Neurogenic orthostatic hypotension (nOH) is common in patients with neurodegenerative disorders such as Parkinson’s disease, multiple system atrophy, pure autonomic failure, dementia with Lewy bodies, and peripheral neuropathies including amyloid or diabetic neuropathy. Due to the frequency of nOH in the aging population, clinicians need to be well informed about its diagnosis and management. To date, studies of nOH have used different outcome measures and various methods of diagnosis, thereby preventing the generation of evidence-based guidelines to direct clinicians towards ‘best practices’ when treating patients with nOH and associated supine hypertension. To address these issues, the American Autonomic Society and the National Parkinson Foundation initiated a project to develop a statement of recommendations beginning with a consensus panel meeting in Boston on November 7, 2015, with continued communications and contributions to the recommendations through October of 2016. This paper summarizes the panel members’ discussions held during the initial meeting along with continued deliberations among the panel members and provides essential recommendations based upon best available evidence as well as expert opinion for the (1) screening, (2) diagnosis, (3) treatment of nOH, and (4) diagnosis and treatment of associated supine hypertension.Electronic supplementary materialThe online version of this article (doi:10.1007/s00415-016-8375-x) contains supplementary material, which is available to authorized users.

Sudden death is an important late outcome in heritable (chromosome 1p1-1q1) cardiac conduction and myocardial disease. Pacemaker therapy is important for the treatment of symptomatic bradycardia, but it does not prevent sudden death. Family members who are beyond the third decade of life with reduced functional capacity, left ventricular dysfunction, pacemakers and who are the offspring of a parent with sudden death appear to be at greatest risk

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.

Bundle branch reentry as a mechanism of reentrant beats was first described in the early 1970s.^-^ When programmed ventricular stimulation became a method used for the induction of tachyarrhythmias, it was observed that a stimulated ventricular premature beat (V2) frequently elicited a spontaneous ventricular response, the "V3 phenomenon." The QRS morphology of V3 was also noted to be similar to that of the stimulated V2 beat. This observation initially suggested that the V3 beat may represent localized intramyocardial reentry near the site of catheter stimulation. However, it was also noted that the occurrence of a V3 beat was associated with those coupling intervals of V2 that generated retrograde conduction delay within the His-Purkinje system {HPS] as demonstrated by a prolonged V2H2 interval. This latter observation led to the snggestion that these V3 beats represented macro reentry within the HPS. As stimulation was commonly performed from the right ventricular apex, the site of block of the V2 beat would be the distal right bundle branch with retrograde conduction occurring via the left bundle branch. As the left bundle branch was capable of generating considerable retrograde conduction delay, the impulse would arrive at the His bundle late enongh to allow antegrade conduction via the right bundle branch and reentry into the right-sided myocardium.Akhtar, et al.,^-^ reported the first electrophysiological findings in hnman studies that supported the hypothesis that macro reentry was the mechanism of the V3 phenomenon. These authors demonstrated that the V3 beats seen following a premaAddress for reprints: