Previous Syncope Research Articles

Has late gadolinium enhancement an incremental value for management of patients with hypertrophic cardiomyopathy?

Purpose: Some authors suggest the presence of fibrosis, identified with Late Gadolinium Enhancement (LGE) in Cardiac Magnetic Resonance (CMR), can be related to the subject arrhythmogenic risk in patients (P) with Hypertrophic Cardiomyopathy (HCM). We aim to examine the association between clinical-morphological variables, risk factors for sudden cardiac death and LGE findings in a population with HCM. Methods: From a population of 74 HCM P, we studied 55 P (51% male; age 63±18 years) who performed CMR. They were divided in 2 groups: LGE+ (with LGE; n=25; 45.5%) and LGE- (without LGE; n=30; 54.5%). Follow-Up (FU) regarding ventricular arrhythmias and Mortality (M) was done. Results: HCM diagnosis was done at a younger age (53±17 vs 61±17; p=0.051) in LGE+. No differences were found regarding gender, cardiovascular risk factors, previous syncope, NYHA class, ambulatory medication, identification of HCM mutation, electrocardiographic criteria for left ventricular hypertrophy or atrial fibrillation. LGE+ more often had family history of sudden death (32% vs 3.4%; p=0.008) and known coronary artery disease (12.0% vs 0%; p=0.088). They also presented a trend towards higher NTproBNP values (5151±7882 vs 1489±2422, p=0.089). Blood pressure response during exercise test was similar. Regarding echocardiogram LGE+ had higher interventricular septum (IVS) thickness (18.8±5.1 vs 15.9±3.09; p=0.017) and left atrium (LA) volume (102.1±33.7 vs 85.4±32.9, p=0.078); more often presented a restrictive pattern of diastolic dysfunction (8.7% vs 4.2%; p=0.021) with a higher E/E' relation (16.5±7.6 vs 12.0±5.9; p=0.022); and left ventricular systolic impairment (24.0% vs 3.3%; p=0.039). No differences were found concerning HCM phenotype, presence of obstruction or mitral regurgitation severity. CMR reinforced the association between LGE+ and previously echocardiographic findings: higher LA volume (32.88±3.6 vs 29.3±5.2; p=0.034); IVS thickness (21.3±4.1 vs 17.9±2.8; p=0.001) and left ventricle ejection fraction (64.1±8.9 vs 68.0±8.6; p=0.064). LGE+ more often had an implantable cardioverter defibrillator (ICD) (36.0% vs 6.7%, p=0.006). At FU (32.0±74.4 months), no differences were found regarding the frequency of ventricular arrhythmias, appropriated ICD therapies or mortality. Conclusions: In this population the presence of LGE emerges as a risk marker, associated with the classical predictors of sudden cardiac death in HCM patients. However its independent association to clinical events requires the study of larger populations, so it can be interpreted as having an incremental value for risk stratification of these P.

第3回不整脈薬物治療フォーラム 失神の既往,ピルジカイニド負荷試験,心室細動誘発性からみたBrugada症候群の生命予後の検討

第3回不整脈薬物治療フォーラム 失神の既往,ピルジカイニド負荷試験,心室細動誘発性からみたBrugada症候群の生命予後の検討

Prognostic Value of Endocardial Voltage Mapping in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

