Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of Inflammatory Cell Subtypes in Heart Failure.

ABSTRACT: Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for heart failure with limited success. A better understanding of the temporal course of the infiltration of the different immune cells and their contribution to the inflammatory process may improve the success for therapy. This brief review outlines the major cell types involved in heart failure, and some of their actions are summarized in the supplementary figure.

SUBMITTER: Strassheim D

PROVIDER: S-EPMC6745095 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Role of Inflammatory Cell Subtypes in Heart Failure.

Strassheim Derek D Dempsey Edward C EC Gerasimovskaya Evgenia E Stenmark Kurt K Karoor Vijaya V

Journal of immunology research 20190902

Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for ...[more]

PMID: 31565659

Similar Datasets

Predicting Heart Failure With Preserved and Reduced Ejection Fraction: The International Collaboration on Heart Failure Subtypes.

Project description:BackgroundHeart failure (HF) is a prevalent and deadly disease, and preventive strategies focused on at-risk individuals are needed. Current HF prediction models have not examined HF subtypes. We sought to develop and validate risk prediction models for HF with preserved and reduced ejection fraction (HFpEF, HFrEF).Methods and resultsOf 28,820 participants from 4 community-based cohorts, 982 developed incident HFpEF and 909 HFrEF during a median follow-up of 12 years. Three cohorts were combined, and a 2:1 random split was used for derivation and internal validation, with the fourth cohort as external validation. Models accounted for multiple competing risks (death, other HF subtype, and unclassified HF). The HFpEF-specific model included age, sex, systolic blood pressure, body mass index, antihypertensive treatment, and previous myocardial infarction; it had good discrimination in derivation (c-statistic 0.80; 95% confidence interval [CI], 0.78-0.82) and validation samples (internal: 0.79; 95% CI, 0.77-0.82 and external: 0.76; 95% CI: 0.71-0.80). The HFrEF-specific model additionally included smoking, left ventricular hypertrophy, left bundle branch block, and diabetes mellitus; it had good discrimination in derivation (c-statistic 0.82; 95% CI, 0.80-0.84) and validation samples (internal: 0.80; 95% CI, 0.78-0.83 and external: 0.76; 95% CI, 0.71-0.80). Age was more strongly associated with HFpEF, and male sex, left ventricular hypertrophy, bundle branch block, previous myocardial infarction, and smoking with HFrEF (P value for each comparison ≤0.02).ConclusionsWe describe and validate risk prediction models for HF subtypes and show good discrimination in a large sample. Some risk factors differed between HFpEF and HFrEF, supporting the notion of pathogenetic differences among HF subtypes.

| S-EPMC4902276 | biostudies-literature

Mendelian Randomization Study of Heart Failure and Stroke Subtypes.

Project description:BackgroundWhether heart failure (HF) is an independent risk factor of ischemic stroke (IS) and hemorrhagic stroke remains controversial. We employed a multivariable Mendelian randomization (MR) to further investigate the causal effects of HF on the risk of stroke and stroke subtypes.MethodsGenetically predicted HF was selected as an instrumental variable (IV) from published genome-wide association studies (GWAS) meta-analyses. Stroke data with different etiologies were extracted as outcome variables from another two GWAS meta-analyses. The random-effects inverse variance-weighted (IVW) model was applied as the main method, along with sensitivity analysis. Atrial fibrillation (AF), coronary heart disease (CHD), and systolic blood pressure (SBP) were controlled for mediating effects in multivariable MR.ResultsGenetically predicted HF was significantly associated with any IS [odds ratio (OR), 1.39; 95% CI, 1.12-1.74; p = 0.03], large artery stroke (LAS; OR, 1.84; 95% CI, 1.27-2.65; p = 0.001), and cardioembolic stroke (CES; OR, 1.73; 95% CI, 1.21-2.47; p = 0.003), but without small vessel stroke (SVS; OR, 1.1; 95% CI, 0.80-1.52; p = 0.56) and intracerebral hemorrhage (ICH; OR, 0.86; 95% CI, 0.41-1.83; p = 0.699) in univariable MR. However, these significant associations were attenuated to the null after adjusting for confounding factor in multivariable MR.ConclusionThere was no direct causal association between HF and stroke in our study. The association between HF and IS can be driven by AF, CHD, and SBP.

| S-EPMC9021833 | biostudies-literature

Inflammatory markers and incident heart failure in older men: the role of NT-proBNP.

Project description:Aim: To determine the relationship between baseline inflammation (CRP and IL-6) with natriuretic peptide (NP) activity (measured by NT-proBNP) and incident heart failure (HF) in older men. Methods & results: In the British Regional Heart Study, 3569 men without prevalent myocardial infarction or HF were followed for mean 16.3 years; 327 developed HF. Baseline CRP and IL-6 were significantly and positively associated with NT-proBNP. Those in the highest CRP and IL-6 quartiles had an elevated risk of HF after age and BMI adjustment (HR = 1.42 [1.01-1.98] and 1.71 [1.24-2.37], respectively), which markedly attenuated after NT-proBNP adjustment (HR = 1.15 [0.81-1.63] and 1.25 [0.89-1.75], respectively). Conclusion: NP activity is associated with pro-inflammatory biomarkers and may explain the link between inflammation and incident HF.

| S-EPMC8559131 | biostudies-literature

Age-Dependent Relationship of Hypertension Subtypes With Incident Heart Failure.

