神经介导性晕厥

晕厥包括神经介导性晕厥、直立性低血压晕厥、心源性晕厥、脑源性晕厥及不明原因的晕厥。其中神经介导性晕厥是最常见的晕厥,包括血管迷走性晕厥、情景性晕厥、颈动脉窦晕厥和精神性晕厥。本文阐述了神经介导性晕厥发病机制及其治疗,对神经介导性晕厥有更深入的了解。     

New approaches to the treatment and prevention of neurally mediated reflex (neurocardiogenic) syncope

Neurally mediated reflex syncope (sometimes referred to as neurocardiogenic syncope), encompasses a group of disorders of which the best known and most frequently occurring forms are the vasovagal (or common) faint, and carotid sinus syndrome. Postmicturition syncope, defecation syncope, cough syncope, and other situational reflex faints are also included among these conditions. With the exception of carotid sinus syndrome in which cardiac pacing is effective, treatment of most neurally mediated reflex faints is shifting from reliance on various drugs to greater emphasis on education and nonpharmacologic therapy. Initial management should include counseling of patients regarding recognition of early warning symptoms, and avoidance of precipitating factors. Volume expansion with salt tablets or electrolyte-containing beverages and patient education on how to perform isometric arm contractions and/or leg crossing in order to abort impending syncope are also important. Thereafter, tilt-training has demonstrated benefit in several clinical studies. When symptoms remain despite the above-noted interventions, pharmacologic therapy with midodrine or a nonselective à-blocker can be considered. the case of most neurally mediated reflex faints, permanent cardiac pacing should be reserved only for those older patients with significant bradycardia or asystole at time of syncope when all other interventions have failed.     

Pathophysiology of reflex syncope: A review

In this correspondence, the pathophysiology of reflex syncope (vasovagal syncope, carotid sinus syndrome, and situational syncope) is reviewed, including clarification of the nomenclature.     

Neurally mediated syncope and unexplained or nonaccidental falls in the elderly

Falls and syncope are among the leading causes for which older patients seek hospital admissions. The prevalence of unexplained or nonaccidental falls is high in this group. The clinical spectrum of falls and syncope has been shown to overlap significantly in the elderly. Carotid sinus syndrome and vasovagal syncope, the two common examples of neurally mediated syncope (NMS), have been increasingly recognised as important attributable causes for unexplained falls and syncope. However, in clinical practice NMS is not widely investigated as a cause of fall and is likely to be underdiagnosed.     

Randomized Clinical Trials of Neurally Mediated Syncope

Evidence for therapy of neurally mediated syncope is generally weak. Many drugs have been used for the treatment of vasovagal syncope (beta-blockers, disopyramide, scopolamine, clonidine, theophylline, fludrocortisone, ephedrine, dihydroergotamine, etilefrine, midodrine, clonidine, serotonin reuptake inhibitors, enalapril). In general, although the results have been satisfactory in uncontrolled trials or short-term controlled trials, the majority of long-term placebo-controlled prospective trials have not been able to show a benefit of the active drug over placebo. Only two well-designed double-blind placebo-controlled randomized trials have been performed—one for etilefrine and the other for atenolol—and both were unable to show a superiority of the active drug versus placebo. Four randomized clinical trials of pacing therapy—three positive and one negative—have been performed in patients affected by vasovagal syncope. The relationship between carotid sinus hypersensitivity and spontaneous, otherwise unexplained, syncope has been demonstrated. Cardiac pacing appears to be beneficial in carotid sinus syndrome; its efficacy has been demonstrated by two randomized controlled trials and confirmed by several pre-post comparative studies, one controlled trial, and one prospective observational study. There is evidence and general agreement that cardiac pacing is useful in patients with cardioinhibitory or mixed carotid sinus syndrome. Usefulness of the treatment is less well established and divergence of opinion exists with regard to cardiac pacing in patients with cardioinhibitory vasovagal syncope. The evidence fails to support the efficacy of beta-blocking drugs. As yet there are insufficient data to support the use of any other pharmacologic therapy for vasovagal syncope. (J Cardiovasc Electrophysiol, Vol. 14, pp. S64-S69, September 2003, Suppl.)     

Hemodynamic significance of heart rate in neurally mediated syncope

BACKGROUND: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. METHODS: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). RESULTS: The baseline hemodynamic data (mean +/- standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 +/- 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 +/- 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 +/- 0.29 vs. 1.97 +/- 0.41 1/min/m2, p < 0.001 and 2098 +/- 615 vs. 1573 +/- 353 dynes x s x cm(-5) x m2, p < 0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. CONCLUSIONS: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope.     

