Summary
This narrative review synthesises emerging evidence on the gut-heart axis in cardiometabolic HFpEF, demonstrating how obesity, hypertension, and type 2 diabetes promote dysbiosis and loss of SCFA-producing bacteria, exacerbating systemic inflammation and cardiac remodelling through upregulation of TLR4- and NLRP3-mediated pathways. The authors propose that therapeutic elevation of beneficial SCFAs (acetate, propionate, butyrate) via dietary intervention could attenuate metainflammation, improve metabolic homeostasis, reinforce intestinal barrier integrity, and directly support failing myocardial function through multiple epigenetic and metabolic mechanisms. The review positions gut microbiota modulation as a biologically plausible, low-risk adjunctive strategy for cardiometabolic HFpEF management.
Regional applicability
The mechanistic evidence and nutritional therapeutic strategies are internationally applicable and relevant to United Kingdom clinical and public health contexts, where cardiometabolic HFpEF prevalence is rising in ageing populations with high obesity and type 2 diabetes burdens. Adoption would require integration with existing NHS guidelines on HFpEF management and dietetic practice.
Key measures
Gut microbiota composition and SCFA-producing taxa; circulating short-chain fatty acids (acetate, propionate, butyrate); inflammatory markers (TLR4, NLRP3 signaling); metabolic markers (lipid and glucose homeostasis); cardiac phenotypes (myocardial fibrosis, diastolic dysfunction); blood pressure and sympathetic tone.
Outcomes reported
This review examines mechanistic pathways linking gut dysbiosis and reduced short-chain fatty acid (SCFA) production to cardiometabolic heart failure with preserved ejection fraction (HFpEF), and evaluates nutritional therapeutic approaches targeting the gut-heart axis.
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