Endocardial voltage mapping (EVM) identifies low-voltage right ventricular (RV) areas, which may represent the electroanatomic scar substrate of life-threatening tachyarrhythmias. We prospectively assessed the prognostic value of EVM in a consecutive series of patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). We studied 69 consecutive ARVC/D patients (47 males; median age 35 years [28-45]) who underwent electrophysiological study and both bipolar and unipolar EVM. The extent of confluent bipolar (<1.5 mV) and unipolar (<6.0 mV) low-voltage electrograms was estimated using the CARTO-incorporated area calculation software. Fifty-three patients (77%) showed ≥1 RV electroanatomic scars with an estimated burden of bipolar versus unipolar low-voltage areas of 24.8% (7.2-31.5) and 64.8% (39.8-95.3), respectively (P=0.009). In the remaining patients with normal bipolar EVM (n=16; 23%), the use of unipolar EVM unmasked ≥1 region of low-voltage electrogram affecting 26.2% (11.6-38.2) of RV wall. During a median follow-up of 41 (28-56) months, 19 (27.5%) patients experienced arrhythmic events, such as sudden death (n=1), appropriate implantable cardioverter defibrillator interventions (n=7), or sustained ventricular tachycardia (n=11). Univariate predictors of arrhythmic outcome included previous cardiac arrest or syncope (hazard ratio=3.4; 95% confidence interval, 1.4-8.8; P=0.03) and extent of bipolar low-voltage areas (hazard ratio=1.7 per 5%; 95% confidence interval, 1.5-2; P<0.001), whereas the only independent predictor was the bipolar low-voltage electrogram burden (hazard ratio=1.6 per 5%; 95% confidence interval, 1.2-1.9; P<0.001). Patients with normal bipolar EVM had an uneventful clinical course. The extent of bipolar RV endocardial low-voltage area was a powerful predictor of arrhythmic outcome in ARVC/D, independently of history and RV dilatation/dysfunction. A normal bipolar EVM characterized a low-risk subgroup of ARVC/D patients.

176: Long-term follow-up after implantable cardioverter defibrillator in patients with Brugada syndrome: a multicenter French experience

Implantation of a cardioverter defibrillator (ICD) is a frequently recommended treatment for symptomatic Brugada syndrome (BrS). However, complications related to the device have been reported. We assessed the benefit / morbidity ratio of this mode of therapy in a cohort of 34 patients implanted in 3 French experienced centers between January 1, 2002 and November 30, 2010. The mean age was 48±14 years, 4 (12%) female. Twenty nine (85%) patients had spontaneous typical coved Type I ECG pattern, 15 (44%) had family history of sudden cardiac death (SCD) and 24 (88%) had positive EP study. ICD implantation was based on aborted sudden cardiac arrest (SCA) in 3 (9%), syncope in 19 (56%) or high risk status (spontaneous type 1 ECG in conjunction with a family history of SCD and/or a positive EP study) in 12 (35%). The median follow-up period was 74±23 (9-127) months. One patient with prior cardiac arrest died of a non-cardiac cause, 5 (15%) patients had appropriate device therapy; all with spontaneous type I ECG and previous syncope but none with prior cardiac arrest. Overall complication rate was 26%. Six (27%) symptomatic and 3 (25%) asymptomatic patients experienced complications. Five (14%) patients (4 with previous syncope and 1 asymptomatic) experienced inappropriate shocks and 4 (12%) had other complications: 2 patients had lead rupture, 1 lead displacement, and 1 pneumothorax during device replacement. These complications occurred in 2 asymptomatic and 2 symptomatic (1 syncope and 1 prior aborted SCA) patients. No case of SCD was observed in ICD carriers. Appropriate device therapy after a median follow-up period of 6 years was observed in patients with prior syncope and none in asymptomatic patients. Complication rate was leading not to recommend ICD implantation in asymptomatic Brugada patients and to carefully evaluate the risk /morbidity ratio in subject with non spontaneous coved type ECG pattern.

Predictors of Hospitalization in Patients with Syncope Assisted in Specialized Cardiology Hospital

