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Vasovagal syncope (VVS) is a common cause of syncope characterised by hypotension, with or without bradycardia, which results in cerebral hypoperfusion and resultant collapse with loss of consciousness. One of the main triggers for VVS (and the pathophysiological cornerstone of the head up tilt table test) is venous pooling in the lower limbs and relative central hypovolaemia.1
Despite uncertainty as to the underlying pathophysiology, stratagems to increase blood volume by increasing fluid and salt intake have been shown to be beneficial in the management of VVS. Salt supplementation improves orthostatic tolerance and increases baroreceptor sensitivity in patients with posturally related syncope.2 The main determinant of response to salt loading appears to be a 24 hour urinary sodium excretion of < 170 mmol.3
The aim of this study was to determine the relation between 24 hour urinary sodium excretion and both symptom severity, and tilt induced haemodynamic changes, in subjects with VVS.
From our database we retrospectively identified 68 consecutive patients who attended our tertiary referral syncope unit with a diagnosis of VVS, defined as positive head up tilt with symptom reproduction and in whom a 24 hour urinary sodium collection had been carried out within six weeks of …