Metabolic and vascular alterations, driven by energy imbalance during rapid electrical activity and metabolic diseases, play a significant role in the pathogenesis of atrial fibrillation.
Atrial fibrillation (AF) is the most common tachyarrhythmia in clinical practice. Over decades of research, a vast amount of knowledge has been gathered about the causes and consequences of AF related to cellular electrophysiology and features of the tissue structure that influence the propagation of fibrillation waves. Far less is known about the role of myocyte metabolism and tissue perfusion in the pathogenesis of AF. However, the rapid rates of electrical activity and contraction during AF must present an enormous challenge to the energy balance of atrial myocytes. This challenge can be met by scaling back energy demand and by increasing energy supply, and there are several indications that both phenomena occur as a result of AF. Still, there is ample evidence that these adaptations fall short of redressing this imbalance, which may represent a driving force for atrial electrical as well as structural remodelling. In addition, several 'metabolic diseases' such as diabetes, obesity, and abnormal thyroid function precipitate some well-known 'culprits' of the AF substrate such as myocyte hypertrophy and fibrosis, while some other AF risk factors, such as heart failure, affect atrial metabolism. This review provides an overview of metabolic and vascular alterations in AF and their involvement in its pathogenesis.
Opačić et al. (Tue,) conducted a review in Atrial fibrillation. Metabolic and vascular alterations, driven by energy imbalance during rapid electrical activity and metabolic diseases, play a significant role in the pathogenesis of atrial fibrillation.