BackgroundRisk stratification of a syncopal episode is necessary to better differentiate patients needing hospitalization of those who can be safely sent home from the emergency department. Currently there are no strict guidelines from our Brazilian medical societies to guide the cardiologist that evaluate patients in an emergency setting.ObjectivesTo analyze the criteria adopted for defining the need for hospitalization and compare them with the predictors of high risk for adverse outcome defined by the OESIL score that is already validated in the medical literature for assessing syncope.MethodsA cross-sectional study of patients diagnosed with syncope during emergency department evaluation at our institution in the year 2011.ResultsOf the 46,476 emergency visits made in that year, 216 were due to syncope. Of the 216 patients analyzed, 39% were hospitalized. The variables associated with the need of hospital admission were - having health care insurance, previous known cardiovascular disease, no history of prior stroke, previous syncope and abnormal electrocardiograms during the presentation. Patients classified in OESIL scores of 0-1 had a greater chance of emergency discharge; 2-3 scores showed greater association with the need of hospitalization. A score ≥ 2 OESIL provided an odds ratio 7.8 times higher for hospitalization compared to score 0 (p <0.001, 95% CI:4,03-15,11). In approximately 39% no etiological cause for syncope was found and in 18% cardiac cause was identified.ConclusionsFactors such as cardiovascular disease, prior history of syncope, health insurance, no previous stroke and abnormal electrocardiograms, were the criteria used by doctors to indicate hospital admission. There was a good correlation between the clinical judgment and the OESIL criteria for high risk described in literature.

Prevalence, Clinical Characteristics and Management of Atrial Fibrillation in Patients With Brugada Syndrome

Atrial fibrillation (AF) can be the first manifestation of latent Brugada syndrome (BS). The aim of our study was to assess the prevalence of AF as the first clinical diagnosis in patients with BS and their demographic and clinical characteristics and diagnosis management in a large cohort of patients. The patient group consisted of 611 patients with BS. The data from those with a diagnosis of AF previous to the identification of BS were analyzed (n = 35). Eleven cases were unmasked after the initiation of a class I antiarrhythmic drug and one during the establishment of general anesthesia. In the remaining population, BS was diagnosed using an ajmaline test performed mainly because of younger age in patients with lone AF (n = 13), previous syncope or sudden cardiac death (n = 3), or a clinical history of sudden cardiac death in the family (n = 5). The mean patient age was 49 ± 15 years, 21 were male patients, 14 had a family history of sudden death, 15 had had previous syncope, and 4 had survived cardiac arrest. Concomitant electrical disorder was found in 13 patients. Remarkably, 21 patients had normal findings on the baseline electrocardiogram. In conclusion, AF could be one of the first clinical manifestations of latent BS in a considerable number of patients. This identification is crucial because the treatment of these patients is subject to relevant changes. The ajmaline test plays an essential role, mainly in young patients with a family history of sudden death, despite having normal findings on a baseline electrocardiogram.

Head-up tilt testing for diagnosing vasovagal syncope: A meta-analysis

BackgroundA systematic evaluation focused on sensitivity and specificity of head-up tilt testing (HUT) for diagnosing vasovagal syncope has not been previously performed. We conducted a meta-analysis of studies comparing HUT outcome between patients with syncope of unknown origin and control subjects without previous syncope. MethodsWe searched Pubmed and Embase databases for all English-only articles concerning case-control studies estimating the diagnostic yield of HUT, and selected 55 articles, published before March 2012, including 4361 patients and 1791 controls. The influence of age, test duration, tilt angle, and nitroglycerine or isoproterenol stimulation on tilt testing outcome was analyzed. ResultsHead-up tilt testing demonstrated to have a good overall ability to discriminate between symptomatic patients and asymptomatic controls with an area under the summary receiver-operating characteristics curve of 0.84 and an adjusted diagnostic odds ratio of 12.15 (p<0.001). A significant inverse relationship between sensitivity and specificity of tilt testing for each study was observed (p<0.001). At multivariate analysis, advancing age and a 60° tilt angle showed a significant effect in reducing sensitivity and increasing specificity of the test. Nitroglycerine significantly raised tilt testing sensitivity by maintaining a similar specificity in comparison to isoproterenol. ConclusionsThe results from this meta-analysis show the high overall performance of HUT for diagnosing vasovagal syncope. Our findings provide useful information for evaluating clinical and instrumental parameters together with pharmacological stressors influencing HUT accuracy. This could allow the drawing of tilt testing protocols tailored on the diagnostic needs of each patient with unexplained syncope.

