Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Abstract

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5 Ϯ 1 episodes/mo, n ϭ 14), age-and sex-matched controls (CON, n ϭ 23), and in healthy subjects who consistently experienced syncope during tilt (FS ϩ , n ϭ 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS ϩ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope. ( J. Clin. Invest. 1997. 99:2736-2744.)

Reduced baroreflex sensitivity in patients with vasovagal syncope

“…TPR at the time of syncope did not differ signifi cantly between the two groups of patients (p = 0.77) (Tab. 3).…”

“…Reduced arterial barorefl ex sensitivity was reported in patients suffering from vasovagal syncope in some studies (1,3,4), whereas another studies did not found differences in barorefl ex sensitivity in these subjects (5). In some reports, an increased baroreceptor refl ex gain was observed in fainting subjects (6, 7).…”

The pathophysiologic mechanisms associated with hypotensive susceptibility

“…In patients who go on to develop near syncope or syncope, acute systemic vasodilatation triggered by forceful cardiac contractions is believed to be the underlying mechanism. This hypothesis has been supported by several studies showing reduction in cardiac volume, increase in fractional shortening [2,3,9,30], forearm vasodilatation and loss of sympathetic tone during syncope [1,11,26,27,33,40]. Increased vagal tone resulting in bradycardia and asystole plays a role but is not always present during reflex syncope [28].…”

Contribuição dos grandes vasos arteriais na adaptação cardiovascular a ortostase

“…Mosqueda-Garcia et al investigated the barorefl ex sensitivity in individuals with vasovagal syncope and positive IT and observed a decreased response of the barorefl ex cardiovagal and sympathetic components when compared to the control group 78 . Some authors have suggested that the function of the barorefl ex is preserved, but it undergoes a sudden suppression due to a depressor refl ex that originates from the heart 79 .…”