ajmaline and Syndrome

We performed incremental atrial pacing immediately after Ajmaline infusion in an asyntomatic female patient whose basal ECG was suggestive of Brugada Syndrome. Ajmaline accentuated the BS ECG pattern. Incremental Atrial pacing induced localized and dynamic repolarization alternans and unequal diastolic intervals (TQ intervals). No ventricular rhythms were elicited (other than short-coupled, monomorphic, low-density ventricular beats.

Topics: Aged; Aged, 80 and over; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Electrocardiography; Female; Humans; Syndrome

The typical Brugada ECG pattern consists of a prominent J-wave associated with ST-segment elevation localized in the right precordial leads V1-V3. In many patients, the ECG presents periods of transient normalization and the Brugada-phenotype can be unmasked by the administration of class-I antiarrhythmics. Reports have documented the heterogeneity of the Brugada syndrome ECG-phenotype characterized by unusual localization of the ECG abnormalities in the inferior leads. Case report A 51-year-old man, without detectable structural heart disease, was referred to us because of a history of syncope, dizziness, and palpitations. The ECG showed a J-wave and ST-segment elevation in the right precordial leads, suggesting Brugada syndrome. As other causes of the ECG abnormalities were excluded, the patient underwent an electrophysiological study that documented easy induction of ventricular fibrillation. During infusion of ajmaline, new prominent J-waves and ST-segment elevation appeared in the inferior leads, whereas the basal ECG abnormalities in the right precordial leads normalized. After infusion of isoprenaline, the ECG-pattern resumed the typical Brugada pattern. An implantable cardioverter-defibrillator was recommended.. In our patient, the double localization of the typical Brugada-pattern and the paradoxical effect of ajmaline on the ECG abnormalities confirmed the possibility of a phenotype heterogeneity in the Brugada syndrome.

Topics: Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Dizziness; Electrocardiography; Humans; Male; Middle Aged; Syncope; Syndrome

Sodium channel-blocking agents are routinely used to unveil the Brugada syndrome in patients in whom the typical electrocardiographic pattern is absent or doubtful. In this article, the authors report a patient with syncopal episodes of unknown origin in whom the conventional electrocardiographic result was normal and a negligibly small "saddle back" type repolarization was present in lead V2 recorded 2 intercostal spaces above the conventional site. Intravenous ajmaline (50 mg) did not elicit the type 1 pattern of the Brugada syndrome in the precordial leads obtained at their usual level, but a clear-cut coved-type repolarization was apparent in high right precordial leads. These findings indicate that high precordial leads should be routinely recorded while assessing the ajmaline test in patients suspected of having the Brugada syndrome.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Defibrillators, Implantable; Electrocardiography; Female; Humans; Injections, Intravenous; Sodium Channel Blockers; Syncope; Syndrome; Vectorcardiography

A patient with a family history of sudden cardiac death and a structurally normal heart presented with a resting ECG intermittently displaying a saddle-type Brugada-ECG, which could be reproducibly converted to a coved-type ECG pattern suggestive of Brugada syndrome. However, no ST-segment changes occurred in the presence of a true right bundle branch block (RBBB) in the same patient. In consideration of the inalienable diagnostic criterion of dynamic ECG abnormalities in the right precordial leads in Brugada syndrome, setting the diagnosis in patients with true RBBB may be unattainable.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Death, Sudden, Cardiac; Diagnosis, Differential; Electrocardiography; Humans; Male; Syndrome

Brugada syndrome is a channelopathy associated with right bundle branch block and ST segment elevation in the right precordial leads. These electrocardiographic signs may not be apparent most of the time but can be unmasked by certain antiarrhythmic agents. Until now, all of the reports on this syndrome have focused on patients with no significant intraventricular conduction delay at baseline electrograms. In this report, we describe a patient with Brugada syndrome with left bundle branch block at baseline ECG. After intravenous ajmaline, the patient developed right bundle branch block and ST segment elevations in the right precordial leads.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Defibrillators, Implantable; Electrocardiography; Female; Humans; Syndrome; Ventricular Fibrillation

The mechanisms responsible for the undulating pattern of ST-segment elevations in the Brugada syndrome are still a matter of discussion. This report describes a young man with a Brugada-like electrocardiographic pattern. The specific ST-segment elevations were unmasked during an episode of anemia due to a duodenal ulcer.

