Neurally-mediated sincope.

Syncope is a syndrome characterized by a relatively sudden, temporary and self-terminating loss of consciousness; the causes may vary, but they have in common a temporary inadequacy of cerebral nutrient flow, usually due to a fall in systemic arterial pressure. However, while syncope is a common problem, it is only one explanation for episodic transient loss of consciousness (TLOC). Consequently, diagnostic evaluation should start with a broad consideration of real or seemingly real TLOC. Among those patients in whom TLOC is deemed to be due to ''true syncope'', the focus may then reasonably turn to assessing the various possible causes; in this regard, the neurally-mediated syncope syndromes are among the most frequently encountered. There are three common variations: vasovagal syncope (often termed the ''common'' faint), carotid sinus syndrome, and the so-called ''situational faints''. Defining whether the cause is due to a neurally-mediated reflex relies heavily on careful history taking and selected testing (e.g., tilt-test, carotid massage). These steps are important. Despite the fact that neurally-mediated faints are usually relatively benign from a mortality perspective, they are nevertheless only infrequently an isolated event; neurally-mediated syncope tends to recur, and physical injury resulting from falls or accidents, diminished quality-of-life, and possible restriction from employment or avocation are real concerns. Consequently, defining the specific form and developing an effective treatment strategy are crucial. In every case the goal should be to determine the cause of syncope with sufficient confidence to provide patients and family members with a reliable assessment of prognosis, recurrence risk, and treatment options.

Analysis of rhythm variation during spontaneous cardioinhibitory neurally-mediated syncope. Implications for RDR pacing optimization: an ISSUE 2 substudy.

BACKGROUND: Little is known of the variations of the heart rate during spontaneous cardioinhibitory neurally-mediated syncope. Their knowledge has both academic and practical implications for the optimization of rate drop response (RDR) pacing mode. METHODS AND RESULTS: We describe variations of the rhythm occurring during 48 syncopal episodes documented by implantable loop recorder. The presyncopal phase of 18 s (interquartile range 9-65) was characterized by a fall in heart rate from 83 +/- 20 bpm to maximal bradycardia or (multiple) asystolic pauses which lasted a median of 19 s (10-30). The recovery phase lasted 22 s (7-52). The total duration of the cardioinhibitory reflex was 85 s (47-116). We then calculated the potential increase in benefit that an optimally programmed drop rate detection could provide compared with a reference Lower Rate detection. Compared with Lower Rate detection (defined as two consecutive beats at 40 bpm), drop rate detection (assumed to be drop size = 20 bpm, detection window = 1 min, and drop rate = 50 bpm) would have been able to introduce intervention pacing, a median of 5.7 s (interquartile range -5.1- -10.4) earlier in 28 cases (58%). CONCLUSION: Cardioinhibitory neurally-mediated reflex varies widely from a few seconds to some minutes. In our data the total duration was <2 min. Optimal RDR programming, being potentially able to anticipate the detection of the cardioinhibitory reflex by a few seconds, could provide an increase in benefit for cardiac pacing therapy in prevention of syncope.

The ACCF/AHA scientific statement on syncope: a document in need of thoughtful revision.

The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have recently published, in both the Journal of the American College of Cardiology (JACC) and Circulation, a Scientific Statement on the Evaluation of Syncope ('Statement'). This Scientific Statement was commissioned to provide guidance for clinicians regarding the evaluation of patients who present with 'syncope'. The Statement was not intended to be a formal set of practice guidelines. However, in the absence of generally accepted practice guidelines in North America, the Statement's potential impact on clinical care may be more far-reaching than expected; it may erroneously be considered to be the authoritative 'de-facto' guideline document. This commentary, submitted by a multidisciplinary consortium of more than 60 physicians with expertise in the management of transient loss of consciousness (TLOC), points out that in many respects the ACCF/AHA Syncope Statement fails to address long-standing clinical errors associated with the evaluation of episodes of apparent TLOC, including syncope. If not appropriately revised, the current Statement may lead to both inadequate patient care as well as a potentially damaging legal environment for physicians undertaking evaluation of patients who present with transient loss of consciousness.

[The adenosine-5'-triphosphate (ATP) test: a diagnostic tool in the management of syncope of unknown origin. Basic and clinical aspects]. / Apport du test à l'adénosine-5'-triphosphate (ATP) dans l'évaluation diagnostique et l'approche therapeutique des syncopes d'origine indéterminée (vasovagale ou neurocardiogénique).

