血管迷走性晕厥的研究进展

血管迷走性晕厥是临床最常见的晕厥病因，其发病机制复杂，目前尚不完全清楚，Bezold-Jarisch反射被认为是血管迷走性晕厥重要的发病机制。压力感受器敏感性下降、心脏自主神经调节、基因等亦在发病中起重要作用。目前血管迷走性晕厥的治疗手段包括一般治疗、药物治疗和射频消融治疗。     

血管迷走性晕厥与基因多态性研究进展

血管迷走性晕厥为最常见的晕厥类型,目前机制尚未完全明确。有学者提出血管迷走性晕厥存在一定的遗传基础。血管迷走性晕厥与候选基因多态性的研究较多,本文对国内外相关的研究进行综述。     

闭环刺激起搏在血管迷走性晕厥治疗中的应用现状分析

起搏器治疗血管迷走性晕厥的获益目前仍存在争议,通常建议用于难治性迷走性晕厥伴发心脏停搏的患者。闭环刺激起搏通过感知程控发现心脏收缩性的变化从而增加心率对血压下降作出应答。目前多项随机观察研究结果表明闭环刺激起搏对于减少心脏抑制型血管迷走性晕厥患者的晕厥发作优于传统起搏治疗,少数研究结果表明闭环刺激起搏对于减少血管抑制型和混合型迷走性晕厥患者的晕厥发作治疗有限。     

硝酸甘油倾斜试验中交感神经活性变化的临床研究

血管迷走性晕厥过去是在排除其他类型晕厥的基础上诊断的，诊断步骤复杂、费时。舌下含化硝酸甘油倾斜试验是诊断血管迷走性晕厥的一项特殊性检查，操作简便，省时。通过对血压、心率及血浆肾上腺素和去甲肾上腺素浓度的测定，以研究舌下含化硝酸甘油倾斜试验中交感神经活性变化，从而对其诱发血管迷走性晕厥的机制进行探讨。     

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。     

血管迷走性晕厥与焦虑抑郁的相关性探讨

血管迷走性晕厥是由多种因素刺激,以心动过缓和周围血管舒张为特征,脑血流灌注不足的一过性自限性发作性晕厥。焦虑、抑郁在血管迷走性晕厥的发病、治疗及预后中扮演重要角色。通过综述近年文献,对二者关系进行概括。     

关于晕厥, 我们还需要做什么？

晕厥是临床常见的问题, 病因纷杂, 常涉及多个学科。晕厥患者的预后也因病因的不同而不同。因此, 如何优化晕厥的诊断流程和危险分层非常重要。另外, 在不明原因晕厥患者中, 植入型心电监测仪(ICM)可以提高晕厥诊断率, ICM指导下的起搏治疗可降低晕厥复发率, 使患者获益, 但在我国存在严重应用不足的问题。血管迷走性晕厥的机制探讨涉及Bezold-Jarish反射学说、神经内分泌调节以及基因多态性等, 但确切机制仍不清楚。血管迷走性晕厥的复发率高, 主要由于缺乏有效的治疗方法。目前药物治疗效果不确切, 而起搏治疗人群受限。因此, 未来仍需开展相关基础和临床研究, 提高晕厥的整体诊断和治疗水平。     

血管迷走性晕厥患者倾斜试验中血浆内皮素内皮舒张因子和心 …

通过研究血管迷走性晕厥患者倾中血皮泊性血管活性物质和心率变异性的变化来了解自主神经及血管内皮功能在血管迷走性晕厥发生机制中的作用。方法２５例患者，斜试验阳性１５例，阴性１０例，于倾斜试验前和倾斜不同时间测定血浆内皮素、一氧化氮水平，脂用动态心电图监测心率变异性的变化。     

血管迷走性晕厥患者和正常人对直立倾斜试验的反应（摘要）

血管迷走性晕厥患者和正常人对直立倾斜试验的反应（摘要）罗杰李俭春张静梅李露言秦丽萍直立倾斜试验对血管迷走性晕厥的诊断提供了较可靠的方法。本试验主要研究血管迷走性晕厥患者和正常人直立倾斜时的心率、血压变化及对异丙肾上腺素（ＩＳＯ）的反应，探讨晕厥发生的...     

