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Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of the heart failure population in the United States. The primary chronic symptom in patients with HFpEF is severe exercise intolerance quantified as reduced peak oxygen uptake during whole body exercise (peak V̇O2). To date, studies have focused almost exclusively on central cardiac limitations of peak V̇O2 in HFpEF. However, in stark contrast to heart failure with reduced ejection fraction (HFrEF), drug therapies targeting central limitations have invariably failed to improve peak V̇O2, quality of life, or survival in HFpEF. Emerging evidence from our lab suggests reduced skeletal muscle oxidative capacity may contribute to exercise intolerance in HFpEF patients. However, the mechanisms responsible for peripheral metabolic inefficiency remain unclear. Reduced blood flow (oxygen delivery), and slowed oxygen uptake kinetics (O2 utilization) may both contribute to reduced peripheral oxidative capacity. Importantly, reduced oxidative capacity may result in increased production of metabolites known to activate muscle afferent nerves and stimulate reflex increases in muscle sympathetic (vasoconstrictor) nervous system activity (MSNA). However, to date there have been no studies specifically investigating the contribution of peripheral metabolic and neural impairments to reduced exercise capacity in HFpEF. The overall aim of this proposal will be 1) to identify impairments in peripheral vascular, metabolic, and sympathetic neural function and 2) to assess the ability of small muscle mass (knee extensor, KE) training, specifically targeting these peripheral skeletal muscle deficiencies, to improve aerobic capacity and exercise tolerance in HFpEF. GLOBAL HYPOTHESIS 1: HFpEF patients will demonstrate reduced skeletal muscle oxygen delivery, slowed oxygen uptake kinetics, and elevated resting and metaboreflex mediated MSNA. Hypothesis 1.1: The vasodilatory response to knee extensor exercise will be impaired in HFpEF patients. Specific Aim 1.1: To measure the immediate rapid onset vasodilatory response to muscle contraction, as well as the dynamic onset, and steady state vasodilatory responses to dynamic KE exercise. Hypothesis 1.2: Skeletal muscle oxygen uptake kinetics will be slowed in HFpEF. Specific Aim 1.2: To measure pulmonary oxygen uptake kinetics during isolated KE exercise in order to isolate peripheral impairments in metabolic function independent of any central impairment. Hypothesis 1.3: HFpEF patients will demonstrate elevated MSNA at rest, and exaggerated metaboreflex sensitivity during exercise. Specific Aim 1.3: To test this hypothesis the investigators will measure MSNA from the peroneal nerve at rest, and during post exercise ischemia to directly assess metaboreflex sensitivity in HFpEF. GLOBAL HYPOTHESIS 2: Isolating peripheral adaptations to exercise training using single KE exercise training will improve peripheral vascular, metabolic, and neural function and result in greater functional capacity in HFpEF. Hypothesis 2.1: Isolated KE exercise training will improve the vasodilatory response to exercise, speed oxygen uptake kinetics, and reduce MSNA at rest HFpEF. Specific Aim 2.1: The assessments of vascular, metabolic, and neural function proposed in hypothesis 1 will be repeated after completing 8 weeks of single KE exercise training. Hypothesis 2.2: Single KE exercise training will improve whole body exercise tolerance, peak V̇O2, and functional capacity in HFpEF. Specific Aim 2.2: To test this hypothesis the investigators will measure maximal single KE work rate, V̇O2 kinetics and peak V̇O2 during cycle exercise, as well as distance covered in the six minute walk test.
Heart failure (HF) has been associated with chronic deleterious effects on skeletal muscle, endocrine system, vasculature and sympathetic nervous system. These alterations have a significant impact on quality of life, leading to a reduction in functional capacity and limited symptoms, which involve dyspnea and fatigue. The investigators tested the hypothesis that hormonal anabolic deficiency associated with neurovascular alterations may worsen the prognosis of patients with heart failure.
The purpose of this study is to evaluate the beta-adrenergic receptor gene polymorphisms in the long-term effects of beta-blockade in patients with chronic heart failure.
This protocol describes a 2-arm randomized controlled pilot study assessing the tolerance, safety and efficacy of sildenafil compared to control. The hypothesis is that sildenafil will be well tolerated and efficacious in patients with chronic heart failure (NYHA class II and III) with evidence of systolic dysfunction (EF ≤40 %) and secondary pulmonary hypertension (SPAP >40mmHg). Patients that satisfy the inclusion criteria will be randomized to sildenafil (40mg x 3) or placebo therapy for 6 months in a 2:1 blinded fashion. The placebo group will be compared to the active therapy group and analyzed for differences in the main study end-points Patient Global Assessment and 6-Minute Walk Test. The study will also assess safety, tolerability, symptoms and quality of life.
The goal of this study is to evaluate the health and social benefit of innovative management - IsereADOM - versus conventional follow-up in patients with heart failure. There is a medico-economic goal too, is to perform a cost-utility analysis of the service bundle (IsereADOM) versus conventional 6-month community-based follow-up in a population with heart failure.
This study is a prospective, single-site, open-label, single-arm intervention study in African-American/Black subjects with HFrEF nested in the Henry Ford Heart Failure Pharmacogenomics Registry, and will be conducted at the Henry Ford Health System in Detroit, MI. There will be a 7-day screening period, a 57-day open-label treatment period, and a safety follow-up at day 87 or 30 days after the last administration of the investigational product.
The purpose of this study is to determine whether 1 year of supervised exercise training in obese individuals at high risk for developing HF, incorporating high intensity interval training (HIIT) two to three times per week in conjunction with daily oral administration of omega-3 poly-unsaturated fatty acids will lead to reduction in visceral adiposity, regression of myocardial triglyceride levels and improvements in cardiac diastolic and vascular function.
The PREPARE-MVR (PRediction of Early PostoperAtive Right vEntricular failure in Mitral Valve Replacement/Repair patients) Study aims to evaluate those preoperative factors which can predict the early postoperative right ventricular failure or determine the functional shift seen in right ventricular function after mitral valve replacement/repair. The PREPARE-MVR study focuses mainly on echocardiographic (both conventional and advanced) parameters and includes right heart catheterization intraoperatively and in the early postoperative period as gold standard method.
The study is designed to repeat an initial training set study conducted at Johns Hopkins Medical Center, comparing a new investigational device, Indicor, a non-invasive tool for estimating left ventricular end diastolic pressure (LVEDP), to the gold standard, invasively measured LVEDP via direct measurement via left heart catheterization. The study is divided into an initial training set, followed by the validation set which is designed to support an FDA 510(k) submission and validate the final algorithm. Patients will be enrolled who are scheduled to undergo a cardiac catheterization and will be asked to perform three tests with the Indicor.
The investigators will examine the effects of 12-weeks of nutritional interventions in older participants who have a symptom of mild to moderate heart failure.