Browse
Submit Data
Databases
API
Help

Dataset Information

26 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Early Changes in Circulating Interleukins and Residual Inflammatory Risk After Acute Myocardial Infarction.

ABSTRACT:

Background

Patients with acute myocardial infarction may have a large infarcted area and ventricular dysfunction despite early thrombolysis and revascularization.

Objective

To investigate the behavior of circulating cytokines in patients with ST-segment elevation myocardial infarction (STEMI) and their relationship with ventricular function.

Methods

In the BATTLE-AMI (B and T Types of Lymphocytes Evaluation in Acute Myocardial Infarction) trial, patients with STEMI were treated with a pharmacoinvasive strategy. The plasma levels of cytokines (IL-1 β , IL-4, IL-6, IL-10, and IL-18) were tested using enzyme-linked immunosorbent assay (ELISA) at baseline and after 30 days. Infarcted mass and left ventricular ejection fraction (LVEF) were examined by 3-T cardiac magnetic resonance imaging. All p-values < 0.05 were considered statistically significant.

Results

Compared to baseline, lower levels were detected for IL-1 β (p = 0.028) and IL-18 (p < 0.0001) 30 days after STEMI, whereas higher levels were observed for IL-4 (p = 0.001) and IL-10 (p < 0.0001) at that time point. Conversely, no changes were detected for IL-6 levels (p = 0.63). The levels of high-sensitivity C-reactive protein and IL-6 correlated at baseline (rho = 0.45, p < 0.0001) and 30 days after STEMI (rho = 0.29, p = 0.009). At baseline, correlation between IL-6 levels and LVEF was also observed (rho = -0.50, p = 0.004).

Conclusions

During the first month post-MI, we observed a marked improvement in the balance of pro- and anti-inflammatory cytokines, except for IL-6. These findings suggest residual inflammatory risk. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0).

SUBMITTER: Coste MER

PROVIDER: S-EPMC8133737 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Association of Circulating, Inflammatory-Response Exosomal mRNAs With Acute Myocardial Infarction.

Project description:Background: Although many cardiovascular disease studies have focused on the microRNAs of circulating exosomes, the profile and the potential clinical diagnostic value of plasma exosomal long RNAs (exoLRs) are unknown for acute myocardial infarction (AMI). Methods: In this study, the exoLR profile of 10 AMI patients, eight stable coronary artery disease (CAD) patients, and 10 healthy individuals was assessed by RNA sequencing. Bioinformatic approaches were used to investigate the characteristics and potential clinical value of exoLRs. Results: Exosomal mRNAs comprised the majority of total exoLRs. Immune cell types analyzed by CIBERSORT showed that neutrophils and monocytes were significantly enriched in AMI patients, consistent with clinical baseline values. Biological process enrichment analysis and co-expression network analysis demonstrated neutrophil activation processes to be enriched in AMI patients. Furthermore, two exosomal mRNAs, ALPL and CXCR2, were identified as AMI biomarkers that may be useful for evaluation of the acute inflammatory response mediated by neutrophils. Conclusions: ExoLRs were assessed in AMI patients and found to be associated with the acute inflammatory response mediated by neutrophils. Exosomal mRNAs, ALPL and CXCR2, were identified as potentially useful biomarkers for the study of AMI.

| S-EPMC8418229 | biostudies-literature

A circulating miRNA signature for early diagnosis of acute kidney injury following acute myocardial infarction.

