Biomarkers of metabolic syndrome, including adiponectin, leptin, TNF-alpha, IL-6, and uric acid, play a significant pathophysiological role in the structural and electrical remodeling that leads to atrial fibrillation.
What is the role of metabolic syndrome biomarkers in the pathogenesis of atrial fibrillation?
Various biomarkers of metabolic syndrome, including inflammatory and metabolic markers, play a significant role in the pathogenesis and pathophysiology of atrial fibrillation.
The relationship between Metabolic syndrome and Atrial Fibrillation is confirmed by many studies. The components of Metabolic syndrome cause remodeling of the atrial. Metabolic syndrome and metabolic derangements of the syndrome could be the cause of the pathogenesis of AF. This review article discusses the major biomarkers of Metabolic syndrome and their role in the pathogenesis of AF. The biomarkers are adiponectin, leptin, Leptin/ Adiponectin ratio, TNF-α, Interleukin-6, Interleukin-10, PTX3, ghrelin, uric acid, and OxLDL.The elevated plasma levels of adiponectin were linked to the presence of persistent AF. Leptin signaling contributes to angiotensin-II evoked AF and atrial fibrosis. Tumor necrosis factor-alpha involvement has been shown in the pathogenesis of chronic AF. Similarly, Valvular AF patients showed high levels of TNF-α. Increased left atrial size was associated with the interleukin-6 because it is a well-known risk factor for AF. Interleukin-10 as well as TNF-α were linked to AF recurrence after catheter ablation. PTX3 could be superior to other inflammatory markers that were reported to be elevated in AF. The serum ghrelin concentration in AF patients was reduced and significantly increased after treatment. Elevated levels of uric acid could be related to the burden of AF. Increased OxLDL was found in AF as compared to sinus rhythm control.
Saira Rafaqat (Sun,) conducted a review in Metabolic Syndrome and Atrial Fibrillation. Biomarkers of metabolic syndrome, including adiponectin, leptin, TNF-alpha, IL-6, and uric acid, play a significant pathophysiological role in the structural and electrical remodeling that leads to atrial fibrillation.