Endothelial dysfunction driven by comorbidity-induced systemic inflammation is a central mechanism in the pathogenesis and cardiac remodeling of HFpEF.
Answers are grounded in this paper and cite their sources.
Supports endothelial inflammation as HFpEF mechanism; leaves open targeted therapies pending prospective trials.
Recently, a new paradigm for the development of heart failure with preserved ejection fraction (HFpEF) has been proposed, which identifies a systemic pro-inflammatory state induced by comorbidities as the origin of microvascular endothelial cell inflammation and subsequent concentric cardiac remodeling and dysfunction. This review further discusses the pivotal role of the inflamed endothelium in the pathogenesis of HFpEF-specific cardiac remodeling. The potential importance of reciprocal interactions of the endothelium with cardiac fibroblasts and cardiomyocytes and with the cardiac neurohumoral response in this cardiac remodeling process is outlined.
No takes yet. Share an insight, caveat, or question.
Tschöpe et al. (2014) conducted a review in Heart failure with preserved ejection fraction (HFpEF).
Synapse has enriched 10 related papers. Consider them for comparative context: