Epicardial Adipose Tissue Composition and Heart Failure With Preserved Ejection Fraction

Trial statusRecruiting
Trial phasePhase 4
Trial typeInterventional
Biological sexAll
Age18-90
SponsorUniversity of Virginia

About this trial

This study seeks to develop improved cardiac MRI (CMR) methods to quantify epicardial adipose tissue (EAT) composition and to demonstrate the advantages of EAT composition imaging (a) in advancing the understanding of the relationship between EAT and heart failure with preserved ejection fraction (HFpEF) and (b) for understanding mechanisms of and guiding medical therapy in HFpEF. The investigators recently developed the first method for quantifying EAT FAC in human subjects, utilizing a rate-6 accelerated radial 2D multi-echo gradient-echo breathhold acquisition with a local low rank reconstruction. In this project the first specific aim is to develop a rapid free-breathing 3D EAT FAC MRI method that reduces motion-related artifacts, increases coverage, and facilitates higher spatial resolution and improved FAC reproducibility. The second specific aim is to show that EAT FAC is more strongly associated than EAT volume with cardiometabolic HFpEF. In this context, individuals with known or suspected HFpEF will undergo CMR, echocardiography, and other testing to (a) diagnose cardiometabolic HFpEF; (b) characterize features associated with the severity of HFpEF; and (c) assess EAT volume and FAC. The investigators will determine if EAT FAC is more strongly associated than EAT volume with HFpEF and with features associated with the severity of HFpEF. The third specific aim is to show, in the context of cardiometabolic HFpEF and pre-HFpEF, (a) that GLP-1 receptor agonism with semaglutide (SEMA) shifts the EAT FAC to a less proinflammatory profile and (b) that baseline EAT FAC is a stronger predictor than EAT volume of improved cardiovascular function due to SEMA. Cardiometabolic HFpEF and pre-HFpEF subjects will undergo echocardiography and CMR with EAT FAC at baseline and after 3 months to serve as a self-control. Subjects will then undergo repeat imaging 6 months after the initiation of SEMA. The change in FAC after treatment with SEMA will be compared to the change in FAC prior to SEMA. Data will be analyzed to show that SEMA changes EAT FAC, and that baseline EAT FAC is a stronger predictor than EAT volume of improvements in severity of HFpEF.

Eligibility criteria

This trial does not accept healthy volunteers

Qualifiers

Age ≥ 18 years - 90 years;

LVEF ≥ 50%;

≥ 2 risk factors for HFpEF or symptoms that could be related to HFpEF (e.g., dyspnea, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, pulmonary edema, etc);

Not currently being treated with GLP-1RA therapy.

Disqualifiers

• Previously or currently reduced EF (<50%), including heart transplant; (2) Obstructive un-revascularized coronary disease by coronary CT or invasive coronary angiography;

MI/PCI/CABG within the past 6 months;

Untreated severe stenotic or regurgitant valvular disease;

Infiltrative cardiomyopathy (Fabry/HCM/sarcoid/amyloid, etc);

Trial design

Design model

Sequential

Treatments tested in this trial

  • GLP-1RA

    Drug

    Receive 6 months of GLP-1RA (Semaglutide) treatment starting at 0.25mg once weekly and then the dose will be up titrated as tolerated every four weeks to once-weekly doses of 0.5, 1.0, 1.7, and 2.4 mg until a maximum dose of 2.4mg (or the subject's maximally tolerated dose, if the subject's maximally tolerated dose is \<2.4 mg) is reached after 16 weeks.

Treatment groups

192 Participants
are divided into 3 treatment groups
Group A: 3D EAT FAC CMR imagingNo intervention 0 interventions
Group B: Imaging acquisition and medical condition overviewNo intervention 0 interventions
Group C: Imaging acquisition and GLP-1RA treatmentExperimental treatment 1 intervention

Trial outcomes

Primary outcomes

1

Epicardial adipose tissue (EAT) fatty acid composition (FAC)

The longitudinal change in epicardial adipose tissue (EAT) fatty acid composition (FAC) \[quantified in terms of the fraction of saturated fatty acids (SFA) in units of %\] that occur after 6 months of treatment with semaglutide will be compared to the change in SFA that occurred during 3 month period prior to the initiation of semaglutide.

Time frame
Baseline, 3 months (self-control period), and 9-months (6 months post semaglutide treatment)

Secondary outcomes

1

EAT Volume

The longitudinal change in epicardial adipose tissue (EAT) volume (ml) that occurs after 6 months of treatment with semaglutide will be compared to the change in SFA that occurred during 3 month period prior to the initiation of semaglutide.

Time frame
Baseline, 3months (self-control period), and 9-months (6 months post semaglutide treatment)
2

Baseline Saturated Fatty Acid Composition of Epicaridal Adipose Tissue and Change in Myocardial Deformation

The cohort will be divided into 2 groups based on the median value of the epicardial adipose tissue saturated fatty acid composition. The change in global strain (%) following treatment with semaglutide will be compared between the groups.

Time frame
Baseline, 3months (self-control period), and 9-months (6 months post semaglutide treatment)
3

Baseline Saturated Fatty Acid Composition of Epicaridal Adipose Tissue and Change in diastolic dysfunction grade

The cohort will be divided into 2 groups based on the median value of the epicardial adipose tissue saturated fatty acid composition. The change in diastolic dysfunction grade following treatment with semaglutide will be compared between the groups.

Time frame
Baseline, 3months (self-control period), and 9-months (6 months post semaglutide treatment)

Other outcomes

1

Myocardial perfusion reserve

The longitudinal change in myocardial perfusion reserve \[quantified in terms of a ratio of stress myocardial blood flow to rest myocardial blood flow\] that occur after 6 months of treatment with semaglutide will be compared to the change in SFA that occurred during 3 month period prior to the initiation of semaglutide.

Time frame
Baseline, 3 months (self-control period), and 9-months (6 months post semaglutide treatment)
2

Stress myocardial blood flow

The longitudinal change in stress myocardial blood flow \[quantified in terms of ml/g/min\] that occur after 6 months of treatment with semaglutide will be compared to the change in SFA that occurred during 3 month period prior to the initiation of semaglutide.

Time frame
Baseline, 3 months (self-control period), and 9-months (6 months post semaglutide treatment)

Sponsors and contacts

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University of Virginia

Lead sponsor

National Institutes of Health (NIH)

Collaborator