The prevalence of syncope increases in elderly population. An inappropriate reflex reaction of the autonomous nervous system in specific circumstances is responsible for symptoms in more than 50% of cases. These neurocardiogenic or vasovagal syncopes are due to a vasoplegia or to a cardio-inhibitory reflex or to the association of both mechanisms. Reproducing the symptoms may contribute to identify the responsible mechanism of syncope; this objective is partly reached by the head-up tilt test--a provocative test--which reproduces symptoms in about half of the cases, mainly by provoking a severe vasodilation with fall of blood pressure. On the opposite, the ATP test (20 mg i.v. bolus)--a descriptive test--provokes a strong cardio-inhibitory reflex independent from external factors like body position but it must be undertaken in a calm environment for preventing any anticipative sympathetic reaction. The test is considered positive if ATP produces a cardiac pause longer than 10 seconds and related symptoms are not taken into account for assessing the final result. ATP test positivity increases with age and with the presence of cardiac diseases. Permanent dual chamber pacing at 70 bpm has been shown to reduce significantly the syncope recurrences in patients with positive ATP test and to have no influence on patients with a negative test. The use of ATP test should be extended to all syncope screening. Its positivity identifies a group of patients in whom the mechanism of the syncope is susceptible to be improved by a permanent dual chamber pacing.

Catecholamine response during haemodynamically stable upright posture in individuals with and without tilt-table induced vasovagal syncope.

AIM: Changes in circulating catecholamine concentrations during vasovagal faints have been the subject of considerable study. However, whether catecholamines are part of the triggering mechanism, or principally reflect attempted compensation for an evolving circulatory crisis is unknown. To address this issue, we determined whether the circulating catecholamine response to upright posture differs among patients with and without inducible vasovagal faints at a time when there is no detectable haemodynamic compromise. METHODS AND RESULTS: Blood samples for measurement of adrenaline and noradrenaline (Norepi) concentrations were obtained in the baseline state, and at both 2-3 min and 4-6 min of upright posture in 22 patients undergoing head-up tilt-table testing for evaluation of syncope of unknown cause. In 11 individuals tilt-testing induced syncope at >5 min head-up posture (Group 1). In 11 other individuals tilt testing did not result in syncope (Group 2). Supine arterial catecholamine levels were comparable in the two groups. However, adrenaline concentrations during upright posture tended to be greater at 2-3 min and were significantly greater at 4-6 min in Group 1 than in Group 2 (P< 0.01). These differences occurred in the absence of significant intergroup differences in mean arterial pressure or cardiac cycle lengths. Norepi concentrations also increased in both groups, but without significant differences. CONCLUSION: Circulating adrenaline concentrations in posturally induced vasovagal faints rise more rapidly in vasovagal fainters than in comparably posturally stressed non-fainters, and were significantly greater in fainters prior to either detectable haemodynamic compromise or diminution of circulating Norepi levels. These findings suggest that a premonitory rise in adrenaline concentrations occurs in vasovagal fainters unassociated with an evolving circulatory crisis.

Improving standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve in a porcine model of cardiac arrest.

To improve the efficiency of standard cardiopulmonary resuscitation (CPR), we evaluated the potential value of impeding respiratory gas exchange selectively during the decompression phase of standard CPR in a porcine model of ventricular fibrillation. After 6 min of untreated cardiac arrest, anesthetized farm pigs weighing 30 kg were randomized to be treated with either standard CPR with a sham valve (n = 11) or standard CPR plus a functional inspiratory impedance threshold valve (ITV(TM)) (n = 11). Coronary perfusion pressure (CPP) (diastolic aortic minus right atrial pressure) was the primary endpoint. Vital organ blood flow was assessed with radiolabeled microspheres after 6 min of CPR, and defibrillation was attempted 11 min after starting CPR. After 2 min of CPR, mean +/- SEM CPP was 14 +/- 2 mm Hg with the sham valve versus 20 +/- 2 mm Hg in the ITV group (P < 0.006). Significantly higher CPPs were maintained throughout the study when the ITV was used. After 6 min of CPR, mean +/- SEM left ventricular and global cerebral blood flows were 0.10 +/- 0.03 and 0.19 +/- 0.03 mL. min(-1). g(-1) in the Control group versus 0.19 +/- 0.03 and 0.26 +/- 0.03 mL. min(-1). g(-1) in the ITV group, respectively (P < 0.05). Fifteen minutes after successful defibrillation, 2 of 11 animals were alive in the Control group versus 6 of 11 in the ITV group (not significant). In conclusion, use of an inspiratory impedance valve during standard CPR resulted in a marked increase in CPP and vital organ blood flow after 6 min of cardiac arrest.

Central clinical research issues in electrophysiology: report of the NASPE Committee.

This article contains the results of an attempt by appointed members of the North American Society of Pacing and Electrophysiology to define the research frontier in electrophysiology and suggest areas of study as an aid in setting the research agenda.

Atrioventricular dissociation exacerbating posturally-induced syncope.

We report a case of an 85-year-old patient with posturally-induced syncope in whom symptoms were reproduced during tilt table testing in conjunction with development of an accelerated junctional rhythm with isorhythmic atrio-ventricular (AV) dissociation. That loss of AV synchrony was crucial to development of hypotension and syncope was demonstrated during electrophysiologic testing in which both an accelerated junctional rhythm and an inducible atypical AV nodal re-entrant tachycardia (AVNRT) were induced. The accelerated junctional rhythm was accompanied by moderate hypotension with the patient in the supine posture, whereas blood pressure was well maintained during atypical AVNRT despite a much faster ventricular rate. Thus, symptomatic hypotension due to AV dissociation, presumably the result of transient autonomic disturbance, may be another manifestation of neurally-mediated syncope.