Fragmented and delayed electrograms within fibrofatty scar predict arrhythmic events in arrhythmogenic right ventricular cardiomyopathy: Results from a prospective risk stratification study

Islets of myocytes within fibrofatty scars represent the substrate for reentrant ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy (ARVC). Electroanatomic mapping can reliably identify such areas. To prospectively test the association between late and fragmented electrograms within scar and arrhythmic events in patients with ARVC. High-density right ventricle electroanatomic mapping was performed in 32 patients with ARVC without history of cardiac arrest or sustained ventricular arrhythmias. Standard definitions of electroanatomic scars and fragmented, isolated, and very late potentials were used. All patients received an implantable cardioverter-defibrillator for the primary prevention of sudden death. After a mean follow-up of 25 ± 7 months, 12 (38%) patients received appropriate implantable cardioverter-defibrillator shock for sustained ventricular arrhythmias. With the exception of a higher rate of previous syncope (P = .053), patients with arrhythmic events at follow-up did not differ from those who remained free from arrhythmic events in terms of other clinical variables, including cardiac magnetic resonance findings. Electroanatomic scars were present in all patients. The distribution and extent of electroanatomic scars were similar in the 2 groups (38 ± 25 cm(2) vs 33 ± 20 cm(2); P = .51). However, patients with implantable cardioverter-defibrillator shock had a higher prevalence of fragmented electrograms (92% vs 20%; P <.001), of isolated late potentials (75% vs 20%; P = .004), and of very late potentials (67% vs 25%; P = .030). Fragmented electrograms were the only variable independently associated with arrhythmic events at follow-up (hazard ratio 21; P = .015). The presence of fragmented and delayed electrograms within the scar predicts arrhythmic events in ARVC.

Early chronotropic response analysis in head up tilt table test

Syncope affects up to a quarter of population [1] and reflex etiology is themost prevalent. The head up tilt test (HUTT)was initially used to evaluate the responses to orthostatic stress in terms of research, and thereafter to investigate syncope [2]. Different protocols have been used showing sensitivity ranging from 30% to 50% and specificity around 90%.We studied the heart rate just after tilting to predict HUTT results in a population under investigation of unexplained syncope referred to our center from March 2005 to December 2009. Subjects were enrolled if there was previous unexplained syncope, no structural heart disease or use of drugs that interfere with cardiac chronotropism, any condition that affects the autonomic system such as diabetes or parkinsonism, and no contraindications to the test. All patients signed a consent form. Positive tests during the first 10 min were excluded from analysis. HUTT was performed after 6 h of fasting and an initial 10 minutes rest period was observed. Patients were tilted to 70°, up to 40 min during which HR and BP were monitored [3–5]. If necessary, 1.25 mg sublingual isosorbide was administered after 20 min. A drop in HR, BP or both followed by symptoms defined test positivity, according to VASIS classification. The HRstart was that in the end of the rest period. Likewise, the HRmax 10 min was the highest seen at monitor during this period. An area under the ROCwas calculated and used to determine the ability of the early chronotropic response-ECR to discriminate HUTT results. AUC greater than 0.7 mean good statistical relation, and not a performance by chance. We calculated sensitivity, specificity, positive likelihood ratio and negative likelihood ratiowith respective 95% CI for all possible cutoff points and determined the optimal using Youden index [6,7]. The quantitative variables with normal distribution were described as mean and standard deviation. The software SAS 9.2 was used in statistical analysis. We enrolled 390 patients with a mean age of 47 y old and 89 had positive HUTT— 39% hadmixed response, 20% vasodepressor, 16% cardioinhibitory and the remainder 25% a POTS or dysautonomic response [Table 1]. ECR was analyzed as the absolute HR increase and as a percentage increase. The absolute ECR in each pattern of response is shown in Table 2. In ROC analysis, a cutoff 21% increase in HRstart discriminated those with negative and positive HUTT with sensitivity of 66.11%, specificity of 75.28%, and AUC of 0.739 (95% CI: 0.692 to 0.782). An absolute cutoff of 15 bpm increase also discriminated groups with sensitivity of 71.43, specificity of 77.53, and AUC of 0.755 (95% CI: 0.709 to 0.796). Comparing both variables using Bootstrap analysis the difference was 0.01615, not statistically significant p=0.114 [Fig. 1]. Statistical analysis demonstrated that a 10% HRstart increase shows specificity of 93.2. A positive HUTT with smaller ECR is a very unusual finding. Spearman correlation coefficient (CI=95%) showed inverse relation between HUTT duration and ECR.We also studied ECR in different age and sex groups [Tables 3 and 4]. Previous studies showed different results on early hemodynamic parameters in HUTT [8–12]. Our paper has a comparatively greater population and we considered the HRstart that immediately before

