Neurocardiogenic syncope

Ward CR, Gray JC, Gilroy JJ, Kenny RA. Midodrine a role in the management of neurocardiogenic syncope. Heart 1998 79(l) 45-9. 

Sra J, Maglio C, Biehl M, Dhala A, Blanck Z, Deshpande S, Jazayeri MR, Akhtar M. Efficacy of midodrine hydrochloride in neurocardiogenic syncope refractory to standard therapy. J Cardiovasc Electrophysiol 1997 8(l) 42-6. 

Perez-Lugones A, Schweikert R, Pavia S, Sra J, Akhtar M, Jaeger F, Tomassoni GF, Saliba W, Leonelli FM, Bash D, Beheiry S, Shewchik J, Tchou PJ, Natale A. LFsefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope a randomized control study. J Cardiovasc Electrophysiol 2001 12(8) 935-8. 

Dysautonomias are conditions in which altered function of the autonomic nervous system adversely affects health. Such conditions range from more common transient episodes in otherwise healthy people (e.g., neurocardiogenic syncope), to progressive neurodegenerative diseases (e.g., multiple system atrophy), and to even more rare genetic disorders, such as dopamine P-hydroxylase deficiency (Table 29-5). 

Sra JS, Vishnubhakta S, Murthy S, et al. Use of intravenous esmolol to predict efficacy of oral beta-adrenergic blocker therapy in patients with neurocardiogenic syncope. J Am Coll Cardiol 1992 19 402 08. 

The current opinion is that neurocardiogenic syncope (NCS) is only one component of a broad and varied group of disturbances in the normal functioning of the ANS. Any one of the disorders may result in orthostatic intolerance, hypotension and, ultimately, syncope. 

There have been numerous studies on the utility of tilt-table testing in the evaluation of neurocardiogenic syncope, that have made it a well-established component in the diagnostic work-up of this disorder (31-36). 

The trials for pacing in neurocardiogenic syncope have gone through several phases. The initial results were based on observational studies. These were followed by historically controlled studies (17-19), randomized open-label controlled studies, and most recently placebo-controUed studies. 

The first reports on the use of permanent pacing for neurocardiogenic syncope demonstrated that VVI mode pacing is almost always ineffective and may actually aggravate syncope because of retrograde ventriculoatrial... 

Finally, Peterson et al. (18) presented data on the long-term effects of permanent pacing in patients with severe recurrent syncope and reproducible tilt-induced neurocardiogenic syncope with a pronounced bradycardic component. Dual-chamber permanent pacemakers were implanted in 37 patients who were then followed for 50 24 months. Approximately 89% had a marked reduction in symptoms, while 27% had complete elimination of symptoms. There was a reduction in the overall frequency of syncopal episodes from 136 to 11 episodes/year. Interestingly, the clinical features that best predicted the usefulness of permanent pacing included a relatively younger age (56 compared to 76 years) and the absence of a prodrome (84). 

As Sutton noted (103), pacing appears to be a very effective means of symptom control, and there is no doubt that it does work in some patients. Based on the physiological processes at play in neurocardiogenic syncope, it should be remembered that a fall in blood pressure usually precedes the fall in heart rate. Thus, pacing determined by rate criteria alone may represent too little too late. The development of newer sensor technology that allows for the direct or indirect measurement of blood pressure would permit the onset of pacing at the earliest point in the syncopal episode. 

Sra (104) has noted that evaluation of any therapy in neurocardiogenic syncope has been undermined by a number of factors. Amongst these he cites difficulty in demonstrating efficacy of therapy under controlled conditions, unreahstic end-points (i.e. a goal of eliminating all symptoms) and inadequate understanding of the natural history of the problem. ... 

While there has been several trials investigating the use of pacemakers in neurocardiogenic syncope, there is less data available on the use of pacing in orthostatic intolerance and autonomic dysfunction. Moss et. al (105) and Weismann et. al (106) initially reported that cardiac tachypacing could be beneficial and improves symptoms in selected patients with severe orthostatic hypotension. Abe et al (107) reported on two patients with severe refractory orthostatic hypotension, in whom tachypacing at 100 bpm improved the blood pressure drop in the upright position and prevented syncope. 

Grubb BP Neurocardiogenic syncope. In Syncope mechanisms and management. Grubb B, Olshansky B (Eds.) Malden, Mass, BlackweU/Futura Pubhshing 47-71 (2005). 

Natale A, Geiger MJ, Maglio C, et al. Recurrence of neurocardiogenic syncope without pharmacologic interventions. Am. J. Cardiol. RF77, 1001-1003 (1996). 

McGrady AV, Bush EG, Grubb BP Outcome of biofeedback-assisted relaxation for neurocardiogenic syncope and headache a cUnical replication series. Appl. Psychophysiol. Biofeedback 22 (1), 63-72 (1997). 

McGrady AV, Kem-Buell C, Bush E, Devonshire R, Claggett AL, Grubb BP Biofeedback-assisted relaxation therapy in neurocardiogenic syncope a pilot study. Appl. Psychophysiol. Biofeedback 28(3), 183-192 (2(X)3). 

Ector H, Reybrouck T, Heidbuchel H, GewUhg M, Van de Werf F Tilt training a new treatment for recurrent neurocardiogenic syncope or severe orthostatic intolerance. Pacing Clin. Electrophysiol. 21, 193-196 (1998). 

Di Girolamo E, Di lorio C, Sabatini P et al. Evaluation of the effects of diverse therapeutic treatments versus no treatment of patients with neurocardiogenic syncope. Cardiologia 43, 833-837 (1998). 

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