Topics: Adult; Ajmaline; Anemia; Anti-Arrhythmia Agents; Bundle-Branch Block; Cardiac Pacing, Artificial; Death, Sudden, Cardiac; Duodenal Ulcer; Electrocardiography; Electrocardiography, Ambulatory; Helicobacter Infections; Helicobacter pylori; Humans; Male; Peptic Ulcer Hemorrhage; Risk Factors; Syndrome; Ventricular Fibrillation

Brugada syndrome (BS) is an electrical cardiac disorder with a right bundle branch block and ST segment elevation in leads V1 to V3 on surface electrocardiograms (ECGs), and is a syndrome that may lead to sudden cardiac death.. The aim of the present study was to screen for mutations in the SCN5A gene in a family with BS, and to characterize the consequences of the mutation on channel function.. A heterozygous nonsense SCN5A mutation (W822X) was identified in the index patient. The mutation was confirmed in the patient's asymptomatic 16-year-old brother and 48-year-old father. The mutation was absent in the index patient's sister and mother. The ECG of the index patient showed a BS type 2 ECG phenotype, which converted into a type 1 ECG phenotype in the presence of flecainide. The ECG of the patient's brother was not typical for BS, but ajmaline treatment unmasked a type 1 ECG phenotype. The ECG of the asymptomatic father was normal at baseline and in the presence of ajmaline. No Na+ currents could be measured in tsA201 cells transfected with W822X mutant channels. Heterozygote expression showed a nearly 50% reduction in Na+ current amplitude with no significant alterations of biophysical properties, indicating a loss of functional Na+ channels, obviously without any dominant-negative activity on wild type channels.. The haploinsufficiency of the Nav1.5 protein is the plausible explanation for the clinical BS phenotype in this family. Because the heterozygous W822X mutation theoretically leads to channel expression at one-half of the normal level, the authors suggest that a modifier gene may influence or rescue the phenotype in the asymptomatic family members.

Topics: Adolescent; Adult; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Cell Line; Codon, Nonsense; Death, Sudden, Cardiac; Electrocardiography; Female; Heart Diseases; Humans; Male; Microscopy, Fluorescence; Middle Aged; Molecular Biology; Muscle Proteins; Mutagenesis; NAV1.5 Voltage-Gated Sodium Channel; Patch-Clamp Techniques; Pedigree; Phenotype; Sodium Channels; Syndrome; Transfection

Brugada syndrome is characterized by sudden death secondary to malignant arrhythmias and the presence of ST segment elevation in leads V(1) to V(3) of patients with structurally normal hearts. This ECG pattern often is concealed but can be unmasked using potent sodium channel blockers. Like congenital long QT syndrome type 3 (LQT3) and sudden unexpected death syndrome, Brugada syndrome has been linked to mutations in SCN5A.. We screened a large European family with Brugada syndrome. Three members (two female) had suffered malignant ventricular arrhythmias. Ten members showed an ECG pattern characteristic of Brugada syndrome at baseline, and eight showed the pattern only after administration of ajmaline (total 12 female). Haplotype analysis revealed that all individuals with positive ECG at baseline shared the SCN5A locus. Sequencing of SCN5A identified a missense mutation, R367H, previously associated with sudden unexpected death syndrome. Two of the eight individuals who displayed a positive ECG after the administration of ajmaline, but not before, did not have the R367H mutation, and sequencing analysis failed to identify any other mutation in SCN5A. The R367H mutation failed to generate any current when heterologously expressed in HEK cells.. Our results support the hypothesis that (1) sudden unexpected death syndrome and Brugada syndrome are the same disease; (2) male predominance of the phenotype observed in sudden unexpected death syndrome does not apply to this family, suggesting that factors other than the specific mutation determine the gender distinction; and (3) ajmaline may provide false-positive results. These findings have broad implications relative to the diagnosis and risk stratification of family members of patients with the Brugada syndrome.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bundle-Branch Block; Comorbidity; Death, Sudden; Electrocardiography; Female; Genetic Predisposition to Disease; Humans; Male; Mutation, Missense; NAV1.5 Voltage-Gated Sodium Channel; Pedigree; Phenotype; Sex Distribution; Sodium Channels; Spain; Syndrome

Topics: Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bundle-Branch Block; Comorbidity; Death, Sudden; Electrocardiography; Genetic Predisposition to Disease; Mutation, Missense; NAV1.5 Voltage-Gated Sodium Channel; Pedigree; Phenotype; Sex Distribution; Sodium Channels; Spain; Syndrome

We present a 56-year-old man who was admitted to an emergency service after receiving an electric shock. The ECG showed a J point and ST segment elevation of up to 5 mm in leads V1 to V3, which normalized in 24 hours. The ajmaline test caused elevation of the J point and of the ST segment up to 12 mm in leads V1 to V3, QTc lengthening, and QTc and T wave alternans. These results denoted alterations in the duration of myocardial action potentials, a common finding in patients with Brugada syndrome and long QT syndrome.