Project description:Background The prevalence of hypertension subtypes changes with age. However, little is known regarding the age-dependent association of hypertension subtypes with incident heart failure (HF). Methods and Results We conducted an observational cohort study including 2 612 570 people (mean age, 44.0 years; 55.0% men). No participants were taking blood pressure-lowering medications or had a known history of cardiovascular disease. Participants were categorized as aged 20 to 49 years (n=1 825 756), 50 to 59 years (n=571 574), or 60 to 75 years (n=215 240). We defined stage 1 hypertension as systolic blood pressure (SBP) 130 to 139 mm Hg or diastolic blood pressure (DBP) 80 to 89 mm Hg and stage 2 hypertension as SBP ≥140 mm Hg or DBP ≥90 mm Hg. Among participants with stage 2 hypertension, isolated diastolic hypertension was defined as SBP <140 mm Hg and DBP ≥90 mm Hg, isolated systolic hypertension as SBP ≥140 mm Hg and DBP <90 mm Hg, and systolic diastolic hypertension as SBP ≥140 mm Hg and DBP ≥90 mm Hg. During a mean follow-up of 1205±934 days, 43 415 HF, 4807 myocardial infarction, 45 365 angina pectoris, 22 179 stroke, and 10 420 atrial fibrillation events occurred. Although the incidence of HF and other cardiovascular disease events increased with age, hazard ratios and relative risk reductions of each hypertension subtype for HF decreased with age. An age-dependent relationship between hypertension subtypes and incident HF was similarly observed in both men and women. Conclusions The contribution of isolated diastolic hypertension, isolated systolic hypertension, and systolic diastolic hypertension to the development of HF and other cardiovascular disease events was attenuated with age, suggesting that preventive efforts for blood pressure control could provide a greater benefit in younger individuals.

| S-EPMC9238621 | biostudies-literature

Skeletal Muscle Mass and Mortality in Heart Failure: Mediation Role of Systemic Immune-Inflammatory Index.

Project description:BackgroundHeart failure (HF)-related skeletal muscle wasting inversely affects the prognosis of HF, in which systemic inflammation may be involved. The relationships among skeletal muscle mass (SMM), systemic inflammation, and cardiovascular outcomes have not been clarified.ObjectivesThis study evaluated the associations of SMM with cardiovascular outcomes, systemic immune-inflammatory index (SII) with cardiovascular outcomes, and the mediation role of SII in the relationship between SMM and outcomes.MethodsWe included inpatients from the RED-CARPET trial (Real-world Data of Cardiometabolic ProtEcTion trial) with a definitive diagnosis of HF. We explored the associations of SMM with prognosis and SII with prognosis stratified by sex. Mediation analysis was applied for the role of SII in the association of SMM and the prognosis.ResultsWith a median follow-up of 4.9 years, 1402 patients with HF had 208 all-cause deaths and 106 cardiovascular deaths. Each 1-SD decrement in SMM was significantly associated with an increased risk of all-cause death (HR: 2.17; 95% CI: 1.20-3.91; P = 0.01 in males and HR: 2.90; 95% CI: 1.27-6.67; P = 0.012 in females). For cardiovascular death, the HR was 3.61 (95% CI: 1.56-8.40; P = 0.003) in males and 6.67 (95% CI: [2.33, 18.9]; P < 0.001) in females. Higher SII was associated with adverse outcomes. In the mediation analyses, SII was partially mediated in the relationship between SMM and cardiovascular death (7.1% [proportion-mediated 95% CI: 0.5%-26%]; P = 0.036 for males, and 5.4% [proportion mediated 95% CI: 0%-18.8%]; P = 0.064 for females).ConclusionsBoth low SMM and increased SII were significantly associated with unfavorable outcomes in HF. SII was partially mediated in the relationship between low SMM and cardiovascular death in HF.

| S-EPMC11877227 | biostudies-literature

Cigarette Smoking, Smoking Cessation, and Heart Failure Subtypes: Insights From the Jackson Heart Study.

