Cerebrovascular blood flow during the near syncopal phase of head-up tilt test: a comparative study in different types of neurally mediated syncope.

AIMS: This study analyses the changes in cerebral blood flow (CBF) velocity occurring in the near syncopal phase of head-up tilt test (HUT) to determine whether their appearance during the premonitory symptoms permits the differentiation of the different types of haemodynamic response. METHODS AND RESULTS: Six hundred and nineteen patients aged 35.9 +/- 16.4 with a prior history of syncope (55%) or presyncope (45%) were studied. Head-up tilt test was positive in 585 patients. The test was interrupted before syncope, once hypotension was evident and CBF changed. A vasovagal reaction (VVR) was observed in 245 patients. They had a 59% fall in diastolic CBF velocity, whereas systolic CBF velocity decreased by 12%. Postural orthostatic tachycardia syndrome (POTS) was observed in 82, systolic and diastolic CBF velocity decreased 44 and 60%, respectively. A similar response was observed in 258 patients with the orthostatic intolerance (OI) pattern. No significant changes were observed in the negative group. CONCLUSION: Patients with VVR had changes in CBF velocity, which are different from those presented by patients with POTS and OI pattern. Cerebral blood flow monitoring is useful to increase the yield of HUT and may allow early interruption before syncope occurs, reducing patient discomfort.     

Tilt testing in neurocardiogenic syncope: isosorbide versus isoproterenol

OBJECTIVE: To compare the diagnostic value of pharmacological stimulation with sublingual isosorbide dinitrate and intravenous isoproterenol during tilt testing in patients with neurocardiogenic syncope and with a negative tilt test without pharmacological provocation. METHODS AND RESULTS: One hundred and twenty patients with a history of neurocardiogenic syncope (aged 15 to 77 years) and 50 healthy volunteers (aged 25 to 70 years) were prospectively submitted to head-up tilt (HUT). Those who did not develop syncope or presyncope during passive HUT for 30 minutes underwent repeated HUT with isoproterenol infusion at 4 microg/min (ISOP HUT), for 10 minutes, and, subsequently, were tilted after sublingual administration of 5 mg of isosorbide dinitrate (ISDN HUT) for another 12 minutes. ISDN HUT was always performed after ISOP HUT. Sensitivity and specificity of passive HUT were 41% (95% C.I. 32.9% to 51.0%) and 100%, respectively. Sensitivity of ISOP HUT was 51.4% (95% C.I. 39.2% to 63.6%) and specificity 70% (95% C.I. 55.4% to 82.1%) and for ISDN HUT were 70% (95% C.I. 57.9% to 80.4%) and 88% (95% C.I. 75.7% to 95.5%), respectively. The accuracy of ISDN HUT was significantly higher than the accuracy of ISOP HUT 77.5% (95% C.I. 68.9% to 84.6%). There were fewer side effects during ISDN HUT. CONCLUSION: Sublingual isosorbide dinitrate is at least as sensitive as isoproterenol to assess patients with suspected neurocardiogenic syncope and with a negative tilt test without provocation. The low rate of side effects and the higher accuracy of ISDN HUT, along with the simplicity of this challenge compared to ISOP HUT, suggest that sublingual isosorbide dinitrate should be preferred as a provocative agent to evaluate neurocardiogenic syncope after a negative passive tilt test.     

Head-up Tilt Testing Predicts Syncope During Ventricular Tachycardia in Implantable Cardioverter Defibrillator Patients