The Clinical Spectrum of Neurocardiogenic Syncope

Neurocardiogenic Syncope. Neurocardiogenic syncope is a collective term used to describe the clinical syndromes of syncope that result from inappropriate, and often excessive, autonomic reflex activity, and manifest as abnormalities in the control of vascular tone and heart rate. These include carotid sinus syndrome, vasovagal syncope, and the syndromes of cough, deglutition, and micturition syncope. Orthostatic hypotension, which, in contrast, results from a failure of autonomic reflexes, is not considered part of this family of closely related syndromes. This review will focus on vasovagal and carotid sinus syndromes.     

Was ist neu in der ESC-Leitlinie von 2009?

The 2009 ESC guideline emphasizes active risk stratification and the diagnostic strategy of prolonged ECG monitoring using an implantable loop recorder. The initial evaluation aims at establishing a prima vista diagnosis or at least a diagnostic hypothesis and risk stratification according to ECG criteria and clinical findings. Carotid sinus massage as a diagnostic procedure remains controversial. Electrophysiological study for evaluation of suspected arrhythmogenic syncope is of decreasing relevance. The loop recorder enables documentation of the rhythm during a subsequent syncope. Neurological work-up is not routinely recommended. A standardized evaluation minimizes the rate of unexplained syncopes. Therapeutic decisions include ICD or pacemaker, as indicated in cases of arrhythmogenic syncope or carotid sinus syncope, and mostly general measures in case of other reflex syncopes.     

A new reflex cardiovascular syndrome: recurrent vasodepressive syncope caused by lesions or tumors of the parapharyngeal space. Etiopathogenesis, clinical picture, differential diagnosis with carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Therapy by intracranial resection of the 9th cranial nerve

An intense vaso-vagal reaction characterizes all the reflex induced cardiovascular syncopes. In these syndromes the vagal cardio-inhibitor effect on heart rate is more evident than the vasodilatation and fall in blood pressure. The vasodepressor mechanism is uncommon even in carotid sinus syndrome. We have studied 6 male patients, age range 56-73 years (mean age: 64) with recurrent vasodepressor syncopes. The following were always present during such episodes: generalized malaise, profound fatigue, pallor, cyanosis, copious sweating, lack of peripheral pulses, severe fall in blood pressure (BP) (systolic BP less than or equal to 50-60 mmHg or unrecordable), mental disorientation and/or syncope. The first diagnosis in our patients was carotid sinus syndrome, but, the clinical picture was quite different from classic carotid sinus syndrome: triggering factors were not present, the vasovagal episodes were longer, the syncopes more frequent and severe, and the VVI pacing uneffective. Further investigations, including computerized axial tomography, showed--in all these patients--a malignant tumour originally localized in or near the parapharyngeal space. We think that the symptoms of our patients can be attributed to parapharyngeal tumour and that the parapharyngeal space lesions are able to cause severe vasovagal attacks and syncope. The pathogenetic mechanism in this syndrome, due to neural irritation of the glossopharyngeal afferent fibres, is similar to the glossopharyngeal neuralgia-asystole syndrome, but it obviously doesn't involve pain-pathways since none of our patients had pain. Therefore, this syndrome differs from glossopharyngeal neuralgia- asystole syndrome in the presence of tumours and in the absence of neuralgia and initiating factors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Kommentar zu der Leitlinie zur Diagnostik und Therapie von Synkopen der Europ?ischen Gesellschaft f��r Kardiologie 2009

The guideline emphasizes active risk stratification and the diagnostic strategy of prolonged ECG monitoring using an implantable loop recorder. The initial evaluation aims at establishing a prima-vista diagnosis or at least a diagnostic hypothesis and risk stratification according to ECG criteria and clinical hints. Carotid sinus massage as a diagnostic procedure remains controversial. Electrophysiological study for evaluation of suspected rhythmogenic syncope is of decreasing relevance. The loop recorder enables documentation of the rhythm during a subsequent syncope. Neurological work-up is not routinely recommended. A standardized evaluation minimizes the rate of unexplained syncopes. Therapeutic decisions include ICD or pacemaker, as indicated in cases of rhythmogenic syncope or carotid sinus syncope, and mostly general measures in cases of other reflex syncopes.     

