were assessed by routine blood count, aggregometry testing, and flow cytometry. Soluble platelet markers were determined by enzyme-linked immunosorbent assay (ELISA) testing. Plasmatic coagulation was measured throughout the study. Platelet count remained unchanged, irrespective of treatment, whereas platelet size decreased in both patient groups. Platelet aggregometry indicated increased platelet reactivity in the MTH group. Furthermore, higher adenosine diphosphate (ADP) plasma levels were found in MTH patients. Expression of glycoprotein IIb/IIIa was increased on platelets of STEMI patients treated with MTH. Lower patient temperatures correlated with longer clotting times and resulted in reduced pH. Lower pH values were positively correlated with longer clotting times. Conclusion: Present data indicate longer clotting times and higher platelet reactivity in STEMI patients treated with MTH. These changes did not correspond to clinical bleeding events or larger infarct size.

SUBMITTER: Scherz T

PROVIDER: S-EPMC8290912 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

ST elevation myocardial infarction.

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

An inspection of therapeutic hypothermia preceding coronary reperfusion in patients with a cardiogenic shock complicating anterior ST-segment elevation myocardial infarction.

Project description:We retrospectively investigated our hypothesis that pre-percutaneous coronary intervention (PCI) procedural therapeutic hypothermia may have clinical advantages in patients with a profound cardiogenic shock complicating anterior ST-segment elevation myocardial infarction (STEMI).Of 483 consecutive patients treated with PCI for a first anterior STEMI including 31 patients with aborted sudden cardiac arrest between 2009 and 2013, a total of 37 consecutive patients with an anterior STEMI complicated with profound cardiogenic shock defined as the presence of hyperlactic acidemia (serum levels of lactate > 4 mmol/L) with mechanical circulatory support were identified. An impaired myocardial tissue-level reperfusion (angiographic myocardial blush grade 0 or 1) and in-hospital mortality were evaluated in accordance with the presence or absence of pre-PCI procedural therapeutic hypothermia.Thirteen patients were treated with pre-PCI procedural therapeutic hypothermia and 24 were not inducted with therapeutic hypothermia. Five patients with and 18 without pre-PCI procedural therapeutic hypothermia impaired myocardial tissue-level reperfusion (38% vs. 75%, p = 0.037). A total of 26 patients with in-hospital death (overall in-hospital mortality 70%) were composed of 6 with and 20 without therapeutic hypothermia (in-hospital mortality 46% vs. 83%, p = 0.028). A multivariate analysis demonstrated a significant association of pre-PCI procedural therapeutic hypothermia (p = 0.021) with in-hospital survival benefit. Adverse events associated with therapeutic hypothermia were not found in 12 patients who completed this treatment.The present study may imply a crucial possibility of clinical benefits of pre-PCI procedural therapeutic hypothermia in patients with a cardiogenic shock complicating anterior STEMI.

| S-EPMC5497289 | biostudies-other

Differential gene expression patterns in ST-elevation Myocardial Infarction and Non-ST-elevation Myocardial Infarction.

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

The platelet phenotype in patients with ST-segment elevation myocardial infarction is different from non-ST-segment elevation myocardial infarction.

Project description:It is assumed that platelets in diseased conditions share similar properties to platelets in healthy conditions, although this has never been examined in detail for myocardial infarction (MI). We examined platelets from patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) compared with platelets from healthy volunteers to evaluate for differences in platelet phenotype and function. Platelet activation was examined and postreceptor signal transduction pathways were assessed. Platelet-derived plasma biomarkers were evaluated by receiver operator characteristic curve analysis. Maximum platelet activation through the thromboxane receptor was greater in STEMI than in NSTEMI but less through protease-activated receptor 1. Extracellular-signal related-kinase 5 activation, which can activate platelets, was increased in platelets from subjects with STEMI and especially in platelets from patients with NSTEMI. Matrix metalloproteinase 9 (MMP9) protein content and enzymatic activity were several-fold greater in platelets with MI than in control. Mean plasma MMP9 concentration in patients with MI distinguished between STEMI and NSTEMI (area under curve [AUC] 75% [confidence interval (CI) 60-91], P = 0.006) which was superior to troponin T (AUC 66% [CI 48-85, P = 0.08), predicting STEMI with 80% sensitivity (95% CI 56-94), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P < 0.0001), and NSTEMI with 50% sensitivity (CI 27-70), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P = 0.03). Platelets from patients with STEMI and NSTEMI show differences in platelet surface receptor activation and postreceptor signal transduction, suggesting the healthy platelet phenotype in which antiplatelet agents are often evaluated in preclinical studies is different from platelets in patients with MI.

| S-EPMC5898983 | biostudies-literature

Thyrotoxicosis Mimicking ST Elevation Myocardial Infarction.

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

Prognosis Between ST-Elevation and Non-ST-elevation Myocardial Infarction in Older Adult Patients.

