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4,008 results for “heart failure”
Data inputs and results from AI-supported title and abstract screening "Lack of evidence regarding markers identifying acute heart failure in patients with COPD: an AI-supported systematic review"
<p>These comma-separated data files were used to conduct the AI supported screening of [Lack of Evidence Regarding Markers Identifying Acute Heart Failure in Patients with COPD: An AI-supported Systematic Review (working title)], following the methodology described in the publication (URL/doi to be uploaded).</p> <p>These files provide insight into the AI-supported screening process and the choices made by the human reviewer.</p>
Age-related proteostatic imbalance exacerbates heart failure with preserved ejection fraction pathogenesis in old mice
<p>Heart failure with preserved ejection fraction (HFpEF) is a leading cause of hospitalization and death in the elderly. While aging strongly increases the incidence of HFpEF, the specific influences of aging on HFpEF at molecular and pathophysiological levels remain unclear. Here, we show that aged mice, when subjected to chronic metabolic and hypertensive stress (2-hit stress), develop an aggravated cardiometabolic HFpEF phenotype compared to younger counterparts. Aged HFpEF mice also display unique pathological characteristics reminiscent of those found in HFpEF patients. We demonstrate that age-related dysfunction in protein quality control (PQC) exacerbates proteostatic stress in HFpEF. Specifically, we demonstrate that increased protein synthesis induced by 2-hit stress combines with age-related impairment in protein degradation in aged HFpEF hearts, culminating in the accumulation of protein aggregates. These findings underscore the importance of incorporating aging into preclinical HFpEF models and support the therapeutic potentials of targeting PQC mechanisms to ameliorate disease outcomes.</p> <p>The deposited data are lc-ms data acquired on the Thermo QEx-Plus system. For any questions, please contact mike kinter mike-kinter at omrf.org</p> <p>This upload contains the bulk of the LC-MS data. But, due to file sizes, and addition group of files can be found at doi 10.5281/zenodo.11094720</p>
Myocardial ultrastructure of human heart failure with preserved ejection fraction
<p>These transmission electron micrographs were obtained from endocardial biopsies of patients with heart failure and preserved ejection fraction, or from non-failling control myocardium. The myocardium is from the right side of the ventricular septum. Images are shown at various magnification levels indicated in the title of the image. Images with titles: HH_DM+ or HH_DM-; Mixed_DM+ or Mixed_DM-; OB_DM+ or OB_DM-; or NF_DM+ or NF_DM- show examples from the primary groups, HH represents HFpEF patients with primarily hypertensive hypertrophic heart disease and the least obesity; OB represents HFpEF patients with primarily severe obesity and the least hypertensive hypertrophic disease; Mixed matches obesity and hypertensive hypertrophic heart disease in HFpEF patients to levels obsserved in the HH and OB groups, and NF is non-failing controls. </p> <p>Additional images are shown for NF, HH, OB, and Mixed from the remaining patients in this study are provided at two magnification levels. These are provided as individual pictures as well. </p> <p> </p>
Heart Failure eQTLs companion to "Pathologic gene network rewiring implicates PPP1R3A as a central cardioprotective factor in pressure overload heart failure"
