Autonomic input

Sympathetic tone increases heart rate and, therefore, maintains atrial fibrillation (AF).11 Parasympathetic activation, such as increased vagal tone, tends to slow heart rate and produce a more variable rhythm.6 However, sympathetic and parasympathetic activation can initiate or exacerbate AF by reducing the duration of the atrial refractory period. This enhances atrial susceptibility to re-entry and promotes spontaneous depolarisation.32 Before the onset of AF, many patients seem to show increased adrenergic (sympathetic) input, followed by abrupt predominance of parasympathetic activity.6

Numerous diseases can influence parasympathetic innervation, including CHF and mitral valve disease, which increases left atrial pressure thereby producing atrial stretch. This, in turn, can facilitate focal electrical activity in the pulmonary vein.11 Strokes can influence the autonomic nervous system innervating the atria, suggesting a role in causing and perpetuating AF after a cerebrovascular event.21 Beta-blockers, which reduce sympathetic drive, are an important treatment for some AF patients.5

In the next section we look at the pathophysiology of stroke in people with atrial fibrillation

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