Neurally mediated syncope

The prevalence and incidence of syncope increases with advancing years due to age related physiological changes in the neurocardiovascular, endocrine and renal systems. Cardiovascular syncope can present as falls because of amnesia for loss of consciousness or postural instability due to hypotension. Drop attacks or non accidental falls should thus be investigated for causes of syncope. The most common causes of neurally mediated syncope in older adults are carotid sinus syndrome, orthostatic hypotension and vasovagal syncope.     

Clinical recognition of neurally mediated syncope

BACKGROUND: Most cases of syncope are due to hypotension, with a vasovagal response the commonest single mechanism. Neurally mediated syncope (NMS) is a vasovagal response evoked by common physical or psychological stress factors in susceptible individuals. Although upright tilt table testing (TTT) has been developed to diagnose this condition, the clinical recognition of this common syndrome in the general community remains poor. AIMS: To evaluate the clinical presentation of patients with NMS and pre-syncope, proven by TTT, and compare them to patients with syncope that have a low probability of having NMS (e.g. older patients with cardiac disease and negative TTT). METHODS: Prospective evaluation by questionnaire at the time of TTT, including documentation of presenting symptoms and signs, and provoking factors in consecutive patients. Comparisons between patient groups analyzed using chi-squared tests and logistic regression. RESULTS: Neurally mediated syncope patients were more likely to present with both syncope and pre-syncope, often with prolonged histories of pre-syncope. Certain provoking stress factors were more common in NMS, with multiple factors often present. Most NMS patients had a hypotensive prodrome before syncope, whereas control patients had a higher incidence of syncope without warning. CONCLUSION: Neurally mediated syncope patients present with situational syncope that is not only stereotypical for the individual, but shares common features with other similar patients. While none of the clinical observations is unique to NMS, a carefully detailed history can elicit a convincing diagnostic pattern that can often obviate the need for extensive and expensive investigation, and in younger patients a TTT may not be required to make the diagnosis.     

Efficacy of tilt training in the treatment of neurally mediated syncope. A randomized study.

Recurrent neurally mediated syncope represents a common clinical event and a therapeutic challenge. Recently tilt training has been proposed for the treatment of recurrent neurally mediated syncope. To evaluate the efficacy of tilt training in preventing tilt-induced syncope and its feasibility, this controlled, randomized study was undertaken. Sixty-eight consenting patients (25 males and 43 females, mean age 40 +/- 19) with recurrent neurally mediated syncope and 2 consecutive positive nitroglycerin-potentiated head-up tilt tests were randomized to tilt training (35 patients) or no treatment (controls, 33 patients). The tilt training programme consisted of daily 30-min sessions of upright standing against a vertical wall 6 days a week for at least 3 weeks, until a reevaluation tilt test (3 patients of both groups dropped out). On this third head-up tilt test, 19 (59%) of 32 tilt trained patients and 18 (60%) of 30 controls still had a positive test. Treated patients performed a mean number of 15 +/- 7 sessions (median 16) and only 11 patients (34%) did all the programmed sessions. Only 1 patient (3%) discontinued treatment because of intolerance, while all other patients did not perform tilt training adequately, because of poor compliance. Thus, in our study tilt training was not effective in reducing tilt testing positivity rate in patients with neurally mediated syncope. Because of poor compliance, tilt training appears to be a feasible treatment only for highly motivated patients, but not for the majority of patients with recurrent neurally mediated syncope.     

Role of the serotonergic system in the genesis of vasovagal syncope.

AIMS: The hypotensive reflex responsible for vasovagal syncope appears related to a reduction in sympathetic neural outflow. Several animal studies suggest that serotonin may play a role in the genesis of this reflex, through inhibition of sympathetic activity. However, the role of the serotonergic system is unknown in humans. The purpose of the study was to investigate the role of the serotonergic system in the genesis of vasovagal syncope by means of the level of platelet and plasma serotonin, as well as plasma catecholamines, during tilt-induced syncope. METHODS AND RESULTS: Fifteen patients (age 34 +/- 16 years) with vasovagal syncope underwent a head-up tilt test (HUT, 60 degrees , 45 min). If syncope did not develop, 300 microg nitroglycerin was administered sublingually and patients continued to be tilted for a further 20 min. Blood samples were obtained in the supine position, and then after 3, 10, 15, 30, 45, 48 and 65 min of HUT. If syncope developed, blood samples were obtained at the beginning of the prodrome, during syncope and after the recovery of consciousness. Platelet and plasma serotonin and plasma catecholamines were measured using high-pressure liquid chromatography with electrochemical detection. Ten patients developed syncope during the unmedicated HUT and four after nitroglycerin. In these patients plasma adrenaline significantly increased from the last programmed sample before the prodrome to its beginning and showed a further increase during loss of consciousness, whereas plasma noradrenaline did not increase, as an expression of inhibition of sympathetic neural outflow. In the patients experiencing syncope, both platelet and plasma serotonin showed no significant change after tilt-up, at the beginning of prodrome, during syncope and after recovery of consciousness. CONCLUSION: These results do not suggest that the serotonergic system plays a role in the pathophysiology of vasovagal syncope.     