Project description:BackgroundAcute kidney injury (AKI) is a common complication of acute myocardial infarction (AMI), and is associated with adverse outcomes. The study aimed to identify a miRNA signature for the early diagnosis of post-AMI AKI.MethodsA total of 108 patients admitted to a coronary care unit (CCU) were divided into four subgroups: AMI-AKI-, AMI+AKI-, AMI+AKI+, and AMI-AKI+. Thirty-six miRNA candidates were selected based on an extensive literature review. Real-time quantitative RT-PCR analysis was used to determine the expression levels of these miRNAs in the serum collected on the day of CCU admittance. TargetScan 7.1 and miRDB databases were used for target prediction and Metacore 6.13 was used for pathway analysis.ResultsThrough a stepwise selection based on abundance, hemolytic effect and differential expression between four groups, 9 miRNAs were found to have significantly differential expression levels as potential biomarkers for post-AMI AKI specifically. Noticeably, the expression levels of miR-24, miR-23a and miR-145 were significantly down-regulated in AMI+AKI+ patients compared to those in AMI+AKI- patients. Combination of the three miRNAs as a panel showed the best performance in the early detection of AKI following AMI (AUC = 0.853, sensitivity 95.65%), compared to the analysis of serum neutrophil gelatinase-associated lipocalin (AUC = 0.735, sensitivity 63.16%). Furthermore, bioinformatic analysis indicated that these three miRNAs regulate the transforming growth factor beta signaling pathway and involve in apoptosis and fibrosis in AKI.ConclusionsFor the first time, this study identify a unique circulating miRNA signature (miR-24-3p, miR-23a-3p, miR-145-5p) that can potentially early detect AKI following AMI and may be involved in renal injury and fibrosis in post-AMI AKI pathogenesis.

| S-EPMC6492315 | biostudies-literature

Peripheral Inflammatory Factors and Acute Myocardial Infarction Risk: A Mendelian Randomization Study.

Project description:BackgroundPrevious observational studies have confirmed the relationship between inflammation and acute myocardial infarction (AMI), but genetic evidence is still lacking. The aim of this study was to explore the bidirectional association of multiple peripheral inflammatory factors with this disease at the genetic level.MethodsSummary data for AMI and several peripheral inflammatory factors (such as interleukin-10 and interleukin-18) were collected from published genome-wide correlation studies. Based on the correlation, independence, and exclusivity assumptions, a total of 9 to 110 instrumental variables were selected from these summary data to predict the above traits. Two-sample Mendelian randomization methods, including inverse-variance weighted (IVW), were used to make causal inferences between exposures and outcomes. Sensitivity analyses including Cochran's Q, MR-Egger intercept, leave-one-out, forest plot, and MR-PRESSO were adopted to assess heterogeneity and horizontal pleiotropy.ResultsThe IVW reported that elevated peripheral levels of interleukin-10 and interleukin-18 were nominally associated with a reduced risk of AMI (OR = 0.876, 95% CI = 0.788 ~ 0.974, P = 0.015; OR = 0.934, 95% CI = 0.875 ~ 0.997, P = 0.040). The IVW also reported that the risk of AMI nominally increased the peripheral level of interleukin-10 (OR = 1.062, 95% CI = 1.003 ~ 1.124, P = 0.040). No significant heterogeneity or horizontal pleiotropy were found by sensitivity analyses.ConclusionBoth interleukin-10 and interleukin-18 were peripheral inflammatory factors genetically associated with AMI. In particular, combined with previous knowledge, interleukin-10 may have a protective effect on the onset, progression, and prognosis of the disease.

| S-EPMC10558024 | biostudies-literature

Characteristics and Outcomes of Early Recurrent Myocardial Infarction After Acute Myocardial Infarction.

