Mechanism-based therapy of non-cardiac syncope: a practical guide.

The term non-cardiac syncope includes all forms of syncope, in which primary intrinsic cardiac mechanism and non-syncopal transient loss of consciousness can be ruled out. Reflex syncope and orthostatic hypotension are the most frequent aetiologies of non-cardiac syncope. As no specific therapy is effective for all types of non-cardiac syncope, identifying the underlying haemodynamic mechanism is the essential prerequisite for an effective personalized therapy and prevention of syncope recurrences. Indeed, choice of appropriate therapy and its efficacy are largely determined by the syncope mechanism rather than its aetiology and clinical presentation. The two main haemodynamic phenomena leading to non-cardiac syncope include either profound hypotension or extrinsic asystole/pronounced bradycardia, corresponding to two different haemodynamic syncope phenotypes, the hypotensive and bradycardic phenotypes. The choice of therapy-aimed at counteracting hypotension or bradycardia-depends on the given phenotype. Discontinuation of blood pressure-lowering drugs, elastic garments, and blood pressure-elevating agents such as fludrocortisone and midodrine are the most effective therapies in patients with hypotensive phenotype. Cardiac pacing, cardioneuroablation, and drugs preventing bradycardia such as theophylline are the most effective therapies in patients with bradycardic phenotype of extrinsic cause.

Simulation training for medical emergencies: Evaluation of dentists' long-term learning skills and confidence.

INTRODUCTION: As the population ages and more patients experience medical emergencies during dental treatments, dentists must competently and confidently manage these situations. We developed a simulation training course for medical emergencies in the dental setting using an inexpensive vital sign simulation app for smartphones/tablets without the need for an expensive simulator. However, the duration for which this effect is maintained is unclear. This study was performed to evaluate the long-term educational effect at 3, 6, and 12 months after taking the course. MATERIALS AND METHODS: Thirty-nine dental residents participated in this course. Scenarios included vasovagal syncope, anaphylaxis, hyperventilation syndrome, and acute coronary syndrome, each of which the participants had to diagnose and treat. The participants were evaluated using a checklist for anaphylaxis diagnosis and treatment skills immediately after and 3, 6, and 12 months after the course. The participants were also surveyed about their confidence in diagnosing and treating these conditions by questionnaire before, immediately after, and 3, 6, and 12 months after the course. RESULTS: The checklist scores for anaphylaxis were significantly lower at 3, 6, and 12 months after the course than immediately after the course. The percentage of participants who provided a correct diagnosis and appropriate treatment for vasovagal syncope, hyperventilation syndrome, and acute coronary syndrome was lower at all reassessments than immediately after the course. CONCLUSION: Because medical emergency management skills and confidence declined within 3 months, it would be useful to introduce a refresher course approximately 3 months after the initial course to maintain skills and confidence.

Diagnosis and treatment of recurrent syncope in a middle-aged women.

A 50-year-old female patient, presented with repeated syncope for more than 2 years. Prior assessments were conducted at different hospitals, but no definite abnormalities were found. The patient's fear and anxiety about possible future attacks were escalating. Through a Head-up tilt test, the cause was finally identified as vasovagal syncope. Following a 5-min administration of nitroglycerin, the patient reported palpitations, nausea, and deep, rapid breathing. The electrocardiogram initially showed a first-degree atrioventricular block, progressing swiftly to a second-degree type I atrioventricular block-high atrioventricular block. Immediate intervention was undertaken, but blood pressure was not instantly ascertainable, coinciding with an abrupt loss of consciousness. Subsequent electrocardiographic findings included paroxysmal third-degree atrioventricular block, sinus arrest, and complete cardiac arrest, prompting the initiation of external cardiac compressions. The longest recorded ventricular arrest approximated 15 s, with sinus rhythm resuming post 10 s of cardiac compressions and the patient regaining consciousness. The patient underwent vagal ablation and no longer experienced syncope.

Tilt table testing, methodology and practical insights for the clinic.

