Age-related electrophysiological changes and increased fibrosis in canine atria slow the conduction of premature beats, providing a mechanistic substrate for the increased propensity to atrial fibrillation in the elderly.
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May explain increased elderly AF susceptibility; extends canine models but leaves open human validation.
Our data show significant differences in contour of AP in adult and old atria. The responses to Bay K8644 and nisoldipine suggest a decreased I(Ca,L) in old atrial tissue. The alterations in AP contour and increased fibrosis may be responsible for slower conduction of early premature beats in old atria. The age-related changes in conduction of premature beats are consistent with those observed in patients with paroxysmal atrial fibrillation and may contribute to the greater propensity to atrial fibrillation in the aged.
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Evgeny P. Anyukhovsky (2002) studied this question.
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