Topics: Ajmaline; Anti-Arrhythmia Agents; Electric Injuries; Electrocardiography; Humans; Long QT Syndrome; Male; Middle Aged; Syndrome

An association between arrhythmogenic right ventricular dysplasia-cardiomyopathy (ARVD/C) and Brugada syndrome can be supposed according to several case reports. In order to examine a possible link between ARVD/C and Brugada syndrome, systematic ajmaline testing with 1 mg/kg body weight intravenously, was done in 55 patients (32 males, mean age 46.7+/-12.3 years) with ISFC/ESC criteria of ARVD/C. In nine patients ajmaline testing could demonstrate coved ST segment elevation of at least 2 mm in at least two right precordial leads. Three of these patients had recurrent syncopes. Electrophysiological study revealed non-sustained ventricular tachycardia with left bundle branch block configuration and inferior axis in only one case. Systematic ajmaline testing could demonstrate a definite link between ARVD/C and Brugada syndrome.

Topics: Adult; Aged; Ajmaline; Anti-Arrhythmia Agents; Arrhythmogenic Right Ventricular Dysplasia; Bundle-Branch Block; Electrocardiography; Female; Germany; Humans; Male; Middle Aged; Prevalence; Syncope; Syndrome; Tachycardia, Ventricular

To determine the prevalence of drug-induced Brugada's syndrome (BrS) electrocardiograms (ECGs) in a healthy population, a sodium channel blockade challenge was performed in previously identified subjects with BrS-compatible (BrC) ECGs. These subjects were detected in 1,000 normal patients in whom first ECGs were systematically recorded. Because of the intermittent nature of electrocardiographic modifications in BrS, second ECGs were also recorded in a representative sample of the population presenting with first ECGs with normal results. The prevalence of typical drug-induced BrS ECGs was 5 of the 1,000 patients. This value was fivefold greater than the reported prevalence of spontaneous BrS ECGs in the healthy population.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Electrocardiography; Female; Humans; Male; NAV1.5 Voltage-Gated Sodium Channel; Polymorphism, Single-Stranded Conformational; Prospective Studies; Sodium Channels; Syndrome; Ventricular Fibrillation

The Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene, SCN5A. The electrocardiographic pattern characteristic of the syndrome is dynamic and is often absent in affected individuals. Sodium channel blockers are effective in unmasking carriers of the disease. However, the value of the test remains controversial.. We studied 147 individuals representing 4 large families with SCN5A mutations. Of these, 104 were determined to be at possible risk for Brugada syndrome and underwent both electrocardiographic and genetic evaluation. Twenty-four individuals displayed an ECG diagnostic of Brugada syndrome at baseline. Of the remaining, 71 received intravenous ajmaline. Of the 35 genetic carriers who received ajmaline, 28 had a positive test and 7 a negative ajmaline test. The sensitivity, specificity, and positive and negative predictive values of the drug challenge were 80% (28:35), 94.4% (34:36), 93.3% (28:30), and 82.9% (34:41), respectively. Penetrance of the disease phenotype increased from 32.7% to 78.6% with the use of sodium channel blockers. In the absence of ST-segment elevation under baseline conditions, a prolonged P-R interval, but not incomplete right bundle-branch block or early repolarization patterns, indicates a high probability of an SCN5A mutation carrier.. In families with Brugada syndrome, the data suggest that ajmaline testing is valuable in the diagnosis of SCN5A carriers. In the absence of ST-segment elevation at baseline, family members with first-degree atrioventricular block should be suspected of carrying the mutation. An ajmaline test is often the key to making the proper diagnosis in these patients.

Topics: Ajmaline; Electrocardiography; Female; Genetic Testing; Heart Block; Heterozygote; Humans; Male; NAV1.5 Voltage-Gated Sodium Channel; Pedigree; Risk; Sensitivity and Specificity; Sodium Channel Blockers; Sodium Channels; Syndrome; Tachycardia, Ventricular

A case of a 33-year-old male who was admitted to the hospital due to recurrent ventricular fibrillation during a febrile illness is presented. Initially, the patient was diagnosed with acute myocardial infarction and received thrombolytic treatment. Echocardiography and coronary angiography were normal. Right precordial ECG leads recorded one and two intercostal spaces higher than normal as well as ECG obtained following ajmaline administration revealed a typical Brugada pattern.