Syncope in pharmacologically unmasked Brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of Brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of Brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of Brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as Brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic Brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.

Left ventricular-based pacing in patients with chronic heart failure: comparison of acute hemodynamic benefits according to underlying heart disease.

BACKGROUND: Acute left ventricular-based pacing has been shown to improve hemodynamics in patients with severe heart failure and left bundle branch block (LBBB). However, it is not known whether the cause of the underlying heart disease influences the potential effect of left ventricular-based pacing. OBJECTIVES: The aim of this study was to determine whether beneficial hemodynamic effects of acute left ventricular-based pacing in severe chronic heart failure are dependent on underlying heart disease. METHODS: After coronary angiography, patients with severe heart failure and LBBB were separated into two groups: dilated (25 patients; 20 male) and ischemic cardiomyopathy (21 patients; 20 male). Hemodynamic parameters were evaluated at baseline and during left ventricular-based pacing. RESULTS: Improvement in hemodynamic parameters were similar in both groups, during acute left ventricular pacing (changes expressed in percentage): pulmonary capillary wedge pressure, -16+/-15% vs. -14+/-10%; V wave amplitude, -25+/-18% vs. -21+/-17%; and biventricular pacing, -15+/-15% vs. -11+/-11% and -23+/-18% vs. -16+/-18%, respectively. CONCLUSION: Underlying heart disease does not influence the response to acute left ventricular-based pacing in patients with severe heart failure and LBBB. This finding provides support for including all patients with enlarged heart and heart failure in future studies evaluating left ventricular-based pacing.

Atrial fibrillation: defining potential curative ablation targets.

The concept that atrial fibrillation (or at least certain forms of the arrhythmia) may be amenable to reversal or amelioration by transcatheter ablation techniques has become increasingly accepted in recent years. As yet, however, the techniques being studied for ablation of atrial fibrillation address neither known critical anatomic elements nor well defined electrophysiologic markers. The approaches, although essentially empirical, are conceptually based on the 'multiple wavelet' or 'focal origin' hypotheses. To date, addressing 'focal origin' atrial fibrillation by transcatheter ablation has been the more encouraging. However, as technology evolves, both in terms of catheter design and possibly endocardial mapping techniques, approaches to wavelet or rotor mechanisms may become similarly effective. This communication examines concepts regarding the manner in which atrial fibrillation is initiated and maintained. The goals are to better understand the encouraging success of empirical ablation methods, and possibly derive insights which may help refine ablation targeting in the future.

Pharmacotherapy of neurally mediated syncope.

A wide variety of pharmacological agents are currently used for prevention of recurrent neurally mediated syncope, especially the vasovagal faint. None, however, have unequivocally proven long-term effectiveness based on adequate randomized clinical trials. At the present time, beta-adrenergic receptor blockade, along with agents that increase central volume (eg, fludrocortisone, electrolyte-containing beverages), appear to be favored treatment options. The antiarrhythmic agent disopyramide and various serotonin reuptake blockers have also been reported to be beneficial. Finally, vasoconstrictor agents such as midodrine offer promise and remain the subject of clinical study. Ultimately, though, detailed study of the pathophysiology of these syncopal disorders and more aggressive pursuit of carefully designed placebo-controlled treatment studies are essential if pharmacological prevention of recurrent neurally mediated syncope is to be placed on a firm foundation.

Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and/or atrial flutter. d,l-Sotalol Atrial Fibrillation/Flutter Study Group.

Currently d,l-sotalol is widely used to prevent recurrence of atrial fibrillation and/or atrial flutter, although a randomized dose-response study has not previously been conducted to guide therapy for this indication. This study summarizes findings of a double-blind, placebo-controlled, multicenter, randomized trial evaluating the efficacy, safety, and dose-response relation of 3 fixed doses of d,l-sotalol (80, 120, and 160 mg twice daily) for the maintenance of sinus rhythm in 253 patients with atrial fibrillation and/or atrial flutter. All patients were in sinus rhythm at randomization. Treatment (69 patients on placebo, 59 on 80 mg, 63 on 120 mg, and 62 on 160 mg given twice daily) was continued for 12 months or until documented recurrence of symptomatic atrial fibrillation and/or flutter. Transtelephonic electrocardiographic monitoring was used to detect symptomatic recurrences. Demographic characteristics were not different in the 4 groups. Structural heart disease was present in 57% of patients. Patients with a history of heart failure were excluded. The time from randomization to symptomatic arrhythmia recurrence was significantly longer in the 2 higher d,l-sotalol dose groups than in the placebo group. The median times to recurrence were 27, 106, 229, and 175 days for the placebo, 80, 120, and 160 mg groups, respectively. There were no deaths or cases of torsade de pointes, sustained ventricular tachycardia, or ventricular fibrillation reported. Thus, d,l-sotalol appeared to be both safe and effective in maintaining sinus rhythm in patients with symptomatic atrial fibrillation and/or flutter. Further, the 120-mg twice daily dose appeared to provide the most favorable benefit and/or risk.