Project description:Background We aimed to understand the characteristics and outcomes of patients readmitted with a recurrent myocardial infarction (RMI) within 90 days of discharge after an acute myocardial infarction (early RMI). Methods and Results We analyzed the timing of reinfarction, etiology, and outcome for all patients admitted with an early RMI within 90 days of discharge after an acute myocardial infarction between January 1, 2010 and January 1, 2017. We identified 6626 admissions for acute myocardial infarction (index myocardial infarction) which led to 168 cases of RMI within 90 days of discharge. The mean patient age was 65.1±13.1 years, and 37% were women. The 90-day probability of readmission with an early RMI was 2.5%. Black race, medical management, higher troponin T, and shorter length of stay were independent predictors of early RMI. Medically managed group had a higher risk for early RMI compared with percutaneous coronary intervention (P=0.04) or coronary artery bypass grafting (P=0.2). Predominant mechanisms for reinfarction were stent thrombosis (17%), disease progression (12%), and unchanged coronary artery disease (11%). At 5 years, the all-cause mortality rate for patients with an early RMI was 49% (95% CI, 40%-57%) compared with 22% (95% CI, 21%-23%) for patients without an early RMI (P<0.0001). Conclusions Early RMI is a life-threatening condition with nearly 50% mortality within 5 years. Stent-related events and progression in coronary artery disease account for most early RMI. Medication compliance, aggressive risk factor management, and care transitions should be the cornerstone in preventing early RMI.

| S-EPMC8475017 | biostudies-literature

Reciprocal Changes of Circulating Long Non-Coding RNAs ZFAS1 and CDR1AS Predict Acute Myocardial Infarction.

Project description:This study sought to evaluate the potential of circulating long non-coding RNAs (lncRNAs) as biomarkers for acute myocardial infarction (AMI). We measured the circulating levels of 15 individual lncRNAs, known to be relevant to cardiovascular disease, using the whole blood samples collected from 103 AMI patients, 149 non-AMI subjects, and 95 healthy volunteers. We found that only two of them, Zinc finger antisense 1 (ZFAS1) and Cdr1 antisense (CDR1AS), showed significant differential expression between AMI patients and control subjects. Circulating level of ZFAS1 was significantly lower in AMI (0.74 ± 0.07) than in non-AMI subjects (1.0 ± 0.05, P < 0.0001), whereas CDR1AS showed the opposite changes with its blood level markedly higher in AMI (2.18 ± 0.24) than in non-AMI subjects (1.0 ± 0.05, P < 0.0001). When comparison was made between AMI and non-AMI, the area under ROC curve was 0.664 for ZFAS1 alone or 0.671 for CDR1AS alone, and 0.691 for ZFAS1 and CDR1AS combination. Univariate and multivariate analyses identified these two lncRNAs as independent predictors for AMI. Similar changes of circulating ZFAS1 and CDR1AS were consistently observed in an AMI mouse model. Reciprocal changes of circulating ZFAS1 and CDR1AS independently predict AMI and may be considered novel biomarkers of AMI.

| S-EPMC4772828 | biostudies-literature

Characterization of circulating endothelial cells in acute myocardial infarction.

Project description:Acute myocardial infarction (MI), which involves the rupture of existing atheromatous plaque, remains highly unpredictable despite recent advances in the diagnosis and treatment of coronary artery disease. Accordingly, a clinical measurement that can predict an impending MI is desperately needed. Here, we characterize circulating endothelial cells (CECs) using an automated and clinically feasible CEC three-channel fluorescence microscopy assay in 50 consecutive patients with ST-segment elevation MI and 44 consecutive healthy controls. CEC counts were significantly elevated in MI cases versus controls, with median numbers of 19 and 4 cells/ml, respectively (P = 1.1 × 10(-10)). A receiver-operating characteristic (ROC) curve analysis demonstrated an area under the ROC curve of 0.95, suggesting near-dichotomization of MI cases versus controls. We observed no correlation between CECs and typical markers of myocardial necrosis (? = 0.02, creatine kinase-myocardial band; ? = -0.03, troponin). Morphological analysis of the microscopy images of CECs revealed a 2.5-fold increase (P < 0.0001) in cellular area and a twofold increase (P < 0.0001) in nuclear area of MI CECs versus healthy controls, age-matched CECs, as well as CECs obtained from patients with preexisting peripheral vascular disease. The distribution of CEC images that contained from 2 to 10 nuclei demonstrates that MI patients were the only subject group to contain more than 3 nuclei per image, indicating that multicellular and multinuclear clusters are specific for acute MI. These data indicate that CEC counts may serve as a promising clinical measure for the prediction of atherosclerotic plaque rupture events.

| S-EPMC3589570 | biostudies-literature

Increased Risk of Acute Myocardial Infarction and Heart Failure in Patients With Inflammatory Bowel Diseases.

