A64-08 Metabolic Reprogramming in Pulmonary Vascular Disease: Insights From Sglt2 Inhibitor Therapy
Abstract
Pulmonary hypertension (PH) involves disordered cellular metabolism that limits oxygen use and forces cells to rely on less efficient glucose pathways. This imbalance raises lactate, uric acid, and brain natriuretic peptide (BNP), reflecting oxidative stress and strain on the right ventricle (RV). Sodium glucose cotransporter 2 (SGLT2) inhibitors improve metabolic efficiency in the heart and kidneys and may also benefit the pulmonary circulation by encouraging oxygen-efficient fuel use. This study examined how SGLT2 therapy affects metabolic and biochemical profiles in patients with PH.
We performed a cross sectional single center study of adults aged 18 years or older with confirmed World Health Organization Group 1 to 3 PH between 2019 and 2024. Data were collected from the institutional PH registry and hospital laboratory system. Patients who received empagliflozin or dapagliflozin for at least six months were compared with matched PH controls. Continuous variables included beta hydroxybutyrate, lactate, uric acid, HbA1c, and BNP. Group comparisons used unpaired t tests. Statistical significance was defined as p < 0.05.
A total of 126 patients were analyzed (52 SGLT2 users and 74 controls). Mean age was 63 ± 10 years, and two thirds were women. At baseline, 71 percent had elevated lactate (>1.8 mmol per L), 65 percent had uric acid above 6 mg per dL, and 78 percent had BNP over 300 pg per mL, indicating tissue hypoxia and oxidative stress. After at least six months of…
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