Implantable cardioverter defibrillator (ICD) programming is usually based on results of supine electrophysiological (EP) testing. However, EP testing does not provide any information about tolerance to ICD therapy in the upright posture. We hypothesized that in addition to the arrhythmia duration and ventricular tachycardia (VT) cycle length, cerebral perfusion may play a role in determining tolerance to tiered ICD therapy. Transcranial Doppler (TCD) and cerebral venous oxygen saturation (rCVOS) are relatively new noninvasive techniques that may be used to assess dynamic changes in cerebral blood flow and metabolism during VT. Sixteen patients with pace-terminable VT and ICDs underwent supine (S) and upright tilt (HUT) ICD testing in conjunction with TCD and rCVOS monitoring. ICDs were programmed to deliver antitachycardia pacing, cardioversion, and defibrillation for VT, in the ascending order of aggressivity. Despite no significant differences in the induced VT cycle length (320 ± 100 msec, S, vs 330 ± 90 msec, HUT) and VT duration (14.6 ± 6.7 sec, S, vs 17 ± 9.2 sec, HUT), cerebral perfusion was more significantly impared during HUT (21 ± 10 [S] vs 29 ± 7% decrease from baseline [HUT], P < 0.001), and rCVOS decreased from baseline (5 ± 6 [S] vs 10 ± 6 [HUT] %, P < 0.001). Five of 16 patients experienced syncope during HUT and none during supine testing. At 1-year follow-up five patients who experienced syncope during HUT experienced at least one episode of syncope, whereas none not so identified did. We conclude that: (1) Supine ICD testing is insufficient to predict individual patient tolerance to ICD therapy; (2) HUT testing predicts tolerance to ICD therapy; and (3) noninvasive neuromonitoring techniques are useful for assessment of cerebral blood flow and metabolism during ICD testing.     

Plasma galanin response to head-up tilt in normal subjects and patients with recurrent vasovagal syncope

Neurohumoral factors may contribute to cardiovascular changes associated with vasovagal syncope (VVS). Galanin (GAL) is a neuropeptide, widely distributed in the central and peripheral nervous systems, that interacts with both sympathetic and vagal systems as well as with neurotransmitters, such as serotonin. We investigated the changes in plasma GAL and catecholamine levels during head-up tilt (HUT) test in patients with recurrent VVS. Twenty-two patients (11 women, aged 33.1 +/- 4.2 years) with a history of VVS and 10 healthy subjects (5 women, aged 38.0 +/- 5.8 years) underwent HUT test (60 degrees, 45 minutes). GAL and catecholamine plasma levels were measured in the supine position, during HUT and, in patients with positive response, at presyncope, syncope, and after recovery of consciousness. Thirteen patients developed syncope during HUT, whereas no healthy subjects had a positive response. In healthy subjects, GAL did not change during HUT. By contrast, in patients with a history of VVS and a negative response to tilting (no syncope), GAL significantly (P <.001) increased in response to tilting (supine, 10.2 +/- 0.6 pmol/L; tilting, 18.1 +/- 1.1 pmol/L at 45 minutes) and correlated positively with the increases in blood pressure (BP) and heart rate (HR). In patients with a positive response, GAL did not change either before the loss of consciousness or during syncope. In patients with a positive response, norepinephrine (NE) significantly (P <.001) increased during tilting and then remained practically unchanged during syncope, whereas epinephrine (E) significantly (P <.001) increased during tilting and then showed further significant increases at presyncope and syncope. In conclusion, this study shows that circulating GAL levels progressively increase in correlation with the cardiovascular parameters during a negative HUT in patients with a history of VVS, whereas they remain unchanged in healthy subjects. Moreover, in the patients with tilting-induced syncope GAL does not change either before or during loss of consciousness. These data suggest a role for endogenous GAL in the adaptive responses to acute orthostatic stress preventing syncope in susceptible individuals.     

Comparative study of cerebral blood flow between postural tachycardia and neurocardiogenic syncope, during head-up tilt test.

