Recent proof-of-concept trials using novel pharmacological agents provide important insight for developing new therapeutic strategies in heart failure with preserved ejection fraction.
This review summarizes the evolving understanding of HFpEF pathophysiology and highlights emerging therapeutic targets from recent proof-of-concept trials.
Heart failure with preserved ejection fraction (HFpEF) is now recognized as a major and growing public health problem worldwide. Yet significant uncertainties still surround its pathophysiology and treatment, leaving clinicians in a dilemma regarding its optimal management. Whether HFpEF and heart failure with reduced ejection fraction (HFrEF) are two distinct entities or two ends of a common spectrum remains a matter of debate. In particular, the lack of benefit observed with renin-angiotensin system blockers has raised questions regarding our understanding of the pathophysiology of HFpEF. New paradigms including a prominent role of co-morbidities, inflammation, endothelial dysfunction, and pro-hypertrophic signalling pathways have been proposed. Recent proof-of-concept trials using a phosphodiesterase inhibitor, a mineralocorticoid receptor antagonist, an angiotensin receptor/neprilysin inhibitor, a soluble guanylate cyclase stimulator, or a sino atria, if current blocker provide important insight for the development of novel therapeutic strategies in HFpEF.
Komajda et al. (2014) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Recent proof-of-concept trials using novel pharmacological agents provide important insight for developing new therapeutic strategies in heart failure with preserved ejection fraction.