Tilt-induced Syncope Research Articles

Influence of Age on Magnitude and Timing of Vasodepression and Cardioinhibition in Tilt-Induced Vasovagal Syncope.

Cardioinhibition may diminish with age, but the changing balance of cardioinhibition and vasodepression with age has not been quantified, leaving the mechanism of vasovagal syncope (VVS) in old ageunclear. This study sought to quantify age-related changes of vasodepression and cardioinhibition in tilt-induced VVS. We studied 163 cases of tilt-induced VVS, evoked using the Italian protocol with blood pressure, heart rate, and video-electroencephalographic monitoring. Presyncope was excluded. Cardioinhibition was defined as the heart rate decrease before syncope; asystolic pauses (≥3 seconds) were divided into early and late asystole, ie, beginning early enough to or too late to be the major cause of loss of consciousness. The log-ratio method was used to quantify contributions of cardioinhibition and vasodepression, assessed in 2 10-second periods before the onset of cardioinhibition and before syncope. With increasing age, cardioinhibition decreased, ie, heart rate decreased less and more slowly near syncope (P< 0.0001), while vasodepression increased. Asystolic pauses were less frequent in the older one-half of the group than the younger one-half (26% vs 57%; P< 0.00001), but when it did, late asystole occurred more often (58% vs 15%; P<0.001). The shift toward less cardioinhibition and more vasodepression with increased age probably reflects a physiological shift in circulatory control. The weakening of cardioinhibition with age may detract from the efficacy of pacing in older patients with VVS. Cardioinhibition-vasodepression balance should be considered in pacing decisions in older subjects with VVS.

New hemodynamic criteria to separate classical orthostatic hypotension from vasovagal syncope.

ObjectiveTo define and evaluate hemodynamic criteria to distinguish between classical orthostatic hypotension (cOH) and vasovagal syncope (VVS) in tilt table testing (TTT).MethodsInclusion criteria for VVS were a history of VVS and tilt‐induced syncope defined as a blood pressure (BP) decrease and electroencephalographic changes during syncope with complaint recognition. Criteria for cOH were a history of cOH and a BP decrease meeting published criteria. Clinical diagnoses were established prior to TTT. We assessed (1) whether the decrease of systolic BP accelerated, “convex,” or decelerated, “concave”; (2) the time from head‐up tilt to when BP reached one‐half its maximal decrease; (3) the difference between baseline heart rate (HR) and HR at BP nadir. We calculated the diagnostic yield of optimized thresholds of these features and their combinations.ResultsWe included 82 VVS cases (40% men, median age 44 years) and 65 cOH cases (66% men, median age 70 years). BP decrease was concave in cOH in 79% and convex in VVS in 94% (p < 0.001). The time to reach half the BP decrease was shorter in cOH (median 34 sec, interquartile range (IQR) 19–98 sec) than in VVS (median 1571 sec, IQR 1381–1775 sec, p < 0.001). Mean HR increased by 11 ± 11 bpm in cOH and decreased by 20 ± 19 bpm in VVS (p < 0.001). When all three features pointed to VVS, sensitivity for VVS was 82% and specificity was 100%. When all three pointed to cOH, sensitivity for cOH was 71% and specificity was 100%.InterpretationThese new hemodynamic criteria reliably differentiate cOH from VVS.