We assessed the cerebral blood flow velocity response to head-up tilt test in patients with typical neurocardiogenic syncope compared with patients showing postural tachycardia. Fifty patients (21 men) with history of orthostatic intolerance, younger than 50 years (mean 27 +/- 10), participated in the study. Transcranial Doppler sonography of the middle cerebral artery, heart rate and brachial blood pressure were recorded during a head-up tilt test. According to the outcome of the test, patients were categorized in two groups: neurocardiogenic syncope (29 patients) and postural tachycardia (21 patients). The clinical history of the two groups was similar. During baseline in the supine position, no differences in haemodynamic parameters were observed. From the first min of tilt, the heart rate was higher in patients with postural tachycardia than in patients with neurocardiogenic syncope. Although, during tilt, the absolute values of the cerebral blood flow parameters were similar in the two groups, throughout tilt, continuous observation of the Doppler recording in patients with postural tachycardia showed intermittent fluctuation of the blood flow velocity, with an oscillatory pattern, which were not observed in the recordings in patients with neurocardiogenic syncope. Comparison of patients with neurocardiogenic syncope, and those with postural tachycardia also showed larger variations of the pulsatility index (P < 0.05) in the postural tachycardia group. These findings support the possibility that abnormalities within the central nervous system play a pivotal role in the pathogenesis of postural tachycardia.     

Physical Training as Non-Pharmacological Treatment of Neurocardiogenic Syncope

Background

Characterized as a sudden and temporary loss of consciousness and postural tone, with quick and spontaneous recovery, syncope is caused by an acute reduction of systemic arterial pressure and, therefore, of cerebral blood flow. Unsatisfactory results with the use of drugs allowed the nonpharmacological treatment of neurocardiogenic syncope was contemplated as the first therapeutic option.

Objectives

To compare, in patients with neurocardiogenic syncope, the impact of a moderate intensity aerobic physical training (AFT) and a control intervention on the positivity of head-up tilting test (HUT) and orthostatic tolerance time.

Methods

Were studied 21 patients with a history of recurrent neurocardiogenic syncope and HUT. The patients were randomized into: trained group (TG), n = 11, and control group (CG), n = 10. The TG was submitted to 12 weeks of AFT supervised, in cycle ergometer, and the CG to a control procedure that consisted in 15 minutes of stretching and 15 minutes of light walk.

Results

The TG had a positive effect to physical training, with a significant increase in peak oxygen consumption. The CG did not show any statistically significant change before and after the intervention. After the intervention period, 72.7% of the TG sample had negative results to the HUT, not having syncope in the revaluation.

Conclusion

The program of supervised aerobic physical training for 12 weeks was able to reduce the number of positive HUT, as it was able to increase tolerance time in orthostatic position during the HUT after the intervention period.     

经食管心房起搏对心脏抑制型血管迷走性晕厥作用的探讨

为评价心脏起搏对心脏抑制型血管迷走性晕厥（ＣＩＶＶＳ）的作用,对２５例首次倾斜试验（ＨＵＴ）阳性并表现为ＣＩＶＶＳ的病人行重复ＨＵＴ,当病人出现心动过缓时,以７２ｂｐｍ的频率经食管心房起搏（ＴＥＡＰ）。２５例中有１８例病人出现心率减慢,其中１例在起搏前即出现晕厥伴低血压;另１７例行ＴＥＡＰ,２例出现房室阻滞伴晕厥,１５例起搏心率维持在７２ｂｐｍ,但起搏７．３７±４．３０（４～１８）ｓ后,病人出现晕厥或先兆晕厥,平均动脉压由８８．８８±１０．０８ｍｍＨｇ降至５５．８６±１２．１８ｍｍＨｇ（Ｐ＜０．０１）。提示ＴＥＡＰ不能预防ＣＩＶＶＳ晕厥的发生。     

Initial experience with an implantable loop recorder in patients with unexplained syncope

