Non-Pharmacological Management of Neurocardiogenic Syncope

AbstractNeurocardiogenic syncope is a common disorder. It is diagnosed by obtaining a detailed history and performing a head-up tilt test, with or without drug provocation. Several studies have been performed pertaining to its management. However, no treatment, whether pharmacological or non-pharmacological, except for counterpressure maneuvers and daily orthostatic tilt training, has been proven effective. Randomized studies of therapies for neurocardiogenic syncope are needed

Sodium Channelopathy Underlying Familial Sick Sinus Syndrome With Early Onset and Predominantly Male Characteristics

Background-Sick sinus syndrome (SSS) is a common arrhythmia often associated with aging or organic heart diseases but may also occur in a familial form with a variable mode of inheritance. Despite the identifcation of causative genes, including cardiac Na channel (SCN5A), the pathogenesis and molecular epidemiology of familial SSS remain undetermined primarily because of its rarity. Methods and Results-We genetically screened 48 members of 15 SSS families for mutations in several candidate genes and determined the functional properties of mutant Na channels using whole-cell patch clamping. We identifed 6 SCN5A mutations including a compound heterozygous mutation. Heterologously expressed mutant Na channels showed loss-of-function properties of reduced or no Na current density in conjunction with gating modulations. Among 19 family members with SCN5A mutations, QT prolongation and Brugada syndrome were associated in 4 and 2 individuals, respectively. Age of onset in probands carrying SCN5A mutations was signifcantly less (mean±SE, 12.4±4.6 years; n=5) than in SCN5A-negative probands (47.0±4.6 years; n=10; P<0.001) or nonfamilial SSS (74.3±0.4 years; n=538; P<0.001). Meta-analysis of SSS probands carrying SCN5A mutations (n=29) indicated profound male predominance (79.3%) resembling Brugada syndrome but with a considerably earlier age of onset (20.9±3.4 years). Conclusions-The notable pathophysiological overlap between familial SSS and Na channelopathy indicates that familial SSS with SCN5A mutations may represent a subset of cardiac Na channelopathy with strong male predominance and early clinical manifestations

Identifying atrial arrhythmias versus pacing-induced rhythm disorders with state-of-the-art cardiac implanted devices

Repetitive non-reentrant ventriculo-atrial synchrony (RNRVAS) is a pacemaker-induced arrhythmia that must be distinguished from atrial fibrillation (AF). Pacemaker-induced arrhythmias are commonly detected as atrial high rate episodes (AHRE) by implanted cardiac devices. Two main types of atrial oversensing are recognized: far-field R-wave (FFRW) oversensing and pacemaker-induced arrhythmias, which include pacemaker-mediated tachycardia and RNRVAS. The presence of ventriculo-atrial conduction is required for both types of pacemaker-induced arrhythmias. The incidence of RNRVAS can increase with the use of various device settings and functions, such as long atrioventricular (AV) interval programming, the rate-adaptive mode, and the atrial overdrive pacing algorithm. The negative aspects of pacemaker-induced arrhythmias, especially RNRVAS, include (1) loss of optimal AV delay, (2) inappropriate increase in ventricular pacing, (3) induction of atrial arrhythmias, and (4) inaccurate diagnosis of AHRE. We review the incidence of arrhythmias, electrophysiological mechanisms, and the clinical diagnosis of RNRVAS identified by using dual-chamber implantable cardiac devices