Project description:Background & aimsThere are conflicting data as to whether inflammatory bowel diseases (IBDs) increase risk for cardiovascular disease. We sought to examine the risk of acute myocardial infarction (AMI) and heart failure in patients with IBD.MethodsWe identified patients diagnosed with IBD in Olmsted County, Minnesota, from 1980 through 2010 (n = 736). For each patient, 2 individuals without IBD (controls, n = 1472) were randomly selected, matched for age, sex, and index date of disease diagnosis. Primary outcomes were AMI and heart failure. Cox proportional hazards analysis was used to estimate the risk of AMI and heart failure.ResultsAfter adjustments for traditional cardiovascular disease risk factors, IBD associated independently with increased risk of AMI (adjusted hazard ratio [aHR], 2.82; 95% CI, 1.98-4.04) and heart failure (aHR, 2.03; 95% CI, 1.36-3.03). The relative risk of AMI was significantly increased in patients with Crohn's disease (aHR vs controls, 2.89; 95% CI, 1.65-5.13) or ulcerative colitis (aHR vs controls, 2.70; 1.69-4.35). The relative risk of AMI was increased among users of systemic corticosteroids (aHR vs controls, 5.08; 95% CI, 3.00-8.81) and nonusers (aHR vs controls, 1.79; 95% CI, 1.08-2.98). The relative risk of heart failure was significantly increased among patients with ulcerative colitis (aHR, 2.06; 95% CI, 1.18-3.65), but not Crohn's disease. The relative risk of heart failure was increased among users of systemic corticosteroids (aHR, 2.51; 95% CI, 1.93-4.57), but not nonusers.ConclusionsIn a population-based cohort study, we found that despite a lower prevalence of traditional risk factors for AMI and heart failure, patients with IBD are at increased risk for these cardiovascular disorders.

| S-EPMC6152828 | biostudies-literature

F13A1 Gene Variant (V34L) and Residual Circulating FXIIIA Levels Predict Short- and Long-Term Mortality in Acute Myocardial Infarction after Coronary Angioplasty.

Project description:Factor XIIIA (FXIIIA) levels are independent predictors of early prognosis after acute myocardial infarction (AMI) and the Valine-to-Leucine (V34L) single nucleotide polymorphism (SNP) seems associated with lower AMI risk. Since the long-term AMI prognosis merits deeper investigation, we performed an observational study evaluating relationships between FXIIIA residual levels, cardiovascular risk-factors, and inherited genetic predispositions. FXIIIA V34L was genotyped in 333 AMI patients and a five-year follow-up was performed. FXIIIA levels assessed at day-zero (d0) and four days after AMI (d4), and conventional risk factors were analyzed, focusing on the development of major adverse cardiovascular events (MACE). FXIIIA assessed at d0 and d4 was also an independent MACE predictor in the long-term follow-up (FXIIIAd0, Odds Ratio (OR) = 3.02, 1.79⁻5.1, p = 0.013; FXIIIAd4, OR = 4.46, 2.33⁻8.55, p = 0.0001). FXIIIAd4 showed the strongest MACE association, suggesting that the FXIIIA protective role is maximized when high levels are maintained for longer time. Conversely, FXIIIA levels stratified by V34L predicted MACE at a lesser extent among L34-carriers (Hazard Risk (HR)VV34 = 3.89, 2.19⁻6.87, p = 0.000003; HRL34-carriers = 2.78, 1.39⁻5.57, p = 0.0039), and V34L did not predict all MACE, only multiple-MACE occurrence (p = 0.0087). Finally, in survival analysis, heart failure and death differed significantly from stroke and recurrent ischemia (p = 0.0013), with FXIIIA levels appreciably lower in the former (p = 0.05). Overall, genetically-determined FXIIIA levels have a significant long-term prognostic role, suggesting that a pharmacogenetics approach might help to select those AMI patients at risk of poor prognosis in the need of dedicated treatments.

| S-EPMC6165350 | biostudies-literature

Culprit-Plaque Morphology and Residual SYNTAX Score Predict Cardiovascular Risk in Acute Myocardial Infarction: An Optical Coherence Tomography Study.

