Brugada syndrome]

In 1992 we described a new syndrome consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and a characteristic electrocardiogram displaying a pattern resembling right bundle branch block with an ST segment elevation in leads V1 to V3. In 1998 it was described that the disease is genetically determined with an autosomal dominant pattern of transmission. Three different mutations have been identified. All three mutations affect the structure and the function of the sodium channel SCN5A. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The disease causes 4 to 10 sudden deaths per 10,000 inhabitants per year in areas like Thailand and Laos. Up to 50% of the yearly sudden deaths in patients with a normal heart might be caused by this syndrome. The diagnosis is easily made by means of the electrocardiogram (ECG). The presence of concealed and intermittent forms, however, makes the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalises the ECG, while i.v. ajmaline, flecainide or procainamide accentuate the ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. The prognosis is poor for patients who do not receive an implantable cardioverter-defibrillator. Antiarrhythmic drugs like amiodarone or beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals.     

The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death--the Brugada syndrome.

In 1992 a new syndrome was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and an electrocardiogram (ECG) characteristic of right bundle branch block with ST segment elevation in leads V1 to V3. The disease is genetically determined, with an autosomal dominant pattern of transmission. Three different mutations that affect the structure and function of the cardiac sodium channel gene SCN5A have been identified. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The incidence of the disease is difficult to estimate, but it causes 4 to 10 sudden deaths per 10000 inhabitants per year in areas like Thailand and Laos. In these countries, the disease represents the most frequent cause of death in young adults. Up to 50% of the yearly sudden deaths in patients with a structurally normal heart are caused by this syndrome. The diagnosis is easily made by means of the ECG. The presence of concealed and intermittent forms, however, make the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the ECG, while intravenous ajmaline, flecainide or procainamide accentuate ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. Recent data suggest that loss of the action potential dome in the right ventricular epicardium but not the endocardium underlies ST segment elevation seen in the Brugada syndrome. Also, electrical heterogeneity within the right ventricular epicardium leads to the development of closely coupled extrasystoles via a phase 2 reentrant mechanism, which then precipitates ventricular tachycardia-ventricular fibrillation. Right ventricular epicardium is preferentially affected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs like amiodarone and beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals. Gene therapy may offer a cure in future years. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy.     

The Brugada Syndrome

In 1992 a syndrome was described consisting of syncopal episodes and/or (resuscitated) sudden death in patients with a structurally normal heart and a characte ristic electrocardiogram (ECG) displaying a pattern resembling a right bundle branch block with ST segment elevation in leads V1 to V3. The disease is genetically determined with an autosomal dominant pattern of transmission in 50% of the familial cases. Several different mutations have been identified affecting the structure, function and trafficking of the sodium channel. The syndrome is ubiquitous. Its incidence and prevalence are difficult to estimate, but this disease may cause 4 to 10 sudden deaths per 10,000 inhabitants per year representing the most frequent cause of natural death in males younger than 50 in South Asia. The disease has been linked to the sudden infant death syndrome (SIDS) and to the sudden unexpected death syndrome (SUDS) by showing that the electrocardiogram and mutations are the same as in Brugada syndrome. The diagnosis is easily made by means of the ECG when it is typical. There exist, however, patients with concealed and intermittent electrocardiographic forms that make the diagnosis difficult. The ECG can be modulated by changes in autonomic balance, body temperature, glucose level and the administration of antiarrhythmic, neuroleptic and antimalaria drugs. Beta adrenergic stimulation normalizes the ECG. Loss of the action potential dome in right ventricular epicardium but not in endocardium underlies the ST segment elevation. Electrical heterogeneity within right ventricular epicardium leads to the development of closely coupled extrasystoles via phase 2 reentry that precipitate ventricular ,fibrillation. Antiarrhythmic drugs do not prevent sudden death in symptomatic or asymptomatic individuals. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy. Patients with frequent electrical storms may even need cardiac transplantation as last resort.     

