|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
|
|
|
|||||||||
|
|||||||||||
|
J Am Coll Cardiol, 2001; 37:1921-1928 © 2001 by the American College of Cardiology Foundation |
* Division of Cardiology, Ospedale Civile, Cento, Italy
Section of Arrhythmology, Department of Cardiology, Ospedali Riuniti, Lavagna, Italy
Section of Arrhythmology, Department of Cardiology, Ospedale S. Maria Nuova, Reggio Emilia, Italy
Division of Cardiology, Ospedale Umberto I, Mestre, Italy
|| Division of Cardiology, Ospedale S. Pietro Igneo, Fucecchio, Italy
Manuscript received September 19, 2000; revised manuscript received January 24, 2001, accepted February 12, 2001.
Reprint requests and correspondence: Dr. Paolo Alboni, Division of Cardiology, Ospedale Civile, 44042 Cento (Fe), Italy
p.alboni{at}ausl.fe.it
 |
Abstract |
|---|
 Top Abstract MethodsResultsDiscussionReferences |
|---|
We sought to establish what historical findings are predictive of the cause of syncope.
BACKGROUND
The clinical features of the various types of syncope have not been systematically investigated.
METHODS
Three hundred forty-one patients with syncope were prospectively evaluated. Each patient was interviewed using a standard questionnaire. A cause of syncope was assigned using standardized diagnostic criteria.
RESULTS
A cardiac cause of syncope was established in 23% of the patients, a neurally mediated cause in 58% and a neurologic or psychiatric cause in 1%, and in the remaining 18%, the cause of syncope remained unexplained. In a preliminary analysis including age, gender and the presence of suspected or certain heart disease after the initial evaluation, only heart disease was an independent predictor of a cardiac cause of syncope (odds ratio 16, p = 0.00001), with a sensitivity of 95% and a specificity of 45%. In contrast, the absence of heart disease allowed us to exclude a cardiac cause of syncope in 97% of the patients. In patients with certain or suspected heart disease, the most specific predictors of a cardiac cause were syncope in the supine position or during effort, blurred vision and convulsive syncope. Significant and specific predictors of a neurally mediated cause were time between the first and last syncopal episode >4 years, abdominal discomfort before the loss of consciousness and nausea and diaphoresis during the recovery phase. In the patients without heart disease, palpitation was the only significant predictor of a cardiac cause.
CONCLUSIONS
The presence of suspected or certain heart disease after the initial evaluation is a strong predictor of a cardiac cause of syncope. A few historical findings are useful to predict cardiac and neurally mediated syncope in patients with and without heart disease.
| ||||||||
The aim of the present study was to establish what historical findings are predictive of the cause of syncope.
|
Methods |
|---|
|
TopAbstractMethodsResultsDiscussionReferences |
|---|
18 years. Three hundred fifty-six consecutive patients with the aforementioned characteristics were referred to the "Syncope Unit" of the Cardiology Division of three hospitals (Cento, Lavagna and Reggio Emilia, Italy) from the emergency room, in-patient service and out-patient clinic between January and July 1999. All patients underwent a standardized initial evaluation consisting of a history, physical and neurologic examinations performed by one of the investigators, evaluation of blood pressure in the supine and standing positions and standard electrocardiogram (ECG). Conventional laboratory tests were performed when a hemorrhagic or metabolic cause was suspected. When the results of the initial evaluation allowed us to define the cause of syncope (i.e., diagnostic [see subsequent text]), the procedures were interrupted. When the results of the initial evaluation were inconclusive, further investigations were performed according to the guidelines of the Italian "Associazione Nazionale Medici Cardiologi Ospedalieri" (1,2) (Fig. 1), with the addition of the adenosine triphosphate (ATP) test when the cause of syncope remained unexplained at the end of the diagnostic work-up. For example, patients with certain or suspected heart disease first underwent noninvasive cardiac examinations, as appropriate, and, in the event of negative results, an electrophysiologic study. Patients without signs of heart disease first underwent carotid sinus massage and the tilt test. In the event of focal neurologic symptoms before or after the loss of consciousness, witnessed prolonged loss of consciousness with tonic-clonic movements or a post-ictal state, migraine or signs of psychiatric disorders, a consultant neurologist or psychiatrist was called in. At his or her discretion, neurologic examinations were performed.