Topics: Adult; Ajmaline; Anti-Arrhythmia Agents; Communicable Diseases; Diagnosis, Differential; Electrocardiography; Heart Conduction System; Humans; Male; Recurrence; Syndrome; Ventricular Fibrillation

Topics: Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Electrocardiography; Humans; Syndrome

The diagnostic ECG pattern in Brugada syndrome (BS) can transiently normalize and may be unmasked by sodium channel blockers such as ajmaline. Proarrhythmic effects of the drug have been well documented in the literature. A detailed protocol for the ajmaline challenge in Brugada syndrome has not yet been described. Therefore, we prospectively studied the risks of a standardized ajmaline test.. During a period of 60 months, 158 patients underwent the ajmaline test in our institution. Ajmaline was given intravenously in fractions (10mg every two minutes) up to a target dose of 1mg/kg. In 37 patients (23%) the typical coved-type ECG pattern of BS was unmasked. During the test, symptomatic VT appeared in 2 patients (1.3%). In all other patients, the drug challenge did not induce VT if the target dose, QRS prolongation >30%, presence/appearance of the typical ECG, or the occurrence of premature ventricular ectopy were considered as end points of the test. A positive response to ajmaline was induced in 2 of 94 patients (2%) with a normal baseline ECG, who underwent evaluation solely for syncope of unknown origin.. The ajmaline challenge using a protocol with fractionated drug administration is a safe method to diagnose BS. Because of the potential induction of VT, it should be performed under continuous medical surveillance with advanced life-support facilities. Due to the prognostic importance all patients with aborted sudden death or unexplained syncope without demonstrable structural heart disease and family members of affected individuals should presently undergo drug testing for unmasking BS.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Child; Clinical Protocols; Death, Sudden, Cardiac; Dose-Response Relationship, Drug; Electrocardiography; Humans; Infusions, Intravenous; Middle Aged; Syncope; Syndrome

We present a Brugada syndrome patient who suffered an aborted sudden death. The ajmaline test (1 mg/kg body weight) induced accentuated alternans ST-segment elevation in V1-V2 without ventricular arrhythmias. It could represent silent ischaemia not detected before, failure of myocardial regions to repolarize in alternate beats due to transmural dispersion of conduction and refractoriness in the right ventricular outflow tract or a rate dependent sodium channel block by ajmaline. We need more studies to know whether this electrocardiographic sign is a risk factor for life-threatening ventricular arrhythmias in Brugada syndrome patients.

Topics: Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Death, Sudden, Cardiac; Electrocardiography; Electrophysiologic Techniques, Cardiac; Humans; Syndrome; Ventricular Fibrillation

The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome.. In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL).. At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (-5+/-8 vs. -16+/-8 mV ms) and a steeper negative ST segment gradient (-0.62+/-0.41 vs. -0.29+/-0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively.. In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome.

Topics: Adult; Aged; Ajmaline; Body Surface Potential Mapping; Case-Control Studies; Electrocardiography; Female; Heart Arrest; Humans; Male; Middle Aged; NAV1.5 Voltage-Gated Sodium Channel; Polymorphism, Single-Stranded Conformational; Prospective Studies; Risk; Signal Processing, Computer-Assisted; Sodium Channel Blockers; Sodium Channels; Statistics, Nonparametric; Syndrome; Ventricular Fibrillation

Topics: Adult; Ajmaline; Cardiac Pacing, Artificial; Diagnosis, Differential; Electrocardiography; Heart Conduction System; Humans; Male; Metaproterenol; Syndrome; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

The syndrome with an electrocardiographic pattern of right bundle branch block, ST segment elevation in leads V(1)to V(3)and sudden death is genetically determined and caused by mutations in the cardiac sodium channel. The inheritance of the disease is autosomal dominant. Sudden death may, however, occur from a variety of causes in relatives and patients with this syndrome.. Twenty-five Flemish families with this syndrome with a total of 334 members were studied. Affected members were recognized by means of a typical electrocardiogram either occurring spontaneously or after the intravenous administration of antiarrhythmic drugs. Sudden deaths in these families were classified as related or not to the syndrome by analysis of the data at the time of the event, mode of inheritance of the disease, and data provided by survivors. Results Of the 25 families with the syndrome, 18 were symptomatic (at least one sudden death related to the syndrome) and seven were asymptomatic (no sudden deaths related to the syndrome). In total, there were 42 sudden cardiac deaths (12% incidence). Twenty-four sudden deaths were related to the syndrome and all occurred in symptomatic families. Eighteen sudden deaths (43% of total sudden deaths) were not related to the syndrome (nine cases) or were of unclear cause (nine cases). Three of them occurred in two asymptomatic families and the remaining 15 in five symptomatic families. Twenty-four of the 50 affected members (47%) suffered (aborted) sudden death and 18 of the 284 unaffected members (6%). This difference in the incidence of sudden death was statistically significant (P<0.0001). Patients with (aborted) sudden death caused by the syndrome were younger than patients with sudden death of other or unclear causes (38+/-4 years vs 59+/-3 years respectively, P=0.0003).. In families at high risk of sudden death because of genetically determined diseases, the main cause of sudden death remains the disease. However, almost the half of sudden deaths are caused by unrelated diseases or are of unclear cause. Accurate classification of the causes of sudden death is mandatory for appropriate analysis of the causes of death when designing preventive treatments.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Ajmaline; Anti-Arrhythmia Agents; Belgium; Bundle-Branch Block; Child; Child, Preschool; Death, Sudden, Cardiac; Electrocardiography; Female; Heart Conduction System; Humans; Infant; Male; Middle Aged; Prospective Studies; Syndrome

