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

V L Thijssen, J Ausma, M Borgers

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes 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 cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.

Original languageEnglish
Pages (from-to)14-24
Number of pages11
JournalCardiovascular Research
Volume52
Issue number1
Publication statusPublished - Oct 2001
Externally publishedYes

Cite this

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title = "Structural remodelling during chronic atrial fibrillation: act of programmed cell survival",
abstract = "Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1{\%}. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes 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 cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.",
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Structural remodelling during chronic atrial fibrillation : act of programmed cell survival. / Thijssen, V L; Ausma, J; Borgers, M.

In: Cardiovascular Research, Vol. 52, No. 1, 10.2001, p. 14-24.

Research output: Contribution to journalReview articleAcademicpeer-review

TY - JOUR

T1 - Structural remodelling during chronic atrial fibrillation

T2 - act of programmed cell survival

AU - Thijssen, V L

AU - Ausma, J

AU - Borgers, M

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N2 - Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes 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 cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.

AB - Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes 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 cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.

KW - Animals

KW - Apoptosis

KW - Atrial Fibrillation/metabolism

KW - Calcium/metabolism

KW - Calcium Channels/metabolism

KW - Cell Death

KW - Chronic Disease

KW - Connexins/metabolism

KW - Contractile Proteins/metabolism

KW - Fibrosis

KW - Goats

KW - Heart Atria

KW - Humans

KW - Microscopy, Electron

KW - Models, Animal

KW - Myocardium/metabolism

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