Project description:AimsCulprit-plaque morphology [plaque rupture (PR) and plaque erosion (PE)] and high-risk plaques (HRP) identified by optical coherence tomography (OCT) and residual SYNTAX score (rSS) have been reported to influence clinical outcomes. Thus, in this study, we aimed to investigate the prognostic implication of culprit-plaque morphology and rSS for major adverse cardiovascular events (MACE) in patients with ST-segment elevation myocardial infarction (STEMI).MethodsBased on plaque morphology and rSS, 274 STEMI patients were divided into 4 groups: PE/low-rSS (n=61), PE/high-rSS (n=58), PR/low-rSS (n=55), and PR/high-rSS (n=100). According to HRP and rSS, patients were stratified to non-HRP/low-rSS (n=97), non-HRP/high-rSS (n=109), HRP/low-rSS (n=19), and HRP/high-rSS (n=49). MACE was defined as the composite of all-cause death, recurrence of myocardial infarction, stroke, and unplanned revascularization of any coronary artery.ResultsDuring the follow-up of 2.2 years, 47 (17.2%) MACE were observed. Patients with PR/high-rSS and HRP/high-rSS presented lower survival probability on revascularization and MACE. In fully adjusted analyses, PR/high-rSS group presented higher MACE risk than PE/low-rSS (HR: 4.80, 95% CI: 1.43-16.11, P=0.025). Patients with non-HRP/high-rSS (HR: 2.90, 95% CI: 1.01-8.38, P=0.049) and HRP/high-rSS (HR: 8.67, 95% CI: 2.67-28.21, P＜0.001) presented higher risk of cardiac events than non-HRP/low-rSS. Adding rSS and HRP to the risk prediction model increased the C-statistic to 0.797 (95% CI: 0.737-0.857), with ΔC-statistic of 0.066 (P=0.002) and the NRI (46.0%, 95% CI: 20.5-56.8%, P＜0.001) and IDI (8.7%, 95% CI: 3.6-18.2%, P＜0.001).ConclusionHigh-risk plaques in combination with rSS enhanced the predictive ability for MACE, indicating culprit-plaque features and residual atherosclerosis burden should be taken into account in risk stratification of STEMI patients.

| S-EPMC9444676 | biostudies-literature

Early biventricular molecular responses to an acute myocardial infarction.

Project description:BackgroundAcute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose.ObjectivesThe aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI.Material and methodsA rat model of left anterior descending coronary artery ligation was used to assess the effect of left ventricular AMI on both the right ventricle as a remote zone and the left ventricle as an ischemic/infarct zone. Microarray technology was applied to detect the gene expression. Gene Ontology and KEGG pathways analysis were done to identify effected pathways and related genes.ResultsWe found that immune response, cell chemotaxis, inflammation, cytoskeleton organization are significantly deregulated in ischemic zone as early response within 30 min. Unexpectedly, there were several affected signaling pathways such as cell chemotaxis, regulation of endothelial cell proliferation, and regulation of caveolea regulation of anti-apoptosis, regulation of cytoskeleton organization and cell adhesion on the remote zone in the right ventricle.ConclusionThis data demonstrates that there is an immediate molecular response in both ventricles after an AMI. Although the ischemia did not histologically involve the right ventricle; there is a clear molecular response to the infarct in the left ventricle. This provides us new insights to understand molecular mechanisms behind AMI and to find more effective drug targets.

| S-EPMC3245415 | 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