Project description:BackgroundCigarette smoking has been associated with incident heart failure (HF). However, the association between cigarette smoking and smoking cessation with HF subtypes has not been well elucidated, particularly among Black people.Methods and resultsWe investigated 4189 (never smoker n=2934, former smoker n=761, current smoker n=464) Black participants (mean age 54 years, 64% women) without a history of HF or coronary heart disease at baseline in the Jackson Heart Study. We examined the association of cigarette smoking with incident HF hospitalization and HF subtypes (HF with preserved ejection fraction and HF with reduced ejection fraction). After adjustment for confounding factors, current smoking was associated with incident HF (both subtypes) compared with never smoking. Smoking intensity among those who identified as currently smoking and smoking burden among those who ever smoked were associated with higher incidence of HF with preserved ejection fraction compared with never smoking. Lung function evaluated by spirometry at baseline did not significantly influence these associations. The risk of developing HF decreased with more years after smoking cessation, and more than 20 years of smoking cessation were required to reach a risk comparable to that of never smoking.ConclusionsSmoking cigarettes was associated with developing both subtypes of HF and it was independent from the influences on baseline lung function. Long-term smoking cessation is necessary to prevent the onset of HF in people who smoke cigarettes.

| S-EPMC11681560 | biostudies-literature

Preventing Heart Failure in Inflammatory and Immune Disorders.

Project description:Patients with chronic inflammatory diseases are at increased risk for heart failure due to ischemic heart disease and other causes including heart failure with preserved ejection fraction. Using rheumatoid arthritis and treated HIV infection as two prototypical examples, we review the epidemiology and potential therapies to prevent heart failure in these populations. Particular focus is given to anti-inflammatory therapies including statins and biologic disease modifying drugs. There is also limited evidence for lifestyle changes and blockade of the renin-angiotensin-aldosterone system. We conclude by proposing how a strategy for heart failure prevention, such as the model tested in the Screening To Prevent Heart Failure (STOP-HF) trial, may be adapted to chronic inflammatory disease.

| S-EPMC4548924 | biostudies-literature

Role of Endothelial and Mesenchymal Cell Transitions in Heart Failure and Recovery Thereafter.

Project description:Background: Mechanisms of myocardial recovery are not well elucidated. Methods: 3-month-old C57/BL6 mice were treated with Angiotensin-II infusion and N (w)-nitro-L-arginine methyl ester in drinking water to induce HF at 5 weeks. These agents were discontinued, and animals studied with echocardiographic, histological and genetic assessment every 2 weeks until week 19. mRNA was extracted from these samples and human pre-post LVAD samples. Results: Histologic and echo characteristics showed progressive worsening of cardiac function by week 5 and normalization by week 19 accompanied by normalization of the transcriptional profile. Expression of 1,350 genes were upregulated and 3,050 genes down regulated in HF compared to controls; during recovery, this altered gene expression was largely reversed. We focused on genes whose expression was altered during HF but reverted to control levels by Week 19. A gene ontology (GO) analysis of this cohort of genes implicated pathways involved in EndoMT and MEndoT. The cohort of genes that were differentially regulated in heart failure recovery in the murine model, were similarly regulated in human myocardial samples obtained pre- and post-placement of a left ventricular assist device (LVAD). Human end stage HF myocardial samples showed cells with dual expressed VE-Cadherin and FSP-1 consistent with cell fate transition. Furthermore, we observed a reduction in fibrosis, and an increase in endothelial cell density, in myocardial samples pre- and post-LVAD. Conclusions: Cell fate transitions between endothelial and mesenchymal types contribute to the pathophysiology of heart failure followed by recovery.

| S-EPMC7874124 | biostudies-literature

The Role of Wearables in Heart Failure.

Project description:Purpose of reviewThis review discusses how wearable devices-sensors externally applied to the body to measure a physiological signal-can be used in heart failure (HF) care.Recent findingsMost wearables are marketed to consumers and can measure movement, heart rate, and blood pressure; detect and monitor arrhythmia; and support exercise training and rehabilitation. Wearable devices targeted at healthcare professionals include ECG patch recorders and vests, patches, and textiles with in-built sensors for improved prognostication and the early detection of acute decompensation. Integrating data from wearables into clinical decision-making has been slow due to clinical inertia and concerns regarding data security and validity, lack of evidence of meaningful impact, interoperability, regulatory and reimbursement issues, and legal liability. Although few studies have assessed how best to integrate wearable technologies into clinical practice, their use is rapidly expanding and may support improved decision-making by patients and healthcare professionals along the whole patient pathway.

| S-EPMC7343723 | biostudies-literature

Role of Exosomal miRNAs in Heart Failure.

Project description:Heart failure is the terminal outcome of the majority of cardiovascular diseases, which lacks specific diagnostic biomarkers and therapeutic targets. It contributes to most of cardiovascular hospitalizations and death despite of the current therapy. Therefore, it is important to explore potential molecules improving the diagnosis and treatment of heart failure. MicroRNAs (miRNAs) are small non-coding RNAs that have been reported to be involved in regulating processes of heart failure. After the discovery of miRNAs in exosomes, the subcellular distribution analysis of miRNAs is raising researchers' attention. Growing evidence demonstrates that exosomal miRNAs may be promising diagnostic and therapeutic molecules for heart failure. This review summarizes the role of exosomal miRNAs in heart failure in the prospect of molecular and clinical researches.

| S-EPMC7773699 | 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