Pomeranian atRial flOw reguLatOr iN conGestive hEart failuRe (PROLONGER): Study protocol.
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ABSTRACT:
SUBMITTER: Lewicki L
PROVIDER: S-EPMC8079108 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: Not available
| S-EPMC8015977 | biostudies-literature
Project description:Congestive heart failure was done by artificial myocardial infarction. After extracting total RNA from control and infarcted ventricles with Triazol, messenger RNA was isolated with Qiagen mRNA isolation kit. About 1.5ug poly A+ RNA was taken for probe preparation. Probe was labeled with Alexa Fluor 546 and 657. Labeled probes were hybridized with Qiagen rat unigene oligo library. After 2 low and 1 high stringency washes Prolong Antifade was added to the slides to prevent bleaching effect. The data ratio was normalized using a location and intensity dependent Lowess formula. Keywords: other
2003-09-08 | GSE632 | GEO
Project description:Canine tachycardia-induced cardiomyopathy caused by several weeks of rapid ventricular pacing is a well-established animal model of congestive heart failure. However, little is known about the underlying changes in gene expression that occur in the canine myocardium after the induction of heart failure. This project aims to compare expression profiles in left ventricular free wall samples from control dogs and dogs with pacing-induced heart failure on the custom MuscleChip. Keywords: other
2003-07-16 | GSE472 | GEO
Project description:Congestive heart failure was done by artificial myocardial infarction. After extracting total RNA from control and infarcted ventricles with Triazol, messenger RNA was isolated with Qiagen mRNA isolation kit. About 1.5ug poly A+ RNA was taken for probe preparation. Probe was labeled with Alexa Fluor 546 and 657. Labeled probes were hybridized with Qiagen rat unigene oligo library. After 2 low and 1 high stringency washes Prolong Antifade was added to the slides to prevent bleaching effect. The data ratio was normalized using a location and intensity dependent Lowess formula.
2010-06-05 | E-GEOD-632 | biostudies-arrayexpress
Project description:Heart failure (HF) continues to be a leading cause of hospital admissions, particularly in underserved patients. We hypothesised that providing individualised self-management support to patients and feedback on use of evidence-based HF therapies (EBT) to physicians could lead to improvements in care and decrease hospitalisations. To assess the feasibility of conducting a larger trial testing the efficacy of this dual-level intervention, we conducted the Congestive Heart failure Adherence Redesign Trial Pilot (CHART-P), a proof-of-concept, quasi-experimental, feasibility pilot study.A large tertiary care medical centre in Chicago.Low-income patients (<US$30,000/year) hospitalised for exacerbation of systolic HF (ejection fraction ?50%) and their physicians. Twenty physicians and 33 patients were enrolled, of whom 23 patients completed the study.Physicians received HF guidelines and periodic individualised feedback on their adherence to EBT. Patients received HF education, support and self-management training for diet and medication adherence by a trained nurse through 11 interactive sessions over a 4-month period. Evaluations were conducted pre-enrolment and 1 month postintervention completion.Feasibility was assessed by the ability to deliver intervention to patients and physicians. Exploratory outcomes included changes in medication and sodium intake for patients and adherence to EBT for physicians.Eighty-seven per cent and 82% of patients received >80% of interventions at 1 month and by study completion, respectively. Median sodium intake declined (3.5 vs 2.0 g; p<0.01). There was no statistically significant change in medication adherence based on electronic pill cap monitoring or the Morisky Medication Adherence Scale (MMAS); however, there was a trend towards improved adherence based on MMAS. All physicians received timely intervention.This pilot study demonstrated that the protocol was feasible. It provided important insights about the need for intervention and the difficulties in treating patients with a variety of psychosocial problems that undercut their effective care.
| S-EPMC4256535 | biostudies-literature
Project description:AimsOver the last decade, major developments in medicine have led to significant changes in the clinical management of heart failure patients. This study was designed to evaluate the recent trends in clinical characteristics, management, and short-term and long-term prognosis of patients with acute decompensated heart failure (ADHF) in Japan.Methods and resultsThe Kyoto Congestive Heart Failure study is a prospective, observational, multicentre cohort study, enrolling consecutive ADHF patients from 19 participating hospitals in Japan from November 2014 to March 2016. A total of 4000 patients will be enrolled into the study and patients' anthropometric, socio-economic, and clinical data from hospital admission to discharge will be collected. In addition, in a pre-determined subgroup of patients (n=1500), a longitudinal follow-up for 2 years is scheduled.ConclusionsThe Kyoto Congestive Heart Failure study will provide valuable information regarding patients with ADHF in the real-world clinical practice of Japan and will be indispensable for future clinical and policy decision-making with respect to heart failure.