Impaired cardiac sympathetic innervation in symptomatic patients with long QT syndrome

Increased sympathetic activation is a key modifier for arrhythmogenesis in patients with long QT syndrome (LQTS), a congenital channelopathy. Therefore, we investigated cardiac sympathetic function using 123I-metaiodobenzylguanidine (MIBG) single photon emission computed tomography (SPECT) in a cohort of symptomatic LQTS patients and correlated these findings with the underlying genotype. [123I]MIBG SPECT was performed in 28 LQTS patients. Among these, 18 patients (64%) had a previous syncope and 10 patients (36%) survived sudden cardiac arrest. Patients were characterized in terms of genetic subtypes and QTc interval on surface ECGs. SPECT images were analysed for regional [123I]MIBG uptake in a 33-segment bullseye scheme and compared to those obtained from 10 age-matched healthy control subjects (43±12 years). An abnormal 123I-MIBG scan was found in 17 of 28 LQTS patients (61%) with a tracer reduction mainly located in the anteroseptal segments of the left ventricle. This finding was independent of the genetic LQTS subtype. In addition, no differences were found between LQTS patients with a QTc>500 ms vs <500 ms or those suffering from syncope vs VF (p>0.05). A distinct regional pattern of impaired cardiac sympathetic function was identified in the majority of symptomatic LQTS patients. This innervation defect was independent of the underlying genotype and clinical disease expression.

Prevalence of HCM and long QT syndrome mutations in young sudden cardiac death-related cases

Cardiomyopathies and channelopathies are major causes of sudden cardiac death. The genetic study of these diseases is difficult because of their heterogenic nature not only in their genetic traits but also in their phenotypic expression. The purpose of the present study is the analysis of a wide spectrum of previously known genetic mutations in key genes related to hypertrophic cardiomyopathy (HCM), long QT syndrome (LQTS), and Brugada syndrome (BrS) development. The samples studied include cases of sudden cardiac death (SCD) in young adults and their relatives in order to identify the real impact of genetic screening of SCD in forensic cases. Genetic screening of described variation in 16 genes implicated in the development of HCM and three more genes implicated in LQTS and BrS was performed by using MassARRAY technology. In addition, direct sequencing of the two most prevalent genes implicated in the development of SQTL type 1 and 2 was also carried out. Genetic screening allowed us to unmask four possibly pathogenic mutation carriers in the 49 SCD cases considered; carriers of mutation represent 9% (2/23) of the probands with structural anomalies found after autopsy and 7% (1/14) of the probands with structurally normal hearts after in depth autopsy protocol. One mutation was found among 12 of the recovered SCD cases considered. In people with direct family history of sudden cardiac death, but not themselves, 11 additional mutation carriers were found. Three different mutations were found in six of the 19 LQTS patients, representing three families and two different mutations were found among six patients with previous syncope. Genetic analysis in sudden cardiac death cases could help to elucidate the cause of death, but it also can help in the prevention of future deaths in families at risk. The study presented here shows the importance and relevance of genetic screening in patients with signs of cardiac hypertrophy and in family cases with more than one relative affected.

