1Meenakshi College of Allied Health Sciences, Meenakshi Academy of Higher Education and Research
2Department of Pedodontics & Preventive Dentistry, Meenakshi Ammal Dental College and Hospital, Meenakshi Academy of Higher Education and Research
3Department of General Medicine, Meenakshi Medical College Hospital & Research Institute, Meenakshi Academy of Higher Education and Research
4Meenakshi College of Nursing, Meenakshi Academy of Higher Education and Research
5Department of Community Medicine, Meenakshi Medical College Hospital and Research Institute, Meenakshi Academy of Higher Education and Research
6Meenakshi College of Physiotherapy, Meenakshi Academy of Higher Education and Research
Background: Heart Failure with preserved Ejection Fraction (HFpEF) is now being recognised as a systemic inflammation-based disease where obesity and metabolic dysfunction functions as the major drivers of cardiac architectural remodelling. Myocardial fibrosis, poor microvascular function, and diastolic stiffness are emerging evidence correlations with excess adiposity.
Objective: Mechanistic pathways through which obesity and metabolic dysregulation mediate cardiac remodeling in HFpEF, as well as clarifying the impact that these processes have on clinical presentation and disease progression.
Method: This is a review of the recent experimental, imaging, longitudinal cohort data assessing metabolic-inflammatory pathways, adipose-myocardial crosstalk, and structural remodelling patterns. Focus is on establishing the connection between the metabolic biomarkers and functional and morphological outcomes of the cardiac functions.
Results: In literature, obesity has been linked to systemic inflammation, dysfunction of endothelium, resistance to insulin and the response of adipokines. The abnormalities were involved in the left-ventricular concentric remodeling, myocardial fibrosis, microvascular rarefaction, and ventricular stiffness. Further mechanical and paracrine influence was caused by the enlarged epicardial adipose tissue which supported the progress of the diastolic dysfunction and atrial remodeling. Symptom severity and low exercise capacity were always associated with metabolic burden.
Conclusion: Obesity and metabolic dysfunction are critical mechanistic pathways of HFpEF, which determines the myocardial structure and clinical course. The interventions involved in the targeted reduce adiposity, enhance metabolic flexibility, and regulate inflammation would provide the most effective solution to remodeling reducing and increasing the outcomes.
Keywords: Obesity, HFpEF, insulin resistance, metabolic dysfunction, systemic inflammation, metabolic burden.
How to cite this article: Ramnath V, Jaiganesh I, Meyammai CT, Kavitha M, Punitha VC, Balamurugan N. Interplay of Obesity, Metabolic Dysfunction and Cardiac Remodelling in HFpEF: Mechanistic Insights. Int J Drug Deliv Technol. 2026;16(10s): 168-173; DOI: 10.25258/ijddt.16.10s.25
Source of support: Nil.
Conflict of interest: None