Structural remodelling during chronic atrial fibrillation: act of programmed cell survival

Atrial fibrillation is the most common cardiac arrhythmia with an overall p revalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable t herapeutic treatment, This has stimulated research to elucidate the pathoph ysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterio ration. Both phenomena are reversible but after prolonged duration of atria l fibrillation, a discrepancy occurs between rapid electrical remodelling a nd slow recovery or contractile function. Recent studies have indicated tha t morphological remodelling might underlie this incongruity. In experimenta l models of lone atrial fibrillation, the remodelling involves cellular cha nges that are reminiscent of dedifferentiation and are characterised by cel lular volume increase, myolysis, glycogen accumulation, mitochondrial chang es and chromatin redistribution. The absence of clear signs of degeneration in these models points towards cardiomyocyte adaptation or a mechanism of programmed cell survival. In patients with atrial fibrillation cardiomyocyt e degeneration does occur along with dedifferentiation which might be the r esult of underlying cardiac pathologies or longer duration of atrial fibril lation. In this review we focus on structural remodelling during atrial fib rillation. The different aspects of histological and ultrastructural change s as well as their role in atrial dysfunction and cardiomyocyte survival ar e discussed, We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented. (C) 2001 Elsevier Science B.V. All rights reserv ed.