Clinical experience of a new rate drop response algorithm in the treatment of vasovagal and carotid sinus syncope.

Dual chamber pacing has proven beneficial in patients with sudden drops in heart rate as seen in vasovagal syncope and carotid sinus syndrome. Newer algorithms for faster detection of an insidious drop in heart rate and short lasting intervention pacing at a high rate, as in the rate drop response algorithm in the Medtronic Kappa series of pacemakers, might improve the effect of pacing. Two case reports, that demonstrate the use of these rate drop response algorithms, are presented. A 24-year-old woman with recurrent episodes of syncope and repeated tilt-table tests with vasovagal cardioinhibitory outcomes had a Medtronic Kappa 400 pacemaker implanted. Syncope was abolished during repeat tilt-table testing following pacemaker implantation and proper functioning of the rate drop response algorithm. The patient has been free of syncope during follow-up apart from a single episode that occurred due to neglect of vasovagal warning symptoms. A 52-year-old man with coronary artery disease developed recurrent blackouts. Carotid sinus massage resulted in 5.5 s of asystole and presyncope. A Medtronic Kappa 700 pacemaker with a rate drop response algorithm was implanted and the patient became asymptomatic. The rate drop response algorithm is discussed in detail based upon the case reports, and recommendations are given for the use of this algorithm in patients with vasovagal syncope and carotid sinus syndrome.     

Neurally-mediated syncope.

"Neurally-mediated (reflex) syncope" refers to a reflex response that, when triggered, gives rise to vasodilation and/or bradycardia; however, the contribution of each of these two factors to systemic hypotension and cerebral hypoperfusion may differ considerably. The initial evaluation may lead to a certain diagnosis in the case of classical vasovagal syncope and of situational syncope. Classical vasovagal syncope is diagnosed if precipitating events such as fear, severe pain, emotional distress, instrumentation or prolonged standing, are associated with typical prodromal symptoms. Situational syncope is diagnosed if syncope occurs during or immediately after urination, defecation, cough or swallowing. In the absence of a certain diagnosis, absence of cardiac disease, long history of syncope, syncope after sudden unexpected unpleasant sight, sound or smell, prolonged standing at attention or crowded, warm places, nausea and vomiting, post-prandial and post-exercise state suggest a neurally-mediated cause which needs to be confirmed by specific tests. Among them, the most useful are carotid sinus massage and tilt testing. In general, education and reassurance are the sufficient initial treatment. Additional treatment may be necessary in high-risk or high-frequency settings. Treatment is not necessary in patients who have sustained a single syncope and are not having syncope in a high-risk setting. It is valuable to assess the relative contribution of cardioinhibition and vasodepression before embarking on treatment as there are different therapeutic strategies for the two aspects. Even if evidence of utility of such an assessment exists only for the carotid sinus massage, it is recommended to extend this assessment also by means of tilt testing or implantable loop recorder. Tilt training and isometric leg and arm counterpressure maneuvers are indicated in patients with recurrent vasovagal syncope. Cardiac pacing is indicated in patients with cardioinhibitory or mixed carotid sinus syndrome and in patients with cardioinhibitory vasovagal syncope with a frequency > 5 attacks per year or severe physical injury or accident and age > 40 years. The evidence fails to support the efficacy of any drug.     

Neurocardiogenic syncope in chronic atrioventricular block

We report a 37-year-old man with type I second-degree atrioventricular (AV) block (atypical Wenckebach's periodicity) referred to our department for pacemaker implantation because of an episode of syncope. After exhaustive evaluation, including electrophysiological test, in which Wenckebach's cycles with block within the AV node was demonstrated, syncope was considered to be neurally mediated. Head-up tilt testing with sublingual isosorbide dinitrate was positive. The decrease in atrial rate at the beginning of the vasovagal reaction was not immediately accompanied by a depressed AV node conduction. Only at the moment of syncope did incomplete AV block appear. This observation illustrates (1) a neurally mediated origin of syncope in a patient with chronic AV block, and (2) the different time-course responses of the sinus and AV nodes to autonomic tone.     