We present the case of a 13-year-old boy with an episode of aborted sudden death, absence of structural heart disease, and a characteristic ECG pattern of right bundle branch block with persistent ST-segment elevation in the right precordial leads, in whom a monomorphic sustained ventricular tachycardia developed spontaneously after the administration of ajmaline. This effect may be related to an increased inhomogeneity of repolarization mediated by the drug and demonstrates the arrhythmogenic potential of Class I antiarrhythmic drugs in patients with Brugada syndrome.

Topics: Adolescent; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Electrocardiography; Humans; Male; Syndrome; Tachycardia, Ventricular; Ventricular Fibrillation

Dynamic variations in electrophysiologic phenomena inherent to the Brugada syndrome may complicate therapy with implantable cardioverter defibrillators (ICDs).. Between 1997 and 1999, 3 of 7 patients with Brugada syndrome (1 man and 2 women, mean age 42 years) received an ICD. During follow-up, 2 patients experienced multiple inappropriate shocks. Simultaneously with dynamic changes in the surface ECG, endocardial ECGs revealed a dynamic decrease in the right ventricular R wave and an increase in the corresponding T wave, resulting in T wave oversensing. With ajmaline administration, these dynamic changes in endocardial signals were reproducible at different right ventricular sites, whereas left ventricular epicardial signals remained stable. Incremental AAI pacing and exercise stress testing resulted in similar changes in right ventricular endocardial signals, but normalization of the surface ECG apart from progressively increasing S waves in leads II, V5, and V6. Orciprenaline administration had no effect on ECG phenomena. After implantation of a left ventricular epicardial lead for sensing and pacing, no inappropriate tachycardia detection recurred.. These findings demonstrate that, in Brugada syndrome, spontaneous or ajmaline-induced changes in the surface ECG may be paralleled by significant variations in the right ventricular endocardial electrogram that may result in ICD malfunction. Implantation of a left ventricular epicardial lead for sensing and pacing may be the ultimate successful approach in certain patients. To assure proper ICD function, ajmaline testing during ICD implantation appears to be helpful.

Topics: Adrenergic beta-Agonists; Adult; Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Cardiac Pacing, Artificial; Death, Sudden, Cardiac; Defibrillators, Implantable; Electrocardiography; Exercise Test; Female; Flecainide; Humans; Injections, Intravenous; Male; Metaproterenol; Middle Aged; Recurrence; Syndrome; Ventricular Fibrillation

A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (MAPs) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. Ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial MAPs may demonstrate regionally different action potential changes that may contribute to the ECG changes in Brugada syndrome.

Topics: Action Potentials; Ajmaline; Anti-Arrhythmia Agents; Defibrillators, Implantable; Electrocardiography; Female; Follow-Up Studies; Humans; Injections, Intravenous; Middle Aged; Syndrome; Tachycardia, Ventricular; Ventricular Fibrillation; Ventricular Function, Right

The Brugada-Brugada syndrome is a rhythmologic disorder which can be diagnosed because of typical ECG criteria. A high-take off descending ST segment localized to the right chest leads, associated with right bundle branch block and ventricular fibrillation or syncopes are characteristic of the syndrome. ECG alterations in the right precordial leads were recorded in a 47 year old female patient who was admitted to hospital because of enteritis and associated syncope. The ECG alterations were initially not realized as Brugada-Brugada syndrome. Because of "recognizing" comparable ECG alterations during a congress lecture, the diagnosis was made. The patient was treated with an ICD.

Topics: Ajmaline; Anti-Arrhythmia Agents; Bundle-Branch Block; Defibrillators, Implantable; Diagnosis, Differential; Electrocardiography; Female; Humans; Middle Aged; Syncope; Syndrome; Ventricular Fibrillation

Topics: Adrenergic beta-Antagonists; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Humans; Lidocaine; Quinidine; Syndrome; Tachycardia, Paroxysmal; Verapamil