Heart failure with preserved ejection fraction: The role of inflammation

Area of Science:

• Cardiology
• Pharmacology
• Immunology

Background:

• Heart failure with preserved ejection fraction (HFpEF) is a growing global health concern, impacting over 64.3 million individuals worldwide.
• HFpEF accounts for more than 50% of all heart failure cases, with increasing prevalence and mortality rates.
• While sodium-glucose co-transporter 2 inhibitors (SGLT2i) show promise, effective pharmacological treatments for HFpEF remain limited.

Purpose of the Study:

• To review current understanding of HFpEF pathogenesis, focusing on the role of inflammation.
• To explore the therapeutic potential of anti-inflammatory strategies in managing HFpEF.
• To address the gap in effective pharmacological therapies for HFpEF.

Main Methods:

• Literature review of current evidence on HFpEF pathogenesis.
• Analysis of the interplay between cardiometabolic comorbidities, inflammation, and RAAS activation in HFpEF.
• Examination of existing and potential anti-inflammatory therapies for HFpEF.

Main Results:

• HFpEF pathogenesis involves complex interactions including inflammation and RAAS activation, leading to cardiac remodelling and diastolic dysfunction.
• Conventional RAAS blockade shows limited efficacy in HFpEF, suggesting a need for alternative therapeutic targets.
• Growing evidence supports the importance of inflammation in HFpEF progression, yet anti-inflammatory therapies are under-explored.

Conclusions:

• Inflammation plays a critical role in HFpEF pathogenesis and cardiac remodelling.
• Targeting inflammation presents a promising therapeutic avenue for HFpEF.
• Further research into anti-inflammatory treatments is crucial for addressing the unmet medical needs in HFpEF.