The Brugada syndrome

The Brugada syndrome is a hereditary disease causing sudden cardiac death in apparently healthy individuals with a structurally normal heart. The disease is caused by mutations in the cardiac sodium channel gene SCN5A. Patients with this disease have a peculiar electrocardiogram with elevation of the ST segment in leads V1 to V3, an electrocardiogram that every doctor should recognize. There exist variants of the electrocardiogram with minimal ST segment elevation and even concealed forms that can only be unmasked by the administration of class I antiarrhythmic drugs. When left untreated or when treated with all known antiarrhythmic drugs, patients with Brugada syndrome have a high mortality (approximately 10% per year). The only effective treatment to prevent sudden death is the implantable defibrillator.     

Brugada-Syndrom

In 1992, a new syndrome (Brugada syndrome, BS) was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and an electrocardiogram characteristic of right bundle branch block with ST segment elevation in leads V₁–V₃. The disease is genetically determined with an autosomal dominant pattern of transmission, and different mutations that affect the structure and function of the cardiac sodium channel gene SCN5A have been identified. BS can be diagnosed by ECG if the manifest form is present; at the present time, three different ECG types of BS are known. In patients with transient forms, the ECG can be modulated by the administration of antiarrhythmic drugs. Application of ajmaline (1 mg/kg i.v.), procainamide (10 mg/kg i.v.) or flecainide (2 mg/kg i.v.) accentuate ST segment elevation or are capable of unmasking concealed or intermittent forms of the disease. BS has been described as being associated with life-threatening ventricular tachyarrhythmias and a high incidence of sudden death. Antiarrhythmic drugs such as amiodarone or beta-blocking agents do not prevent sudden death in symptomatic or asymptomatic individuals. Implantation of an automatic cardioverter defibrillator is the only form of treatment currently proven to be effective. Gene therapy may offer a cure in the future.     

Brugada syndrome: From cell to bedside

In 1992, a new syndrome was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and a characteristic electrocardiogram (ECG) displaying a pattern resembling right bundle branch block with an ST-segment elevation in leads V1 to V3. The disease is genetically determined with an autosomal dominant pattern of transmission. Three different mutations have been identified in one individual and 2 families afflicted with the disease. All 3 mutations affect the structure and the function of the sodium channel SCN5A. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The syndrome appears to be ubiquitous. The incidence of the disease is difficult to estimate, but it causes 4 to 10 sudden deaths per 10,000 inhabitants per year in areas such as Thailand and Laos. In these countries, the disease represents the most frequent cause of death in young adults. Up to 50% of the yearly sudden deaths in patients with a normal heart are caused by this syndrome. The diagnosis is easily made by means of the ECG. The presence of concealed and intermittent forms, however, makes the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the ECG, while intravenous ajmaline, flecainide, or procainamide accentuate the ST-segment elevation and are capable of unmasking concealed and intermittent forms of the disease. Recent data suggest that loss of the action potential dome in right ventricular epicardium but not endocardium underlies the ST-segment elevation seen in the Brugada syndrome and that electrical heterogeneity within right ventricular epicardium leads to the development of closely coupled extrasystoles via a phase 2 reentrant mechanism which then precipitates ventricular tachycardia-ventricular fibrillation (VT/VF). Right ventricular epicardium is preferentially affected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs such as amiodarone and beta blockers do not prevent sudden death in symptomatic or asymptomatic individuals. Gene therapy may offer a cure in future years. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy.     

The Brugada Syndrome

The Brugada syndrome is a genetically determined disease caused by mutations of the cardiac sodium channel. The disease affects mainly males in their forties and causes sudden cardiac death because of polymorphic ventricular tachycardia. These patients have a structurally normal heart. The electrocardiogram of this syndrome shows, spontaneously or after Class 1 antiarrhythmic drugs, ST segment elevation in leads V₁ to V₃ and a pattern resembling a right bundle branch block. Phase 2 reentry between epi‐ and endocardiac layers is responsible for the arrhythmias. The only effective treatment at present is implantation of a cardioverter defibrillator. A.N.E. 2000;5(1):88–91     

Sudden death in patients and relatives with the syndrome of right bundle branch block, ST segment elevation in the precordial leads V(1)to V(3)and sudden death.

BACKGROUND: 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. PATIENTS AND METHODS: 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). CONCLUSIONS: 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.     

