Atrial fibrillation is associated with significant morbidity and an estimated two-fold increase in premature death, exerting adverse effects on the left ventricular myocardium beyond the atrium.
Atrial fibrillation extends beyond atrial remodeling to cause systemic inflammation, endothelial dysfunction, and ventricular myocardial damage, which may have important prognostic implications for rate versus rhythm control strategies.
Atrial fibrillation (AF) is the most common sustained clinical arrhythmia and is associated with significant morbidity, mostly secondary to heart failure and stroke, and an estimated two-fold increase in premature death. Efforts to increase our understanding of AF and its complications have focused on unravelling the mechanisms of electrical and structural remodelling of the atrial myocardium. Yet, it is increasingly recognized that AF is more than an atrial disease, being associated with systemic inflammation, endothelial dysfunction, and adverse effects on the structure and function of the left ventricular myocardium that may be prognostically important. Here, we review the molecular and in vivo evidence that underpins current knowledge regarding the effects of human or experimental AF on the ventricular myocardium. Potential mechanisms are explored including diffuse ventricular fibrosis, focal myocardial scarring, and impaired myocardial perfusion and perfusion reserve. The complex relationship between AF, systemic inflammation, as well as endothelial/microvascular dysfunction and the effects of AF on ventricular calcium handling and oxidative stress are also addressed. Finally, consideration is given to the clinical implications of these observations and concepts, with particular reference to rate vs. rhythm control.
Wijesurendra et al. (Mon,) conducted a review in Atrial fibrillation. Atrial fibrillation is associated with significant morbidity and an estimated two-fold increase in premature death, exerting adverse effects on the left ventricular myocardium beyond the atrium.