Vasovagal syncope interrupting sleep?

Clinical data are reported for 13 patients who were referred with recurrent loss of consciousness at night interrupting their sleep. Most of the patients were women (10 of 13) with a mean age of 45 years (range 21-72 years). The histories were more consistent with vasovagal syncope than with epilepsy. This was supported by electroencephalographic and tilt test results. More polysomnographic monitoring data are required to confirm the diagnosis of vasovagal syncope interrupting sleep. This will be difficult because, although the condition may not be rare, the episodes are usually sporadic.     

Are treatments for vasovagal syncope effective? A meta-analysis

Background

Therapies used to treat vaso-vagal syncope (VVS) recurrence have not been proven effective in single studies.

Methods

Comprehensive search of PubMed, EMBASE and Cochrane Central databases of published trials was done. Randomized or non-randomized studies, comparing the intervention of interest to control group(s), with the endpoint of spontaneous recurrence or syncope on head-up tilt test, were included. Data were extracted on an intention-to-treat basis. Study heterogeneity was analyzed by Cochran's Q statistics. A random-effect analysis was used.

Results

α-adrenergic agonists were found effective (n = 400, OR 0.19, CI 0.06–0.62, p < 0.05) in preventing VVS recurrence. β-blockers were not found to be effective when only randomized studies comparing β-blockers to non-pharmacologic agents were assessed (9 studies, n = 583, OR 0.48, CI 0.22–1.04, p = 0.06). Tilt-training had no effect when only randomized studies were considered (4 studies, n = 298, OR 0.47, CI 0.21–1.05, p = 0.07). Selective serotonin reuptake inhibitors were found effective (n = 131, OR 0.28, CI 0.10–0.74, p < 0.05), though the analysis contained only 2 studies. Pacemakers were found effective in preventing syncope recurrence when all studies were analyzed (n = 463, OR 0.13, CI 0.05–0.36, p < 0.05). However, studies comparing active pacemaker to sensing mode only did not show benefit (3 studies, n = 162, OR 0.45, CI 0.09–2.14, p = 0.32).

Conclusions

This meta-analysis highlights the totality of evidence for commonly used medications used to treat VVS, and the requirement for larger, double-blind, placebo controlled trials with longer follow-up.     

How is syncope studied in the Italian hospitals?]

BACKGROUND: The aim of this study was to evaluate how the main tests for the diagnostic assessment of syncope are currently performed in the Italian hospitals. METHODS: During the early 2003 dedicated questionnaires were administered to about 400 Italian hospitals. About each test information was requested relative to: test protocol, laboratory equipment, patients evaluated during 2002. RESULTS: Eighty-four hospitals answered the questionnaire. A syncope-dedicated ambulatory (at least once a week) was available during 2002 in 59/84 hospitals, and 56 were dependent on the Cardiology Division. Carotid sinus massage was performed either in clinostatic and in orthostatic position in 60 Centers and was repeated after atropine in 15. To define the test positivity, 35 Centers followed the "symptom method". Only 15 Centers performed > 100 procedures during 2002 (range 3-500). Tilt testing was performed in 72 hospitals. A dedicated tilting bed was available in 65 Centers, continuous beat-to-beat pressure measurement in 22. Out of the 72 Centers, 55 followed the so-called "Italian protocol" as the main methodology of the test. Only 17 Centers performed > 100 procedures during 2002 (range 3-500). Adenosine test was performed in 26 hospitals, the median dose of drug was 18 mg (range 6-20 mg); 25 out 26 Centers considered the test as positive when an asystolic pause > or = 6 s was observed. Only 6 Centers performed > 15 procedures during 2002 (range 1-204). An implantable loop recorder was available in 48 Centers. The number of implant procedures during 2002 varied among the Centers from 1 to 22. CONCLUSIONS: A great variability was observed concerning the methodology of each test and the number of procedures performed. Thus, a standardization effort about the methodology of syncope study is still needed by the medical associations.     

Should we treat severe vasovagal syncope with a pacemaker?

Cardiac pacing for vasovagal syncope (VVS) addresses the cardioinhibitory component of the reflex but cannot directly affect vasodepression, which occurs in every reflex even when hidden by dominant cardioinhibition. The randomized controlled trials of pacing in VVS have, after almost 2 decades, determined that a small number of patients can benefit because their vasodepressor component is not severe. Early studies compared pacing with no therapy yielding highly significant benefits. Subsequently, all study patients had implanted devices with half being switched off. No benefit was seen. The ISSUE‐3 study found significant benefit (P < 0.039) in prevention of syncope recurrence in older patients. A sub‐study later showed those with negative tilt tests, otherwise indistinguishable from tilt‐positives, had 5% recurrence in 21 months (P < 0.004). There is acceptance that pacing must be dual chamber, but the question of how pacing is delivered remains open. Relying on falling heart rate is insufficient, probably because it occurs too late. Other algorithms which indirectly detect neuroendocrine changes earlier than heart rate fall may have useful application. In clinical terms, the patient to be considered for pacing should not be young and have severe symptoms. Ideally, tilt testing should be negative implying vasodepression of lesser severity and, therefore, yielding fewer syncope recurrences. When selecting pacing, additional concern must be given to regression to the mean of symptoms, severe to less severe. Patients seek help when they are at their worst. Moreover, many years of pacing are unlikely to be free of complications related to implanted hardware.     

Cerebral autoregulation in neurally mediated syncope: victim or executioner?

Involvement of cerebral vasoconstriction confirms the complexity of the pathophysiology of neurally mediated syncope, and the need to adopt a comprehensive approach to the study of this problem.     

Do symptoms predict cardiac arrhythmias and mortality in patients with syncope?

BACKGROUND: Patients with syncope frequently present with multitude of other symptoms but their significance in predicting morbidity or mortality has not been previously studied. OBJECTIVE: To determine if certain symptoms can be used to identify syncope patients at risk for cardiac arrhythmias, mortality, or recurrence of syncope. PATIENTS AND METHODS: From August 1987 to February 1991, we prospectively evaluated patients with syncope from outpatient, inpatient, and emergency department services of a university medical center. These patients were interviewed, charts were reviewed, and detailed information on 19 symptoms and comorbidities was obtained. A cause of syncope was assigned using standardized diagnostic criteria. All patients were followed up at 3-month intervals for at least 1 year for recurrence of syncope and mortality. Patients in whom the cause of syncope was determined by medical history and physical examination alone were not included in our analysis. RESULTS: History and physical examination led to the cause of syncope in 222 of 497 patients enrolled. In the remaining 275 patients, the absence of nausea and vomiting before syncope (odds ratio, 7.1) and electrocardiographic abnormalities (odds ratio, 23.5) were predictors of arrhythmic syncope. Underlying cardiac disease was the only predictor of 1-year mortality. No symptom remained as independent predictor for 1-year mortality or syncope recurrence. CONCLUSIONS: Symptoms, although important in assigning many noncardiac causes, are not useful in risk-stratifying patients whose cause of syncope cannot be identified by other history and physical examination. Triage decisions and management plans should be based on pre-existing cardiac disease or electrocardiographic abnormalities, which are important predictors of arrhythmic syncope and mortality.