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).
Inclusion Criteria:
- 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.
5. 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)
Exclusion Criteria:
• 1. Pregnancy
Metabolic Remodeling in Pulmonary Arterial Hypertension (PAH)
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Hormonal, Metabolic, and Signaling Interactions in PAH
The Effect of Glucagon-Like Peptide-1 (GLP-1) on Pulmonary Vascular Resistance (PVR) in Patients With Heart Failure
Skeletal Muscle Mitochondrial Abnormalities and the Metabolic Syndrome in PAH