Why the study?
Heart failure with preserved ejection fraction has emerged as the predominant form of heart failure, motivating a review of recent progress in its molecular pathogenesis and emerging treatment approaches.
Meta-Analysis (n=30,882)
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This review provides a comprehensive overview of the molecular mechanisms driving HFpEF, particularly inflammation and oxidative stress, and outlines current and emerging targeted therapies.
Heart failure with preserved ejection fraction (HFpEF) has progressively emerged as the predominant form of heart failure. Thus, studies on the underlying mechanisms of HFpEF have shifted from pathophysiological to molecular factors. Meanwhile, previous studies have primarily focused on inflammation, oxidative stress, metabolic dysregulation, and impaired cardiac compliance (manifesting as ventricular hypertrophy and interstitial fibrosis). In addition to conventional guideline-directed medical therapies, novel therapeutic strategies targeting these aforementioned pathogenic pathways have been investigated. This review aimed to summarize recent progress in HFpEF pathogenesis and emerging treatment approaches, offering insights for developing novel diagnostic and management strategies.
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Fan et al. (2026) conducted a meta-analysis in Heart Failure with Preserved Ejection Fraction (HFpEF) (n=30,882). RAS inhibitors vs. placebo was evaluated on Composite outcome of cardiovascular death and hospitalization for heart failure (OR 0.87, 95% CI 0.82-0.93, p=null).
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