Sympathetic dysfunction in vasovagal syncope and the postural orthostatic tachycardia syndrome

Orthostatic hypotension (OH) is a common cardiovascular disorder, with or without signs of underlying neurodegenerative disease. OH is diagnosed on the basis of an orthostatic challenge and implies a persistent systolic/diastolic blood pressure decrease of at least 20/10 mm Hg upon standing. Its prevalence is age dependent, ranging from 5% in patients <50 years of age to 30% in those >70 years of age. OH may complicate treatment of hypertension, heart failure, and coronary heart disease; cause disabling symptoms, faints, and traumatic injuries; and substantially reduce quality of life. Despite being largely asymptomatic or with minimal symptoms, the presence of OH independently increases mortality and the incidence of myocardial infarction, stroke, heart failure, and atrial fibrillation. In this review, we outline the etiology and prevalence of OH in the general population, summarize its relationship with morbidity and mortality, propose a diagnostic and therapeutic algorithm, and delineate current challenges and future perspectives.

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“…(23,24). Both reflex syncope and postural orthostatic tachycardia syndrome have been discussed in detail elsewhere (22,(25)(26)(27).…”

Section: The Homeostatic Regulation Of Blood Pressurementioning

confidence: 99%

Orthostatic Hypotension

Ricci

Caterina

Fedorowski

2015

Journal of the American College of Cardiology

374

161

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“…OH is defined as a decrease in systolic blood pressure or diastolic pressure on standing compared to a sitting or supine position. The POTS is characterized by an excessive increase in the heart rate upon standing and is associated with symptoms of OI [2]. OI may cause injury, and epidemiological studies have confirmed that OI is an independent risk factor for coronary heart disease, stroke, and renal failure [1].…”

Section: Introductionmentioning

confidence: 99%

“…Conversely, an impairment of the compensatory response to upright posture can lead to decreased cerebral perfusion and an inability to tolerate the upright posture, termed orthostatic intolerance (OI) [1]. The symptoms of OI are fatigue, blurred vision, dizziness, nausea, abdominal pain, and syncope [2]. The main types of OI consist of orthostatic hypotension (OH) and postural orthostatic tachycardia syndrome (POTS) according to response to head-up tilt table test (HUT) [3].…”

Section: Introductionmentioning

confidence: 99%

Cortical Morphology in Patients with Orthostatic Intolerance

Shin

Kim²,

Han³

et al. 2015

Eur Neurol

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Background: We evaluated the cortical morphology in patients with orthostatic intolerance. Methods: Thirty patients with orthostatic intolerance, as well as age- and sex-matched normal controls, were enrolled in this study. We divided the patients into orthostatic hypotension (n = 22) and postural tachycardia syndrome (n = 8) groups based on their response to a head-up tilt table test. We analyzed whole-brain T1-weighted MRI images using FreeSurfer 5.1. The measures of cortical morphology were compared between the groups. Results: The cortical thickness in the right hemisphere, including the medial orbitofrontal, peri-calcarine, post-central, inferior temporal, and lateral occipital cortex, and in the peri-calcarine cortex of the left hemisphere was thinned in patients with orthostatic hypotension compared to normal controls. The other measures of cortical morphology, including the surface area, volume, and curvatures, did not differ between patients with orthostatic hypotension and normal controls. However, none of the measures of cortical morphology differed between patients with postural tachycardia syndrome and normal controls. Conclusions: We demonstrated that the cortical morphology significantly changed in patients with orthostatic hypotension but not in patients with postural tachycardia syndrome compared to normal controls. These findings support the hypothesis that orthostatic intolerance is a heterogeneous syndrome.

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“…1,3 Clinical management is complex, largely due to lack of knowledge about pathophysiological mechanisms. Previous studies have shown that neurohumoral changes, 4 deconditioning, 5 and hypovolemia 6 may be involved.…”

Section: Introductionmentioning

confidence: 99%

Reduced Systolic Volume: Main Pathophysiological Mechanism in Patients with Orthostatic Intolerance?

Távora-Mehta¹,

Mehta²,

Magajevski³

et al. 2016

Arquivos Brasileiros De Cardiologia

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BackgroundOrthostatic intolerance patients' pathophysiological mechanism is still obscure, contributing to the difficulty in their clinical management.ObjectiveTo investigate hemodynamic changes during tilt test in individuals with orthostatic intolerance symptoms, including syncope or near syncope.MethodsSixty-one patients who underwent tilt test at - 70° in the phase without vasodilators were divided into two groups. For data analysis, only the first 20 minutes of tilting were considered. Group I was made up of 33 patients who had an increase of total peripheral vascular resistance (TPVR) during orthostatic position; and Group II was made up of 28 patients with a decrease in TPVR (characterizing insufficient peripheral vascular resistance). The control group consisted of 24 healthy asymptomatic individuals. Hemodynamic parameters were obtained by a non-invasive hemodynamic monitor in three different moments (supine position, tilt 10' and tilt 20') adjusted for age.ResultsIn the supine position, systolic volume (SV) was significantly reduced in both Group II and I in comparison to the control group, respectively (66.4 ±14.9 ml vs. 81.8±14.8 ml vs. 101.5±24.2 ml; p<0.05). TPVR, however, was higher in Group II in comparison to Group I and controls, respectively (1750.5± 442 dyne.s/cm5 vs.1424±404 dyne.s/cm5 vs. 974.4±230 dyne.s/cm5; p<0.05). In the orthostatic position, at 10', there was repetition of findings, with lower absolute values of SV compared to controls (64.1±14.0 ml vs 65.5±11.3 ml vs 82.8±15.6 ml; p<0.05). TPVR, on the other hand, showed a relative drop in Group II, in comparison to Group I.ConclusionReduced SV was consistently observed in the groups of patients with orthostatic intolerance in comparison to the control group. Two different responses to tilt test were observed: one group with elevated TPVR and another with a relative drop in TPVR, possibly suggesting a more severe failure of compensation mechanisms.

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Sympathetic dysfunction in vasovagal syncope and the postural orthostatic tachycardia syndrome

Cited by 51 publications

References 75 publications

Orthostatic Hypotension

Orthostatic Hypotension

Cortical Morphology in Patients with Orthostatic Intolerance

Reduced Systolic Volume: Main Pathophysiological Mechanism in Patients with Orthostatic Intolerance?

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