Patients with recurrent syncope undiagnosed after extensive noninvasive and invasive testing pose a diagnostic and therapeutic dilemma. Holter monitoring is non-diagnostic in 90% of cases. Recent developments in loop recorder technology permit longterm ECG monitoring in patients with recurrent unexplained syncope. The implantable loop recorder monitors a single lead electrogram continuously using 2 sensing electrodes on the device shell. The device was implanted in 20 patients (11 male, 9 female) with the history of recurrent syncope. During a mean follow-up of 12+/-6 months after device implantation, 11 patients (55%) experienced syncope (8 pts) or presyncope (3 pts). In the remaining 9 patients, no syncope occurred. In all 11 patients with syncope or presyncope during follow-up, loop recording definitively determined whether an arrhythmia was the cause of symptoms or not. Diagnosis included bradycardia in one patient, tachycardia in two patients, in one patient two rhythm disturbances were revealed: frequent ventricular premature beats with bigemini and atrial flutter. Two patients had a neurocardiogenic syncope. Syncope was nonarrhythmic in 5 patients. An implantable loop recorder is useful for establishing the diagnosis if symptoms are recurrent but too infrequent for conventional monitoring techniques.     

Efficacy of Midodrine Hydrochloride in Neurocardiogenic Syncope Refractory to Standard Therapy

Midodrine for Refractory Neurocardiogenic Syncope. introduction : Some patients with neurocardiogenic syncope continue to have recurrent syncope or presyncope despite the use of currently available drug therapy. The purpose of this study was to determine whether midodrine hydrochloride, a selective adrenergic agonist, could he effective in patients resistant to, or intolerant of, currently used medications in the treatment of neurocardiogenic syncope.
Methods and Results : Eleven patients with a history of recurrent syncope or presyncope in whom hypotension with syncope or presyncope could be provoked during head-up tilt testing were included. There were 4 men and 7 women with a mean age (± SD) age of 34 ± 13 years. In all patients, standard therapy with beta-adrenergic receptor blocking agents, ephedrine, theophylline, disopyramide, fludrocortisone, and sertraline hydrochloride, was either ineffective, poorly tolerated, or contraindicated. Midodrine was initially administered orally at a dose of 2.5 mg three times daily. After adjustment of dosage over 2 to 4 weeks, patients were followed-up clinically. Midodrine was discontinued in one patient because of side effects. Frequency of syncope or presyncope during the 3 months prior to starting treatment was compared during a mean follow-up of 17 ± 4 weeks after starting treatment with midodrine. There was significant (P < 0.01) reduction in syncopal and presyncopal episodes on midodrine. Five patients had complete resolution of symptoms, while four patients had significant improvement. Symptoms did not improve in one patient.
Conclusions : Midodrine hydrochloride can he effective in preventing recurrent symptoms in selected patients with neurocardiogenic syncope unresponsive to, or intolerant of, standard drug therapy.     

心脏抑制型血管迷走性晕厥患者倾斜试验阳性的重复性观察

目的　总结心脏抑制型血管迷走性晕厥倾斜试验阳性重复性。方法　对 46例首次倾斜试验阳性并表现为心脏抑制型血管迷走性晕厥的患者在 1或 3 d相同的时间进行重复倾斜试验。结果　39例诱发出晕厥或晕厥前症状 ,倾斜试验阳性 ,其阳性重复性为 84.4% ,其中 ,30例表现为心脏抑制型 ,6例表现为混合型 ,3例表现为血管减压型。结论　心脏抑制型血管迷走性晕厥患者倾斜试验阳性的类型可以发生变化     

Frequency of arrhythmic events during head-up tilt testing in patients with suspected neurocardiogenic syncope or presyncope

Head-up tilt testing (HUT) is a useful diagnostic tool for evaluating suspected neurocardiogenic syncope. Although arrhythmic events during HUT have been occasionally reported, their incidence in a large number of patients is unknown. We aimed to assess the incidence and clinical significance of arrhythmic events in patients with suspected neurocardiogenic syncope who underwent HUT with isoproterenol provocation. For 2,242 patients who underwent HUT, the incidence of total arrhythmic events was 31%: bradyarrhythmias 24%, premature beats 4%, and tachyarrhythmias 3%. For 547 patients who developed bradyarrhythmias during HUT, the incidence of junctional arrhythmias was 92%. For 702 arrhythmic events, the incidence of arrhythmic events during the first phase of HUT was significantly lower than the second phase (p <0.001). The incidence of arrhythmic events in patients with positive HUT responses was significantly higher than in those with negative responses (p <0.001). In patients with positive responses, bradyarrhythmias were noted in 85%, and junctional arrhythmia was the most common arrhythmic event. Of the positive responses, 353 patients (61%) had the vasodepressive type, 181 (32%) patients the mixed type, and the remaining 39 (7%) the cardioinhibitory type. Of 2,242 patients, ventricular fibrillation occurred in 1 patient (0.04%). Thus, bradyarrhythmias were the most common arrhythmic events during HUT with isoproterenol provocation. Serious ventricular tachyarrhythmia rarely occurred.     

