The diagnosis of vasovagal syncope

The diagnosis of vasovagal syncope is usually based on a combination of careful history taking, clinical examination, and a surface electrocardiogram to exclude cardiac and non-cardiac causes of syncope [3,4]. When the etiology of syncope is uncertain, head-up tilt-table testing (HUTT) is commonly used to reproduce symptoms in patients with suspected vasovagal syncope [3,5]. Nitroglycerin (NTG) challenge during HUTT is often utilized to determine the etiology of unexplained syncope [5,6]. NTG may facilitate syncope through various pathways, but the precise mechanism of its contribution to syncope remains unclear [7]. Traditionally, venodilation and the venous pooling of blood into the low extremities and splanchnic and mesenteric vasculature along with the subsequent reduction of left ventricular preload have been regarded as the main hemodynamic effects of NTG, while arterial dilatation is thought to play a smaller role [8,9]. Some studies showed that sublingual NTG provokes a cardiac output-mediated vasovagal response that is not preceded by a fall in systemic vascular resistance (SVR) [10,11]. However, conflicting results concerning NTG-induced hemodynamic changes have been reported. Several studies revealed decreases in SVR without a marked change in cardiac output (CO) or ganciclovir rate (HR) during NTG administration [12].
Materials and methods
Results
Discussion Small doses of nitrates have traditionally been considered potent venodilators, leading to decreased ventricular preload and CO with a lesser impact on arterial resistance, and this effect of nitrate compounds has generally been assumed to be the main mechanism of nitrate-induced vasovagal syncope [8]. Several studies that used pulsations of indirect finger arterial pressure to show a reduced CO in subjects with presyncope during nitrate-stimulated HUTT support this concept [9–11]. However, Koole et al. found no evidence of increased venous pooling during nitrate-stimulated tilt testing in patients with a history of vasovagal syncope using a radionuclide technique [14]. Moreover, two reports that used thoracic bioimpedance and echocardiography did not reveal a decreased CO after NTG administration [12,15]. Consistent with our results, a recent study also suggested that the determinant of nitrate-induced presyncopal symptoms decreased SVR by means of thoracic bioimpedance [16]. These researchers examined the influence of body position on the response to NTG, and found that SVR decreased to a greater extent in subjects with presyncope than in the non-syncope group regardless of whether NTG was administrated in the supine position or upright position. They also observed a greater increase in aortic reflection time and decrease in pulse pressure in response to NTG in the presyncope group, which suggested decreased arterial resistance. In this study, we evaluated beat-to-beat hemodynamic changes with ICG during 3 phases of HUTT: in the supine position, in the upright position, and during NTG administration. While passive tilting was insufficient to reproduce presyncopal symptoms, a marked decrease in MAP was observed in the NTG+ group and an HR increment that may be explained by the baroreflex mechanism was observed. After the administration of NTG, a more profound decrease in MAP with presyncopal symptoms was observed in the NTG+ group along with a minimal increase in HR. The relatively small increment of HR in the NTG+ group suggests that NTG can influence the autonomic response. Previous literature revealed that nitrate-induced vasovagal syncope is related not only to a vasodilatory effect but also to baroreceptor-mediated stimulation of autonomic tone and neurohormonal activation [7,13]. NTG can stimulate sympathetic tone and induce vasovagal syncope by increasing cardiac contractility and subsequently triggering intraventricular pressure receptors, leading to the Bezold–Jarisch reflex [7]. However, we did not assess the effect of NTG on autonomic nervous tone and are unable to evaluate its contribution to presyncopal symptoms. Further studies of the role of baroreflex activity in vasovagal syncope are needed [13].