补中益气汤加味治疗血管迷走性晕厥的疗效观察

目的探讨中药治疗血管迷走性晕厥的疗效.方法两组病例均口服美托洛尔,治疗组加服补中益气汤,观察血压心率及晕厥发作情况,治疗前后对比经直立倾斜试验(TTT)结果.结果治疗组总有效率91.7%,无不良反应.结论补中益气汤对血管迷走性晕厥的疗效较好.     

Pro position: syncope - a tilt test is indispensable

Summary The most frequent kind of syncope is the so-called "neurally mediated" (vasovagal) syncope; head-up tilt testing has become an effective, safe and non-invasive test for the diagnosis and study of vasovagal syncope. Most authors define the hemodynamic pattern triggered by the tilt test by describing the relation between heart rate and blood pressure. The diagnostic value of tilt table testing is high: in patients with unexplained syncope the percentage of positive reactions to tilt testing lies between 82 and 85%. The specificity of the method is between 95 and 95%. Tilt table testing significantly reduces the number of patients with unexplained syncope. The objective findings of the test provide insight into the mechanism of vasovagal syncope, a differentiated choice of therapy and possibly an evaluation of the applied therapy. Thus tilt table testing is an indispensable diagnostic tool for unexplained syncope.     

Syncope in the elderly

Syncope is defined as a self-limited loss of consciousness, usually combined with falling due to the inability to maintain postural tone. The underlying mechanism is a transient global cerebral hypoperfusion. The aetiology essentially includes cardiac disorders (structured heart disease or arrhythmias), neurally-mediated reflex syndromes, orthostatic hypotension and carotid sinus syndrome. History and physical examination will lead to the diagnosis in up to 50%. The most important step is to differentiate patients with heart disease from others, since the mortality of these patients is doubled. Echocardiography, Holter-monitoring and electrophysiological study are useful to approach this population. In patients with suspected neurally-mediated syncope (vasovagal syncope) tilt testing is indicated. Treatment depends on the aetiology. The diagnostic work-up and the therapeutic approach of patients with syncope are outlined. For patients with vasovagal syncope conventional therapeutic strategies include an increased salt/fluid intake, moderate exercise training, tilt-sleeping or tilt-training. Beta-blockers failed to show efficacy in a number of randomised trials. Recently, pacemaker implantation in selected patients with recurrent vasovagal syncopical episodes showed a significant increase in syncope-free survival, compared to no therapy and compared to beta-blocker therapy. In contrast to the increased mortality risk for patients with cardiac syncope, patients with vasovagal syncope have a benign prognosis.     

Permanent cardiac pacing to prevent vasovagal syncope.

Patients with frequent vasovagal syncope have a poor quality of life and often resist treatment with standard pharmacologic approaches. Although the evidence is weak, clinical vasovagal syncope is probably associated with some degree of bradycardia. Studies of temporary pacing during tilt table tests showed that pacing prevented syncope in a little over half of patients who developed a vasovagal response. Six open-label studies of permanent pacing show that permanent pacemaker therapy is associated with substantial improvement over medical therapy. The roles of specific pacemaker modes have not been determined, although there is some evidence that rate-drop responsiveness helps. The second Vasovagal Pacemaker Study will quantify the true benefits of pacing for vasovagal syncope and assess the role of rate-drop response algorithms.     

Role of pacemakers in treating neurocardiogenic syncope

Patients with frequent vasovagal syncope have a poor quality of life and often resist treatment with standard pharmacologic approaches. Clinical vasovagal syncope may be associated with some degree of bradycardia. Studies of temporary pacing during tilt table tests showed that pacing prevented syncope in a little more than half of patients who developed a vasovagal response. Six open-label studies of permanent pacing show that permanent pacemaker therapy is associated with substantial improvement over medical therapy. The roles of specific pacemaker modes have not been determined, although there is some evidence that rate-drop responsiveness helps. The second Vasovagal Pacemaker Study will quantify the true benefits of pacing for vasovagal syncope and assess the role of rate-drop response algorithms.     

