Summary
This contemporary review consolidates evidence for obesity cardiomyopathy as a pathological entity that develops independent of hypertension, coronary heart disease, and other comorbidities. The authors synthesise epidemiological, clinical, and experimental findings to characterise the disease's phenotype and examine multiple interconnected mechanisms—including adipose tissue dysfunction, metabolic disturbances, mitochondrial calcium dysregulation, oxidative stress, mitophagy defects, and microvascular disease—that drive myocardial dysfunction in obesity. The review critically evaluates both pharmacological and lifestyle modification approaches to therapeutic management.
UK applicability
Given the rising prevalence of obesity and obesity-related heart failure in the United Kingdom, this review's characterisation of obesity cardiomyopathy as an independent disease entity has direct relevance to UK clinical practice, diagnostic protocols, and public health strategy. The emphasis on lifestyle modification interventions may inform UK cardiovascular disease prevention and management guidelines.
Key measures
Left ventricular dysfunction; myocardial structure and function; adipose tissue dysfunction markers; systemic inflammation; insulin resistance; glucose transport; free fatty acid spillover; lipotoxicity; mitochondrial calcium homeostasis; oxidative stress; autophagy/mitophagy; myocardial fibrosis; coronary flow reserve; coronary microvascular function; endothelial function
Outcomes reported
The review consolidates epidemiological, clinical, and experimental evidence for obesity cardiomyopathy as a distinct disease entity, documenting left ventricular dysfunction and identifying underlying cellular and molecular mechanisms independent of comorbid conditions.
Topic tags
Dig deeper with Pulse AI.
Pulse AI has read the whole catalogue. Ask about this record, its theme, or how the findings apply to UK farming and policy — every answer cites the underlying studies.