This review provides an overview of the molecular and cellular pathways in HFPEF and potential therapeutic targets to address its phenotypic heterogeneity.
Heart failure (HF) with preserved ejection fraction (HFPEF) is responsible for half of all HF cases and will be the most common form of HF within the next 5 years. Previous studies of pharmacological agents in HFPEF have proved neutral or negative, in part due to phenotypic heterogeneity and complex underlying mechanisms. This review summarizes the key molecular and cellular pathways characterized in HFPEF as well as current and future therapies that target these mechanisms.
Nanayakkara et al. (Wed,) studied this question.
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