Cardiac Pacing During Neurocardiogenic (Vasovagal) Syncope

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

Different treatments for different mechanisms in vasovagal syncope

The treatment of vasovagal syncope has been by far unsatisfactory. Beta-blockers may prevent vasovagal syncope, but they exacerbates heart asystole. Cardiac pacing prevents syncope but notpresyncope. The frequent, serious vasovagal syncope attacks of a 63- year-old woman patient were completely prevented by administration of 100 mg metoprolol (b.i.d) for 3 months until the patient experienced a complete heart block. A DDD pacemaker implantation abolished syncope but not the presyncope, which was eventually prevented in a follow-up period of 24 months by adding 75 mg atenalol twice a day. This case suggests a different mechanism involved in vasovagal syncope. (J Geriatr Cardiol; 2006; 3(1):61-64)     

Evaluation of beta-adrenergic blockader therapy in vasovagal syncope reproduced by head-up tilt test]

Increased sympathetic tone is one physiopathological mechanism of vasovagal syncope. In this case, betablocker therapy is logical. The reports in the literature suggest that the head-up tilt test can reliably reproduce vasovagal syncope. Ten patients (4 men and 6 women, mean age 59 +/- 18 years) who suffered from recurrent vasovagal syncopes (2 to 10 attacks in 6 patients and more than 10 in the other 4) with a positive initial head-up tilt test (syncope or severe dizziness with marked hypotension after a maximum of 40 minutes at 60 degrees) were treated with atenolol (200 mg daily in 7 cases and 100 mg daily in the other 3). A second head-up tilt test was performed 15 +/- 6 days later under betablocker therapy; this test was negative in 7 and remained positive in 3 cases. Irrespective of the result, the 10 patients followed the same therapy at the same dosage. After 9 +/- 5 months, 3 patients had another syncopal attack; 2 stopped taking their medication and the third patient continued the betablocker because there was a marked reduction in the frequency of his attacks. There were no further syncopal episodes during follow-up of the other 7 patients. The medium-term efficacy could not be predicted from the results of the second head-up tilt test. The following conclusions may be drawn from this study: The head-up tilt test becomes negative in 70% of cases after introducing betablocker therapy, assuming a 100% reproductivity. This treatment is effective in over half the patients at medium term and should be considered in patients with recurrent vasovagal syncope.     

Management and therapy of vasovagal syncope: A review

Vasovagal syncope is a common cause of recurrent syncope. Clinically, these episodes may present as an isolated event with an identifiable trigger, or manifest as a cluster of recurrent episodes warranting intensive evaluation. The mechanism of vasovagal syncope is incompletely understood. Diagnostic tools such as implantable loop recorders may facilitate the identification of patients with arrhythmia mimicking benign vasovagal syncope. This review focuses on the management of vasovagal syncope and discusses the non-pharmacological and pharmacological treatment options, especially the use of midodrine and selective serotonin reuptake inhibitors. The role of cardiac pacing may be meaningful for a subgroup of patients who manifest severe bradycardia or asystole but this still remains controversial.     

Cost-utility analysis of pacemakers for the treatment of vasovagal syncope

Dual-chamber pacing is a promising treatment for patients with very frequent vasovagal syncope, but its cost utility is unknown. We report that the incremental cost per quality-adjusted life-year gained is $13,159 Canadian dollars (about $8,600 US dollars), and therefore this pacemaker therapy for vasovagal syncope has a favorable cost-utility ratio.     

How and When to Pace in Vasovagal Syncope

Pacing in Vasovagal Syncope. This article discusses the indications for pacing in vasovagal syncope. It also reviews the literature on pacing results; notably, there are two small randomized controlled trials of pacing versus no therapy (or continued nondevice therapy) that show a clear benefit for pacing. The mode of benefit is, as yet, unclear. Pacing has to be dual chamber with some form of rate hysteresis. Ways of improving pacemaker therapy delivery in vasovagal syncope are anticipated.