Chronic low‐grade inflammation in heart failure with preserved ejection fraction

Abstract

Heart failure (HF) with preserved ejection fraction (HFpEF) is currently the predominant form of HF with a dramatic increase in risk with age. Low‐grade inflammation, as occurs with aging (termed “inflammaging”), is a common feature of HFpEF pathology. Suppression of proinflammatory pathways has been associated with attenuated HFpEF disease severity and better outcomes. From this perspective, inflammasome signaling plays a central role in mediating chronic inflammation and cardiovascular disease progression. However, the causal link between the inflammasome‐immune signaling axis on the age‐dependent progression of HFpEF remains conjectural. In this review, we summarize the current understanding of the role of inflammatory pathways in age‐dependent cardiac function decline. We will also evaluate recent advances and evidence regarding the inflammatory pathway in the pathophysiology of HFpEF, with special attention to inflammasome signaling.

Abstract

Heart failure (HF) with preserved ejection fraction (HFpEF) is a complex syndrome characterized by multisystem disorders. Despite the increasing age‐dependent prevalence, there are very few effective therapies. Considered now as the greatest unmet medical need in cardiovascular disease, comorbidity‐driven inflammation has emerged as a critical component of HFpEF pathogenesis. Thus, chronic low‐grade inflammation may drive key pathophysiological changes in HFpEF.