Cardiac pacing in severe recurrent reflex syncope and tilt-induced asystole

AimThe benefit of cardiac pacing in patients with severe recurrent reflex syncope and asystole induced by tilt testing has not been established. The usefulness of tilt-table test to select candidates for cardiac pacing is controversial.Methods and resultsWe randomly assigned patients aged 40 years or older who had at least two episodes of unpredictable severe reflex syncope during the last year and a tilt-induced syncope with an asystolic pause longer than 3 s, to receive either an active (pacing ON; 63 patients) or an inactive (pacing OFF; 64 patients) dual-chamber pacemaker with closed loop stimulation (CLS). The primary endpoint was the time to first recurrence of syncope. Patients and independent outcome assessors were blinded to the assigned treatment. After a median follow-up of 11.2 months, syncope occurred in significantly fewer patients in the pacing group than in the control group [10 (16%) vs. 34 (53%); hazard ratio, 0.23; P = 0.00005]. The estimated syncope recurrence rate at 1 year was 19% (pacing) and 53% (control) and at 2 years, 22% (pacing) and 68% (control). A combined endpoint of syncope or presyncope occurred in significantly fewer patients in the pacing group [23 (37%) vs. 40 (63%); hazard ratio, 0.44; P = 0.002]. Minor device-related adverse events were reported in five patients (4%).ConclusionIn patients aged 40 years or older, affected by severe recurrent reflex syncope and tilt-induced asystole, dual-chamber pacemaker with CLS is highly effective in reducing the recurrences of syncope. Our findings support the inclusion of tilt testing as a useful method to select candidates for cardiac pacing.Study registrationClinicalTrials.gov identifier NCT02324920, Eudamed number CIV-05-013546.

A higher proportion of men than of women fainted in the phase without nitroglycerin in tilt-induced vasovagal syncope

PurposeVasovagal syncope (VVS) affects more women than men. We determined whether this sex ratio affects tilt table test (TTT) results.MethodsWe retrospectively studied TTT outcomes in suspected VVS. TTT consisted of supine rest, a maximum 20 min of head-up tilt without and, if nitroglycerin was needed, a further maximum 20 min after nitroglycerin administration. TTT was terminated if VVS occurred. We used binary logistic regression for the entire TTT and for each phase, with VVS as outcome and age and sex as predictors.ResultsTTT provoked vasovagal (pre)syncope in 494 out of 766 tests (64%). The proportion of men and women who fainted during the entire TTT did not differ significantly between the sexes (p = 0.13, corrected for age). A lower proportion of women than men had VVS in the phase without nitroglycerin (odds ratio 0.54; 95% confidence interval 0.37–0.79; p = 0.002, corrected for age), whereas a higher proportion of women than men fainted after nitroglycerin (odds ratio 1.58; 95% confidence interval 1.13–2.21; p = 0.008, corrected for age). These sex differences remained significant after correction for a history of orthostatic versus emotional triggers. The effect of sex on TTT outcome was closely associated with differences of blood pressure change upon tilt-up (lower in men in both TTT phases: without nitroglycerin p = 0.003; with nitroglycerin p = 0.05), but not with heart rate changes.ConclusionMen were more susceptible to induction of VVS without nitroglycerin and women after it. The unexpected findings may be due to sex-specific pathophysiological differences.

Skin sympathetic nerve activity as a biomarker for syncopal episodes during a tilt table test

Autonomic imbalance is the proposed mechanism of syncope during a tilt table test (TTT). We have recently demonstrated that skin sympathetic nerve activity (SKNA) can be noninvasively recorded using electrocardiographic electrodes. The purpose of this study was to test the hypothesis that increased SKNA activation precedes tilt-induced syncope. We studied 50 patients with a history of neurocardiogenic syncope undergoing a TTT. The recorded signals were band-pass filtered at 500-1000 Hz to analyze nerve activity. The average SKNA (aSKNA) value at baseline was 1.38 ± 0.38 μV in patients without syncope and 1.42 ± 0.52 μV in patients with syncope (P = .77). On upright tilt, aSKNA was 1.34 ± 0.40 μV in patients who did not have syncope and 1.39 ± 0.43 μV in patients who had syncope (P = .65). In all 14 patients with syncope, there was a surge of SKNA before an initial increase in heart rate followed by bradycardia, hypotension, and syncope. The peak aSKNA immediately (<1 minute) before syncope was significantly higher than baseline aSKNA (2.63 ± 1.22 vs 1.39 ± 0.43 μV; P = .0005). After syncope, patients were immediately placed in the supine position and aSKNA dropped significantly to 1.26 ± 0.43 μV; (P = .0004). The heart rate variability during the TTT shows a significant increase in parasympathetic tone during syncope (low-frequency/high-frequency ratio: 7.15 vs 2.21; P = .04). Patients with syncope do not have elevated sympathetic tone at baseline or during the TTT except immediately before syncope when there is a transient surge of SKNA followed by sympathetic withdrawal along with parasympathetic surge.

A proof of principle study of atomoxetine for the prevention of vasovagal syncope: the Prevention of Syncope Trial VI.