|
20 mm Hg during 5 min after the patient assumed the upright position, associated with dizziness or syncope (3,4); typical vasovagal if a precipitating event, such as fear, severe pain, strong emotion or instrumentation, could be identified in the absence of another competing diagnosis for the cause of syncope (3); situational syncope when the loss of consciousness occurred during or immediately after urination, defecation, coughing or swallowing (3); tilt-induced syncope when the loss of consciousness was induced during the tilt test, as previously described (5); carotid sinus syncope when carotid sinus massage, performed both in the supine and upright positions, induced syncope in the presence of bradycardia or hypotension, or both (6); drug-induced syncope when a clear temporal relationship between drug assumption and syncope could be proven; adenosine-sensitive syncope if a bolus of 20 mg of ATP induced a cardiac pause 6 s (7); and mechanical cardiac syncope in the presence of severe valvular stenosis or other flow obstruction. Arrhythmic syncope was diagnosed on the basis of standard ECG or 24-h Holter recordings or during the electrophysiologic study. The following findings of standard ECG were considered diagnostic: sinus bradycardia <40 beats/min or repetitive sinoatrial blocks or sinus pauses >3 s; Mobitz II or advanced (2:1, 3:1, etc.) second-degree atrioventricular (AV) block or third-degree AV block; atrial fibrillation with a slow ventricular response (mean heart rate <50 beats/min); and sustained supraventricular or ventricular tachyarrhythmias. The following findings of 24-h Holter recording were considered diagnostic: any arrhythmia associated with syncope or presyncope, or, in the absence of neurologic symptoms, Mobitz II or advanced degree or third-degree AV block; and sustained ventricular tachyarrhythmias. The following electrophysiologic findings were considered diagnostic: sinus node recovery time >3 s; baseline HV interval 100 ms or appearance of infra-hisian second- or third-degree AV block during atrial pacing or after ajmaline administration; and induction of syncopal or hypotensive supraventricular or ventricular tachyarrhythmias. Metabolic syncope due to hypoglycemia was diagnosed when the loss of consciousness was preceded by tremors, confusion, salivation, hunger and a hyperadrenergic state, and glycemia was <40 mg/dl.
|
|
Statistical analysis. Comparisons between groups were performed by means of the Fisher exact test, t test or rank-sum test, as appropriate. The logistic regression test was used to find those variables that were independent predictors of the cause of syncope. The data were analyzed with the StatSoft software (Version 5.1, 1997, Tulsa, Oklahoma).
|
Results |
|---|
|
TopAbstractMethodsResultsDiscussionReferences |
|---|
|
|
Comparison of clinical features during syncope. The clinical features of the patients with cardiac, neurally mediated and unexplained causes of syncope are reported in Table 2. There were some significant differences between cardiac and neurally mediated syncope. In contrast, the clinical features of unexplained syncope were very similar to those of neurally mediated syncope; indeed, among the variables examined, only male gender, time between the first and last syncopal episode and tremors showed significant differences between the two types of syncope.
We first performed a statistical analysis of the variables that were not part of the presentation of syncope: age, gender and the presence of suspected or certain heart disease after the initial evaluation. On univariate analysis, these were found to differ. Among these three variables, on multivariate analysis, the presence of suspected or certain heart disease was the only independent predictor of a cardiac cause of syncope (odds ratio 16, 95% confidence interval 5 to 48, p = 0.00001). Consequently, the patients were classified into two subgroups: one comprising the 191 patients with heart disease and the other comprising the 146 patients without it. We analyzed the historical variables of syncope separately in these two subgroups. The results are reported in Tables 4 and 5. Suspected or certain heart disease after the initial evaluation was present in 74 (95%) of 78 patients with a final diagnosis of cardiac syncope, but also in 117 (45%) of 259 of patients who did not have a cardiac cause of syncope (Fig. 2). In contrast, the absence of suspected or certain heart disease allowed us to exclude a cardiac cause of syncope in 142 (97%) of these 146 patients (Fig. 2).