Responses to the prolonged head-up tilt followed by sublingual nitrate provocation in asymptomatic older adults

BACKGROUND: prolonged head-up tilt testing and sublingual nitrate provocation are increasingly used in the diagnosis of neurocardiogenic syncope. However there are few data regarding the results of these tests in asymptomatic older subjects. OBJECTIVE: to assess the responses to the prolonged head-up tilt test followed by sublingual glyceryl trinitrate provocation in asymptomatic subjects over the age of 60 years. DESIGN: observational study. METHODS: we recruited 64 asymptomatic subjects over the age of 60 (39 men, 25 women) from two general practice lists in Nottingham and Leicester. Exclusion criteria were: history of syncope, ischaemic heart disease, cerebrovascular disease, marked aortic stenosis, carotid artery disease and being unable to stand for the duration of the test. All subjects underwent a full clinical examination, a 12-lead electrocardiogram and a 30-40-min head-up tilt test, during which we monitored the heart rate and blood pressure continuously. We ended the test prematurely if the subjects developed syncope or symptoms of presyncope associated with hypotension with or without bradycardia. If they remained asymptomatic at the end of this period, they received 400 microg of sublingual glyceryl trinitrate and monitoring continued for another 15 min. SETTINGS: two teaching hospitals in Nottingham and Leicester. RESULTS: six (9%) of the subjects had a positive response (syncope or presyncope) to the prolonged head-up tilt test prior to glyceryl trinitrate provocation. After provocation, 30 (52%) of the remaining 58 subjects had a positive response. CONCLUSION: the role of sublingual glyceryl trinitrate provocation following prolonged head-up tilt testing in the diagnosis of neurocardiogenic (vasovagal) syncope in older people is questionable, as many asymptomatic older subjects demonstrate syncopal or presyncopal symptoms.     

Cardiac Pacing During Neurocardiogenic (Vasovagal) Syncope

Cardiac Pacing and Neurocardiogenic Syncope. Head-up tilt testing is increasingly being used as a diagnostic modality in patients with unexplained syncope who are thought to have neurocardiogenic (vasovagal) mechanisms of syncope. Although large-scale placebo-controlled trials are still awaited, pharmacologic therapy is usually effective in preventing syncope or presyncope in this patient population. However, the role of permanent pacemaker therapy remains controversial. Because hypotension is usually associated with paradoxical bradycardia and occasionally asystole, it has been argued that permanent pacemaker therapy may be useful in preventing syncope and, thus, injury, in the so-called "malignant vasovagal cardioinhibitory response" in which the onset of syncope is thought to be abrupt. The onset of hypotension, however, usually precedes bradycardia during neurocardiogenic syncope, and pacing may thus not prevent syncope or presyncope in these patients. The role of cardiac pacing in patients with neurocardiogenic syncope is reviewed.     