Tilt table testing (TTT) has been used for decades to study short-term blood pressure (BP) and heart rate regulation during orthostatic challenges. TTT provokes vasovagal reflex in many syncope patients as a background of widespread use. Despite the availability of evidence-based practice syncope guidelines, proper application and interpretation of TTT in the day-to-day care of syncope patients remain challenging. In this review, we offer practical information on what is needed to perform TTT, how results should be interpreted including the Vasovagal Syncope International Study classification, why syncope induction on TTT is necessary in patients with unexplained syncope and on indications for TTT in syncope patient care. The minimum requirements to perform TTT are a tilt table with an appropriate tilt-down time, a continuous beat-to-beat BP monitor with at least three electrocardiogram leads and trained staff. We emphasize that TTT remains a valuable asset that adds to history building but cannot replace it, and highlight the importance of recognition when TTT is abnormal even without syncope. Acknowledgement by the patient/eyewitness of the reproducibility of the induced attack is mandatory in concluding a diagnosis. TTT may be indicated when the initial syncope evaluation does not yield a certain, highly likely, or possible diagnosis, but raises clinical suspicion of (1) reflex syncope, (2) orthostatic hypotension (OH), (3) postural orthostatic tachycardia syndrome or (4) psychogenic pseudosyncope. A therapeutic indication for TTT in the patient with a certain, highly likely or possible diagnosis of reflex syncope, may be to educate patients on prodromes. In patients with reflex syncope with OH TTT can be therapeutic to recognize hypotensive symptoms causing near-syncope to perform physical countermanoeuvres for syncope prevention (biofeedback). Detection of hypotensive susceptibility requiring therapy is of special value.

High spinal cord injury precipitating syncope: a rare indication for pacemaker insertion.

The current evidence for vasovagal syncope management is that cardiac pacing is only indicated in a highly select group of patients where symptoms can be linked to bradycardic episodes. High spinal cord injury can lead to autonomic dysfunction and sympathetic nervous system hypoactivity. A high spinal cord injury can theoretically precipitate profound bradycardia leading to haemodynamic instability and syncope. A patient in his 50s with a history of C2 spinal injury was admitted to our tertiary centre for management of what was initially thought to be septic shock causing hypotension and syncope. With evidence to suggest this patient's presentation may be profound reflex syncope in the context of unopposed parasympathetic signalling, consensus was reached to implant a permanent pacemaker. Remarkably, the patient's haemodynamics stabilised and there were no further episodes of syncope.

Twenty-five years of research on syncope.

Over the last 25 years, the Europace journal has greatly contributed to dissemination of research and knowledge in the field of syncope. More than 400 manuscripts have been published in the journal. They undoubtedly improved our understanding of syncope. This symptom is now clearly differentiated from other forms of transient loss of consciousness. The critical role of vasodepression and/or cardioinhibition as final mechanisms of reflex syncope is emphasized. Current diagnostic approach sharply separates between cardiac and autonomic pathways. Physiologic insights have been translated, through rigorously designed clinical trials, into non-pharmacological or pharmacological interventions and interventional therapies. The following manuscript is intended to give the reader the current state of the art of knowledge of syncope by highlighting landmark contributions of the Europace journal.

Prospective randomized study comparing permanent pacing with rate drop response and closed loop stimulation in patients with vasovagal syncope where permanent pacing is indicated and selected as the appropriate treatment option.

BACKGROUND: Pacing for vasovagal syncope is established. Two pacing algorithms are available. The rate-drop-response (RDR-Medtronic) is triggered by falling heart rate acting with modified rate-hysteresis. The closed loop stimulation or system (CLS-Biotronik) is triggered by impedance changes in the right ventricle reflecting falling volume and rising contractility. These are very different physiologically. Both algorithms carry favorable reports in clinical use. METHODS: A randomized-controlled superiority trial is proposed to compare the two algorithms for the control of vasovagal syncope in patients for whom pacing is indicated by current guidelines in North America and Europe. Available recent evidence may be seen as supporting superiority of CLS. No comparison between the two algorithms has been made. In this trial, patients will be centrally randomized to one or other algorithm on a 1:1 basis. Two-hundred-seventy-six patients in each group will be recruited. Sample size is determined using a confidence interval of 95%, a power of 90%, and a drop-out rate of 10% to detect an 11% difference between CLS and RDR. Recurrent symptom comparison will be made by an independent committee. The Co-primary endpoints will be recurrent syncope burden compared with that in 24-months preimplant, and occurrence of syncope in 24-months follow-up. Each outcome will be compared between the two algorithms. Secondary endpoints will be program and drug therapy changes over 24-months follow-up and quality of life by questionnaire at baseline,1 and 2 years. RESULTS AND CONCLUSIONS: These are anticipated to clarify the device algorithm choice and, therefore, to improve patient care.