|
|
4 years, 2 syncopal episodes, syncope during effort or in the supine position, blurred vision before the loss of consciousness and convulsive syncope. On multivariate analysis, duration of symptoms 4 years, syncope in the supine position and blurred vision remained independent predictors (Table 4). Significant univariate predictors of a neurally mediated cause of syncope were time between the first and last syncopal episode >4 years, history of presyncope, abdominal discomfort and pallor before the loss of consciousness and nausea and diaphoresis during the recovery phase. On multivariate analysis, duration of symptoms >4 years, history of presyncope and nausea remained independent predictors (Table 4).
Patients without suspected or diagnosed heart disease.
In the 146 patients without suspected or diagnosed heart disease after the initial evaluation, the only significant univariate predictor of a cardiac cause of syncope was palpitations before the loss of consciousness. The significant univariate predictors of a neurally mediated cause of syncope were 3 syncopal episodes and duration of prodromes >10 s. On multivariate analysis, duration of prodromes >10 s remained an independent predictor (Table 5).
Diagnostic value. Sensitivity, specificity and post-test probability (8) of the significant predictors are reported in Table 6.
|
|
Discussion |
|---|
|
TopAbstractMethodsResultsDiscussionReferences |
|---|
Comparison with previous studies. Two previous prospective studies have evaluated the clinical features during syncope (9,10). Martin et al. (9) obtained the clinical histories of 170 patients presenting with syncope on arrival at the emergency room. These authors reported that the duration of prodromal symptoms was longer for neurally mediated syncope than for cardiac syncope. We could not confirm this finding. However, in this study, a presumed diagnosis was established only at the time of the emergency room evaluation. Calkins et al. (10) evaluated the clinical histories in three selected groups of patients with neurally mediated syncope, syncope due to ventricular tachycardia and syncope due to AV block. The clinical histories of patients with syncope due to ventricular tachycardia or AV block were similar. In contrast, the clinical histories of patients with neurally mediated syncope differed from those of patients with cardiac syncope. We confirmed some features suggestive of neurally mediated syncope, such as diaphoresis before and after the loss of consciousness and nausea after the loss of consciousness. Other features suggestive of neurally mediated syncope, such as longer duration of prodromes, palpitations, nausea and lightheadedness before syncope and fatigue after the loss of consciousness, were not confirmed. In the study of Calkins et al. (10), patients were asked to give a description of their two most recent syncopal episodes. For this reason, the prevalence of symptoms was very likely overestimated, and the description could not be precise, as the time between two syncopal episodes is often long. Moreover, it is not clear how the duration of prodromes was evaluated. It must also be considered that the results will be different according to whether a study is carried out in a selected group of patients or in an unselected group (consecutive patients).
Results of the present study. On the basis of specific diagnostic criteria, the cause of syncope was established in 281 patients (82%) and remained unexplained in 60 (18%); the prevalence in the latter group was lower than that reported in five previous studies performed in the 1980s (mean 34%) (9,11–14), probably because of a more extensive utilization of carotid sinus massage, tilt testing and electrophysiology.
The clinical features of unexplained syncope and neurally mediated syncope were very similar (Table 2). This suggests that unexplained syncope is, at least in the vast majority of patients, a neurally mediated syncope that is difficult to diagnose with currently utilized tools.
The absence of prodromal symptoms was similar between cardiac and neurally mediated syncope (41% and 33%, respectively); therefore, this factor is not useful for diagnosing the cause of syncope. The duration of the loss of consciousness and the duration of the recovery phase were also similar between these two types of syncope.