Project description:Background: Whether there is a difference in prognosis between elderly patients with ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) remains mysterious. Methods: We conducted a retrospective cohort study by analyzing the data in the Longitudinal Health Insurance Database (LHID) in Taiwan to explore differences between STEMI and NSTEMI with respect to in-hospital and long-term (3-year) outcomes among older adult patients (aged ≥65 years). Patients were further stratified based on whether they received coronary revascularization. Results: In total, 5,902 patients aged ≥65 years with acute myocardial infarction (AMI) who underwent revascularization (2,254) or medical therapy alone (3,648) were included. In the revascularized group, no difference was observed in cardiovascular (CV) and all-cause mortality during hospitalization or at 3-year follow-up between the two AMIs. Conversely, in the non-revascularized group, patients with NSTEMI had higher crude odds ratio (cOR) for all-cause death during hospitalization [cOR: 1.33, 95% confidence interval (CI) = 1.07-1.65] and at 3-year follow-up (cOR: 1.47, 95% CI = 1.21-1.91) relative to patients with STEMI. However, after multivariable adjustments, only NSTEMI indicated fewer in-hospital CV death [adjusted odds ratio (aOR): 0.75, 95% CI = 0.58-0.98] than STEMI in non-revascularized group. Moreover, major bleeding was not different between patients with STEMI or NSTEMI aged ≥65 years old. Conclusion: Classification of AMI is not associated with the difference of in-hospital or 3-year CV and all-cause death in older adult patients received revascularization. In a 3-year follow-up period, STEMI was an independent predictor of a higher incidence of revascularization after the index event. Non-ST-elevation myocardial infarction had more incidence of MACE than patients with STEMI did in both treatment groups.

| S-EPMC8761910 | biostudies-literature

Hypothermia for Cardioprotection in Patients with St-Elevation Myocardial Infarction: Do Not Give It the Cold Shoulder Yet!

Project description:The timely revascularization of an occluded coronary artery is the cornerstone of treatment in patients with ST-elevation myocardial infarction (STEMI). As essential as this treatment is, it can also cause additional damage to cardiomyocytes that were still viable before reperfusion, increasing infarct size. This has been termed "myocardial reperfusion injury". To date, there is still no effective treatment for myocardial reperfusion injury in patients with STEMI. While numerous attempts have been made to overcome this hurdle with various experimental therapies, the common denominator of these therapies is that, although they often work in the preclinical setting, they fail to demonstrate the same results in human trials. Hypothermia is an example of such a therapy. Although promising results were derived from experimental studies, multiple randomized controlled trials failed to do the same. This review includes a discussion of hypothermia as a potential treatment for myocardial reperfusion injury, including lessons learned from previous (negative) trials, advanced techniques and materials in current hypothermic treatment, and the possible future of hypothermia for cardioprotection in patients with STEMI.

| S-EPMC8878494 | biostudies-literature

Selective intracoronary hypothermia in patients with ST-elevation myocardial infarction. Rationale and design of the EURO-ICE trial.

Project description: Not available

| S-EPMC9725036 | biostudies-literature

Whole blood transcriptional profiling by RNA sequencing in patients with ST-elevation and non-ST elevation myocardial infarction

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

Out-of-hospital initiation of hypothermia in ST-segment elevation myocardial infarction: a randomised trial.

Project description:ObjectiveTo evaluate the effect of prereperfusion hypothermia initiated in the out-of-hospital setting in awake patients with ST-segment elevation myocardial infarction (STEMI) on myocardial salvage measured by cardiac MRI (CMR).MethodsHypothermia was initiated within 6 hours of symptom onset by the emergency medical service with surface cooling pads and cold saline, and continued in the cath lab with endovascular cooling (target temperature: ≤35°C at time of reperfusion). Myocardial salvage index (using CMR) was compared in a randomised, controlled, open-label, endpoint blinded trial to a not-cooled group of patients at day 4±2 after the event.ResultsAfter postrandomisation exclusion of 19 patients a total of 101 patients were included in the intention-to-treat analysis (control group: n=54; hypothermia group: n=47). Target temperature was reached in 38/47 patients (81%) in the intervention group. Study-related interventions resulted in a delay in time from first medical contact to reperfusion of 14 min (control group 89±24 min; hypothermia group 103±21 min; p<0.01). Myocardial salvage index was 0.37 (±0.26) in the control group and 0.43 (±0.27) in the hypothermia group (p=0.27). No differences in cardiac biomarkers or clinical outcomes were found. In a CMR follow-up 6 months after the initial event no significant differences were detected.ConclusionOut-of-hospital induced therapeutic hypothermia as an adjunct to primary percutaneous coronary intervention did not improve myocardial salvage in patients with STEMI.Trial registration numberNCT01777750.

| S-EPMC6580740 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data