There are few effective therapies for vasovagal syncope (VVS). Pharmacological norepinephrine transporter (NET) inhibition increases sympathetic tone and decreases tilt-induced syncope in healthy subjects. Atomoxetine is a potent and highly selective NET inhibitor. We tested the hypothesis that atomoxetine prevents tilt-induced syncope. Vasovagal syncope patients were given two doses of study drug [randomized to atomoxetine 40 mg (n = 27) or matched placebo (n = 29)] 12 h apart, followed by a 60-min drug-free head-up tilt table test. Beat-to-beat heart rate (HR), blood pressure (BP), and cardiac haemodynamics were recorded using non-invasive techniques and stroke volume modelling. Patients were 35 ± 14 years (73% female) with medians of 12 lifetime and 3 prior year faints. Fewer subjects fainted with atomoxetine than with placebo [10/29 vs. 19/27; P = 0.003; risk ratio 0.49 (confidence interval 0.28-0.86)], but equal numbers of patients developed presyncope or syncope (23/29 vs. 21/27). Of patients who developed only presyncope, 87% (13/15) had received atomoxetine. Patients with syncope had lower nadir mean arterial pressure than subjects with only presyncope (39 ± 18 vs. 69 ± 18 mmHg, P < 0.0001), and this was due to lower trough HRs in subjects with syncope (67 ± 30 vs. 103 ± 32 b.p.m., P = 0.006) and insignificantly lower cardiac index (2.20 ± 1.36 vs. 2.84 ± 1.05 L/min/m2, P = 0.075). There were no significant differences in stroke volume index (32 ± 6 vs. 35 ± 5 mL/m2, P = 0.29) or systemic vascular resistance index (2156 ± 602 vs. 1790 ± 793 dynes*s/cm5*m2, P = 0.72). Norepinephrine transporter inhibition significantly decreased the risk of tilt-induced syncope in VVS subjects, mainly by blunting reflex bradycardia, thereby preventing final falls in cardiac index and BP.

Mechanisms of tilt-induced vasovagal syncope in healthy volunteers and postural tachycardia syndrome patients without past history of syncope.

Upright tilt table testing has been used to test for vasovagal syncope (VVS) but can result in “false positives” in which tilt‐induced fainting (tilt+) occurs in the absence of real‐world fainting. Tilt+ occurs in healthy volunteers and in patients with postural tachycardia syndrome (POTS) and show enhanced susceptibility to orthostatic hypotension. We hypothesized that the mechanisms for hypotensive susceptibility differs between tilt+ healthy volunteers (Control‐Faint (N = 12)), tilt+ POTS patients (POTS‐Faint (N = 12)) and a non‐fainter control group of (Control‐noFaint) (N = 10). Subjects were studied supine and during 70° upright tilt while blood pressure (BP), cardiac output (CO), and systemic vascular resistance (SVR), were measured continuously. Impedance plethysmography estimated regional blood volumes, flows, and vascular resistance. Heart rate was increased while central blood volume was decreased in both Faint groups. CO increased in Control‐Faint because of reduced splanchnic vascular resistance; splanchnic pooling was similar to Control‐noFaint. Splanchnic blood flow in POTS‐Faint decreased and resistance increased similar to Control‐noFaint but splanchnic blood volume was markedly increased. Decreased SVR and splanchnic arterial vasoconstriction is the mechanism for faint in Control‐Faint. Decreased CO caused by enhanced splanchnic pooling is the mechanism for faint in POTS‐Faint. We propose that intrahepatic resistance is increased in POTS‐Faint resulting in pooling and that both intrahepatic resistance and splanchnic arterial vasoconstriction are reduced in Control‐Faint resulting in increased splanchnic blood flow and reduced splanchnic resistance.

