Abstract
Atrial fibrillation (AF) is the most common persistent arrhythmia, and can lead to systemic thromboembolism and heart failure. Aging and metabolic syndrome (MetS) are major risks for AF. One of the most important manifestations of MetS is dyslipidemia, but its correlation with AF is ambiguous in clinical observational studies. Although there is a paradoxical relationship between fasting cholesterol and AF incidence, the benefit from lipid lowering therapy in reduction of AF is significant. Here, we reviewed the health burden from AF and MetS, the association between two disease entities, and the metabolism of triglyceride, which is elevated in MetS. We also reviewed scientific evidence for the mechanistic links between very low density lipoproteins (VLDL), which primarily carry circulatory triglyceride, to atrial cardiomyopathy and development of AF. The effects of VLDL to atria suggesting pathogenic to atrial cardiomyopathy and AF include excess lipid accumulation, direct cytotoxicity, abbreviated action potentials, disturbed calcium regulation, delayed conduction velocities, modulated gap junctions, and sarcomere protein derangements. The electrical remodeling and structural changes in concert promote development of atrial cardiomyopathy in MetS and ultimately lead to vulnerability to AF. As VLDL plays a major role in lipid metabolism after meals (rather than fasting state), further human studies that focus on the effects/correlation of postprandial lipids to atrial remodeling are required to determine whether VLDL-targeted therapy can reduce MetS-related AF. On the basis of our scientific evidence, we propose a pivotal role of VLDL in MetS-related atrial cardiomyopathy and vulnerability to AF.
Highlights
Atrial fibrillation (AF) develops upon a complex of genetic impacts and additional disease-related remodeling, and can be clinically manifested with electrical and/or structural remodeling, which is defined as atrial cardiomyopathy [10]
Following secretion from liver into the circulation, the size and contents of very low density lipoproteins (VLDL) change by interacting with several enzymes, such as phospholipid transfer protein (PLTP), cholesteryl ester transfer protein (CETP), and lipoprotein lipase (LPL)
According to the aforementioned results, we suggest that the atrial cardiomyopathy in metabolic syndrome (MetS) is related to VLDL-induced lipotoxicity
Summary
AF develops upon a complex of genetic impacts and additional disease-related remodeling, and can be clinically manifested with electrical and/or structural remodeling, which is defined as atrial cardiomyopathy [10]. The following working definition of atrial cardiomyopathy has been proposed and published, and is based on experts’ consensus: “any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations” [10]. With this new definition, atrial cardiomyopathy can precede the onset of AF by a couple of decades [11]. Unlike AF-induced remodeling, in which the atria are affected selectively, most pathological processes that affect the atria involve the ventricles to a greater or lesser extent [10]
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