Key result
Metabolic alterations in atrial fibrillation cause metabolic stress due to an imbalance between energy demand and supply, presenting novel therapeutic opportunities to modulate cardiac metabolism.
This review highlights the pathophysiological role of AF-associated cellular metabolic changes and their potential value as novel therapeutic targets.
Metabolic targeting in AF warrants further study; this review extends mechanistic insights but leaves clinical adoption open.
Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice and is associated with morbidity and mortality. Over the past 2 decades, there have been major advances in understanding AF pathophysiology, but important knowledge gaps, particularly about targetable basic mechanisms, remain. Recent metabolomic and proteomic studies have shown changes in the expression of molecules involved in metabolic pathways in human and experimental AF, indicating a role for metabolic alterations in AF pathophysiology. AF is characterized by irregular high-frequency excitation and contraction that affect atrial energy demands, circulation and oxygen supply, and change the balance between metabolic demand and supply, causing metabolic stress. Here, we review the information available about AF-induced metabolic changes and their pathophysiological contribution. We also discuss the possibilities of developing novel therapeutic strategies that act by modulating cardiac metabolic processes during AF.
No takes yet. Share an insight, caveat, or question.
Harada et al. (2017) conducted a review in Atrial fibrillation. Metabolic alterations in atrial fibrillation cause metabolic stress due to an imbalance between energy demand and supply, presenting novel therapeutic opportunities to modulate cardiac metabolism.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:
More on Atrial fibrillationMore from Circulation Journal