Clinical Management of Arrhythmogenic Right Ventricular Cardiomyopathy: An Update

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic heart muscle disease characterized by the peculiar right ventricular (RV) involvement. Distinctive pathologic features are myocardial atrophy and fibro-fatty replacement of the RV free wall, and clinical presentation is usually related to ventricular tachycardias with a left bundle branch block pattern or ventricular fibrillation leading to cardiac arrest, mostly in young people and athletes. Later in the disease evolution, progression and extension of RV muscle disease and left ventricular involvement may result in right or biventricular heart failure. In the 1994 an International Task Force proposed standardized diagnostic criteria designed to guarantee an adequate specificity and based on the presence of major and minor criteria encompassing electrocardiographic, arrhythmic, morphofunctional, histopathologic, and genetic factors; more recently, Task Force criteria have been modified to increase their diagnostic sensitivity. Retrospective analysis of clinical and pathologic series including fatal cases identified a series of risk factors such as malignant familial background, youthful age, previous syncope or cardiac arrest, competitive sport activity, severe RV disease with left ventricular involvement, and episodes of complex ventricular arrhythmias or VT. The therapeutic options include beta blockers, antiarrhythmic drugs, catheter ablation, and implantable cardioverter defibrillator (ICD). The ICD is the most effective safe-guard against arrhythmic sudden death. In patients in whom ARVC has progressed to severe RV or biventricular systolic dysfunction with risk of thromboembolic complications, treatment consists of current therapy for heart failure including anticoagulant therapy. In case of refractory congestive heart failure, patients may become candidates for heart transplantation.

What can be done when asymptomatic patients discover they have Brugada syndrome? A case report of Brugada syndrome

Brugada syndrome is an inherited cardiac disorder associated with a specific electrocardiographic pattern, involving ST segment elevation in leads V1 to V3. When not spontaneously terminated, it can lead to ventricular fibrillation and sudden death. We present a case report of a young male whose brother suffered a sudden cardiac arrest while playing soccer. A novel mutation c.2678G>A was detected on the gene SCN5A through molecular diagnosis. The mutation was shown to be present in the individual, his daughter and his other brother. For patients with previous ventricular fibrillation and/or syncope, implantable cardiac device (ICD) is recommended. However, how can patients without symptoms but with a clear diagnosis prevent cardiac arrest?

Novel mutation (H402R) in the S1 domain of KCNH2-encoded gene associated with long QT syndrome in a Spanish family

Long-QT syndrome is a congenital cardiac disease resulting in ventricular arrhythmias and sudden death. Genetic mutations in two protein ion-channel genes, KCNQ1 and KCNH2. The mutations position in these genes provides additional information about the evaluation of the risk-stratification. In a Spanish family in whom previous repetitive syncope episodes, sudden death and pathological prolongation of the QT interval were documented, a novel heterozygous mutation in the KCNH2 gene (A1218 > G) was identified. This mutation loading to amino acid substitution H420R in the S1 transmembrane domain of KCNH2. The new A1218 > G mutation in the KCNH2 gene detected in this Spanish family causes arrhythmia manifestation in the carriers.

Risk stratification of the patients with Brugada type electrocardiogram: a community-based prospective study

Risk stratification of patients with Brugada electrocardiogram (ECG) is being strongly debated. Conflicting results have been suggested from international registries, which enrolled non-consecutive cases, studied with different programmed electrical stimulation (PES) protocols. The aim of this study was to prospectively evaluate the incidence of arrhythmic events and the prognostic role of clinical presentation, ECG, and of a standardized PES protocol in consecutive cases from a community-based population. A total of 166 consecutive patients (45 +/- 14 years) with Brugada ECG were enrolled. Type 1 ECG was observed spontaneously in 72 (43%) and after pharmacological testing in 94 (57%). One hundred and three (62%) were asymptomatic, 58 (35%) had syncope, and five (3%) had a prior cardiac arrest. One hundred and thirty-five (81%) underwent PES with two extra stimuli up to ventricular refractoriness and 34% had ventricular fibrillation (VF) induced. Arrhythmic events occurred in nine patients at a mean follow-up of 30 +/- 21 months (2.2 events per 100 person-year): in three (60%) patients with aborted sudden death (aSD), five (8.6%) of those with syncope, and one (1%) of the asymptomatic. The only predictors of events were a history of syncope or aSD (P = 0.02) and induction at PES (P = 0.004). Clinical presentation is the most important parameter in the risk stratification of patients with Brugada ECG. Programmed electrical stimulation seems valuable, particularly in patients with previous syncope.