Transcatheter Leadless Pacemaker for the Treatment of Vasovagal Syncope.

Vasovagal syncope (VVS) is largely a benign condition focused on patient education, lifestyle modification, and avoidance of triggers. However, a subset of patients may benefit from permanent pacemaker placement. Commonly, patients with VVS are younger and those requiring pacing have symptoms associated with severe cardioinhibitory syncope. With the advent of leadless pacemaker systems, a lot of the risks associated with traditional transvenous pacemaker systems are mitigated. In this article, we provide a comprehensive review of the data available for the treatment of cardioinhibitory vasovagal syncope using leadless pacemaker systems.

Glossopharyngeal neuralgia with cardioinhibitory syncope: Is a permanent pacemaker required?

Glossopharyngeal neuralgia is a rare facial pain syndrome, which in more rare cases can be associated with syncope. We present the outcome of a case report that combines this rare association that received medical therapy with anti-epileptic medication and permanent dual chamber pacemaker implantation. In this case, syncope episodes were associated with both vasodepressor and cardioinhibitory reflex syncope types. The patient found relief from syncope, hypotension, and pain after initiation of anti-epileptic therapy. Although a dual chamber pacemaker was implanted, the pacemaker interrogation revealed no requirement for pacing at one-year follow-up. As far as we know, this is the first case that reports pacemaker interrogation during follow-up and, taking into account the absence of pacemaker activation at one-year follow-up, the device was not needed to prevent bradycardia and syncope episodes. This case report supports the current guidelines for pacing in neurocardiogenic syncope, by demonstrating a lack of requirement for pacing in the event of both cardioinhibitory and vasodepressor responses.

Tests for the identification of reflex syncope mechanism.

INTRODUCTION: Treatment efficacy of reflex syncope is mainly related to the mechanism underlying syncope rather than its etiology or clinical presentation. The predominant mechanism underlying reflex syncope can be assigned to hypotensive or to bradycardic phenotypes. AREAS COVERED: Methodology and diagnostic criteria of the most useful tests for the identification of hypotensive and bradycardic phenotypes are discussed. Diagnostic tests for the hypotensive phenotype include office blood pressure measurement with active standing test, home, and wearable blood pressure monitoring, 24-h ambulatory blood pressure monitoring and tilt table test. Diagnostic tests for the bradycardic phenotype include carotid sinus massage, tilt table test and prolonged ECG monitoring. EXPERT OPINION: In reflex syncope, the documentation of bradycardia/asystole during a syncopal episode does not rule out the possibility that a preceding or parallel hypotensive reflex plays an important role. Similarly, even when a hypotensive mechanism is established, the possibility of an associated cardioinhibitory reflex should be investigated. Investigating the mechanism of reflex syncope is mandatory in patients with severe recurrent episodes, with the final aim to develop a personalized treatment strategy. Recent trials have demonstrated the benefits of personalized mechanism-based therapy, thus highlighting the importance of a comprehensive assessment of the mechanisms underlying syncope.

Current approach to the treatment of vasovagal syncope in adults.

Vasovagal syncope (VVS) is the most common cause of transient loss of consciousness. Although not associated with mortality, it causes injuries, reduces quality of life, and is associated with anxiety and depression. The European and North American cardiac societies recently published syncope clinical practice guidelines. Most patients with VVS do well after specialist evaluation, reassurance and education. Adequate hydration, increased salt intake when not contraindicated, and careful withdrawal of diuretics and specific hypotension-inducing drugs are a reasonable initial strategy. Physical counterpressure maneuvers might be helpful but can be of limited efficacy in older patients and those with short or no prodromes. Orthostatic training lacks long term efficacy and is troubled by non-compliance. Yoga might be helpful, although the biomedical mechanism is unknown. Almost a third of VVS patients continue to faint despite these conservative measures. Metoprolol was not helpful in a pivotal randomized clinical trial. Fludrocortisone and midodrine significantly reduce syncope recurrences with tolerable side effects, when titrated to target doses. Pacing therapy with specialized sensors appears promising in carefully selected population who have not responded conservative measures. Cardioneuroablation may be helpful but has not been studied in a formal clinical trial.

[Vasovagal Syncope: Mechanisms and Treatments].

