Plasma Exosome Profile in ST-Elevation Myocardial Infarction Patients with and without Out-of-Hospital Cardiac Arrest.
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ABSTRACT:
SUBMITTER: Zara M
PROVIDER: S-EPMC8347807 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundCirculating microRNAs (miRNAs) have been found to have different expressions in different phases of acute myocardial infarction. The profiles of plasma exosome miRNAs in patients with ST-segment elevation myocardial infarction (STEMI) at 3-6 months postinfarction are unknown.ObjectiveThe aim of this study was to assess the profiles of plasma exosome miRNAs in patients with STEMI in comparison with healthy volunteers and to select specific exosome miRNAs related to pathophysiological changes post-STEMI.MethodsPlasma and echocardiography parameters were collected from 30 patients 3-6 months after STEMI and 30 healthy volunteers. Plasma exosome miRNAs were assessed by using high-throughput sequence (Illumina HiSeq 2500) and profile of the plasma exosome miRNAs was established in 10 patients and 6 healthy volunteers. The specific exosome miRNAs related to heart diseases were selected according to the TargetScan database. The specificity of the selected exosome miRNAs was evaluated in additional 20 post-STEMI patients and 24 healthy volunteers by using quantitative PCR (qPCR). Left ventricular remodeling (LVR) was defined using the European Association of Cardiovascular Imaging criteria according to echocardiography examination. Correlations between expression of the specific miRNAs and echocardiography parameters of LVR were assessed using the Spearman correlation analysis.ResultsTwenty eight upregulated miRNAs and 49 downregulated miRNAs were found in patients 3-6 months after STEMI (p < 0.01) in comparison with the healthy volunteers. The two least expressed and heart-related exosome miRNAs were hsa-miR-181a-3p (0.64-fold, p < 0.01) and hsa-miR-874-3p (0.50-fold, p < 0.01), which were further confirmed by using qPCR and demonstrated significant specificity in another 20 patients with post-STEMI comparing to 24 healthy volunteers [area under the curve (AUC) = 0.68, p < 0.05; AUC = 0.74, p < 0.05]. The expression of hsa-miR-181a-3p was downregulated in patients with LV adverse remodeling in comparison with patients without LV adverse remodeling and healthy volunteers.ConclusionCirculating exosome miR-874-3p and miR-181a-3p were downregulated in patients with STEMI postinfarction. Exosome hsa-miR-181a-3p might play a potential role in the development of LVR in patients with post-STEMI.
| S-EPMC9240753 | biostudies-literature
Project description:BackgroundPatients with ST-elevation myocardial infarction (STEMI) complicated by an out-of-hospital-cardiac-arrest (OHCA) may vary widely in their probability of dying. Large variation in mortality may have implications for current national efforts to benchmark operator and hospital mortality rates for coronary angiography. We aimed to build a risk-adjustment model of in-hospital mortality among OHCA survivors with concurrent STEMI.MethodsWithin the Cardiac Arrest Registry to Enhance Survival (CARES), we included adults with OHCA and STEMI who underwent emergent angiography within 2 hours of hospital arrival between January 2013 and December 2019. Using multivariable logistic regression to adjust for patient and cardiac arrest factors, we developed a risk-adjustment model for in-hospital mortality and examined variation in patients' predicted mortality.ResultsOf 2,999 patients (mean age 61.2 ± 12.0, 23.1% female, 64.6% white), 996 (33.2%) died during their hospitalization. The final risk-adjustment model included higher age (OR per 10-year increase, 1.50 [95% CI: 1.39-1.63]), unwitnessed OHCA (OR, 2.51 [1.99-3.16]), initial non-shockable rhythm [OR, 5.66 [4.52-7.13]), lack of sustained pulse for > 20 minutes (OR, 2.52 [1.88-3.36]), and longer resuscitation time (increased with each 10-minute interval) (c-statistic = 0.804 with excellent calibration). There was large variability in predicted mortality: median, 25.2%, inter-quartile-range: 14.0% to 47.8%, 10th-90th percentile: 8.2 % to 74.1%.ConclusionsIn a large national registry, we identified 5 key predictors for mortality in patients with STEMI and OHCA and found wide variability in mortality risk. Our findings suggest that current national benchmarking efforts for coronary angiography, which simply adjusts for the presence of OHCA, may not adequately capture patient case-mix severity.
| S-EPMC8840945 | biostudies-literature
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: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
Project description:Whether ST-segment (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) should be regarded as distinct pathophysiological entities is a matter of debate. We tested the hypothesis that peripheral blood gene-expression profiles at presentation distinguish STEMI from NSTEMI. We performed a case-control study collecting whole-blood from 60 STEMI and 58 NSTEMI (defined according to the third universal definition of MI) consecutive patients on hospital admission. We used RNA-sequencing for the discovery phase, comparing 15 STEMI vs. 15 NSTEMI patients, matched for age, sex, and cardiovascular risk factors, and quantitative PCR in the remaining unmatched patients for validating top-significant genes. Gene-level differential expression analysis identified significant differences in the expression of 323 genes: 153 genes withstood correction for admission cardiac troponin I (cTnI), differentiating the two conditions independently of myocardial necrosis extent. Functional annotation analysis uncovered divergent modulation in leukocyte and platelet activation, cell migration, and mitochondrial respiratory processes. Linear regression analysis revealed gene expression patterns on admission predicting infarct size, as indexed by cTnI peak (R2 = 0.58-0.75). Our results unveil distinctive pathological traits for these two MI subtypes and provide insights into the early assessment of injury extent. This could translate into RNA-based disease-specific biomarkers for precision diagnosis and risk stratification.
