View clinical trials related to Heart Failure.
Filter by:The study aims 1) to determine autoantibody titers against the AGTR1 receptor and against the ETA receptor, 2) to characterize cytokine expression profiles of heart-specific activated T cells in patients with systolic heart failure. Auto-antibody titers and specific cytokine expression profiles in heart-specific activated T cells will then be correlated with heart failure progression and outcome.
The prevalence of sleep-disordered breathing is common in patients with stable chronic heart failure (up to 83%). Basically, the SAS is divided into two categories: central SAS (CSAS) and obstructive SAS (OSAS). The two can coexist. In patients with CHF, the presence of SAS is associated with higher mortality. CHF is associated with a high rate of re-hospitalization and significant morbidity and mortality and is considered as a major medical and economic problem. To date, few studies have investigated the prevalence, severity, persistence and the role of SAS during cardiac decompensation. For different pathophysiological considerations, it is assumed that SAS is exacerbated during AHF. Therefore SAS is not conventionally screened during this phase. This assumption has been questioned recently by some studies which showed stability of the type of SAS and its severity between the decompensation episode and the stable HF. Our hypothesis is that SAS during an AHF episode of CHF will remain stable both in terms of severity and type at three months of decompensation. Thus early polygraphy may be reliable for identifying HF patients with SAS.
Sleep apnea, characterized by abnormal breathing at night, is often untreated in patients with heart failure. Helping patients to effectively use the most common form of treatment for sleep apnea, positive airway pressure therapy, can improve their heart function. This can reduce the likelihood that the patient will be re-admitted to the hospital. AirCareLabs has developed an innovative solution that allows patients to communicate with health care providers 24 hours a day, thus allowing them to get the help they need to effectively use positive airway pressure and thereby reduce the risk of being re-admitted to the hospital.
We thought to investigate the influence of DPP-4 inhibitor on the serum BNP level of diabetic patients with congestive heart failure. This study consists of two protocols. In the first protocol, diabetic patients with high level of serum BNP (100-2000 pg/ml) receiving outpatient treatment with any type of DPP-4 inhibitor at our institution will be enrolled. After baseline data collection, DPP-4 inhibitor will be suspended for one month and serum BNP will be measured. The DPP-4 inhibitor will be resumed and after another month, serum BNP will be measured again. In the other protocol, diabetic patients who were hospitalized due to heart failure were enrolled. DPP-4 inhibitor will be started (if the patient is not taking a DPP-4 inhibitor) or suspended (if the patient is taking a DPP-4 inhibitor) after stabilization of heart failure, and serum BNP will be measured before and after the drug administration or suspension.
This Phase I, open label, study will investigate the effects of VentriGel injection in patients who have experienced a first, large ST elevation myocardial infarction (STEMI) treated by PCI within the past 3 years and have evidence of left ventricular remodeling.
The response to therapy with a fixed dose combination of isosorbide dinitrate and hydralazine (FDC I/H) is enhanced in African Americans with heart failure and reduced ejection fraction (HFrEF) when compared to similar white cohorts. This study will seek to confirm the previous genetic sub-study from AHeFT which suggested a functional polymorphism of guanine nucleotide binding protein beta polypeptide 3 subunit (GNB3), C825T in exon 10, influences the therapeutic efficacy of FDC I/H. This study will initiate treatment with FDC I/H in 500 self designated African American subjects with systolic heart failure. They will be followed for up to two years on therapy. Clinical outcomes (survival, heart failure hospitalizations, and change in quality of life) on FDC I/H will be compared by GNB3 genotype subset. The hypothesis to be confirmed is that subjects homozygous for the T allele (those with the GNB3 TT genotype which is present in approximately 50% of black subjects) demonstrate enhanced therapeutic benefit from FDC I/H.
Pilot study in patients with continuous flow left ventricular assist device (cfLVAD) to proof the feasibility of a specific individual training at home aimed to increase pulse pressure above a predefined threshold which might attenuate the loss of arterial wall thickness. Hypothesis: Increasing daily physical activity near to normal (> 10.000 steps per day) with a pre-defined level of pulse pressure (intensity) is a realizable and feasible approach to investigate changes in arterial wall thickness and cardio-respiratory capacity in cfLVAD patients.
Establishing the association between biological markers and exercise capacity in continuous-flow left ventricular assist device patients.
Patients admitted as an unscheduled hospital admission with either a acute heart failure syndrome (ACF) or acute coronary syndrome (ACS) will be eligible if their 6-12 month mortality risk is estimated to be 20% or greater at the time of discharge. Mortality risk is estimated using GRACE (for ACS) or EFFECT (for AHF) scores. Patients are randomly allocated to receive a holistic care intervention based around the creation of a detailed Future (anticipatory) Care Plan which is agreed with the patient and their family and which is shared with the Family Doctor and Emergency Services including ambulance teams. Primary endpoint is quality of life assessed by questionnaire.
The SchlaHF XT Registry is a longitudinal study of patients with heart failure (HF). The study aims to understand the importance of diagnosis and treatment of sleep disordered breathing (SDB) on HF with the following questions: How often does SDB occur in HF? What forms of SDB occur and how are they treated? How does SDB develop over time? How does the heart failure therapy affect SDB? What is the treatment adherence of patients treated? Does SBD and its treatment affect the survival of heart failure patients?