Phenotypic characterization of a large European family with Brugada syndrome displaying a sudden unexpected death syndrome mutation in SCN5A:

INTRODUCTION: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.     

Brugada syndrome--an under-recognized electrical disease in patients with sudden cardiac death

In 1992, Brugada and Brugada described 8 patients with a history of aborted sudden death and a distinct ECG pattern of right bundle-branch block with ST segment elevation in leads V1-V3 and normal QT interval in the absence of any structural heart disease. It is called Brugada syndrome now and is believed to be responsible for 4-12% of all sudden deaths and around 20% of deaths in patients with structurally normal hearts. Although this syndrome is observed worldwide and the exact prevalence is unknown, it is more common in the Southeast Asian countries. Repeated syncope, ventricular fibrillation, and sudden cardiac death have been reported in patients with Brugada syndrome. The clinical presentation of Brugada syndrome is distinguished by a male predominance and the appearance of arrhythmic events at an average age of 40 years. The Brugada syndrome is inherited in an autosomal dominant manner with incomplete penetrance and an incidence ranging between 5 and 66 per 10,000. The surface ECG manifestations of the syndrome can transiently disappear, but can be unmasked by potent sodium channel blockers in some cases. Mutations of the cardiac sodium channel SCN5A have been detectable in <20% of patients with Brugada syndrome. Recent genetic studies have confirmed the genetic heterogeneity of the disorder. Antiarrhythmic drugs appear to be of little use in prolonging survival and in preventing recurrences of ventricular arrhythmias. To date, implantable cardioverter defibrillator remains the best therapy to prevent sudden death in these patients.     

The Brugada syndrome: clinical, genetic, cellular, and molecular abnormalities

The Brugada syndrome is an arrhythmic syndrome characterized by a right bundle branch block pattern and ST segment elevation in the right precordial leads of the electrocardiogram in conjunction with a high incidence of sudden death secondary to ventricular tachyarrhythmias. No evidence of structural heart disease is noted during diagnostic evaluation of these patients. In 25% of families, there appears to be an autosomal dominant mode of transmission with variable expression of the abnormal gene. Mutations have been identified in the gene that encodes the alpha subunit of the sodium channel (SCN5A) on chromosome 3. This genetic defect causes a reduction in the density of the sodium current and explains the worsening of the above electrocardiographic abnormalities when patients are treated with sodium channel blocking antiarrhythmic agents, which further diminish the already reduced sodium current. The prognosis is poor with up to a 10% per year mortality. Antiarrhythmic drugs including beta-blockers and amiodarone have no benefit in prolonging survival. The treatment of choice is the insertion of an implantable cardioverter-defibrillator.     

Brugada syndrome

The Brugada syndrome is an autosomal dominant disease with incomplete penetrance that may cause syncope and sudden cardiac death in young individuals with a normal heart. It is characterized by an electrocardiographic pattern of complete or incomplete right bundle branch block and ST segment elevation in leads V1-V3. One of the genes linked to this syndrome is SCN5A, the gene encoding for the cardiac sodium channel. Mutations in SCN5A cause a functional reduction in the availability of cardiac sodium current in Brugada syndrome. However, only 20-25% of patients affected by this syndrome have mutations on this gene. A novel gene locus on chromosome 3, distinct from SCN5A, has been identified recently. The relative male preponderance of the phenotype, despite equal inheritance of the gene in males and females, has led to the speculation of a role for testosterone in the phenotype. The disease could manifest at first time as cardiac arrest without any previous symptom, and the electrocardiographic pattern could be intermittent, requiring a pharmacological challenge with Class I antiarrhythmic drugs to unmask ST elevation. Several conditions producing Brugada-like electrocardiographic patterns should be borne in mind and excluded while making a diagnosis of the Brugada syndrome. The management is difficult as pharmacological agents are not universally effective. The mode of treatment recommended by the majority of cardiac electrophysiologists is the implantation of a cardioverter defibrillator. Symptomatic patients with inducible ventricular arrhythmias and a positive family history should be considered for prophylactic implantation of a cardioverter defibrillator.     