False positive head-up tilt: hemodynamic and neurohumoral profile

OBJECTIVES: This study examined differences in mechanisms of head-up tilt (HUT)-induced syncope between normal controls and patients with neurocardiogenic syncope. BACKGROUND: A variable proportion of normal individuals experience syncope during HUT. Differences in the mechanisms of HUT-mediated syncope between this group and patients with neurocardiogenic syncope have not been elucidated. METHODS: A 30-min 80 degrees HUT was performed in eight HUT-negative volunteers (Group I), eight HUT-positive volunteers (Group II) and 15 patients with neurocardiogenic syncope. Heart rate and blood pressure (BP) were monitored continuously. Epinephrine and norepinephrine plasma levels, as well as left ventricular dimensions and contractility determined by echocardiography, were measured at baseline and at regular intervals during the test. RESULTS: The main findings of this study were the following: 1) All parameters were similar at baseline in the three groups; and 2) During tilt: a) the time to syncope was shorter in Group III than in group II (9.5 +/- 3 vs. 17 +/- 3 min p < 0.05); b) there was an immediate, persisting drop in mean BP in Group III; c) the decrease rate of left ventricular end-diastolic dimensions was greater in Group III than in Group II or Group I (-1.76 +/- 0.42 vs. -0.87 +/- 0.35 and -0.67 +/- 0.29 mm/min, respectively, p < 0.05); d) the leftventricular shortening fraction was greater in Group III than in the other two groups (39 +/- 1 vs. 34 +/- 1 and 32 +/- 1%, respectively, p < 0.05); and e) although the norepinephrine level remained comparable among the groups, there was a significantly higher peak epinephrine level in Group III than in Group II and Group I (112.3 +/- 34 vs. 77.6 +/- 10 and 65 +/- 12 pg/ml, p < 0.05). CONCLUSIONS: Mechanisms of syncope during HUT appeared to be different in normal volunteers and patients with neurocardiogenic syncope. In the latter, there was evidence of an impaired vascular resistance response from the beginning of the orthostatic challenge. Furthermore, in the patients there was more rapid peripheral blood pooling, as indicated by the echocardiographic measurements of left ventricular end-diastolic changes, leading to more precocious symptoms. In syncopal patients, the higher level of plasma epinephrine probably mediated the increased cardiac contractility and possibly contributed to the impaired vasoconstrictive response.     

Long QT syndrome patients may faint due to neurocardiogenic syncope.

AIMS: Syncope in long QT syndrome (LQTS) is expected to be due to Torsades de Pointes ventricular tachycardia (TdP). Often these patients faint in situations with emotional stress. The aim of the present study was to evaluate whether neurocardiogenic syncope occurs in LQTS. METHODS AND RESULTS: Ten untreated consecutive LQTS patients (age 11-72 years, median 37.5 years, five males and five females from five different families (one KvLQT1 mutation, two HERG mutations in three families and one without established genetic background)) were examined by a head-up tilt-table test (HUT). If syncope did not occur within 25 min, the patient received 0.25 mg nitroglycerine sublingually and the HUT was continued for 20 min. Nine out of 10 patients had a positive HUT. The syncope resulted from a combined vasodepressor and bradycardiac response. There were no cases of TdP. No syncope occurred in a 42-year-old asymptomatic male LQTS patient with a borderline prolonged QTc of 0.45 s and a HERG mutation. In 11 of 21 patients referred for syncope without LQTS a positive HUT was found (P < 0.10). CONCLUSION: Syncope in LQTS can be of neurocardiogenic origin and is not necessarily due to TdP. The reason for neurocardiogenic syncope in LQTS is unknown, but involvement of the autonomic nervous system outside the heart is possible.     

Cerebral blood flow velocity declines before arterial pressure in patients with orthostatic vasovagal presyncope

