Is There Still a Role for Drug Therapy in Vasovagal Syncope

By definition, syncope is not a disease, but a symptom clinically characterised by transient loss of consciousness, which generally leads to falling, followed by spontaneous recovery [1]. It can be due to neuromediated mechanisms as well as to cardiac or cerebrovascular causes. The Framingham study [2], which investigated 5209 patients with 26 years’ follow-up, indicated that syncope occurring in patients without cardiovascular or neurological pathology is likely to be neuromediated in nature, with a proportion ranging from 0.8% in the age group between 35 and 44 years to 4% in the oldest patients (age > 75 years). No increase in the incidence of sudden death, acute myocardial infarction, or cerebral stroke was noticed with respect to the syncope-free group throughout the follow-up. Nevertheless, some authors [3] define particular forms of vasovagal syncope as ‘malignant’, not because they carry an increased likelihood of sudden death, but because they can result in severe trauma, especially when the syncope is not preceded by relevant prodromes, as frequently happens in the elderly. Therefore, therapy against neuromediated syncope should essentially be aimed at preventing trauma and improving quality of life, especially in patients involved in risky professional activities, such as public transport drivers and aircraft pilots. All patients should be reassured as to the benign nature of the disorder and receive behavioural advice. They should be trained to avoid syncopetriggering conditions (such as over-warm or crowded environments, or prolonged standing up) and to recognise possible prodromes and all signs and symptoms preceding the event, in order to react with appropriate manoeuvres to abort the syncope and prevent any injury. A volume increase is necessary, which can be achieved by liquid (2–3 l water) [4] and salt injection (up