Left Ventricular Geometry and Function Preceding Neurally Mediated Syncope

Abstract

Background-Neurally mediated syncope has been associated with increased left ventricular (LV) fractional shortening (FS) during tilt testing, which is consistent with the hypothesis that the stimulation of LV mechanoreceptors leads to reflex hypotension and/or bradycardia. However, FS does not represent true LV contractility because of its dependence on afterload and preload. Methods and Results-To elucidate the role of increased contractility in the mediation of neurally mediated syncope, we compared echocardiographic measures of LV performance corrected for end-systolic stress (ESS) in 21 patients (13 women and 8 men) with unexplained syncope who had either positive (nϭ10) or negative (nϭ11) responses to a tilt-table test. Two-dimensional echocardiographic LV imaging was performed at baseline and during the initial 5 minutes of upright tilt. In the supine position, both groups had similar LV end-diastolic volume indexes, stroke volumes, FS, circumferential ESS, and afterload-independent measures of LV performance (stress-corrected midwall and FS). However, after 5 minutes of upright tilt, patients who subsequently had a positive test had a lower stroke volume, lower stress-corrected midwall shortening, and endocardial FS. The tilt-positive group also had a greater fall in ESS and FS early during upright tilt. Conclusions-Reduced ESS, LV volume, and chamber function during initial upright tilt are associated with a subsequent positive tilt response in patients with unexplained syncope. These data suggest that if paradoxic activation of LV mechanoreceptors has a role in mediating neurally mediated syncope, it is not triggered by LV hypercontractility or increased systolic wall stress during the initial period of upright tilt. (Circulation. 2000;101:777-783.)

The venous system is the main determinant of hypotension in patients with vasovagal syncope

“…15 During the first and intermediate phases of TT, the reduction or the rate of reduction in SV or end-diastolic volume has been seen to be greater in patients with positive TT than in controls. 11,12,14,17,18 In the studies by de Jong-de Vos van Steenwijk et al 21 and Novak et al, 23 a decrease in SV and CO was not observed in patients with positive TT before loss of consciousness, and hypotension appeared secondary to a fall in calculated TPR. However, the former study investigated paediatric subjects without a history of spontaneous syncope, who might show a different haemodynamic behaviour.…”

Enhanced plasma catecholamine and cAMP response during the head-up tilt test in patients with vasovagal syncope

“…In contrast, other studies have not found a significant increase of adrenaline in VVS [13,15,25]. Myocardial hypercontractility, which could be expected as a possible result of an adrenaline surge preceding VVS, was not documented by echocardiography [26]. By measuring peak ventricular acceleration, Brignole et al showed that VVS may occur at both low and high levels of ventricular contractility [27].…”

Left Ventricular Hypercontractility Immediately after Tilting Triggers a Disregulated Cardioinhibitory Reaction in Vasovagal Syncope: Echocardiographic Evaluation during the Head-Up Tilt Test

“…Also, it has been assumed that vigorous LV contractions due to increased sympathetic tone stimulate afferent C receptors which in turn activate vagal tone [19], and some investigators have reported LV hypercontractility before syncope during the HUTT [7,8,9]. However, other previous studies have failed to verify the increased LV contractility as the initiating factor of hemodynamic changes in HUTT-induced VVS [5,10]. The current study was designed to give an account of those conflicting results and we postulated that a disregulated activation of the autonomic nervous system might promptly begin at the time of venous pooling.…”

“…However, that pathophysiologic concept and therapies in patients with VVS are largely based on assumptions or logical deductions made without sufficient data [2]. The Bezold-Jarisch reflex is believed to be triggered by venous pooling, a compensatory activation of the sympathetic nervous system, and/or reflex hypercontractility of the LV which is relatively underfilled [3,4,5,6]. In fact, there have been some reports observing the vigorous LV contractions before syncope [7,8,9].…”

“…In fact, there have been some reports observing the vigorous LV contractions before syncope [7,8,9]. On the other hand, other investigations have failed to find any prior hypercontractility of the LV in patients who experienced loss of consciousness during the head-up tilt test (HUTT) [5,10]. To date, there is no acceptable explanation for the discrepant results of these previous studies.…”