Quantitative electroencephalography characteristics of tilt-induced neurally-mediated syncope among youth

ObjectiveTo characterize the quantitative electroencephalographic (QEEG) patterns associated with tilt-induced syncope in youth. MethodsSeveral QEEG parameters were analyzed. Data were calculated for peak or nadir changes with syncope for amplitude-EEG, fast Fourier transform (FFT) power in several frequency ranges, 8–13 Hz/1–4 Hz frequency ratio, and FFT edge. ResultsChanges in QEEG parameters were present among all patients with tilt-induced syncope (n = 76). These changes included increases in the low frequency FFT power (1–4 Hz range), decreases in the power ratio (8–13 Hz/1–4 Hz) and decreases in the FFT edge (95%, 1–18 Hz). All patients had suppression of EEG amplitudes that closely followed loss of consciousness. Asymmetry indices demonstrated cerebral hemisphere lateralization at multiple periods during the evolution of syncope, but the side of lateralization did not differ from 0.5 probability. ConclusionsQEEG parameters can be used to characterize EEG changes associated with tilt-induced, neurally-mediated syncope. SignificanceQEEG may serve as a useful tool for the study of syncope neurophysiology, and the modeling of changes with syncope may improve our understanding of other neurologic disorders caused by defects in cerebral perfusion.

Clinical features of prolonged tilt-induced hypotension with an apparent vasovagal mechanism, but without syncope.

A previous study of electroencephalography (EEG) changes with syncope led to a finding that some young patients develop prolonged periods of tilt-induced hypotension, but they do not lose consciousness. The present study aim was to compare patterns of hemodynamic changes, measures of duration, and sweating between these patients and patients with tilt-induced vasovagal syncope. In an observational study, qualitative changes in hemodynamic parameters were compared between patients with prolonged hypotension (n = 30) and with syncope (n = 30). To demonstrate that periods of hypotension far-exceed the typical presyncope period, several parameters were used to compare the durations of events between groups. Differences in sweating patterns were explored. Parallels in hemodynamic changes were present in both groups suggesting similar vasovagal mechanisms. Patients with prolonged hypotension had longer durations of hypotension (165 ± 44 versus 57 ± 13 s, p < 0.001), diminished cardiac output (109 ± 38 versus 32 ± 9 s, p < 0.001), and EEG slowing (85 ± 31 versus 9 ± 4 s, p < 0.001) compared to patients with syncope. While all patients generated an increase in sweat rate, those with hypotension only developed a robust sweat response that always preceded the plateau in hypotension compared to 14 (47%) patients with syncope who developed an increase in sweating prior to syncope, p < 0.001. Similarities are present among hemodynamic changes with prolonged hypotension and with tilt-induced vasovagal syncope, suggesting a possible vasovagal mechanism for prolonged hypotension. If true, understanding why some individuals develop a vasovagal response that does not culminate in rapid syncope may help to elucidate the physiologic underpinnings of the vasovagal reflex.

Differentiating Motor Phenomena in Tilt-Induced Syncope and Convulsive Seizures: Shmuely S, Bauer PR, van Zwet EW, et al. Neurology. 2018;90e1339-e1346

Differentiating Motor Phenomena in Tilt-Induced Syncope and Convulsive Seizures: Shmuely S, Bauer PR, van Zwet EW, et al. Neurology. 2018;90e1339-e1346

Differentiating motor phenomena in tilt-induced syncope and convulsive seizures.

We assessed motor phenomena in syncope and convulsive seizures to aid differential diagnosis and understand the pathophysiologic correlates. We studied video-EEG recordings of tilt-induced syncope and convulsive seizures in participants aged 15 years and older. Syncope was defined as (1) loss of consciousness (video-assessed), (2) circulatory changes (accelerating blood pressure decrease with or without bradycardia/asystole), and (3) EEG changes ("slow" or "slow-flat-slow"). We assessed myoclonic jerks and tonic postures of the arms and noted time of occurrence, laterality, synchrony, and rhythmicity (mean consecutive differences of interclonic intervals). Video-EEG records of 65 syncope cases and 50 convulsive seizures were included. In syncope, postures occurred in 42 cases (65%) and jerks in 33 (51%). Fewer jerks occurred in syncope (median 2, range 1-19) compared to convulsive seizures (median 48, range 20-191; p < 0.001). Jerks were more rhythmic in seizures compared to syncope (p < 0.001). Atonia was seen in all syncope cases, while this was not observed in any seizure. Jerks predominantly occurred during the slow and postures during the flat EEG phase. Jerks and tonic postures were common in syncope, but semiology differed from convulsive seizures. The lack of overlap in the number of jerks suggests that less than 10 indicates syncope and more than 20 a convulsive seizure: the "10/20 rule." Loss of tone strongly favors syncope. The EEG correlates imply that jerks in syncope are likely of cortical origin, whereas tonic postures may result from brainstem disinhibition.