The characteristics of neurocardiogenic syncope in children

Purpose : Syncope is relatively common in children and adolescents. Among the etiologies of syncope, neurocardiogenical syncope is the most common, but it is often confounded with seizure. We investigated the clinical features of patients under the age of 15 with neurocardiogenical syncope, compared to patients with neurologic disorders including epilepsy. Methods : Among the children who visited the Department of Pediatrics at Cheongju St. Mary's Hospital and Chungbuk National University Hospital from March 2005 to February 2007, we retrospectively analyzed 69 patients whose chief complaint was syncope. We classified the patients by syncope etiology and made comparisons between the neurocardiogenical syncope (NCS) group and the neurological disorders (ND) group regarding to age; location; time and season in which syncope occurred; associated symptoms, including seizures, provocation factors; prodromes; duration of syncope; frequency of previous syncope; birth history; associated disease; past medical history; family history; neurological exam; physical exam; laboratory findings; electrocardiography; electroencephalography (EEG); head-up tilt test; brain CT; and MRI. Results : Among 69 syncope patients, 53 (76.8%) were in the NCS group and 11 (15.9%) were in the ND group. There were no statistically significant differences between the two study groups except for the presence of prodromes and EEG abnormalities. The presence of prodromes in the NCS group was more common than in the ND group [46.9% (23/49) vs. 9.1% (1/11), (P=0.038)]. The EEG abnormality in the ND group was more common than in the NCS group [90% (9/10) vs. 5.8% (3/52), (P

Endothelial function in young subjects with vaso-vagal syncope

Background The aim of this study was to determine whether endothelial function and inappropriate peripheral vasomotion have a significant role in the pathogenesis of neurally mediated syncope. Methods In 16 patients (mean age 28.2 ± 5.8 years) with previous vaso-vagal syncope and in matched healthy subjects, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent response to glyceryl trinitrate (GTN), 25 μg, were measured in the brachial artery from high-resolution ultrasonography. Heart rate variability (HRV) analysis at rest and during tilt test was compared between two groups. Results In the subjects with positive tilt test, all HRV parameters were significant higher respect to subjects with negative tilt test ( P < 0.001). The patients with positive tilt test, showed persistent, marked variability of heart rate (HR), due to increased vagal activity with withdrawal sympathetic tone and consequently reduction of blood pressure (BP) (−30.4 ± 4.2 mmHg, P < 0.001) accompanied by a decrease in HR (−24.3 ± 4.5 beats/min, P < 0.001) compared to negative tilt test subjects. These findings prove the real presence of vagal hypertone in patients with syncope. In our study, HR reached values lower than 40 beats/min. FMD in patients with neurally mediated syncope were significantly greater than those in controls (respectively, 9.2 ± 2.8% vs. 4.6 ± 1.4%, P < 0.01) whereas no differences were shown in the response to GTN (18.4 ± 4.4% vs. 16.1 ± 4.2%, n.s.). Conclusions The augmented endothelial function and the abnormal vasodilation of peripheral arteries in association with bradycardia play an important role in the development of vaso-vagal syncope in young subjects.

Evolução clínica de pacientes com síncope neurocardiogênica (SNC) após suspensão da terapia específica

To evaluate the outcome of patients with NCS after interruption of pharmacological therapy and to investigate the possible clinical variables predicting recurrence. Thirty-seven patients (age 31+/-16 years) with refractory recurrent NCS being 19 females where prospectively studied. All patients became asymptomatic and had a negative tilt table test (TT) after pharmacological therapy. The treatment was interrupted and one month later, a new TT with no medication was carried out. The probability free of symptoms recurrence was analyzed according to sex, age, number of syncope episodes previously to the treatment, clinical history time, treatment time, drug free from treatment time and TT result. Twenty-two patients (59%) presented recurrence during a mean follow-up of 21+/-19.7 months. The variables related to greater recurrence were number of previous syncope (p=0.0248), positive TT after interruption of the therapy (p=0.0002) and female gender (p=0.0131). Most of the very symptomatic patients with NCS present recurrence after the suppression of a specific therapy. A TT carried out after treatment discontinuation can identify patients with higher risk of recurrence, specially in the first year of follow-up.

