Neurocardiogenic, vasovagal syncope

Dual chamber pacing with rate-drop response is one of the latest therapeutic innovations. It significantly reduces the likelihood of syncope but not the occurrence of presyncope. We concur with Benditt that it seems prudent to be cautious about the present status of cardiac pacing in vasovagal syncope. One of the most extensive overviews on pharmacological treatment is by Atiga et al.. The agents most likely to be effective include beta-blockers, fludrocortisone, and alpha-adrenergic agonists. Education on avoiding trigger situations, increasing salt and fluid intake, regular meals, sitting or lying down quickly if warning symptoms occur, are other general recommendations. For unproved treatments, it is a standard requirement that a properly designed randomized clinical trial be performed. Unfortunately, not every question in medicine can be solved by this approach. This applies to the syndrome of neurocardiogenic syncope. In this field, large controlled studies are difficult to undertake due to the variable frequency of spontaneous symptoms and apparent long periods of remission. This contrasts with the urgency of decision making after frequent or dramatic syncopal attacks. The clinical spectrum varies widely between ‘malignant’ and ‘benign’. In their paper in this issue Santini et al. suggest coupling the best available cardiac pacing mode with the possibility of delivering an active drug. New sophisticated devices are supposed to have: (i) a diagnostic element; (ii) a patient activated intervention algorithm; (iii) an automatic drug-delivery element; (iv) a dual chamber pacemaker; (v) a data-storage unit. In this respect, atropine proved to be effective in the prevention of the cardio-inhibitory type of syncope. For the vasodepressor type, there was a statistically nonsignificant trend in favour of atropine. So, even when the ‘pharmaco-pacemaker’ is available, one drug would probably not suffice in every incident in every patient. Moreover, the type of syncope will vary from one patient to another and from one moment to another. So, more than one ‘ideal’ drug would have to be available in the automatic pharmaco-