Gastric myoelectrical and neurohormonal changes associated with nausea during tilt-induced syncope.

Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery. Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n=18) and control subjects (n=6) without symptoms or hemodynamic changes during tilt-table testing. Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P=.003) and tachygastria (P=.014) power ratios, while the dominant frequency (P<.001) and the percent normogastria (P=.004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P=.001), tachygastria (P=.005), and normogastria (P=.03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5±122.8 vs 91.2±15.3pg/mL, P=.012) and epinephrine (434±91.3 vs 48.7±2.5pg/mL, P=.03), but not norepinephrine (P>.05), also differed with syncope between cases and controls. The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.

Temporal Relationship of Asystole to Onset of Transient Loss of Consciousness in Tilt-Induced Reflex Syncope.

The purpose of this study was to investigate the relationship between the onset of asystole and transient loss of consciousness (TLOC) in tilt-induced reflex syncope and estimate how often asystole was the principal cause ofTLOC. The presence of asystole in vasovagal syncope (VVS) may prompt physicians to consider pacemaker therapy for syncope prevention, but the benefit of pacing is limited in VVS. We evaluated electrocardiography, electroencephalography, blood pressure, and clinical findings during tilt-table tests. Inclusion required TLOC (video), electroencephalographic slowing, accelerating blood pressure decrease, and an RR interval≥3 s. We excluded cases with nitroglycerin provocation. Asystole after onset of TLOC (group A) or within 3 s before TLOC (group B) was unlikely to cause TLOC, but an earlier start of asystole (group C) could be the cause of TLOC. In one-third of 35 cases (groups A [n= 9] and B [n = 3]), asystole was unlikely to be the primary cause of TLOC. The median of the mean arterial pressure at the onset of asystole was higher when asystole occurred early (45.5 mmHg, group C) than when it occurred late (32.0 mmHg, groups A and B), which suggests that vasodepression was not prominent at the start of asystole in early asystole, further suggesting that early asystole was the prime mechanism of syncope. In one-third of cases of tilt-induced asystolic reflex syncope, asystole occurred too late to havebeenthe primary cause of TLOC. Reliance on electrocardiography data only is likely to overestimate the importanceofasystole.

Benefit of dual-chamber pacing with Closed Loop Stimulation in tilt-induced cardio-inhibitory reflex syncope (BIOSync trial): study protocol for a randomized controlled trial

BackgroundThe efficacy of dual-chamber cardiac pacing in neuro-mediated reflex syncope with a cardio-inhibitory response to the Tilt-Table test (TT) has not been definitively assessed so far. The lack of reproducibility of results from previous studies may be partially explained by discrepancies in subject selection and some weaknesses in design and methods. The European Society of Cardiology (ESC) has set a class IIb indication to pacemaker implantation in this population recommending further research.Methods/designThe BIOSync study is a multicenter, patient- and outcome-assessor-blind, randomized, parallel-arm, placebo-controlled trial with the objective of assessing the clinical benefit of cardiac pacing in patients with frequently recurrent reflex syncope, suspected (but not proven) to be triggered by asystolic pauses as showing a VASIS 2B response to the TT (>3-s pause regardless of blood pressure drop). The primary and secondary endpoints are time to first post-implantation recurrence of syncope or the combination of pre-syncope or syncope, respectively. One hundred and twenty-eight consenting patients will be 1:1 randomized to dual-chamber cardiac pacing ‘on’ or ‘off’ after pacemaker implantation, and followed up until the first adjudicated primary endpoint event for a maximum of 2 years. The so-called Closed Loop Stimulation function on top of dual-chamber pacing is the pacing mode selected in the study active arm. Participating patients are asked to self-report syncopal symptoms at least every 3 months with self-administered questionnaires addressed to an independent Adjudication Committee. Patients and members of the Adjudicating Committee are blinded to randomization. The study is designed to detect a 40% relative reduction in the 2-year incidence of syncopal recurrences with 80% statistical power.DiscussionThe BIOSync study is designed to definitively assess the benefit of pacing against placebo in reflex syncope patients with a cardio-inhibitory response to the TT. The study will also provide important information on the efficiency of the TT in appropriately selecting reflex syncope patients for cardiac pacing.Trial registrationClinicalTrials.gov, identifier: NCT02324920 (27 October 2016, date last accessed).

