Why the study?
Is the regression of established cardiac fibrosis in hypertensive heart disease feasible and will stiffness and symptomatic failure be improved?
Is the regression of established cardiac fibrosis in hypertensive heart disease feasible and will stiffness and symptomatic failure be improved?
This review highlights the unmet clinical need and potential cellular/molecular mechanisms for regressing established cardiac fibrosis in hypertensive heart failure with preserved ejection fraction.
Does not yet support fibrosis regression in hypertensive HFpEF; leaves open whether targeting mechanisms improves stiffness or symptoms.
Established cardiac fibrosis (ECF) with symptomatic heart failure preserved ejection fraction represents an ever-increasing segment of the hypertensive population. The regression of ECF with attendant improvement in myocardial stiffness and symptomatic failure represents an unmet health care need. Is the regression of ECF in hypertensive heart disease feasible and will stiffness and symptomatic failure be improved? What is the cellular/molecular signaling involved in its regression? What incremental knowledge is needed to proceed effectively? These issues are addressed in this Review.
No takes yet. Share an insight, caveat, or question.
Weber et al. (2017) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: