Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.
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Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and frequently co-occurs with metabolic diseases, such as diabetes and obesity. Due to the intricate and multifactorial pathophysiology of AF, this disorder often eludes effective prevention and durable control with current therapeutic strategies; thus, these strategies may not consistently mitigate the onset, persistence, and related adverse outcomes of AF. Moreover, atrial metabolic remodeling and mitochondrial stress can promote the development of atrial cardiomyopathy and AF through electrophysiological and structural changes. Hence, targeting these metabolic alterations may prevent the onset of this arrhythmia. A contemporary therapeutic paradigm prioritizes restoration of metabolic homeostasis, led by sodium–glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists and complemented by emerging mitochondria-targeted strategies with potential for incremental disease modification. Concurrently, integrative multi-omics is mapping atrial metabolic diversity in AF to support biomarker-guided, individualized interventions, while next-generation imaging is enhancing the detection of pathologic substrates and refining risk assessment. This review provides a comprehensive analysis of the mechanisms through which metabolic remodeling and mitochondrial stress cause AF, evaluates current experimental and diagnostic methods, and discusses emerging substrate-targeted therapies.
Grigoriou et al. (Thu,) reported a other. Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.
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