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PubMed2006

Prevention of Syncope Trial (POST): a randomized, placebo-controlled study of metoprolol in the prevention of vasovagal syncope.

BACKGROUND: Previous studies that assessed the effects of beta-blockers in preventing vasovagal syncope provided mixed results. Our goal was to determine whether treatment with metoprolol reduces the risk of syncope in patients with vasovagal syncope. METHODS AND RESULTS: The multicenter Prevention of Syncope Trial (POST) was a randomized, placebo-controlled, double-blind, trial designed to assess the effects of metoprolol in vasovagal syncope over a 1-year treatment period. Two prespecified analyses included the relationships of age and initial tilt-test results to any benefit from metoprolol. All patients had >2 syncopal spells and a positive tilt test. Randomization was stratified according to ages <42 and > or =42 years. Patients received either metoprolol or matching placebo at highest-tolerated doses from 25 to 200 mg daily. The main outcome measure was the first recurrence of syncope. A total of 208 patients (mean age 42+/-18 years) with a median of 9 syncopal spells over a median of 11 years were randomized, 108 to receive metoprolol and 100 to the placebo group. There were 75 patients with > or =1 recurrence of syncope. The likelihood of recurrent syncope was not significantly different between groups. Neither the age of the patient nor the need for isoproterenol to produce a positive tilt test predicted subsequent significant benefit from metoprolol. CONCLUSIONS: Metoprolol was not effective in preventing vasovagal syncope in the study population.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Syncope and work. STePS study (Short Term Prognosis of Syncope)].

BACKGROUND: Recurrent syncope is a common medical problem responsible for 3-5% of emergency department (ED) accesses and 1-6% of hospital admissions. If syncope occurs in a subject working in a critical safety task, the consequences of this event might be very dangerous for the worker, colleagues, others or for the environment. Therefore, syncope management is a major problem for occupational medicine, converning the general safety at work. AIMS: To evaluate the syncope events in a group of potential workers aged 18 to 65 years; to evaluate the symptoms preceding syncope and the presence of associated illnesses and recurrent events. POPULATION AND RESULTS: This study is part of the prospective study STePS (Short Term Prognosis of Syncope), and included 305 consecutive patients (aged 18-65 years, female 56%) who had syncope as a main symptom and presented at ED of four general hospitals in the Milan area, Italy, between the 23rd of January and 30th of June 2004. The 24% of subjects were hospitalized. In 21% the syncope occurs suddenly without any preceding symptom. The 67% of subjects didn't have any important illness at the time. 50% of subjects had recurrent syncope. In four subjects another syncope occurred in a 10 day follow-up. CONCLUSIONS: occupational medicine should consider syncope scrupulously. Proper diagnostic management is important to permit a correct evaluation of work safety issues.

Adolescent↗
PubMed2002

Comparison of hemodynamic adaptation to orthostatic stress in patients with hypertrophic cardiomyopathy with or without syncope and in vasovagal syncope.

This study was designed to investigate whether, in patients with hypertrophic cardiomyopathy (HC), tilt-induced volume unloading triggers a peripheral reflex similar to that seen in patients with a history of vasovagal syncope or rather acts through an intrinsic cardiac mechanism secondary to diastolic dysfunction. Thirty-seven patients with HC (10 with and 27 without a history of syncope), 10 patients with vasovagal syncope, and 9 controls underwent 70 degrees head-up tilt for 45 minutes during continuous radionuclide monitoring of left ventricular function. We focused on the initial 5 minutes into the tilt test, well before symptoms occurred, to exclude that the observed hemodynamic changes were the consequence rather than the cause of syncope. HC patients with previous syncope and vasovagal patients experienced significant hypotension after the initial 5 minutes of tilt. Only HC patients with a history of syncope had a significant decrease in cardiac output, which began at the initial stage of the test. Systemic vascular resistance decreased in vasovagal patients, but increased in the HC syncopal group. Baseline peak filling rate was lower (2.4 +/- 0.5 vs 3.3 +/- 1.1 stroke counts/s, p = 0.03) and a "pseudonormal" or a restrictive pattern of left ventricular filling was more frequent (70% vs 26%, p = 0.02) in HC patients with than without a history of syncope. Thus, significant hypotension or frank syncope during orthostatic stress in HC patients with a history of syncope is due to an early decrease in cardiac output, which occurs well before the onset of symptoms; such impaired hemodynamic adaptation seems to be related to diastolic dysfunction.

