Key result
A systemic pro-inflammatory state induced by comorbidities drives microvascular endothelial cell inflammation, which subsequently triggers concentric cardiac remodeling and dysfunction in HFpEF.
Design
Review
Authors
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Supports endothelial inflammation as HFpEF mechanism; leaves open targeted therapies pending prospective trials.
Endothelial dysfunction driven by comorbidity-induced systemic inflammation is a central mechanism in the pathogenesis and cardiac remodeling of HFpEF.
Tschöpe et al. (2014) conducted a review in Heart failure with preserved ejection fraction (HFpEF). A systemic pro-inflammatory state induced by comorbidities drives microvascular endothelial cell inflammation, which subsequently triggers concentric cardiac remodeling and dysfunction in HFpEF.
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