Responses to Tilt test in young and elderly patients with syncope of unknown origin

The aim of the present study was to assess the cardiovascular autonomic function and responses to tilt test in young and elderly patients with syncope of unknown origin. We evaluated two groups of patients with previous unexplained syncope: 192 older subjects (112 males, 80 females, mean age 67.2 ± 6.8 years) and 188 young subjects (102 males, 86 females, mean age 25 ± 9 years). All patients underwent ambulatory electrocardiogram (ECG) monitoring, to evaluate time domain indices of heart rate variability (HRV), and head-up tilt test in the morning after an overnight fast. The responses of positive tilt test were classified using the VAsovagal Syncope International Study (VASIS) criteria: mixed (VASIS-1), cardioinhibition (VASIS-2A), severe cardioinhibition/asystole (VASIS-2B), pure vasodepression (VASIS-3). All the time-domain HRV indexes were lower in the older than in young subjects. The rate of positive responses was not different in the two groups. In elderly group the positive head-up tilt test responses showed: a pure vasodepressive response (VASIS 3) in 126 patients (65%), a mixed (VASIS-1) response in 25 patients (13%), a cardioinhibitory (VASIS-2A) response in 13 patients (7%). Only 28 (14.6%) of elderly group patients had negative head-up tilt test response. In contrast, in young group the positive head-up tilt test responses showed: 114 patients (61.2%) a mixed (VASIS-1) vasovagal response, 40 patients (22.3%) a cardioinhibitory (VASIS-2A) response, four (2.1%) patients a severe cardioinhibitory (VASIS-2B) and four (2.1%) patients a pure vasodepression (VASIS-3) response, respectively. The tilt test was negative in response in 26 young patients (12.2%). Our results confirm that the head-up tilt test may be useful in assessing unexplained syncope, since it is seen to be positive in 85% of elderly patients and 86% in young patients. In our subjects, vasodepressive response was the most frequent cause of syncope in older subjects, while vasovagal response is the commonest cause of syncope of young patients. This different behaviour in the elderly may be is explained with physiological aging, which is associated with a reduction of sympathetic-parasympathetic control on the cardiac rhythm, demonstrated by reduction in all the time domain HRV indices.

Efecto del tiempo transcurrido tras el síncope sobre el rendimiento diagnóstico de la prueba de basculación

The propensity for spontaneous and tilt-induced neurocardiogenic syncope may exhibit temporal variations. Therefore the diagnostic performance of the head-up tilt test could be improved if it were performed soon after the occurrence of spontaneous syncope. The objective of this study was to assess whether the time interval between the last syncopal episode and tilt table testing influenced the outcome of the test. Three hundred and fifteen patients undergoing diagnostic tilt table testing potentiated with nitroglycerin for suspected neurocardiogenic syncope were included in the study. The time between the last spontaneous syncope and the tilt table test was recorded and its relationship with the results of the test was analyzed. The tilt table test was positive in 211 patients (67.0%). The time from syncope to test was similar for patients with positive and negative tilt table test results: 28 (1-500) vs 32 (2-700) days (NS). No significant relation was observed between the results of the test and the occurrence of spontaneous syncope during the week, the month or the three months previous to the procedure. However, in men and in patients older than 50 years a higher rate of positive tests was observed if the tilt test was performed within the first month after the last spontaneous syncope. The time from the last previous spontaneous syncope to the head-up tilt test does not have a significant impact on test outcome in the overall population with suspected neurocardiogenic syncope. However, the rate of positivity might decrease in men and patients older than 50 years if the test is performed later than one month after the spontaneous syncopal episode.