Tilt-induced vasovagal syncope and psychogenic pseudosyncope: Overlapping clinical entities

In the article “Tilt-induced vasovagal syncope and psychogenic pseudosyncope: Overlapping clinical entities” by H. Blad et al.,1 there is one error in the risk calculation of having both conditions (VVS …

Time- and frequency-domain analysis of beat to beat P-wave duration, PR interval and RR interval can predict asystole as form of syncope during head-up tilt

To seek possible differences in short-period temporal RR interval, P-wave and PR interval dispersion and spectral coherence in patients with a head-up tilt test positive for vasovagal syncope with or without prolonged asystole, severe symptoms and at high risk of trauma.We retrospectively reviewed 5 min ECG and blood pressure recordings obtained at baseline, at rest and during head-up tilt in 40 patients diagnosed as having recurrent vasovagal syncope confirmed at a head-up tilt test. We analysed autoregressive spectral power for all the ECG-derived variables, focusing on temporal P-wave and PR interval dispersion indexes as well as their spectral coherence calculated on the same 5 min recordings at rest and during tilt.ECG recordings obtained during tilt before syncope showed significantly lower P → PR spectral coherence and higher RR standard deviations in patients with tilt-induced asystole than in those without (0.567 ± 0.097 versus 0.670 ± 0.127, p: 0.010 and 84 ± 36 versus 46 ± 22 ms2, p < 0.0001). Differences in the RR standard deviations persisted also on the last hundred beats (−100) (113 ± 54 versus 34 ± 17 ms2, p < 0.0001). Multiple regression analysis identified a significantly negative association between the maximum RR intervals and P → PR coherence at rest (β: −0.3, p < 0.05) and positive association with RR−100 standard deviation during tilt-induced syncope (β: 0.621, p < 0.001).P → PR spectral coherence could be used to assess the risk of prolonged asystole in patients with tilt-induced vasovagal syncope as well as as a possible surrogate for tilt-testing during these patients’ follow-up.

Cardiac arrest during recovery after tilt-induced vasodepressor syncope in a 76-year old man

A 76-year-old man with a history of frequent syncope in youth and in the last 5 years was referred for a head-up tilt test. During the head-up tilt test, he developed a classical vasovagal reflex syncope. On immediate return to the supine position, the patient regained consciousness. Shortly afterward, the heart rate slowed distinctly and the patient became unresponsive with undetectable blood pressure. Chest compressions were initiated with return of spontaneous circulation 2 minutes later. Thereafter, the patient regained consciousness without neurological sequelae. This case illustrates cardiac arrest due to prolonged vasovagal reflex.

Sweat patterns differ between tilt-induced reflex syncope and tilt-induced anxiety among youth.

Profound sweating can occur with reflex-syncope and with emotional distress, but little is known about the similarities and differences between these sweat responses when they occur during orthostatic challenge. We sought to characterize and compare the sweat patterns related to tilt-induced syncope, presyncope, anxiety, and normal tilt testing. In a prospective observational study, quantitative sweat rate was measured from the abdomen, forearm, ankle, and thigh during head-upright tilt. Sweat characteristics were compared across tilt diagnoses of syncope, presyncope, anxiety, and normal testing. When anxiety and syncope/presyncope occurred during the same study (separated by≥6min), both were diagnosed. Our cohort comprised150 patients (15.1±2.3years; 82.9% female) with 156 diagnoses: 76 with reflex-syncope, 31 with presyncope, 23 with anxiety, and 26 with normal results. All syncope/presyncope patients and 20 (87%) of the anxiety patients had corresponding sweat responses. Minimal or negligible sweating occurred among patients with normal tests. Neither basal sweat (19.4±4.7 versus 18.3±3.7 versus 18.5±3.7nL/min/cm(2)) nor peak sweat (171±47.4 versus 149.4±64.4 versus 154.4±59.2 nL/min/cm(2)) differed between patients with syncope, presyncope, or anxiety, p=.32 and p=.12, respectively. However, the qualitative sweat patterns related to syncope/presyncope (diffuse, smoothly contoured, symmetrical, single peaks) differed considerably from the sweat patterns related to anxiety (heterogeneous, asymmetrical, roughly contoured single-peak, multi-peak, or progressive sweat changes). The sweat patterns related to syncope/presyncope are distinguishable from the sweat patterns related to anxiety. Recognition of the different sweat patterns can inform how signs and symptoms are interpreted during clinical orthostatic challenge.