Síncope e padrão de Brugada intermitente

Brugada syndrome is a rare syndrome, with an estimated prevalence in Europe of 1-5/10 000 population, whose initial clinical presentation can be sudden death. Although it has a characteristic electrocardiographic pattern, this can be intermittent. The authors present the case of a 32-year-old man, with no family history of syncope or sudden death, who went to the emergency department for syncope without prodromes. The initial electrocardiogram (ECG) in sinus rhythm documented an isolated and non-specific ST-segment elevation in V2. During further diagnostic studies, a repeat ECG revealed type 1 Brugada pattern. This pattern was later seen in a more marked form during a respiratory infection. The patient subsequently underwent electrophysiological study, followed by implantation of an implantable cardioverter-defibrillator (ICD), with an episode of ventricular fibrillation converted via ICD shock two months after implantation.     

Chest pain and ST elevation associated with fever in patients with asymptomatic Brugada syndrome: fever and chest pain in Brugada syndrome

Brugada syndrome is a disease with a high risk of sudden cardiac death. Genetic mutations of the cardiac sodium channel are linked to the characteristic electrocardiogram abnormality of Brugada syndrome. Dysfunction of the mutated sodium channel is reported to be temperature-sensitive. We experienced two patients with asymptomatic Brugada syndrome who showed significant ST elevation in precordial leads while they were in a febrile state. Moreover, these patients had chest pain during precordial ST elevation. From these cases, asymptomatic Brugada syndrome should be considered as one of differential diagnoses when we examine the patients who complained of fever and chest pain. Furthermore, we should lower the elevated body temperature in patients with Brugada syndrome, because fever caused spontaneous ST elevation leading to fatal ventricular arrhythmias.     

Diagnosis and management of Brugada Syndrome

Brugada Syndrome (BS) is a cardiac ion channel disorder linked to loss of function mutation in the SCN5A gene which affects the sodium current. The diagnosis is made on the ECG showing characteristic cove-shaped ST elevation in leads V(1) to V(3) in the absence of structural heart disease, electrolyte disturbance or ischaemia. This condition is genetically transmitted as an autosomal dominant syndrome with incomplete penetrance. It is responsible for 20% of all sudden deaths in those without structural heart disease. Diagnosis of BS can be difficult as the ECG changes are dynamic and variable. Genetic mutation in SCN5A gene is found in 25-30% of patients with Brugada Syndrome. Patients may present with syncope due to polymorphic VT or resuscitated sudden death in the third or fourth decade of life. Symptoms frequently occur at night or at rest and fever is a common trigger in children. Patients presenting with syncope or resuscitated sudden cardiac death should have an implantable defibrillator. Management of asymptomatic patients is controversial and risk stratification is required. www.brugadadrugs.org gives a list of drugs that should be avoided by patients suffering from BS.     

An Unusual Case of Brugada Syndrome in a 10-year-old Child with Fevers

Brugada syndrome is an arrhythmogenic disease characterized by a pattern of ST segment elevation in the right precordial leads on an electrocardiogram with an increased risk of sudden cardiac death. It is primarily reported in adults with limited data about the prevalence, prognosis, and long-term management in children. We describe a 10-year-old boy with a family history of sudden cardiac death, who had near syncope associated with a febrile illness. A screening electrocardiogram revealed ST segment elevation in the right precordial leads consistent with Type-1 Brugada syndrome. An electrocardiogram after recovery from his illness showed Type-2 “saddle-back” ST segment changes. An echocardiogram and a cardiac magnetic resonance imaging revealed a normal heart without myocardial fibrofatty infiltration, scar, or ischemia. A tilt-table test was negative. Implantable cardioverter-defibrillator placement remains the only effective treatment for patients with symptomatic Brugada syndrome; however, risk stratification of asymptomatic patients continues to remain a challenge. Although some investigators have reported the use of electrophysiological studies for distinguishing between high and low risk patients with Brugada syndrome, there are no precise predictors of risk for sudden cardiac death in pediatric patients. After careful discussion, this patient was considered intermediate to high risk for sudden cardiac death and had successful implantation of a transvenous defibrillator. Although Brugada syndrome is a rare diagnosis in the pediatric population, such patients should be referred for further evaluation and management.     

