Background-Prior reports on patients with ARVC/D focused on individuals with advanced forms of the disease. There are limited data regarding diagnostic performance of various testing modalities in newly identified individuals suspected of having ARVC/D.

Arrhythmia frequency and number of appropriate ICD treatments were reduced after upgrade to CRT-ICD for HF treatment. Thus, apart from hemodynamic benefits, CRT may also ameliorate ventricular tachyarrhythmia susceptibility in HF patients.

Unanesthetized, unrestrained kangaroo rats (Dipodomys) were studied to examine the changes in the frequency and duration of sleep states caused by long-term manipulations of hypothalamic temperature (Thy) at a thermoneutral (30 degrees C) and a low (20 degrees C) ambient temperature (Ta). A cold stimulus present in either the hypothalamus or the skin decreased both the total sleep time (TST) and the ratio of paradoxical sleep (PS) to TST. At a low Ta, TST, but not the PS-to-TST ratio, was increased by raising Thy, indicating that a cold peripheral stimulus could differentially inhibit PS. At a thermoneutral Ta, cooling Thy decreased both TST and the PS/TST. Changes in the amount of PS were due largely to changes in the frequency, but not the duration, of individual episodes of PS, suggesting that the transition to PS is partially dependent on the thermoregulatory conditions existing during slow-wave sleep (SWS). These results are consistent with the recent findings that the thermoregulatory system is functional during SWS but is inhibited or inactivated during PS.

Circulating adrenaline concentrations in posturally induced vasovagal faints rise more rapidly in vasovagal fainters than in comparably posturally stressed non-fainters, and were significantly greater in fainters prior to either detectable haemodynamic compromise or diminution of circulating Norepi levels. These findings suggest that a premonitory rise in adrenaline concentrations occurs in vasovagal fainters unassociated with an evolving circulatory crisis.

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Abstract-A wide variety of pharmacological agents are currently used for prevention of recurrent neurally mediated syncope, especially the vasovagal faint. None, however, have unequivocally proven long-term effectiveness based on adequate randomized clinical trials. At the present time, ␤-adrenergic receptor blockade, along with agents that increase central volume (eg, fludrocortisone, electrolyte-containing beverages), appear to be favored treatment options. The antiarrhythmic agent disopyramide and various serotonin reuptake blockers have also been reported to be beneficial. Finally, vasoconstrictor agents such as midodrine offer promise and remain the subject of clinical study. Ultimately, though, detailed study of the pathophysiology of these syncopal disorders and more aggressive pursuit of carefully designed placebo-controlled treatment studies are essential if pharmacological prevention of recurrent neurally mediated syncope is to be placed on a firm foundation. (Circulation. 1999;100:1242-1248.)Key Words: syncope Ⅲ nervous system Ⅲ pharmacology Ⅲ Cardiovascular Drugs N eurally mediated (neurocardiogenic) syncope comprises a number of clinical conditions in which symptomatic systemic hypotension occurs as a result of a transient disturbance of neural reflex cardiovascular control (Table 1). [1][2][3] The vasovagal faint, carotid sinus syndrome, and postmicturition syncope are the most common forms of the neurally mediated faint. Others, including cough syncope and postexertional syncope, are less frequently encountered.This communication focuses on the pharmacological options that have been proposed for preventing neurally mediated faints, and especially the vasovagal faint, because it has been the most thoroughly studied. The objective is to provide an overview of the pharmacology and pertinent proposed modes of action of those agents that may be of benefit. Drug Therapy of Neurally Mediated Syncope: Basic PrinciplesMost individuals who experience a neurally mediated faint (particularly vasovagal fainters) require no additional therapy beyond education (ie, recognition of premonitory symptoms, avoidance of triggering events, and awareness of useful evasive actions) and reassurance regarding the non-lifethreatening nature of the condition. On occasion, stress and anxiety management may be warranted. Various more aggressive nonpharmacological (eg, support hose, extended exposure to upright posture, pacemakers) and pharmacological treatment options are usually reserved for those relatively few individuals who experience frequent syncope and/or when symptoms cause excessive lifestyle difficulties, threaten employment, or result in unacceptable risk of physical injury to the patient or others.Currently, drugs are used for both diagnostic and therapeutic purposes in the patient with neurally mediated syncope. [1][2][3] In terms of diagnostic applications, agents such as isoproterenol, edrophonium, nitroglycerin, and adenosine have been reported to be helpful during tilt-table testing (ie, so-called pharmacolog...

Compared with individuals who do not manifest VVS during HUT, VVS prone individuals appear to demonstrate functional diminution of baroreceptor responsiveness. This altered response may undermine the normal expected compensatory response to evolving systemic hypotension. The basis for this transient disturbance in baroreceptor responsiveness is currently unknown.

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