The Clinical and Electroencephalographic Spectrum of Tilt-Induced Syncope and “Near Syncope” in Youth

BackgroundThe aim of the study was to characterize the clinical and electroencephalographic (EEG) patterns associated with tilt-induced reflex syncope and delayed orthostatic hypotension without syncope in youth. MethodsWe conducted a prospective observational study of 95 patients referred to a pediatric neurology clinic for head-upright tilt testing. Clinical signs, symptoms, video EEG, and continuous blood pressure and heart rate were monitored. ResultsEighty patients had reflex syncope, and 15 had delayed-onset hypotension without syncope. The mean age was 15.3 (standard deviation ±2.3) years; 75 (78.9%) were female. All patients with hypotension only had corresponding signs and symptoms; 13 (86.7%) had corresponding EEG slowing. The duration of EEG slowing with hypotension far exceeded the presyncope interval from onset of slowing to loss of consciousness among patients with syncope (P < 0.001). Although prior near-syncope and presyncope episodes were reported commonly in both groups, patients with delayed hypotension without syncope were less likely to have experienced loss of consciousness during episodes of orthostatic intolerance (P < 0.001). Patients with syncope had either slow-flat-slow (n = 23) or slow-only (n = 57) EEG patterns. Compared to those with slow-only EEG patterns, patients with the slow-flat-slow pattern had greater rates of asystole (P < 0.001), myoclonic movements (P < 0.001), facial grimace (P = 0.003), vocalizations (P = 0.002), and arm flexion (P < 0.001) or extension (P = 0.006) during tilt-induced syncope. ConclusionsAmong otherwise healthy youth, orthostatic signs and symptoms vary across the spectrum of tilt-induced reflex syncope and delayed hypotension without syncope. Delayed hypotension without syncope may represent the poorly defined phenomenon of “near syncope” in some patients.

The Role of the Baroreflex in TiltTableTesting: Outcome and Type of Response.

The purpose of this study was to better understand the role of the baroreflex in tilt-induced vasovagal syncope (VVS). The role of the baroreflex in tilt-induced VVS remains controversial. The authors hypothesized that: 1)patients with positive tilt table test (TTT) results have greater baroreflex gain (BRG) compared with patients with negative TTT results; and 2) patients with tilt-induced asystole have greater BRG compared with patients without asystole. Using the sequence method, BRG measurements were obtained in 438 consecutive patients undergoing TTT. Two hundred sixty-eight patients (61%) had positive TTT results (mean age 50 ± 21 years; 34% men), and 170 patients (39%) had negative TTT results (mean age 48 ± 21 years; 35% men). Mean BRG was significantly higher in patients with positive TTT results compared with those with negative TTT results (12.9 ± 6.0ms/mmHg vs. 11.5 ± 6.0ms/mmHg; p= 0.01). Among the 268 patients with positive TTT results, 23 (9%) had more than 3 s of asystole (mean age 37 ± 17; 30% men), and 245 patients had a mixed vasodepressor or cardioinhibitory response without asystole (mean age 51 ± 17 years; 34% men). Mean BRG was greater in patients with tilt-induced asystole (>3 s) compared with patients without asystole (15.3 ± 5.9ms/mmHg vs. 12.7 ± 5.9ms/mmHg; p= 0.03). The results of this study demonstrate that baseline BRG was higher in patients with positive TTT resultscompared with those with negative TTT results, with greater values noted in patients with tilt-induced asystole (>3 s) compared with those without asystole.