The mechanisms underlying VVS remain poorly understood. The current wisdom suggests that orthostasis results in venous pooling and a reduction in venous return (19), although debate continues on this issue (20- 21). It is believed that the vigorous contraction of the myocardium against an inadequately filled chamber then precipitates the Bezold-Jarisch reflex, which results in paradoxical hypotension and bradycardia (19). In younger patients, investigations using cardiac imaging, neurochemical assays, and electrophysiological analyses performed during HUT have found an increase in sympathetic nerve activity, serum epinephrine, and renin resulting in tachycardia and an initial rise in blood pressure in response to upright tilt (22). Before the onset of syncope, a sudden withdrawal in sympathetic drive evidenced by a reduction in sympathetic nerve activity (23), myocardial contractility (24), circulating norepinephrine, renin, and endothelin is observed (22). Increased cardiac vagal tone (25) and vasopressin levels (26) are observed after the onset of syncope. The mean age of subjects in the above studies was 42.5 years. Their generalizability to the older patient with VVS must, therefore, be open to question.