Predictive models of syncope causes in an outpatient clinic

The investigation of unexplained syncope remains a challenging clinical problem. In the present study we sought to evaluate the diagnostic value of a standardized work-up focusing on non invasive tests in patients with unexplained syncope referred to a syncope clinic, and whether certain combinations of clinical parameters are characteristic of rhythmic and reflex causes of syncope. METHODS AND RESULTS: 317 consecutive patients underwent a standardized work-up including a 12-lead ECG, physical examination, detailed history with screening for syncope-related symptoms using a structured questionnaire followed by carotid sinus massage (CSM), and head-up tilt test. Invasive testings including an electrophysiological study and implantation of a loop recorder were only performed in those with structural heart disease or traumatic syncope. Our work-up identified an etiology in 81% of the patients. Importantly, three quarters of the causes were established non invasively combining head-up tilt test, CSM and hyperventilation testing. Invasive tests yielded an additional 7% of diagnoses. Logistic analysis identified age and number of significant prodromes as the only predictive factors of rhythmic syncope. The same two factors, in addition to the duration of the ECG P-wave, were also predictive of vasovagal and psychogenic syncope. These factors, optimally combined in predictive models, showed a high negative and a modest positive predictive value. CONCLUSION: A standardized work-up focusing on non invasive tests allows to establish more than three quarters of syncope causes. Predictive models based on simple clinical parameters may help to distinguish between rhythmic and other causes of syncope.     

Disease-related syncope. Analysis of a community-based hospital registry

Syncope is characterized by sudden and transient loss of consciousness that follows a reduction or interruption of cerebral blood flow. The present study was designed to assess the prevalence of disease-related syncope in a wide sample of in-patients admitted for different diseases. A total of 16 809 patients (age range 18-99 years) were recruited from three hospitals in Florence in 1998. The community-based registry was reviewed to identify all patients suffering from complaints associated with syncope. Each disease-related syncope was matched with the number of patients suffering from that disease. Furthermore, each disease was expressed as a percentage of total cases included in the study. The odds ratio was calculated to determine the index of significant correlation between syncope and occasional diseases. Total syncopes were 775 (prevalence 4.46%), vasovagal syncopes were 336 (1.9% of total sample and 44% of total syncopes), and the disease-related syncopes were 439 (56% of total syncopes). We found a significant association between syncope and orthostatic hypotension, complete heart block, chronic cerebral disease, migraine, acute gastrointestinal haemorrhages and aortic stenosis. Furthermore, we found a significant association with acute gastrointestinal haemorrhage, which has not been described previously. Significant relationships emerged from our data which yield a new insight into the association between syncope and a wide range of systemic diseases.     

The incidence of malignant vasovagal syndrome in patients with recurrent syncope

We reviewed 322 patients with recurrent syncope between 1984 and 1988. Investigation included limited intracardiac electrophysiological study in all cases with programmed extra-stimulus studies in 48 cases. In 93 patients (29%), all investigations were normal, (including negative extrastimulus in 30). In the other 229 cases syncope was explained by AV-block (n = 111, 34%), sinus node disease (n = 68, 21%), carotid sinus syndrome (n = 32, 10%) and inducible sustained tachyarrhythmia (n = 18, 6%). Prolonged 60 degrees head-up tilt was performed in 71 out of 93 patients with unexplained syncope, and reproduced vasovagal syncope and presenting symptoms in 53 (75%), or 16% of the whole population reported. These patients were diagnosed as having malignant vasovagal syndrome. Positive tilts were significantly less common in a group of 27 subjects of similar age without a history of syncope (7%), and a random sample of 37 patients with atrioventricular block (n = 16), sick sinus syndrome (n = 18) and inducible tachyarrhythmia (n = 3), (19%, 11% and 0% respectively, P less than 0.01). From this retrospective review it appears, therefore, that tilt testing is a valuable provocative tool for vasovagal syncope and may reduce the number of syncopal patients that remain undiagnosed, although these early observations do not allow an exact appraisal of the sensitivity and specificity of the tilt test.