OBJECTIVES: We studied hemodynamic changes leading to orthostatic vasovagal presyncope to determine whether changes of cerebral artery blood flow velocity precede or follow reductions of arterial pressure. BACKGROUND: Some evidence suggests that disordered cerebral autoregulation contributes to the occurrence of orthostatic vasovagal syncope. We studied cerebral hemodynamics with transcranial Doppler recordings, and we closely examined the temporal sequence of changes of cerebral artery blood flow velocity and systemic arterial pressure in 15 patients who did or did not faint during passive 70 degrees head-up tilt. METHODS: We recorded photoplethysmographic arterial pressure, RR intervals (electrocardiogram) and middle cerebral artery blood flow velocities (mean, total, mean/RR interval; Gosling's pulsatility index; and cerebrovascular resistance [mean cerebral velocity/mean arterial pressure, MAP]). RESULTS: Eight men developed presyncope, and six men and one woman did not. Presyncopal patients reported light-headedness, diaphoresis, or a sensation of fatigue 155 s (range: 25 to 414 s) before any cerebral or systemic hemodynamic change. Average cerebral blood flow velocity (CBFV) changes (defined by an iterative linear regression algorithm) began 67 s (range: 9 to 198 s) before reductions of MAP. Cerebral and systemic hemodynamic measurements remained constant in nonsyncopal patients. CONCLUSIONS: Presyncopal symptoms and CBFV changes precede arterial pressure reductions in patients with orthostatic vasovagal syncope. Therefore, changes of cerebrovascular regulation may contribute to the occurrence of vasovagal reactions.     

Clinical efficacy of propantheline bromide in neurocardiogenic syncope: Pharmacodynamic implications

Summary The pharmacological response with tilt-table testing predicts long-term efficacy in neurocardiogenic syncope. However, beta-blockers for neurocardiogenic syncope are often not tolerated or are ineffective. Since cholinergic tone is important in the efferent part of the neurocardiogenic reflex, we investigated the pharmacodynamics and efficacy of propantheline bromide in preventing neurocardiogenic syncope. We studied 16 patients (11 males) with a mean age of 48.8 (± 15.1) years with presyncope or syncope and who had positive baseline tilt-table studies at a mean of 15.8 (± 10.3) minutes into the upright 60° tilt. They were given propantheline bromide orally, an anticholinergic agent, at a dose of 64.3 (± 21.8) mg/day for 7 days, and tilt-table testing was repeated 1 hour after readministration of propantheline bromide, 30 mg orally. After propantheline bromide treatment, 13 of 16 patients (81%) had no inducible presyncope or syncope on repeat tilt-table testing. In this group of responders, the mean minimum heart rate during upright tilt-table testing increased from 43.2 (± 77.3) beats/min to 77.3 (± 17.2) beats/min after propantheline bromide (p<0.005). More significantly, the minimum mean arterial blood pressure increased from 42.2 (± 25) mmHg to 81.3 (± 16.7) mmHg (p<0.0005) during upright tilt. At a follow-up of 15.2 (± 7.4) months, in the responder group (12 patients with long-term follow-up), the average dose of propantheline bromide was 32.5 (± 23.8) mg/day, which was significantly reduced from the initial dose (p<0.05). A clinical recurrence of symptoms occurred in only 4 out of 12 patients on propantheline bromide (33%), none of which were directly attributable to drug failure. It was concluded from this study that propantheline bromide is highly effective in preventing neurocardiogenic syncope. In addition, propantheline bromide's effectiveness is more than would be expected by prevention of cardioinhibition in neurocardiogenic syncope and would support a role for direct cholinergic control of vascular tone.This work was presented in part at the American Heart Association 67th Scientific Sessions, Dallas, Texas, November 14, 1994.     

Utility of mobile cardiac outpatient telemetry for the diagnosis of palpitations, presyncope, syncope, and the assessment of therapy efficacy

Introduction: Continuous mobile cardiac outpatient telemetry (MCOT) may have several advantages over traditional ambulatory monitoring systems in the diagnostic evaluation of symptoms such as palpitations, dizziness, and syncope. However, only limited published data are available showing its advantages.
Methods and Results: We reviewed the records of 122 consecutive patients evaluated using MCOT for palpitations, presyncope/syncope, or to monitor the efficacy of a specific antiarrhythmic therapy. Ten of 17 patients (59%) studied for presyncope/syncope had a diagnosis made with MCOT. Eight of these 17 patients had a previous negative evaluation for presyncope/syncope and five had an event correlated with the heart rhythm during the monitoring period. Nineteen patients monitored for palpitations or presyncope/syncope were asymptomatic during monitoring but had a prespecified arrhythmia detected. When MCOT was used as the first ambulatory monitoring system to evaluate palpitations (n = 18), 73% of patients correlated their symptoms with the underlying cardiac rhythm. Seven of 21 patients monitored for medication titration had dosage adjustments during outpatient monitoring.
Conclusions: MCOT can detect asymptomatic clinically significant arrhythmias, and was especially useful to identify the cause of presyncope/syncope, even in patients with a previous negative workup. This outpatient monitoring system allows patients to undergo daily medication dose titration in the outpatient setting, thus avoiding hospitalization.     

