Background

Heart failure with preserved ejection fraction (HFpEF), also known as diastolic heart failure, is estimated to affect 1.1 to 5.5% of the general population1 (at least 85 million people worldwide). Patients with HFpEF are commonly very symptomatic, with an elevated risk of rehospitalization and reduced quality of life due to its complex pathophysiology and the lack of proven effective therapies. With a rapidly increasing prevalence (AGR +2.6%), the management of patients with HFpEF is extremely challenging and associated with a high economic burden (>$3B in Australia only).

Inflammation is a critical contributor of HFpEF, being a key driver of cardiac fibrosis and therefore cardiac dysfunction. Breaking down the pathogenesis of such underlying mechanisms of HFpEF constitutes a promising therapeutic