Introduction
Sleep deprivation (SD) is known to be
associated with an increased incidence of adverse
cardiovascular and metabolic disorders in humans.
nervous system in the heart,9 and also is associated
with increased mortality.10,11
On the other hand, atrial conduction abnormalities
obtained by tissue Doppler imaging (TDI)
has been associated with the left atrial enlargement
in various clinical conditions.12–14 And also, the
prolongation of intraatrial and interatrial conduction
times and the inhomogeneous propagation
of sinus impulses are typical electrophysiological
features of the atrium prone to fibrillate.15–17
Moreover, atrial electromechanical delay (AEMD)
as measured by TDI has been shown to detect atrial
impairment in paroxysmal atrial fibrillation.17,18
And importantly, AEMD may also predict the
development of new-onset atrial fibrillation.19
Since atrial fibrillation is a reentrant arrhythmia,
it is logical that the triggering factor generally
is a critically timed atrial activation that may
give rise to reentry in a vulnerable structure.
The autonomic nervous system may act in this
respect as an external factor by modulating atrial
refractoriness through both atria and modifying
intraatrial conduction.20 Because autonomic tone
is affected by sleep and sleep duration, there might
Introduction
Sleep deprivation (SD) is known to be
associated with an increased incidence of adverse
cardiovascular and metabolic disorders in humans.
nervous system in the heart,9 and also is associated
with increased mortality.10,11
On the other hand, atrial conduction abnormalities
obtained by tissue Doppler imaging (TDI)
has been associated with the left atrial enlargement
in various clinical conditions.12–14 And also, the
prolongation of intraatrial and interatrial conduction
times and the inhomogeneous propagation
of sinus impulses are typical electrophysiological
features of the atrium prone to fibrillate.15–17
Moreover, atrial electromechanical delay (AEMD)
as measured by TDI has been shown to detect atrial
impairment in paroxysmal atrial fibrillation.17,18
And importantly, AEMD may also predict the
development of new-onset atrial fibrillation.19
Since atrial fibrillation is a reentrant arrhythmia,
it is logical that the triggering factor generally
is a critically timed atrial activation that may
give rise to reentry in a vulnerable structure.
The autonomic nervous system may act in this
respect as an external factor by modulating atrial
refractoriness through both atria and modifying
intraatrial conduction.20 Because autonomic tone
is affected by sleep and sleep duration, there might
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