Brugada electrocardiographic pattern due to tricyclic antidepressant overdose

The Brugada syndrome is an arrhythmogenic disease with characteristic coved ST-segment elevation 2 mm or greater in the right precordial leads (type 1 Brugada electrocardiogram [ECG] pattern or “Brugada sign”] and is estimated to be responsible for at least 20% of sudden deaths in patients with structurally normal hearts [Circulation 2005;111(5):659-70]. The Brugada sign has been described in asymptomatic patients after exposure to various drugs. As published reports of the drug-induced Brugada sign have become increasingly prevalent, there is growing interest in the mechanisms responsible for this acquired ECG pattern and its clinical significance.We report a case of a patient who developed the type 1 Brugada ECG pattern after intentional overdose of a tricyclic antidepressant agent, review the literature concerning tricyclic antidepressant agent-induced Brugada sign, discuss potential mechanisms, and evaluate the clinical significance of this ECG abnormality.     

Brugada syndrome

The Brugada syndrome is a clinical-electrocardiographic diagnosis characterized by syncopal episodes or sudden death (caused by ventricular tachycardia and ventricular fibrillation) in patients with a structurally normal heart with a characteristic electrocardiographic pattern consisting of ST segment elevation in precordial leads (Vl-V3) and a morphology of the QRS complex resembling right bundle branch block (the latter can transiently disappear). Timely diagnosis and adequate treatment may essentially decrease mortality of this disease. In our review we have summarized results of recent studies of etiology, pathogenesis, clinical picture, diagnosis and treatment of the Brugada syndrome.     

Brugada and Long QT‐3 Syndromes: Two Phenotypes of the Sodium Channel Disease

Brugada and long QT‐3 syndromes are two allelic diseases caused by different mutations in SCN5A gene inherited by an autosomal dominant pattern with variable penetrance. Both of these syndromes are ion channel diseases of the heart manifest on surface electrocardiogram by ST‐segment elevation in the right precordial leads and prolonged QT_c interval, respectively, with predilection for polymorphic ventricular tachycardia and sudden death, which may be the first manifestation of the disease. Brugada syndrome usually manifests during adulthood with male preponderance, whereas long QT3 syndrome usually manifests in teenage years, although it can also manifest in adulthood. Class IA and IC antiarrhythmic drugs increase ST‐segment elevation and predilection for polymorphic ventricular tachycardia and ventricular fibrillation in Brugada syndrome, whereas these agents shorten the repolarization and QT_c interval, and thus may be beneficial in long QT‐3 syndrome. Beta‐blockade also increases the ST‐segment elevation in Brugada syndrome but decreases the dispersion of repolarization in long QT‐3 syndrome. Mexiletine, a class IB sodium channel blocker decreases QT_c interval as well as dispersion of repolarization in long QT‐3 syndrome but has no effect on Brugada syndrome. The only effective treatment available at this time for Brugada syndrome is implantable cardioverter defibrillator, although repeated episodes of polymorphic ventricular tachycardia can be treated with isoproterenol. In symptomatic patients of long QT‐3 syndrome in whom the torsade de pointes is bradycardia‐dependent or pause‐dependent, a pacemaker could be used to avoid bradycardia and pauses and an implantable cardioverter defibrillator is indicated where arrhythmia is not controlled with pacemaker and beta‐blockade. However, the combination of new devices with pacemaker and cardioverter‐defibrillator capabilities appear promising in these patients warranting further study.     

Brugada Syndrome with atypical characteristics: Case report

The Brugada Syndrome (BrS) is a heterogeneous genetic disease characterized by persistent or transient ST-segment elevation in the right precordial electrocardiography (ECG) leads and a high incidence of sudden death and life-threatening ventricular tachyarrhythmias in patients with structurally normal hearts. The syndrome generally manifests in men during adulthood. The ECG manifestations can be overt or concealed. We report a case of BrS whose type 1 ECG pattern during febrile state converted to type 2 ECG after alleviation of fever with atypical characteristics (78-year-old woman with monomorphic ventricular tachycardia on holter monitoring, a history of the sudden infant death of her child, and without inducible ventricular arrhythmia by programed ventricular stimulation [PVS]).