Heart failure with preserved ejection fraction: The role of inflammation

Heart failure (HF) is a debilitating clinical syndrome affecting 64.3 million patients worldwide. More than 50% of HF cases are attributed to HF with preserved ejection fraction (HFpEF), an entity growing in prevalence and mortality. Although recent breakthroughs reveal the prognostic benefits of sodium-glucose co-transporter 2 inhibitors (SGLT2i) in HFpEF, there is still a lack of effective pharmacological therapy available. This highlights a major gap in medical knowledge that must be addressed. Current evidence attributes HFpEF pathogenesis to an interplay between cardiometabolic comorbidities, inflammation, and renin-angiotensin-aldosterone-system (RAAS) activation, leading to cardiac remodelling and diastolic dysfunction. However, conventional RAAS blockade has demonstrated limited benefits in HFpEF, which emphasises that alternative therapeutic targets should be explored. Presently, there is limited literature examining the use of anti-inflammatory HFpEF therapies despite growing evidence supporting its importance in disease progression. Hence, this review aims to explore current perspectives on HFpEF pathogenesis, including the importance of inflammation-driven cardiac remodelling and the therapeutic potential of anti-inflammatory therapies.