<p>These are the results of a QTL analysis companion to "Pathologic gene network rewiring implicates PPP1R3A as a central cardioprotective factor in pressure overload heart failure". We performed RNA expression measurements and obtained genotype information in genome-wide markers for 313 patients (177 failing hearts , 136 donor, non-failing [control] hearts) using Affymetrix expression and Affymetrix Human 6.0 respectively.<strong> </strong>Prior to eQTL discovery, we used PEER to find hidden covariates that could confound signals in our data as well as filtering any genotypes with major allele frequencies less than 5%. To test associations between gene expression in each cohort separately, we used QTLTools with an additive model accounting for gender, age, sample site, and the PEER factors as covariates. We corrected for eQTL multiple association testing using a 10000 permutations per locus in a 2 megabase window and a false discovery rate cutoff of 5%. To select the number of PEER factors, we performed the full analysis multiple times from 1 to 15 PEER factors and observed a saturation of new QTLs being discovered when using 10 factors.</p> <p>Four files are provided, two for each cohort (cases and controls):</p> <p>- peer_[cases|controls]_nominal.txt: Nominal associations with a p-value threshold of 0.001</p> <p>- peer_[cases|controls]_permutations_all.significant.txt: All significant associations detected after the QTLtools permutation test.</p> <p>The column names are those from QTLtools, in order:</p> <p><br> 1. The phenotype ID<br> 2. The chromosome ID of the phenotype<br> 3. The start position of the phenotype<br> 4. The end position of the phenotype<br> 5. The strand orientation of the phenotype<br> 6. The total number of variants tested in cis<br> 7. The distance between the phenotype and the tested variant (accounting for strand orientation)<br> 8. The ID of the tested variant ( in Affy 6.0 SNP ids)<br> 9. The chromosome ID of the variant<br> 10. The start position of the variant<br> 11. The end position of the variant<br> 12. The nominal P-value of association between the variant and the phenotype<br> 13. The corresponding regression slope<br> 14. A binary flag equal to 1 is the variant is the top variant in cis</p>
KG for heart failure gene expression data
<p>Pre processed gene expression data for different heart failure. Includes count table, gene patiens metadata, gene lenght</p>
A Novel Approach to Heart Failure Prediction and Classification through Advanced Deep Learning Model
<p>A Novel Approach to Heart Failure Prediction and Classification through Advanced Deep Learning Model</p>
A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling
<p>Collection of auxiliary data to reproduce the results from "<strong>A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling</strong>". Source code is available at: https://github.com/saezlab/reheat2_pub<br><br>We provide processed data to facilitate access to the results, for the original count data, please see the associated manuscript for references to the original datasets. </p> <p> </p> <p> </p>
Neuromodulation to Treat Patients With Heart Failure With Preserved Ejection Fraction
ClinicalTrials.gov study NCT03327649. IPD Sharing: YES. Countries: 1. Publications: 2.
A Proof of Concept and Dose-finding Study of XXB750 in Patients With Heart Failure
ClinicalTrials.gov study NCT06142383. IPD Sharing: YES. Countries: 12. Publications: 0.
Prospective ARNI vs ACE Inhibitor Trial to DetermIne Superiority in Reducing Heart Failure Events After MI
ClinicalTrials.gov study NCT02924727. IPD Sharing: YES. Countries: 41. Publications: 9.
Effect of Sotagliflozin on Cardiovascular Events in Participants With Type 2 Diabetes Post Worsening Heart Failure (SOLOIST-WHF Trial)
ClinicalTrials.gov study NCT03521934. IPD Sharing: YES. Countries: 32. Publications: 6.
Comparison of Sacubitril/Valsartan Versus Enalapril on Effect on NT-proBNP in Patients Stabilized From an Acute Heart Failure Episode.
ClinicalTrials.gov study NCT02554890. IPD Sharing: YES. Countries: 1. Publications: 8.
Efficacy and Safety of LCZ696 Compared to Valsartan, on Morbidity and Mortality in Heart Failure Patients With Preserved Ejection Fraction
ClinicalTrials.gov study NCT01920711. IPD Sharing: YES. Countries: 43. Publications: 55.
Data deposition for Complex electrophysiological remodeling in postinfarction ischemic heart failure
Open the record for dataset details and reuse information.
