View clinical trials related to Heart Failure.
Filter by:The purpose of the study is to collect data from the two implanted sensors simultaneously to the surface ECG and echocardiographic measurements of electromechanical parameters, in CRT patients.
The present study will examine the comparative effectiveness of two treatment strategies currently used in the treatment of patients with systolic heart failure presenting with pleural effusion. Patients will be randomized to standard medical treatment only or medical treatment and referral to thoracentesis. Study hypothesis: A strategy of referring patients with heart failure-related pleural effusion to thoracentesis increases number of days alive outside of hospital over the following 90 days.
Physical activity is a key element in cardiac rehabilitation and prevention of cardiovascular mortality and hospitalizations. After cardiac rehabilitation programs end, physical activity levels and participation in continued cardiac rehabilitation declines. The aim of this study is to evaluate the feasibility a mobile health intervention with text messages and behavior change theory in patients with cardiovascular disease for a duration of 3 months after completion of a cardiac rehabilitation program. An intervention consisting of action planning, text messages, and coordinator support is tested in a feasibility trial design with 40 expected participants.
Heart Failure (HF) is a complex disease associated with the highest burden of cost to the healthcare system. The cardiopulmonary exercise test (CPET) is instrumental in determining the prognosis of patients with HF. This study will evaluate whether aggregate biometric data from the Apple Watch combined with demographic, cardiac, and biomarker testing can improve our ability to predict heart failure outcomes among a diverse ambulatory HF population
Heart failure (HF) is a complex syndrome with increasing incidence and high rates of mortality and hospitalization. Although inhibitors of angiotensin converting enzyme (ACE), β-blockers and aldosterone-receptor blockers have improved the treatment of heart failure, mortality of HF remains unacceptably high. Recently, we identified a key metabolite N-acetylneuraminic acid (Neu5Ac) increased in the plasma of patients with heart failure. Also, elevated plasma Neu5Ac, independent of other traditional risk factors, is associated with poor prognosis in patients with HF in long-term follow up. Neu5Ac levels, the most common sialic acid in mammals, generated from sialylated glycoconjugates by neuraminidase. Neu5Ac and its regulatory enzyme neuraminidase play a key role in heart failure. We found neuraminidase inhibitor could reduce Neu5Ac levels and improve heart failure in mice model, providing opportunity for a novel therapeutic strategy in HF. Neuraminidase inhibitor oseltamivir is also an old anti-influenza drug. Using oseltamivir may be a new therapeutic strategy in heart failure. Based on above information, we designed the randomized, open-label, blank-controlled study in patients with chronic HF to receive either oseltamivir or placebo, in addition to standard HF therapy to Identify the effect of oseltamivir on serum Neu5Ac level in patients with heart failure and assess the clinic outcomes of level in patients with heart failure using oseltamivir.
This is a prospective interventional study to better understand i) the prevalence of Obstructive Sleep Apnea (OSA) in Heart Failure with preserved Ejection Fraction (HFpEF), ii) its hemodynamic correlates, and iii) the impact of intervention with Continuous Positive Airway Pressure (CPAP) on quality of life.
Background: CKD in patients with heart failure (HF) is common and associated with poor prognosis. Despite evidence of benefit with Renin-Angiotensin-Aldosterone-System inhibitor (RAASi) agents, they are avoided due to fear of hyperkalaemia. New potassium binders, e.g. Sodium Zirconium Cyclosilicate (SZC), reduce incidence of hyperkalaemia in CKD-HF patients and hence may help RAASi maximisation, which has not been investigated in an RCT. Purpose: The proposed study will randomise HFrEF patients with stable CKD 3-5 and serum potassium 5-5.0 mmol/L, to receive SZC or placebo while RAASi therapy is maximised. The aim of the study is to examine if SZC is superior to placebo in achieving maximal doses of ACEi/ARB, e.g. Ramipril 10 mg, Candesartan 32 mg; and mineralocorticoid receptor antagonist, e.g. Epleronone 50 mg or Spironolactone 50 mg, avoiding hyperkalaemia. Methods: Eligible patients with eGFR<60 mL/min/1.73m2, heart failure (EF<40%) on none/submaximal dose of RAASi will be randomised to receive 10g TDS of investigational medicinal product (IMP), either SZC or placebo, for 48 hours and in 10 or 5g OD guided by laboratory serum potassium (K+). Every two weeks the RAASi dose will be increased and IMP adjusted according to a strict protocol and guided by laboratory potassium and creatinine. The primary endpoint of the study is achievement of maximal dose of RAASi in randomised patients avoiding hyperkalaemia, i.e. K+≤5.6 mmol/L. Patients will be allowed to continue with RAASi maximisation to K+<6.0mmol/L. Patients will be tested at baseline and follow-up visits for hyperkalaemia, AKI, symptomatic hypotension and QT prolongation on ECG. Results: The study results will show if SZC is superior to placebo for RAASi maximisation in CKD-HF patients while maintaining safe levels of serum potassium without any adverse impact on quality of life. The study will demonstrate if SZC allows higher RAASi dose and more dose escalations than placebo. It will also examine the impact of RAASi escalation on creatinine, proteinuria, and cardiac blood biomarkers. Conclusion: If positive, the results of this study will demonstrate that SZC enables RAASi up titration in CKD-HF patients, which potentially can help achieve optimal treatment and improve quality of life of the patient.
The aim of our study is to understand the biological pathways involved in the occurrence of IDy in patients with HF since ID is very common and supposes a negative impact in terms of clinical outcomes in these patients. In this context, a deeper understanding of the mechanisms involved in the development of ID in these patients and the impact on the altered biological pathways after iron replenishment will pave the way for an improvement and simplification of the preventive strategies in patients with HF.
Autophagy is considered an important component of Heart failure progression. Deubiquitination enzymes play an important role in autophagy. An important regulatory process within the autophagy pathway is ubiquitination. Ubiquitination targets proteins for degradation. On the contrary, de-ubiquitinating proteins (such as UCHL1) reverses this process. Studies have demonstrated deubiquitination to be linked to certain pathological processes, such as heart failure. UCHL1 will be examined as a potential marker of disease progression in acute decompensated heart failure.
This research is being done to better understand the relationship between information collected by wearable devices and clinical measurements in people with heart failure with preserved ejection fraction (HFpEF) and others without HFpEF. This is an observational study with no study intervention or randomization. Participants will undergo baseline history and physical, 12-lead EKG, laboratory studies of blood/serum/urine, echocardiography, activity questionnaire, 6 minute walk test, and placement of wearable devices to be worn for up to 14 days (activity monitors, EKG monitor and continuous glucose monitor). Participants will return after ~14 days of wearing the devices and repeat of physical examination, 12-lead EKG, 6 minute walk test, activity questionnaire. Additionally, participants will undergo magnetic resonance imaging (MRI) of their leg with exercise, cardiopulmonary exercise testing (CPET) and, for those who qualify, magnetic resonance imaging (MRI) of their heart with exercise.