Adaptation, Physiological↗
PubMed2000

Clinical features of adenosine sensitive syncope and tilt induced vasovagal syncope.

AIM: To evaluate the possible relation between adenosine sensitive syncope and tilt induced vasovagal syncope. METHODS: An ATP test and a head up tilt test were performed in 175 consecutive patients with syncope of uncertain origin. The ATP test consisted of the rapid intravenous injection of 20 mg of ATP; a positive response was defined as the induction of a ventricular pause (maximum RR interval) >/= 6000 ms. The head up tilt test was performed at 60 degrees for 45 minutes; if negative, 0.4 mg oral glyceryl trinitrate spray was given and the test continued for a further 20 minutes; a positive response was defined as induction of syncope in the presence of bradycardia, hypotension, or both. RESULTS: Of the 121 patients with a positive response, 77 (64%) had a positive head up tilt alone, 18 (15%) had a positive ATP test alone, and in 26 (21%) both ATP and head up tilt were positive. Compared with the patients with isolated positive head up tilt, those with isolated positive ATP were older (mean (SD) age, 68 (10) v 45 (20) years), had a lower median number of syncopal episodes (2 v 3), a shorter median duration of syncopal episodes (4 v 36 months), a lower prevalence of situational, vasovagal, or triggering factors (11% v 64%), a lower prevalence of warning symptoms (44% v 71%), and a higher prevalence of systemic hypertension (22% v 5%) and ECG abnormalities (28% v 9%). The patients with a positive response to both tests had intermediate features. Of the 44 positive responses to the ATP test, atrioventricular block was the cause of the ventricular pause in 43; of the 29 positive cardioinhibitory responses to head up tilt, sinus arrest was present in 23 cases and atrioventricular block in six. CONCLUSIONS: ATP and head up tilt tests identify different populations of patients affected by syncope; these have different general clinical features, different histories of syncopal episodes, and different mechanism sites of action. Therefore, adenosine sensitive syncope and tilt induced vasovagal syncope are two distinct clinical entities.

Adenosine Triphosphate↗
PubMed2005

Left ventricular outflow tract obstruction provoked during dobutamine stress echocardiography predicts future chest pain, syncope, and near syncope.

BACKGROUND: Although dobutamine stress echocardiography (DSE) is associated with dynamic left ventricular (LV) obstruction, it is unknown whether such obstructive event, in general, and the specific site of obstruction, in particular, have unique clinical prognostic significance. We sought to determine whether dynamic LV outflow tract (LVOT) versus LV midcavitary obstruction provoked during DSE would predict future chest pain, syncope, and/or near syncope. METHODS: Two hundred thirty-seven patients (145 men and 92 women, mean age 58 +/- 13 [+/-SD] years) without DSE-provoked ischemia underwent continuous wave Doppler interrogation to detect any inducible dynamic flow obstruction. Patients were prospectively followed for a mean duration of 31 +/- 13 months. RESULTS: One hundred fifty-four of 237 patients had no provoked LV obstruction (group 1). Fifty-four (22.8%) had provoked LV midcavitary (group 2) obstruction, and 29 (12.2%) had outflow tract (group 3) obstruction. During follow-up, chest pain occurred more frequently in groups 2 (46%, P < .05) and 3 (52%, P = .05) as compared with group 1 (31%). A higher incidence of syncope and/or near syncope was noted in group 3 (21% vs 9% in group 1). LVOT obstruction but not midcavitary obstruction was a significant predictor of future chest pain (relative risk 2.63, P = .0021) and syncope and/or near syncope (relative risk 3.11, P = .036). Kaplan-Meier analysis showed a significantly less event-free survival (P = .025) for the combined end point of chest pain, syncope, and/or near syncope in patients with LVOT obstruction. CONCLUSIONS: This is the first prospective study to identify the differential prognostic implications of the site of dynamic obstruction noted during DSE. Our results demonstrate that DSE-provoked LVOT obstruction is an independent positive predictor of future episodes of chest pain and syncope and/or near syncope. These findings warrant larger studies addressing treatment options to ameliorate symptoms in this subgroup of patients.

