SGLT2 inhibitors, GLP1 agonists, and ARNI therapy show potential to improve hemodynamics and metabolic dysfunction in patients with pulmonary hypertension based on preclinical and early clinical data.
Do SGLT2 inhibitors, GLP1 agonists, and ARNIs improve outcomes in patients with pulmonary hypertension (PH-LHD and PAH)?
SGLT2 inhibitors, GLP1 agonists, and ARNIs represent promising emerging therapies for pulmonary hypertension by targeting underlying metabolic dysfunction and adverse remodeling.
Pulmonary hypertension (PH) is a highly morbid condition. PH due to left heart disease (PH-LHD) has no specific therapies and pulmonary arterial hypertension (PAH) has substantial residual risk despite several approved therapies. Multiple lines of experimental evidence link metabolic dysfunction to the pathogenesis and outcomes in PH-LHD and PAH, and novel metabolic agents hold promise to improve outcomes in these populations. The antidiabetic sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP1) agonists targeting metabolic dysfunction and improve outcomes in patients with LHD but have not been tested specifically in patients with PH. The angiotensin receptor/neprilysin inhibitors (ARNIs) produce significant improvements in cardiac hemodynamics and may improve metabolic dysfunction that could benefit the pulmonary circulation and right ventricle function. On the basis of promising preclinical work with these medications and clinical rationale, we explore the potential of SGLT2 inhibitors, GLP1 agonists, and ARNIs as therapies for both PH-LHD and PAH.
King et al. (Sat,) conducted a review in Pulmonary hypertension (PH-LHD and PAH). SGLT2 inhibitors, GLP1 agonists, and ARNIs was evaluated. SGLT2 inhibitors, GLP1 agonists, and ARNI therapy show potential to improve hemodynamics and metabolic dysfunction in patients with pulmonary hypertension based on preclinical and early clinical data.