Online supplement for "T cell costimulation blockade blunts age-related heart failure"
<p><strong>ONLINE SUPPLEMENT FOR:</strong></p> <p><strong>Research Letter:</strong></p> <p><strong>T cell costimulation blockade blunts age-related heart failure</strong></p>
The Ubiquitin Ligase WWP1 Contributes to Shifts in Matrix Proteolytic Profiles and a Myocardial Aging Phenotype with Diastolic Heart Failure
<p><strong><em>Aims</em></strong>. Ubiquitylation is a key event that regulates protein turnover, and induction of the ubiquitin ligase E3 WWP1 has been associated with age. Left ventricular hypertrophy (LVH) commonly occurs as a function of age and can cause heart failure with a preserved ejection fraction (EF; HFpEF). We hypothesized that overexpression (O/E) of WWP1 in the heart would cause LVH as well as functional and structural changes consistent with the aging HFpEF phenotype.</p> <p><strong><em>Methods and Results.</em></strong> Global WWP1 O/E was achieved in mice (n=11) and echocardiography (40 MHz) performed to measure LV mass, EF, Doppler velocities (early-E, late/atrial-A), myocardial relaxation (E’), and isovolumetric relaxation time (IVRT) at 4, 6, and 8 weeks. Age matched wild type animals (n=15) were included as referent controls. LV EF was identical (60+1% vs 60+1%, p>0.90) with no difference in LV mass (67+3 vs 75+5, p>0.25) at 4 weeks. However, at 8 weeks of age, LV mass increased by over two-fold, E/A fell (impaired passive filling), and E/E’ was lower and IVRT prolonged (impaired LV relaxation) - all p<0.05. Collagen percent area increased by over two-fold and fibrillar collagen expression (rtPCR) by over 1.5 fold (p<0.05) with WWP1 O/E. WWP1 with an anti-WWP1 antibody could be identified in isolated cardiac fibroblasts with WWP1 increased by over two-fold in O/E fibroblasts (p<0.05).</p> <p><strong><em>Conclusion.</em></strong> Inducing WWP1 expression caused LVH, preserved systolic function, but impaired diastolic dysfunction, consistent with the HFpEF phenotype. Targeting the WWP1 pathway may be a novel therapeutic target for this intractable form of HF associated with aging.</p>
Raw Data or the article: Physiopathology and Diagnosis of Congestive Heart Failure: Consolidated Certainties and New Perspectives
<p>Volume overload and fluid congestion are a fundamental issue in the assessment and management of patients with heart failure (HF). Recent studies have found that in acute decompensated heart failure (ADHF), right and left-sided pressures generally start to increase before any notable weight changes take place preceding an admission. ADHF may be a problem of volume redistribution among different vascular compartments instead of, or in addition to, fluid shift from the interstitial compartment. Thus, identifying heterogeneity of volume overload would allow guidance of tailored therapy. A comprehensive evaluation of congestive HF needs to take into account myriad parameters, including physical examination, echocardiographic values, and biomarker serum changes. Furthermore, potentially useful diagnostic tools include bioimpedance to measure intercompartmental fluid shifts, and evaluation of ultrasound lung comets to detect extravascular lung water.</p>
Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure
<p>Genome-wide association study summary statistics.</p>
The Ubiquitin Ligase WWP1 Contributes to Shifts in Matrix Proteolytic Profiles and a Myocardial Ageing Phenotype with Diastolic Heart Failure
<p><strong><em>Aims</em></strong>. Ubiquitylation is a key event that regulates protein turnover, and induction of the ubiquitin ligase E3 WWP1 has been associated with age. Left ventricular hypertrophy (LVH) commonly occurs as a function of age and can cause heart failure with a preserved ejection fraction (EF; HFpEF). We hypothesized that overexpression (O/E) of WWP1 in the heart would cause LVH as well as functional and structural changes consistent with the ageing HFpEF phenotype.</p> <p><strong><em>Methods and Results.</em></strong> Global WWP1 O/E was achieved in mice (n=11) and echocardiography (40 MHz) performed to measure LV mass, EF, Doppler velocities (early-E, late/atrial-A), myocardial relaxation (E’), and isovolumetric relaxation time (IVRT) at 4, 6, and 8 weeks. Age matched wild type animals (n=15) were included as referent controls. LV EF was identical (60+1% vs 60+1%, p>0.90) with no difference in LV mass (67+3 vs 75+5, p>0.25) at 4 weeks. LVH and diastolic dysfunction occurred with WWP1 O/E wherein LV mass increased by over two-fold, E/A fell (impaired passive filling), and E/E’ was lower and IVRT prolonged (impaired LV relaxation). Collagen percent area increased by over two-fold with WWP1 O/E and increased expression of determinants of fibrosis and growth (qPCR) were also concomitantly increased.</p> <p><strong><em>Conclusion.</em></strong> Inducing WWP1 expression caused LVH with significant diastolic dysfunction, consistent with the HFpEF phenotype. Thus, targeting the WWP1 pathway may be a novel therapeutic target for this intractable form of HF associated with ageing</p>
Interleukin-1 Blockade in Recently Decompensated Heart Failure
ClinicalTrials.gov study NCT01936909. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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