Adult↗
PubMed2006

The Second Prevention of Syncope Trial (POST II)--a randomized clinical trial of fludrocortisone for the prevention of neurally mediated syncope: rationale and study design.

BACKGROUND: Neurally mediated syncope is a common and frequently distressing problem. It is associated with a poor quality of life, which improves when the frequency of syncope is reduced. Few therapies for neurally mediated syncope have been proven effective. Fludrocortisone is commonly used to prevent recurrences of syncope but with little evidence to support its use. A placebo-controlled clinical trial of fludrocortisone for the prevention of neurally mediated syncope is needed. STRUCTURE OF STUDY: POST II is a multicenter, international, randomized, placebo-controlled study of fludrocortisone in the prevention of neurally mediated syncope. The primary end point is the time to first recurrence of syncope. Patients will be randomized 1:1 to receive fludrocortisone 0.05 to 0.2 mg or matching placebo and followed for 1 year. Secondary end points include syncope frequency, presyncope, and quality of life. Primary analysis will be performed with an intention-to-treat approach, with a secondary on-treatment analysis. POWER CALCULATIONS: Assuming a 40% risk of syncope in the control arm, a relative reduction of 40% by fludrocortisone, and a dropout rate of 20%, the enrollment of 310 patients will give an 80% power of reaching a positive conclusion about fludrocortisone therapy, with P = .05. REGISTRATION: POST II is registered with both (ISRCTN 51802652) and (NCT00118482). IMPLICATIONS: This study will be the first adequately powered trial to determine whether fludrocortisone is effective in preventing neurally mediated syncope. If it is effective, then fludrocortisone may become the first-line medical therapy for this condition.

Fludrocortisone↗
PubMed1995

Syncope associated with exercise, a manifestation of neurally mediated syncope.

A retrospective review of patients evaluated at a university-based referral hospital was performed to assess the basis for syncope associated with exercise in young patients. Over an 8-year period, 54 consecutive young patients (aged 12 to 30 years) were referred for evaluation of frank syncope. Twelve patients had syncope associated with exercise (group I) and 42 patients had syncope not associated with exercise (group II). Patients underwent physical examination, chest x-ray, 2-dimensional echocardiography, and in selected cases, cardiac catheterization. Head-up tilt-table testing was performed in 11 of 12 group I patients. Ten group I patients had no evidence of structural heart disease: 9 of these 10 (90%) developed syncope with tilt-table testing. Head-up tilt-table testing was performed in 41 of 42 group II patients: 34 (83%) developed syncope with tilt-table testing. Standard cardiac electrophysiologic study was performed in 9 of 12 group I and in 30 of 42 group II patients, and identified a basis for syncope in only 2 group I and 1 group II patients. Among 9 group I patients with a positive result on head-up tilt-table testing and no evidence of structural heart disease (mean follow-up 4.3 years), 7 are without further episodes of syncope; 3 have discontinued medication and 5 have resumed at least limited exercise. In conclusion, susceptibility to tilt-induced syncope was the most frequent finding in young patients without structural heart disease referred for evaluation of exercise-associated syncope. Tilt-table testing may be an important diagnostic tool for the evaluation of these patients.

Adolescent↗
PubMed1998

Role of endogenous opioids in syncope induced by head-up tilt test and its relationship with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope.