Syncope is defined as the transient loss of consciousness due to cerebral hypoperfusion. Reflex syncope (neurally mediated syncope) is among all syncope, vasovagal syncope is among reflex syncope in addition. We frequently treated several patients with vasovagal syncope in our clinical situation. We report here the mechanisms and treatments of vasovagal syncope. Although this syncope has a low risk, the diagnosis and the treatments are complicated. Therefore, invasive treatments are necessary in selected patients. This article discusses the management procedures of syncope according to the guidelines and our clinical experience.

Biomarkers and Hemodynamic Parameters in the Diagnosis and Treatment of Children with Postural Tachycardia Syndrome and Vasovagal Syncope.

In children, vasovagal syncope and postural tachycardia syndrome constitute the major types of orthostatic intolerance. The clinical characteristics of postural tachycardia syndrome and vasovagal syncope are similar but their treatments differ. Therefore, their differential diagnosis is important to guide the correct treatment. Therapeutic methods vary in patients with the same diagnosis because of different pathomechanisms. Hence, in patients with vasovagal syncope or postural tachycardia syndrome, routine treatments have an unsatisfactory efficacy. However, biomarkers could increase the therapeutic efficacy significantly, allowing for an accurate and detailed assessment of patients and leading to improved therapeutic effects. In the present review, we aimed to summarize the current state of research into biomarkers for distinguishing the diagnosis of pediatric vasovagal syncope from that of postural tachycardia syndrome. We also discuss the biomarkers that predict treatment outcomes during personalized therapy for each subtype.

Pacing for vasovagal syncope: Tips for use in practice.

Vasovagal syncope (VVS) continues to be the most frequent cause of syncope in all age groups. Recent randomized double-blinded trials (RCTs) provide further support for pacing in selected cases of patients with recurrent refractory VVS with significant cardio-inhibitory response either documented spontaneously or induced during head-up tilt testing (HUTT). Cardiac pacing is the only therapy of proven efficacy for the predominant cardio-inhibitory phenotype of vasovagal (reflex) syncope; however, several questions regarding the best candidates remain. The current review focuses on practical tips for use of cardiac pacing in practice.

A leadless pacemaker matched with a vasovagal syncope: how long can it last?

BACKGROUND: Guidelines recommend that cardiac pacing should be considered in patients suffering from frequent vasovagal syncopal (VVS) episodes. Studies have demonstrated the safety and efficacy of leadless pacemakers (LP) in cardioinhibitory vasovagal populations specifically, rendering them a reasonable alternative to transvenous pacing in these patients. However, due to the paucity of data on extraction and the number of concomitant LPs that can be safely implanted, there are concerns regarding LPs' battery longevity, especially in younger patients who may require decades of pacing therapy. METHODS: This is a retrospective analysis of the first 100 LPs implanted at a tertiary cardiac centre in the UK. Demographical data and device parameters at implant and follow-ups were obtained from the hospital's medical records. The battery life of the LPs in the VVS patients was compared to that of patients with other pacing indications. RESULTS: Ninety patients were included in the analysis. 14 patients (15.6%) had VVS, and 76 patients (84.4%) had other indications for pacing. Mean ages were 34 ± 13 years and 62 ± 20 years for the VVS and the other group, respectively. The estimated total battery life was 15.22 ± 0.35 and 13.65 ± 2.97 years in the VVS and the other indications group respectively (p = .04). There were no complications in the VVS group. CONCLUSION: LPs provide a promising treatment for patients with vasovagal syncope with reassuring battery performance at the short/intermediate term. Further longer-term follow-up data are needed to identify the true battery potential in this patient cohort.

[Transient loss of consciousness]. / Wegrakingen.

Although transient loss of consciousness (TLOC) is a common problem, hospital care for patients with TLOC is characterised by high rates of no diagnosis and misdiagnosis, accompanied by unnecessary hospital admissions and tests. We attribute these problems to increasing specialisation as well as to a blind spot for vasovagal syncope, a condition not claimed by any specialty. We suggest that all doctors seeing patients with TLOC, both in primary and secondary care, should be familiar with the presentations of the relatively harmless vasovagal syncope and the alarm symptoms of potentially life-threatening cardiac syncope. In this article we present some practical pointers to recognise these conditions and answer some frequently-asked questions regarding the diagnosis and treatment of TLOC.