| S-EPMC7250845 | biostudies-literature
Project description:BackgroundIn-hospital left ventricular (LV) thrombus following acute ST-elevation myocardial infarction (STEMI) has not been evaluated on a national scale and was the focus of this investigation.MethodsWe used the 2003 to 2013 Nationwide Inpatient Sample database to identify adults ?18?years old with a principal diagnosis code of ST-elevation myocardial infarction. Patients were divided into two groups defined by the presence or absence of LV thrombus. Clinical characteristics and in-hospital outcomes were studied using relevant statistics. Multiple linear and logistic regression models were conducted to identify factors associated with LV thrombus.ResultsOf 1,035,888 STEMI patients hospitalized in the U. S from 2003 to 2013, 1982 (0.2%) developed acute in-hospital LV thrombus. Compared to no LV thrombus, patients with LV thrombus were more likely to have in-hospital complications; acute ischemic and hemorrhagic stroke, acute renal failure, gastrointestinal bleed, cardiogenic shock, in-hospital cardiac arrest and mortality. They also had longer mean length of stay and higher hospital charges. Factors associated with LV thrombus included: anterior/anterolateral STEMI, acute or chronic heart failure with reduced ejection fraction, atrial fibrillation, LV aneurysm, Left heart valvular disease, acute or chronic deep venous thrombosis/pulmonary embolism and alcohol abuse. Patients with LV thrombus were less likely to be female [AOR 0.66, 95% CI (0.51-0.84)].ConclusionThe identification of factors associated with early development of LV thrombus following STEMI, will help direct resources for specific high-risk group and prompt cost-effective therapies. Gender variability in LV thrombus development warrants further investigations.
| S-EPMC6891157 | biostudies-literature
Project description:BackgroundIn-hospital ischemic stroke following acute ST-elevation myocardial infarction (STEMI) has not been evaluated on a national scale in the United States.MethodsWe used 2003 to 2014 Nationwide Inpatient Sample data to identify adults with a principal diagnosis of STEMI. Patients were divided into two groups defined by presence or absence of ischemic stroke. Clinical characteristics and in-hospital outcomes were studied using relevant statistics. Multiple linear and logistic regression models identified factors associated with ischemic stroke, national trend of in-hospital stroke incidence and in-hospital mortality.ResultsOf 1,842,529 STEMI patients hospitalized from 2003 to 2014, 22,268 (1.2%) developed acute in-hospital ischemic stroke. Those with acute strokes were older (age ≥ 65 years: 70% vs 46%), more likely female (51% vs 33%), and had higher rates of atrial fibrillation (28.9% vs 12.2%) and heart failure (40.5% vs 21.1%). Age and gender adjusted incidence of in-hospital ischemic stroke following STEMI remained stable; 1.4% in 2003 and 1.5% in 2014 (P trend = 0.50). However, age and gender adjusted in-hospital mortality declined in STEMI patients with and without in-hospital ischemic stroke [AOR 0.97 (0.95-0.99) P trend = 0.03, and AOR 0.98 (0.98-0.99) P trend < 0.001, respectively]. Patients with ischemic strokes had higher in-hospital mortality (25.7% Vs 7.2%, p < 0.001), [AOR 2.11, 95% CI (1.92-2.32)].ConclusionIn the United States, the incidence of acute in-hospital stroke remained stable from 2003 to 2014 following STEMI with significant decrease of in-hospital mortality trends. Despite slight improvement in mortality trends, in-hospital mortality rates remained elevated calling for interventions to optimize health care delivery.
| S-EPMC7736913 | biostudies-literature
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:BackgroundWhether sex differences exist in the inflammatory response after ST-elevation myocardial infarction (STEMI) remains to be elucidated. We studied leukocyte profiles and their prognostic value in men and women presenting with STEMI.MethodsFrom a total of 552 consecutive STEMI patients, blood samples were collected at hospital admission. Linear regression was used to assess the relationship between leukocyte profiles and enzymatic infarct size. Cox regression was used to assess the association between leukocyte profiles and one-year mortality.ResultsWomen presented with higher lymphocyte counts (2.3·109 cells/L (IQR 1.6-3.1) vs. 1.8·109 cells/L (IQR 1.4-2.5), p = 3.00 ∙ 10-4) and percentages (21.1% (IQR 14.4-28.1) vs. 17.1% (IQR 12.3-24.3), p = 0.004). Lymphocyte to monocyte ratio (LMR) was also higher in women (3.25 (IQR 2.56-4.5) vs. 2.68 (IQR 2.08-3.59), p = 7.28 ∙ 10-7). Higher LMR was associated with lower peak CK-MB (β = -0.27 (95% CI: -0.50, -0.03), p = 0.026), lower peak troponin T (β = -0.45 (95% CI: -0.77, -0.13), p = 0.006) and lower one-year mortality risk (HR 0.35 (95% CI: 0.13, 0.96), p = 0.042).ConclusionAt admission for STEMI, women present with higher lymphocyte count and LMR. Higher LMR is associated with smaller infarct size and decreased one-year mortality risk and could be used as a biomarker to predict outcome.
| S-EPMC7176674 | 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