This study was designed to evaluate the role of endogenous opioids in neurally-mediated syncope. Head-up tilt test was performed on 35 patients with syncope of unknown origin. Plasma beta-endorphin was measured (1) at baseline, (2) at the end of tilt test or at time of syncope, (3) 15 min before isoproterenol-test, (4) at the end of the isoproterenol-test or at time of syncope. Subjects with a positive tilt testing showed a larger rise in plasma beta-endorphin concentrations at time of syncope (baseline 13.7+/-8.0 vs. syncope 41.4+/-26.4 pmol l(-1); P<0.01). On the contrary, patients with a positive isoproterenol-test showed no rise in plasma beta-endorphin levels (baseline 7.9+/-3.6 vs. syncope 7.4+/-2.7 pmol l(-1); P=ns). Patients with a passive negative tilt test (baseline 6.7+/-2.8 vs. end of test 7.0+/-3.3 pmol l(-1); P=ns) and negative isoproterenol tilt test (baseline 7.4+/-3.8 vs. end of test 8.1+/-3.4 pmol l(-1); P=ns) showed no changes in beta-endorphin concentrations. To further examine the efficacy of i.v. naloxone to prevent syncope, 10 patients were randomized to naloxone (0.02 mg/kg) or placebo. Second head-up tilt testing was negative in 1/5 patients with naloxone and in 2/5 patients with placebo. We conclude that, (1) endogenous opioids seem to be involved in vasovagal syncope induced by baseline head-up tilt test, (2) changes in plasma beta-endorphin concentrations show significant differences between patients who have isoproterenol-dependent and isoproterenol-independent syncope, this finding might occur in the setting of different pathophysiologic mechanisms, and (3) intravenous naloxone at a dose of 0.02 mg/kg was not superior to placebo in order to prevent positive responses to baseline tilt test.

Adolescent↗
PubMed2003

Prevention of Syncope Trial (POST): a randomized clinical trial of beta blockers in the prevention of vasovagal syncope; rationale and study design.

BACKGROUND: Few therapies for vasovagal syncope have been proven effective. A large, placebo-controlled clinical trial of beta-blockers is needed. STRUCTURE OF STUDY: The Prevention of Syncope Trial (POST) is a multicentre, randomized, placebo-controlled, study of metoprolol in the prevention of vasovagal syncope. The primary hypothesis is that beta-blockers will increase the time to the first recurrence of syncope when compared with placebo. Patients will be randomized 1:1 to receive metoprolol or placebo, and followed for 1 year. The primary endpoint is the time to first syncope recurrence, and secondary endpoints include syncope frequency, presyncope, and quality of life. INCLUSION AND EXCLUSION CRITERIA: Patients are eligible if they have a positive tilt test and 3 syncopal spells preceding the tilt test. They are excluded if they have seizures or other causes of syncope; important heart disease; a contraindication to or need for beta blockers; a permanent pacemaker; a major noncardiovascular disease; or previous use of beta blockers at a dose greater than the equivalent of metoprolol 25mg twice daily for the purpose of suppressing vasovagal syncope. POWER CALCULATIONS: We assume a 40% risk of syncope in the control arm, an absolute reduction of 20% by metoprolol, and a dropout of 20%. Entry of 220 patients will result in an 80% chance of reaching a positive conclusion about beta-blocker therapy with 2p=0.05.

Adrenergic beta-Antagonists↗
PubMed2000

Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope : pacemaker versus no therapy: a multicenter randomized study. The Vasovagal Syncope International Study (VASIS) Investigators.

BACKGROUND-This study was performed to compare implantation of a DDI pacemaker with rate hysteresis with no implant in respect to syncopal recurrences in patients with severe cardioinhibitory tilt-positive neurally mediated syncope. METHODS AND RESULTS-Forty-two patients from 18 European centers were randomized to receive a DDI pacemaker programmed to 80 bpm with hysteresis of 45 bpm (19 patients) or no pacemaker (23 patients). Inclusion criteria were >/=3 syncopes over the last 2 years and a positive cardioinhibitory (Vasovagal Syncope International Study types 2A and 2B) response to tilt testing. The median number of previous syncopal episodes was 6; asystolic response to tilt testing was present in 36 patients (86%) (mean asystole, 13.9+/-10.2 seconds). All patients were followed up for a minimum of 1.0 years and a maximum of 6.7 years (mean, 3.7+/-2.2). One patient (5%) in the pacemaker arm experienced recurrence of syncope compared with 14 patients (61%) in the no-pacemaker arm (P=0.0006). In the no-pacemaker arm, the median time to first syncopal recurrence was 5 months, with a rate of 0.44 per year. On repeated tilt testing performed within 15 days after enrollment, positive responses were observed in 59% of patients with pacemakers and in 61% of patients without pacemakers (P=NS). CONCLUSIONS-In a limited, select group of patients with tilt-positive cardioinhibitory syncope, DDI pacing with hysteresis reduced the likelihood of syncope. The benefit of the therapy was maintained over the long term. Even in untreated patients, the syncopal recurrence burden was low. A negative result of tilt testing was not a useful means to evaluate therapy efficacy.