Predictive value of presyncope in patients monitored for assessment of syncope

BACKGROUND: The purpose of this study was to assess the diagnostic value of recording the cardiac rhythm during presyncope in patients undergoing monitoring for undiagnosed syncope. METHODS AND RESULTS: Eighty-five patients (age, 59 +/- 18 years; 44 men, 41 women) with recurrent unexplained syncope underwent prolonged monitoring with an implantable loop recorder. Patients were examined for syncope, which was either recurrent or associated with at least 2 presyncopal episodes. Patients had a mean of 5.1 +/- 5.5 syncopal episodes in the previous 12 months, and 70% of patients had symptoms for >2 years. Sixty-two (73%) patients had recurrent symptoms during a 12-month follow-up period. Of 150 recurrent events captured by the implantable loop recorder, there were 38 (25%) episodes of syncope and 112 (75%) episodes of presyncope. Syncope alone recurred in 12 patients, presyncope in 25, and both in 16. An arrhythmia was present in 64% of syncopal events (bradycardia in 16, tachycardia in 2) versus 25% for presyncopal events (bradycardia in 7, tachycardia in 3, P =.001). An arrhythmia was detected in 9 (56%) of the 16 patients with both syncope and presyncope, which was present in all recorded episodes of syncope compared with 6 of 9 presyncopal episodes. Patient-related failure to freeze the device after symptoms occurred in 21 (36%) of 59 syncopal events compared with 15 (12%) of 127 presyncopal events (P =.0001). CONCLUSIONS: Syncope is more likely to be associated with an arrhythmia than is presyncope in patients undergoing extended monitoring. Presyncope is a nonspecific end point that is frequently associated with sinus rhythm. Patients undergoing extended monitoring for syncope should continue to be monitored after an episode of presyncope unless an arrhythmia is detected.     

Upright postures and isoproterenol infusion for provocation of neurocardiogenic syncope: A comparison of standing and head-up tilting

Head-up tilt testing has proved to be useful in provocation of neurocardiogenic syncope. The purpose of this study was to examine whether simply assuming an upright posture by standing can be an alternative to the head-up tilt testing for diagnosis of neurocardiogenic syncope. Eight-four patients with recurrent unexplained syncope and 22 normal volunteers were recruited into the study. Forty-seven patients with syncope and all normal volunteers received the standing test. Thirty-seven of the patients with syncope received head-up tilt testing (90 degrees). All subjects lay down for 5 minutes and then assumed an upright posture until syncope or presyncope occurred or until a maximum of 10 minutes was reached in each stage of the test. The tests included four stages: baseline and infusion of 1, 2, or 3 μg/min isoproterenol in each of the successive stages. Five subjects could not tolerate the procedure, and further testing was terminated. Overall, the standing test was positive in 83% of the patients with syncope, and its specificity was 74%. The head-up tilt testing was positive in 75% of the patients with syncope. The duration of assuming an upright posture before occurrence of syncope or presyncope was significantly longer in the syncope-tilting group in the third stage (p < 0.01) and the fourth stage (p < 0.05) compared with the syncope-standing group. However, the curves of the time course for cumulative positive rates were not significantly different (p = 0.0739) in the two groups. The standing test can serve as an alternative to head-up tilt testing and can be applied to patients with recurrent unexplained syncope for confirmation of the diagnosis.