Symptoms and signs, such as nausea, vomiting before the loss of consciousness, pallor, weakness, lightheadedness and yawning, which have been used up to now in clinical practice and considered very suggestive of neurally mediated syncope, even in the absence of a clinical investigation, show a similar prevalence in cardiac and neurally mediated syncope (Table 2) and, therefore, are not indicative of the type of syncope. These results suggest that activation of the autonomic system occur in all types of syncope. In addition, the prevalence of incontinence and injury was similar in all types of syncope.
Study limitations. In syncope, there is no diagnostic "gold" standard against which other diagnostic tests may be measured; therefore, no set of criteria and no algorithm for diagnosing syncope may be considered ideal. The diagnostic criteria we employed in the present study are those most commonly used; they were also officially accepted by the Italian Cardiological Association (1,2).
The prevalence of neurologic or psychiatric loss of consciousness was low (1%). It is possible that this result does not express the true prevalence of this type of loss of consciousness, because it is presumable that patients with seizure disorders or with loss of consciousness associated with focal neurologic symptoms went directly, or through the emergency room, to the neurology department. A similar low prevalence was reported in previous studies (9,12,15,16). The prevalence of typical vasovagal syncope may also be underestimated, as a population study showed that only 23% of patients with this type of syncope are referred to the hospital (17). For these reasons, the results of the present study seem to reflect the distribution of patients who are referred to the syncope unit, rather than the distribution of patients with syncope in the general population.
Abnormal neural reflexes have been shown to play an important role in the genesis of syncope in patients with sinus node dysfunction or with paroxysmal supraventricular tachyarrhythmias (18–21). Therefore, the diagnosis of arrhythmic syncope may constitute a simplification.
Clinical implications. In clinical practice, patients with syncope undergo several examinations, very often with negative results. The results of the present study suggest a practical strategy for evaluation of patients with syncope. We have demonstrated that the presence of suspected or certain heart disease after the initial evaluation is a predictor of a cardiac cause of syncope, as already reported by Martin et al. (22), although its specificity is low.
Thus, the presence or absence of heart disease should be investigated first. In the presence of heart disease, some variables (e.g., blurred vision, syncope occurring in the supine position or during effort or convulsive syncope) suggest a cardiac cause of syncope, with a high specificity. The presence of these variables increases the pre-test probability of a cardiac cause of syncope. For example, in a patient with suspected or certain heart disease, the diagnosis of a cardiac cause of syncope is increased from a pre-test probability of 39% (Fig. 2) to a post-test probability of 79% when syncope occurs in the supine position (Table 6). Therefore, these patients should probably be admitted to the hospital, and cardiac examinations should be given priority. In contrast, a long duration (>4 years) of symptoms and syncope preceded by abdominal discomfort or followed by nausea and diaphoresis suggest a neurally mediated cause of syncope, with a high specificity and an increased post-test probability. In these cases, autonomic tests should be given priority, and, if they are positive, a neurally mediated mechanism is likely, and the diagnostic work-up should be stopped. However, it must be emphasized that the sensitivity of the most specific predictors is quite low (Table 6), and, therefore, they can be useful only in a minority of patients.
When heart disease is absent, a cardiac cause is unlikely, unless palpitations precede syncope. In the latter case, the possibility that a tachyarrhythmia is the cause of syncope should be evaluated. In the other cases, autonomic tests should be performed to evaluate the possible neurally mediated nature of syncope. Patients usually do not need to be admitted to the hospital, given the benign outcome of this type of syncope.
The results of the present study can optimize the work-up of syncope, avoiding useless tests and reducing the high diagnostic costs in patients with syncope (23).