Aged↗
PubMed1996

Risk factors for syncope recurrence after a positive tilt-table test in patients with syncope.

BACKGROUND: Recent work with head-up tilt-table testing has suggested that many patients with syncope may have recurrent neurally mediated episodes of bradycardia, hypotension, or both. The purpose of this study was to determine how to identify patients at high risk of a recurrence of neuromediated syncope after a positive isoproterenol/tilt-table test. METHODS AND RESULTS: A cohort of 101 drug-free patients in a university hospital outpatient clinic with syncope and a positive isoproterenol/tilt-table test underwent baseline assessment of demographic variables, symptomatic burden, and hemodynamic and clinical responses to tilt testing. The primary outcome measure was the time to the first recurrent syncopal spell. The actuarial probabilities of remaining syncope free after 1 and 2 years were 72% and 60%, respectively. Multivariate proportional hazards analysis demonstrated that the most powerful predictor of a recurrence of syncope was the logarithm of the number of preceding syncopal spells (P<.001). Other predictive variables included the duration of syncopal symptoms, tilt test symptomatic outcome, and trough heart rate. The probability of a recurrence of syncope also varied with the logarithm of the frequency of preceding spells (P=.008). The median frequency of pretest spells was 0.3/month; after the tilt test, the median frequency dropped approximately 90% to 0.03 per month. CONCLUSIONS: The risk of a recurrence of syncope after a positive tilt-table test can be predicted with simple pretest and intratest variables.

Adult↗
PubMed1986

Cardiogenic syncope. Seizure versus syncope.

Our recommendations for the evaluation of the patient with suspected cardiogenic syncope are as follows: An initial thorough history and physical examination of the patient will suggest the diagnosis of cardiogenic syncope in at least 50 per cent of patients. A sudden occurrence of syncope, or "drop attack", is most suggestive of an arrhythmic cause for syncope. If there is no evidence of neurologic, metabolic, or obvious cardiac (for example, aortic stenosis) cause for syncope, a 24-hour ambulatory ECG should be performed. If the patient has had repeated syncopal episodes or if the patient has had seizures that are difficult to control with anticonvulsant therapy, ambulatory ECG monitoring may reveal an arrhythmia in these preselected patients. If the initial 24-hour ambulatory ECG is negative and if the patient has had multiple episodes of syncope, multiple days of recording will be necessary before typical symptoms occur that correlate with arrhythmias. Seventy-two hours of ambulatory ECG monitoring should be sufficient in most instances to establish an arrhythmic cause for syncope. Echocardiography and exercise stress testing are not routinely indicated in the evaluation of syncope unless the clinical history and examination suggest valvular or coronary disease. Rarely, an atrial myxoma will be visualized by echocardiography that is not apparent clinically. Those patients who still have unexplained recurrent syncopal episodes, despite all noninvasive studies, can benefit from invasive electrophysiologic studies, although the expected yield from electrophysiologic testing is low.

Arrhythmias, Cardiac↗
PubMed2004

A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The vasovagal syncope and pacing trial (SYNPACE).

