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Updated: Nov 29, 2025
09:20
Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
Published on: February 13, 2021
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Left ventricular dysfunction in heart failure with preserved ejection fraction-molecular mechanisms and impact on
Frank R Heinzel1,2,3, Niklas Hegemann1,4, Felix Hohendanner1,2,3
1Department of Internal Medicine and Cardiology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany.
Cardiovascular Diagnosis and Therapy
|November 23, 2020
Summary
Heart failure with preserved ejection fraction (HFpEF) affects many patients but lacks targeted therapies. This review explores cardiomyocyte dysfunction and right ventricular issues in HFpEF for better classification and treatment.
Area of Science:
- Cardiology
- Molecular Biology
- Pathophysiology
Background:
- Heart failure with preserved ejection fraction (HFpEF) presents significant morbidity and mortality.
- Current HF therapies offer limited benefit for HFpEF patients.
- Comorbidities like hypertension, diabetes, and obesity are prevalent in HFpEF.
Purpose of the Study:
- To review alterations in cardiomyocyte function and cellular pathways in HFpEF.
- To outline upstream signaling pathways contributing to HFpEF.
- To summarize the prevalence and mechanisms of right ventricular dysfunction (RVD) in HFpEF.
Main Methods:
- Review of preclinical and clinical studies on HFpEF mechanisms.
- Analysis of molecular alterations in cardiomyocytes and extracellular matrix.
- Examination of systemic and regional signaling pathways.
Main Results:
- HFpEF is characterized by left ventricular (LV) diastolic dysfunction and structural remodeling.
- Pulmonary hypertension and RVD are common and increase mortality in HFpEF.
- Alterations in ion homeostasis, sarcomere function, and metabolism contribute to diastolic dysfunction.
Conclusions:
- Understanding molecular mechanisms of LV and RV dysfunction is crucial for HFpEF.
- Improved classification and targeted therapies for HFpEF are needed.
- Investigating cellular pathways may lead to novel therapeutic strategies for HFpEF.
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