血管迷走性晕厥的机制、诊断及治疗进展

晕厥是指由于脑血流低灌注导致一过性意识丧失和姿势紧张丧失 ,可由多种不同原因引起。其中 ,与神经反射有关的晕厥统称为神经介导性晕厥 ,包括血管迷走性晕厥 (vasovagalsyncope ,VVS)、颈动脉窦过敏综合征和排尿性晕厥等。神经介导性晕厥的共同特点是某些触发因素引起反射性交感神经张力下降或伴有一定程度的迷走神经张力升高 ,从而导致血管扩张、血压下降、心率减慢 ,引起大脑缺血 ,发生晕厥。几种不同类型的神经介导性晕厥的区别在于触发因素及反射弧的传入途径不同。VVS是神经介导性晕厥中的一种常见类型。据统计 ,在院外发生晕厥事…     

起搏治疗神经介导性晕厥

神经介导性晕厥（综合征）又称神经反射性晕厥是指多种因素触发的过强的神经反射，引起低血压和心动过缓，从而导致晕厥发作。神经介导性晕厥包括：（1）血管迷走性晕厥（vasovagal syncope，VVS）；（2）颈动脉窦综合征（carotid sinus syndromes，CSS）；（3）其他反射性晕厥。     

心脏电生理学新概念 (17)倾斜试验

晕厥在临床中常见 ,多与心脏、代谢疾病以及神经反射有关。一般地说 ,与心脏和代谢疾病有关的晕厥依靠目前的临床检查技术多数可以明确原因 ,但与神经反射有关的晕厥诊断比较困难。以往所谓不能解释的晕厥 (Ｕｎｅｘｐｌａｉｎｅｄｓｙｎｃｏｐｅ)中绝大部分与神经反射有关 ,现在统称其为神经介导性 (Ｎｅｕｒａｌｌｙｍｅｄｉａｔｅｄｓｙｎｃｏｐｅ)晕厥。神经介导性晕厥包括许多不同类型 ,这些类型的共同特点是某些触发因素引起反射性交感神经张力下降或伴一定程度的迷走神经张力升高 ,从而导致血管扩张、血压降低 (伴有或不伴心率减慢 )…     

倾斜试验的应用及评价

晕厥在临床中常见，多与心脏、代谢疾病以及神经反射有关。一般地说，与心脏和代谢疾病有关的晕厥依靠目前常用的临床检查技术多数可以明确原因，但与神经反射有关的晕厥诊断比较困难。以往所谓不能解释的晕厥（ｕｎｅｘｐｌａｉｎｅｄ ｓｙｎｃｏｐｅ）中绝大部分与神经反射有关，现在统称其为神经介导性（ｎｅｕｒａｌｌｙ　ｍｅｄｉａｔｅｄ　ｓｙｎｃｏｐｅ）晕厥。神经介导性晕厥包括许多不同类型，这些类型的共同特点是某些触发因素引起反射性交感神经张力下降或伴一定程度的迷走神经张力升高，从而导致血管扩张、血压降低（伴有或不…     

晕厥的评估与诊断

正晕厥是指一过性全脑血流低灌注导致的突发、短暂、完全性意识丧失,特点是发生迅速、一过性、自限性并能够完全恢复。晕厥是常见临床症状,在美国每年有大约75万人因晕厥而就诊[1]。Framingham研究显示,晕厥发生率为每年每千人6.2人次,70岁以后发病率急剧增加[2]。预估晕厥终生累积发病率为30%~40%[3]。晕厥的病因多种,包括神经介导的反射性晕厥(包括血管迷走性晕厥、情境性晕厥、颈动脉窦过敏综合征)、体     

直立倾斜试验的研究进展

直立倾斜试验是用于诊断不明原因晕厥和先兆晕厥的常用方法。该试验已经应用于临床30多年,主要诊断神经介导性晕厥,但其在诊断过程中的确切作用尚不确定。公认的局限性包括再现性差,缺乏预后的作用和足够的随机研究来指导治疗的选择。     

��������������񾭽鵼�����ʵķ��ζԲ�

目的探讨心脏介入治疗过程中发生神经介导性晕厥的机制和防治对策。方法2000-06-2004-03对吕梁市医院368例冠状动脉成型介入治疗的病人随机分防治组(n=187)与对照组(n=181)。防治组在术后拔管时给予2%利多卡因对血管鞘周围局部浸润麻醉,对照组拔管时不给予局部浸润麻醉。结果神经介导性晕厥对照组发生率11.04%,防治组发生率为3.20%。两组间差异有显著性(P<0.05)。结论心脏介入治疗中发生的神经介导性晕厥与导管刺激血管,心脏及血管受压有关。术后拔管过程中局部浸润麻醉能够有效地减少神经介导性晕厥的发生。     