| S-EPMC5542729 | biostudies-literature
Project description: Not available
| S-EPMC8016002 | biostudies-literature
Project description:Anthracycline-induced congestive heart failure (CHF) is a rare but serious toxicity associated with this commonly employed anticancer therapy. The ability to predict which patients might be at increased risk prior to exposure would be valuable to optimally counsel risk-to-benefit ratio for each patient. Herein, we present a genome-wide approach for biomarker discovery with two validation cohorts to predict CHF from adult patients planning to receive anthracycline.We performed a genome-wide association study in 3,431 patients from the randomized phase III adjuvant breast cancer trial E5103 to identify single nucleotide polymorphism (SNP) genotypes associated with an increased risk of anthracycline-induced CHF. We further attempted candidate validation in two independent phase III adjuvant trials, E1199 and BEATRICE.When evaluating for cardiologist-adjudicated CHF, 11 SNPs had a P value <10-5, of which nine independent chromosomal regions were associated with increased risk. Validation of the top two SNPs in E1199 revealed one SNP rs28714259 that demonstrated a borderline increased CHF risk (P = 0.04, OR = 1.9). rs28714259 was subsequently tested in BEATRICE and was significantly associated with a decreased left ventricular ejection fraction (P = 0.018, OR = 4.2).rs28714259 represents a validated SNP that is associated with anthracycline-induced CHF in three independent, phase III adjuvant breast cancer clinical trials. Clin Cancer Res; 23(1); 43-51. ©2016 AACR.
| S-EPMC5215621 | biostudies-literature
Project description:Congestive heart failure (CHF) and atrial fibrillation (AF) frequently coexist and are associated with increased risk of cardiovascular events.To compare baseline characteristics, comorbidities and pharmacotherapy in AF patients with concomitant CHF to those without CHF.The study included 3506 real-life AF patients with (37.1%) and without CHF - participants of the multicentre, retrospective MultiCenter expeRience in AFib patients Treated with OAC (CRAFT) trial (NCT02987062).All patients were treated with non-vitamin K antagonist oral anticoagulants (NOAC) or vitamin K antagonists (VKA). The frequency of NOAC among patients with and without CHF was 45.6% and 43.2%, respectively (P = .17). Patients with CHF were older (73.3 vs 64.7 years, P <.001), less likely to be women (37.4% vs 42%, P = .007), had higher CHA2DS2-VASc score (3.8 ± 1.7 vs 2.6 ± 1.8, P <.001), more often had permanent AF (53.0% vs 13.4%, P <.001), chronic obstructive pulmonary disease (16.7% vs 4.9%, P <.001), coronary artery disease (64.3% vs 29.8%, P <.001), peripheral vascular disease (65.3% vs 31.4%, P <.001), chronic kidney disease (43.1% vs 10.0%, P <.001), liver fibrosis (5.7% vs 2.6%, P <.001), neoplasm (9.6% vs 7.3%, P = .05), history of composite of stroke, transient ischemic attack or systemic embolization (16.2% vs 10.7%, P <.001), pacemaker (27.4% vs 22.1%, P = .004), implantable cardioverter-defibrillator (22.7% vs 0.8%, P <.001) or transaortic valve implantation (4.0% vs 0.8%, P <.001), cardiac resynchronization therapy (8.7% vs 0.3%, P <.001), composite of kidney transplantation, hemodialysis or creatinine level > 2.26 mg/dL (3.6% vs 0.8%, P <.001) and had less often hypertension (69.4% vs 72.5%, P = .05).Patients with AF and CHF had a higher thromboembolic risk and had more concomitant diseases.
| S-EPMC6250503 | biostudies-other
Project description:Compromised gut health and dysbiosis in people with heart failure has received a great deal of attention over the last decade. Whether dogs with heart failure have a similar dysbiosis pattern to what is described in people is currently unknown. We hypothesised that dogs with congestive heart failure have quantifiable dysbiosis compared to healthy dogs that are similar in sex and age. A total of 50 dogs (15 healthy dogs and 35 dogs with congestive heart failure) were prospectively recruited, and their faecal gut microbiome was assessed using 16S rRNA sequencing (Illumina MiSeq platform). There was no significant change in the microbial diversity and richness in dogs with congestive heart failure. However, there was an increase in abundance of Proteobacteria in the congestive heart failure group (p = 0.014), particularly due to an increase in the family Enterobacteriaceae (p = 0.002) and Escherichia coli (p = 0.033). We conclude that dogs with congestive heart failure have dysbiosis, and we show additional trends in our data suggesting that dogs may have a similar pattern to that described in people. The results of this study provide useful preliminary information and raise the possibility that dogs represent a clinically relevant animal model of dysbiosis in people with heart failure.
| S-EPMC7426839 | biostudies-literature