AIMS: Recently, some studies revealed the efficacy of pacemaker implantation in decreasing recurrences in patients with vasovagal syncope. As these studies were not blinded or placebo-controlled, the benefits observed might have been due to a bias in the assessment of outcomes or to a placebo effect of the pacemaker. We performed a randomized, double-blind, placebo-controlled study in order to ascertain if pacing therapy reduces the risk of syncope relapse. METHODS AND RESULTS: Twenty-nine patients (53 +/- 16 years; 19 women) with severe recurrent tilt-induced vasovagal syncope (median 12 syncopes in the lifetime) and 1 syncopal relapse after head-up tilt testing underwent implantation of a pacemaker, and were randomized to pacemaker ON or to pacemaker OFF. During a median of 715 days of follow-up, 8 (50%) patients randomized to pacemaker ON had recurrence of syncope compared to 5 (38%) of patients randomized to pacemaker OFF (p = n.s.); the median time to first syncope was longer in the pacemaker ON than in pacemaker OFF group, although not significantly so (97 [38-144] vs 20 [4-302] days; p = 0.38). There was also no significant difference in the subgroups of patients who had had a mixed response and in those who had had an asystolic response during head-up tilt testing. CONCLUSION: Our data were unable to show a superiority of active pacing versus inactive pacing in preventing syncopal recurrence in patients with severe recurrent tilt-induced vasovagal syncope.

Cardiac Pacing, Artificial↗
PubMed2003

Management of syncope referred urgently to general hospitals with and without syncope units.

OBJECTIVE: We tested the hypothesis that management of patients with syncope admitted urgently to a general hospital may be influenced by the presence of an in-hospital structured syncope unit. BACKGROUND: The management of syncope is not standardized. Methods We compared six hospitals equipped with a syncope unit organized inside the department of cardiology with six matched hospitals without such facilities. The study enroled all consecutive patients referred to the emergency room from 5 November 2001 to 7 December 2001 who were affected by transient loss of consciousness as their principal symptom. RESULTS: There were 279 patients in the syncope unit hospitals and 274 in the control hospitals. In the study group, 30 (11%) patients were referred to the syncope unit for evaluation. In the study group, 12% fewer patients were hospitalized (43 vs 49%, not significant) and 8% fewer tests were performed (3.3+/-2.2 vs 3.6+/-2.2 per patient, not significant). In particular, the study group patients underwent fewer basic laboratory tests (75 vs 86%, P=0.002), fewer brain-imaging examinations (17 vs 24%, P=0.05), fewer echocardiograms (11 vs 16%, P=0.04), more carotid sinus massage (13 vs 8%, P=0.03) and more tilt testing (8 vs 1%, P=0.000). In the study group, there was a +56% rate of final diagnosis of neurally mediated syncope (56 vs 36%, P=0.000). CONCLUSION: Although only a minority of patients admitted as an emergency are referred to the syncope unit, overall management is substantially affected. It is speculated that the use of a standardized approach, such as that typically adopted in the syncope unit, is able to influence overall practice in the hospital.

Adult↗
PubMed2006

An implantable loop recorder study of highly symptomatic vasovagal patients: the heart rhythm observed during a spontaneous syncope is identical to the recurrent syncope but not correlated with the head-up tilt test or adenosine triphosphate test.

OBJECTIVES: The aim of this study was to analyze the heart rhythm during spontaneous vasovagal syncope (VVS) in highly symptomatic patients with implantable loop recorders (ILR) and to correlate this rhythm with the heart rhythm observed during head-up tilt test (HUT). BACKGROUND: Heart rhythm obtained during provocative condition is often used to guide therapy in VVS. To date there is no conclusive evidence that the heart rhythm observed during a positive HUT can predict heart rhythm during VVS or that the heart rhythm observed during a spontaneous syncope will be identical to the recurrent syncope. METHODS: Twenty-five consecutive VVS patients (age 60.2 +/- 17.1 years; 14 women,) presenting with frequent syncopes (6.9 +/- 4.6 episodes/year) and a positive HUT (cardioinhibitory in 8 patients) were implanted with an ILR. Seven of them also had a positive adenosine triphosphate (ATP) test. RESULTS: Follow-up was 17.0 +/- 3.6 months. Thirty VVS were observed in 12 patients. Nine episodes showed bradycardia of <40 beats/min or asystole; progressive sinus bradycardia preceding sinus arrest was the most frequent electrocardiographic finding. Twenty-one syncopes occurred without severe bradycardia. The heart rhythm observed during the first syncope was identical to the recurrence. No correlation was found between slow heart rate at the ILR interrogation and a cardioinhibitory HUT response (p = 1.0) or a positive ATP test (p = 1.0). CONCLUSIONS: In highly symptomatic patients with VVS, the heart rhythm observed during spontaneous syncope does not correlate with the HUT. The heart rhythm during the first spontaneous syncope is identical to the recurrent syncope.