96例晕厥患者的病因分析

目的对晕厥患者进行病因分析,寻找晕厥诊疗方向。方法选择2014年1月1日~2016年12月21日以晕厥收入我院神经内科的患者96例,分析患者的病因构成。结果所有患者中,神经介导的反射性晕厥50例,占52.1%,体位性低血压及直立不耐受综合征性晕厥31例,占32.3%,心源性晕厥如心律失常、冠状动脉粥样硬化性心脏病、肺栓塞等引起的10例,占10.4%。非晕厥5例,占5.2%。结论晕厥的主要病因是神经介导的反射性晕厥,其次为体位性低血压晕厥、心源性晕厥;需重视神经系统疾病引起的晕厥病因的查找;对病因进行危险分层有助于降低潜在的风险。     

131例老年性晕厥的病因分析

目的探讨老年性晕厥常见的发病病因。方法选择大连医科大学附属第二医院以晕厥待查收住院的患者252例,年龄≥60岁并符合2009年欧洲心脏病学会诊断标准的老年性晕厥患者131例,统计年龄、性别、晕厥发生时体位、诱发因素、伴随症状、意识丧失的持续时间、既往史及相关辅助检查等资料,分析各类晕厥的病因和危险因素。结果 131例老年性晕厥患者占同期全部晕厥的52.0%(131/252),神经介导性晕厥为43.5%(57例),其中血管迷走性晕厥38例,情境性晕厥15例,颈动脉窦高敏性晕厥3例,精神疾病所致晕厥1例。心源性晕厥为32.8%(43例),其中病态窦房结综合征、Ⅱ度及以上房室传导阻滞19例,阵发性室性心动过速5例,阵发性心房颤动4例,快-慢综合征1例,急性冠状动脉综合征2例,冠心病、心绞痛或心肌梗死5例,泵衰竭4例,束支传导阻滞3例。神经系统疾病所致晕厥为12.2%(16例)。其他原因晕厥为7.6%(10例)。原因不明为3.8%(5例)。二分类logistic回归分析显示,家族史、治疗依从性、糖尿病及血脂异常为神经源性晕厥、心源性晕厥患者发生的高危因素。结论老年性晕厥的主要原因为神经介导性晕厥,其次为心源性晕厥,其他原因较少见。     

Clinical spectrum of neurally mediated reflex syncopes.

AIMS: The clinical features of the various types of neurally mediated reflex syncope have not been systematically investigated and compared. We sought to assess and compare the clinical spectrum of neurally mediated reflex syncopes. METHODS AND RESULTS: Four hundred sixty-one patients with syncope were prospectively evaluated and 280 had neurally mediated reflex syncope. Each patient was interviewed using a standard questionnaire. A cause of syncope was assigned using standardized diagnostic criteria. Typical vasovagal syncope was diagnosed in 39 patients, situational syncope in 34, carotid sinus syncope in 34, tilt-induced syncope in 142 and complex neurally mediated syncope (positive response to both carotid sinus massage and tilt test) in 31. The clinical features of situational, carotid sinus, tilt-induced and complex neurally mediated syncope were very similar. By contrast, typical vasovagal syncope differed from other neurally mediated syncopes not only in terms of its precipitating factors (fear, strong emotion, etc.), which constituted predefined diagnostic criteria, but also in the variety of its clinical features (lower age and prevalence of organic heart disease, higher prevalence of prodromal symptoms, and of autonomic prodromes, longer duration of prodromes, higher prevalence of symptoms during the recovery phase and lower prevalence of trauma). CONCLUSION: The clinical spectrum of neurally mediated reflex syncopes demonstrates much overlap between them. However, when the afferent neural signals are localized in cortical sites, as in typical vasovagal syncope, symptoms are more frequent and of longer duration.     

Cardioinhibitory carotid sinus hypersensitivity predicts an asystolic mechanism of spontaneous neurally mediated syncope.

