Myocardial Metabolic Flux in Pulmonary Arterial Hypertension
Starting soon · Phase 2
Conditions studied: Pulmonary Arterial Hypertension
In brief
The rationale for this study is that GLP-1 agonist treatment is likely to influence myocardial substrate utilisation, changing the predominant source of metabolic energy within the heart to a more energetically efficient form. This is represented by a surrogate for improved mitochondrial efficiency with reduction in myocardial lactate levels (produced by inefficient myocardial glycolysis, prevalent in the ventricles of patients with pulmonary hypertension), which can be measured by 31P-magnetic resonance spectroscopy (31P-MRS).
Key facts
- Study ID
- NCT07737522
- Run by
- Imperial College London
- People needed
- 32
- Starts
- 2026-10-01
- Expected to finish
- 2029-04-01
- Last updated by the study team
- 2026-07-30
Who can join
Age: 18 and older, up to 85. Sex: any. Healthy volunteers: not accepted.
You may qualify if…
- 1. Diagnosis of Group 1 PAH confirmed by right heart catheterisation under the National Pulmonary Hypertension Service, Royal Brompton Hospital, part of GSTT Foundation Trust 2. Age over 18, less than 85 years 3. Able to give informed consent 4. On a stable dose of PAH-specific therapies (e.g., ERA, PDE5i) for at least 3 months.
- Clinically justified prescription of GLP-1 agonist Semaglutide based on following criteria: BMI > 30 or BMI > 27 with at least one cardiovascular co-morbidity (systemic hypertension, diabetes, pre-diabetes, COPD, atrial fibrillation, dyslipidaemia, sleep disordered breathing)
You may not qualify if…
- • 1. Pregnancy
- 2. Myocardial infarction within the previous 3 months
- 3. Contraindications to MRI: Pacemakers, metallic implants, or severe claustrophobia.
- 4. Severe renal impairment: eGFR < 15ml/min/1.73m.
- 5. Current use of SGLT2 inhibitors or GLP-1 agonist therapy (which significantly alter fuel substrate preference) or insulin therapy that cannot be held for the fasting scan
Full record on ClinicalTrials.gov
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