Adenosine Triphosphate↗
PubMed2003

International Study on Syncope of Uncertain Etiology 2: the management of patients with suspected or certain neurally mediated syncope after the initial evaluation rationale and study design.

STUDY DESIGN: Multi-centre, prospective observational study. OBJECTIVES: Main objective is to verify the value of implantable loop recorder (ILR) in assessing the mechanism of syncope and the efficacy of the ILR-guided therapy after syncope recurrence. INCLUSION CRITERIA: Patients who met the following criteria are included: suspected or definite neurally mediated syncope based on initial evaluation; >/=3 syncope episodes in the last 2 years; severe clinical presentation of syncope requiring treatment initiation in the judgement of the investigator and age >30 years. EXCLUSION CRITERIA: Patients with one or more of the following are excluded: carotid sinus syndrome; suspected or definite heart disease and high likelihood of cardiac syncope; symptomatic orthostatic hypotension diagnosed by standing blood pressure measurement; loss of consciousness different from syncope (e.g. epilepsy, psychiatric, metabolic, drop-attack, TIA, intoxication, cataplexy) and subclavian steal syndrome. END-POINTS: The primary end-points are the ECG-documented syncopal events and the syncope recurrences after application of ILR-guided therapy. SAMPLE SIZE AND DURATION: A minimum of 400 patients will be enrolled during an anticipated period of 3 years.

Clinical Protocols↗
PubMed2004

Syncope Evaluation in the Emergency Department Study (SEEDS): a multidisciplinary approach to syncope management.

BACKGROUND: The primary aim and central hypothesis of the study are that a designated syncope unit in the emergency department improves diagnostic yield and reduces hospital admission for patients with syncope who are at intermediate risk for an adverse cardiovascular outcome. METHODS AND RESULTS: In this prospective, randomized, single-center study, patients were randomly allocated to 2 treatment arms: syncope unit evaluation and standard care. The 2 groups were compared with chi2 test for independence of categorical variables. Wilcoxon rank sum test was used for continuous variables. Survival was estimated with the Kaplan-Meier method. One hundred three consecutive patients (53 women; mean age 64+/-17 years) entered the study. Fifty-one patients were randomized to the syncope unit. For the syncope unit and standard care patients, the presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P<0.001), respectively, hospital admission was required for 22 (43%) and 51 (98%) patients (P<0.001), and total patient-hospital days were reduced from 140 to 64. Actuarial survival was 97% and 90% (P=0.30), and survival free from recurrent syncope was 88% and 89% (P=0.72) at 2 years for the syncope unit and standard care groups, respectively. CONCLUSIONS: The novel syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope and all-cause mortality among intermediate-risk patients. Observations from the present study provide benchmark data for improving patient care and effectively utilizing healthcare resources.

Aged↗
PubMed1997

Neurally mediated syncope and syncope due to autonomic failure: differences and similarities.

Syncope is a transient loss of consciousness and postural tone caused by a global reduction of blood flow to the brain. Abnormalities in autonomic cardiovascular control can impair blood supply to the brain and produce syncope in two different disorders: autonomic failure and neurally mediated syncope. In autonomic failure, sympathetic efferent activity is chronically impaired so that vasoconstriction is deficient, upon standing blood pressure always falls (i.e., orthostatic hypotension), and syncope or presyncope occurs. Conversely, in neurally mediated syncope, the failure of sympathetic efferent vasoconstrictor traffic (and hypotension) occurs episodically and in response to a trigger. Between syncopal episodes, patients with neurally mediated syncope have normal blood pressure and orthostatic tolerance. This article reviews the characteristics of autonomic failure and describes in more detail the pathophysiology, diagnosis, and treatment of neurally mediated syncope.

Autonomic Nervous System Diseases↗