Myocardial Perfusion, Oxidative Metabolism, and Fibrosis in HFpEF
Condition: Heart Failure, Diastolic; Diastolic Heart Failure; Hypertension
MeSH terms: Heart Failure; Heart Failure, Diastolic
Study type: Interventional
Phase: Phase 4

Summary: 
      Unlike heart failure with reduced ejection fraction (HFrEF) where several medicines and
      devices have been demonstrated to reduce mortality, no such therapies have been identified in
      HFpEF. This may be in part due to incomplete understanding of the underlying mechanisms of
      HFpEF.

      Recently, impaired myocardial blood flow, reduced myocardial energy utilization, and
      increased myocardial fibrosis have been postulated to play important pathophysiologic roles
      in HFpEF. The investigators and others have demonstrated that HFrEF may be associated with
      altered myocardial energy utilization and "energy starvation." However, there are limited
      data regarding "energy starvation" in HFpEF and the relationships between myocardial blood
      flow, energy utilization, and fibrosis in HFpEF are largely unknown. Therefore, the purposes
      of this study are to use non-invasive cardiac imaging techniques to describe cardiac
      structure, function, blood flow, energetics, and fibrosis, and the relationships between
      these in order to better understand underlying mechanisms in HFpEF.
    

Detailed description: 
      The investigators hypothesize that HFpEF is associated with reductions in myocardial blood
      flow and energy utilization and increased myocardial fibrosis as compared to age and gender
      matched hypertensive and healthy controls. The investigators will test their hypotheses by
      comparing measurements of myocardial blood flow, energy utilization, and fibrosis between
      three subject groups (HFpEF vs hypertension vs healthy). Myocardial blood flow will be
      quantitated from nitrogen (N)13-Ammonia positron emission tomography (PET) and gadolinium
      enhanced cardiac magnetic resonance (CMR) imaging, both at rest and stress following coronary
      vasodilation with regadenoson. Myocardial energy utilization will be quantified with
      11C-acetate PET imaging and myocardial fibrosis will be assessed with gadolinium enhanced CMR
      and alterations in myocardial T1. Echocardiography will be utilized to quantify cardiac
      diastolic function.

      It is anticipated that the results of this proposed study will provide a foundation that will
      inform future studies aimed at identifying novel preventive or therapeutic agents in HFpEF.
    

Intervention name(s): regadenoson
Intervention type(s): Drug
Intervention description(s): evaluation of myocardial blood flow, interstitial fibrosis and oxidative metabolism in HFpEF, compared to hypertensive and normal participants
Other intervention name(s): positron emission tomography; echocardiography; cardiac magnetic resonance imaging
Intervention MeSH terms: Regadenoson
Allocation: Non-Randomized
Intervention model: Factorial Assignment
Masking: None (Open Label)
Primary purpose: Diagnostic
Keywords: magnetic resonance imaging; positron-emission tomography; echocardiography; myocardial blood flow; energy metabolism