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Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous, multi-organ syndrome driven by comorbidity-induced systemic inflammation. In acute and critical illness, such as sepsis, acute diastolic dysfunction is common. Its prognostic significance is debated and is complicated by hemodynamic instability and diagnostic challenges. Survivors of acute illness face a long-term risk of major adverse cardiovascular events, yet the transition from critical illness to acquired diastolic dysfunction to chronic HFpEF remains an underexplored area requiring further research. Recent landmark trials have established new therapeutic options for chronic HFpEF, including sodium glucose co-transporter 2 inhibitors, mineralocorticoid receptor antagonists, and glucagon-like peptide-1 receptor agonists. Here, we review the pathophysiology of HFpEF across the continuum from chronic stable HFpEF to acute decompensation, identify long-term sequelae, and highlight future advancements.
Fisher et al. (Tue,) studied this question.