|
References |
|---|
|
TopAbstractMethodsResultsDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  T Pezawas, G Stix, J Kastner, B Schneider, M Wolzt, and H Schmidinger Implantable loop recorder in unexplained syncope: classification, mechanism, transient loss of consciousness and role of major depressive disorder in patients with and without structural heart disease Heart, April 1, 2008; 94(4): e17 - e17. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Tan and S. W. Parry Vasovagal syncope in the older patient. J. Am. Coll. Cardiol., February 12, 2008; 51(6): 599 - 606. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Brignole Diagnosis and treatment of syncope Heart, January 1, 2007; 93(1): 130 - 136. [Full Text] [PDF]
|
|
|
|
|
|
Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) J. Am. Coll. Cardiol., September 5, 2006; 48(5): e247 - e346. [Full Text] [PDF]
|
|
|
|
 |
|
 Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]
|
|
|
|
|
|
M. Brignole, A. Ungar, A. Bartoletti, I. Ponassi, A. Lagi, C. Mussi, M. A. Ribani, G. Tava, M. Disertori, F. Quartieri, et al. Standardized-care pathway vs. usual management of syncope patients presenting as emergencies at general hospitals. Europace, August 1, 2006; 8(8): 644 - 650. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Perennes, M. Fatemi, M. L. Borel, Y. Lebras, C. L'Her, and J.-J. Blanc Epidemiology, Clinical Features, and Follow-Up of Patients With Syncope and a Positive Adenosine Triphosphate Test Result J. Am. Coll. Cardiol., February 7, 2006; 47(3): 594 - 597. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Sheldon, S. Rose, S. Connolly, D. Ritchie, M.-L. Koshman, M. Frenneaux, and for the Syncope Symptom Study Investigators Diagnostic criteria for vasovagal syncope based on a quantitative history Eur. Heart J., February 1, 2006; 27(3): 344 - 350. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. D. Binder, M. A. Fifer, M. E. King, and J. R. Stone Case 26-2005 - A 48-Year-Old Man with Sudden Loss of Consciousness while Jogging N. Engl. J. Med., August 25, 2005; 353(8): 824 - 832. [Full Text] [PDF]
|
|
|
|
 |
|
 C M Gavin and J T Gray 15 Assessment and management of neurological problems (2) Emerg. Med. J., August 1, 2005; 22(8): 564 - 571. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Bloomfield and S. Jazrawi Shear Hilarity Leading to Laugh Syncope in a Healthy Man JAMA, June 15, 2005; 293(23): 2863 - 2864. [Full Text] [PDF]
|
|
|
|
|
|
M. Brignole, C. Menozzi, R. Maggi, A. Solano, P. Donateo, N. Bottoni, G. Lolli, F. Quartieri, F. Croci, D. Oddone, et al. The usage and diagnostic yield of the implantable loop-recorder in detection of the mechanism of syncope and in guiding effective antiarrhythmic therapy in older people Europace, January 1, 2005; 7(3): 273 - 279. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-J. Blanc, C. L'her, G. Gosselin, J.-C. Cornily, and M. Fatemi Prospective evaluation of an educational programme for physicians involved in the management of syncope Europace, January 1, 2005; 7(4): 400 - 406. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. K. Shen, W. W. Decker, P. A. Smars, D. G. Goyal, A. E. Walker, D. O. Hodge, J. M. Trusty, K. M. Brekke, A. Jahangir, P. A. Brady, et al. Syncope Evaluation in the Emergency Department Study (SEEDS): A Multidisciplinary Approach to Syncope Management Circulation, December 14, 2004; 110(24): 3636 - 3645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Task Force members, M. Brignole, P. Alboni, D. G. Benditt, L. Bergfeldt, J.-J. Blanc, P. E. B. Thomsen, J. G. van Dijk, A. Fitzpatrick, S. Hohnloser, et al. Guidelines on management (diagnosis and treatment) of syncope - Update 2004: The task force on Syncope, European Society of Cardiology Eur. Heart J., November 2, 2004; 25(22): 2054 - 2072. [Full Text] [PDF]
|
|
|
|
|
|