AIMS: We correlated the finding of cardioinhibitory carotid sinus hypersensitivity (CSH) with that observed during a spontaneous syncopal relapse by means of an implantable loop recorder (ILR). METHODS AND RESULTS: We included 18 consecutive patients with suspected recurrent neurally mediated syncope and positive cardioinhibitory response during carotid sinus massage (max pause 5.5 +/- 1.6 s) who had subsequent documentation of a spontaneous syncope by means of an ILR. They were compared with a 2:1 age- and sex-matched group of 36 patients with a clinical diagnosis of recurrent neurally mediated syncope and negative response to carotid sinus massage, tilt testing and ATP test. Asystole >3 s was observed at the time of the spontaneous syncope in 16 (89%) of CSH patients and in 18 (50%) of the control group (P = 0.007). Sinus arrest was the most frequent finding among CSH patients but not among controls (72 vs. 28%, P = 0.003). After ILR documentation, 14 CSH patients with asystole received dual-chamber pacemaker implantation; during 35 +/- 22 months of follow-up, 2 syncopal episodes recurred in 2 patients (14%), and pre-syncope occurred in another 2 patients (14%). Syncope burden decreased from 1.68 (95% confidence interval 1.66 - 1.70) episodes per patient per year before to 0.04 (0.038-0.042) after pacemaker implant (98% relative risk reduction). CONCLUSIONS: In patients with suspected neurally mediated syncope, the finding of cardioinhibitory CSH predicts an asystolic mechanism at the time of spontaneous syncope and, consequently, suggests a possible benefit of cardiac pacing therapy.     

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.     

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.     

Current management of syncope: Treatment alternatives

Opinion statement Syncope, defined as a transient loss of consciousness and postural tone with spontaneous recovery and no neurologic sequelae, is among one of the most common causes of consultation with a physician. The diagnostic workup is complex but can be simplified if focused on the underlying condition. Prognosis is highly dependent on the presence or absence of structural heart disease, primarily the presence of cardiomyopathy regardless of etiology, particularly if the left ventricular (LV) function is less than 35%. The diagnostic approach to the patient with recurrent syncope and no structural heart disease is targeted to rule out neurally mediated causes. This approach usually includes a tilt table test (ie, head-up tilt), carotid sinus massage in patients older than 55 years, and an adenosine challenge test in patients who remain with unexplained syncope. Unexplained syncope in patients with reduced LV function (< 35%) may be potentially life-threatening. Infrequent causes of syncope should be sought in younger patients with a family history of sudden cardiac death. Channelopathies such as the long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia are among this variety. Therapy should address the potential mechanism of syncope. In neurally mediated causes, restoration of orthostatic tolerance, primarily by increasing volume during orthostatic stress, is recommended. Physiologic countermaneuvers and increase in salt and water intake are usually the initial therapy. With syncope in patients with an LV dysfunction (< 35%), an ICD is frequently recommended after ruling out common causes of syncope. Syncope in the elderly is usually multifactorial and therapy should include reassessment of multiple medications, which can promote neurally mediated syncope as well as searching for bradycardic causes. Empiric pacing may be used in this complex group of patients.     

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.)     

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.     

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.     

Carotid sinus syncope: the most frequent neurally mediated syncope in the elderly

The present work reviews current literature and the authors' experience of carotid sinus syndrome (CSS), which is considered to be the most common cause of neurally mediated acute disorders of consciousness in the elderly. Although no definitive consensus about its nosology has yet been reached, most groups agree that three features fulfill the diagnosis: anamnestic presence of syncope or its minor equivalents, and their reproduction by carotid sinus massage associated with defined values of cardioinhibition or vasodepression or both. The technique for performing carotid sinus massage used by the authors is described; this manoeuvre seems very safe and reproducible as long as simple rules are followed, and it allows the classification of CSS types. The treatment of CSS is varied, according to several factors. No pharmacological therapy has yet been demonstrated to be effective. While severe cardioinhibitory forms require an appropriate pacing, vasodepressive ones and types with only minor symptoms show a more favourable natural history. Pacing is advised in mixed CSS with either frequent and invalidating relapses, or 'high risk' attacks (severe, abrupt, with major traumas, etc.). Finally, the protocol for choosing the adequate mode of pacing is illustrated. In most cases VVI is sufficient, but the decision requires a careful individual examination.     

Reproducibility of tilt-table test result in patients with malignant neurocardiogenic syncope

The indication for permanent pacemaker remains controversial in malignant neurocardiogenic syncope. A highly reproducible prolonged pause during a repeat head-up tilt-table testing may identify a subgroup of neurally mediated syncope with a prominent and consistent cardioinhibitory component. Seven patients (3 females) with a mean age of 30 years (23-44 years) were diagnosed to have malignant neurocardiogenic -syncope; all are classified according to the Vasovagal Syncope International Study as 2B type, with observed sinus pauses ranged from 3 s to 26 s of which only 1 demonstrated a reproducible sinus pause. No recurrence of syncope was clinically observed in patients during the follow-up period. Of 6 patients treated non--pharmacologically, one required a beta-blocker and none required a permanent pacemaker. Prolonged asystole manifest during head-up tilt-table testing is a poorly reproducible phenomenon and permanent pacemaker implantation in malignant neurocardiogenic syncope should not be a first line therapy.