R. C. Ziegelstein Near-Syncope After Exercise JAMA, September 8, 2004; 292(10): 1221 - 1226. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Brembilla-Perrot, C. Suty-Selton, D. Beurrier, P. Houriez, M. Nippert, A. Terrier de la Chaise, P. Louis, O. Claudon, M. Andronache, A. Abdelaah, et al. Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing J. Am. Coll. Cardiol., August 4, 2004; 44(3): 594 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Solano, C. Menozzi, R. Maggi, P. Donateo, N. Bottoni, G. Lolli, C. Tomasi, F. Croci, D. Oddone, E. Puggioni, et al. Incidence, diagnostic yield and safety of the implantable loop-recorder to detect the mechanism of syncope in patients with and without structural heart disease Eur. Heart J., July 1, 2004; 25(13): 1116 - 1119. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. O. Cheng, C.-C. Lu, C.-S. Tung, A. Diedrich, S. Y. Paranjape, P. A. Harris, D. W. Byrne, D. Robertson, and J. Jordan Simple Self-Help Maneuvers Are Effective in Aborting Vasovagal Syncope * Response Circulation, May 11, 2004; 109(18): e217 - e217. [Full Text] [PDF]
|
|
|
|
 |
|
 N. Nathani, G. D Perkins, and D. R Thickett Medical emergencies in trauma Trauma, April 1, 2004; 6(2): 135 - 142. [Abstract] [PDF]
|
|
|
|
|
|
P. Alboni, M. Brignole, C. Menozzi, A. Raviele, A. Del Rosso, M. Dinelli, K. Bettiol, N. Bottoni, and A. Solano Clinical spectrum of neurally mediated reflex syncopes Europace, January 1, 2004; 6(1): 55 - 62. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Croci, M. Brignole, C. Menozzi, A. Solano, P. Donateo, D. Oddone, E. Puggioni, and G. Lolli Efficacy and feasibility of isometric arm counter-pressure manoeuvres to abort impending vasovagal syncope during real life Europace, January 1, 2004; 6(4): 287 - 291. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Guidelines on Management (diagnosis and treatment) of syncope - update 2004: The Task Force on Syncope, European Society of Cardiology Europace, January 1, 2004; 6(6): 467 - 537. [Full Text] [PDF]
|
|
|
|
|
|
D J Farwell and A N Sulke Does the use of a syncope diagnostic protocol improve the investigation and management of syncope? Heart, January 1, 2004; 90(1): 52 - 58. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. C. Kurer Implantable looprecorders: dollars and sense J. Am. Coll. Cardiol., August 6, 2003; 42(3): 502 - 504. [Full Text] [PDF]
|
|
|
|
 |
|
 J. E. David, S. H. Yale, and H. J. Vidaillet Hyperventilation-Induced Syncope: No Need to Panic Clin. Med. Res., April 1, 2003; 1(2): 137 - 139. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Garcia-Civera, R. Ruiz-Granell, S. Morell-Cabedo, R. Sanjuan-Manez, F. Perez-Alcala, E. Plancha, A. Navarro, S. Botella, and A. LLacer Selective use of diagnostic tests inpatients with syncope of unknown cause J. Am. Coll. Cardiol., March 5, 2003; 41(5): 787 - 790. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. G. Benditt and M. Brignole Syncope: is a diagnosis a diagnosis? J. Am. Coll. Cardiol., March 5, 2003; 41(5): 791 - 794. [Full Text] [PDF]
|
|
|
|
|
|
M. Disertori, M. Brignole, C. Menozzi, A. Raviele, P. Rizzon, M. Santini, A. Proclemer, C. Tomasi, A. Rossillo, F. Taddei, et al. Management of patients with syncope referred urgently to general hospitals Europace, January 1, 2003; 5(3): 283 - 291. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Brignole, M. Disertori, C. Menozzi, A. Raviele, P. Alboni, M. V. Pitzalis, P. Delise, E. Puggioni, M. Del Greco, V. Malavasi, et al. Management of syncope referred urgently to general hospitals with and without syncope units Europace, January 1, 2003; 5(3): 293 - 298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Brignole, F. Croci, C. Menozzi, A. Solano, P. Donateo, D. Oddone, E. Puggioni, and G. Lolli Isometric arm counter-pressure maneuvers to abort impending vasovagal syncope J. Am. Coll. Cardiol., December 4, 2002; 40(11): 2053 - 2059. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
|
