The prevalence, incidence and prognostic value of the Brugada-type electrocardiogram: a population-based study of four decades. (65/664)

OBJECTIVES: We sought to demonstrate the prevalence, incidence and prognostic value of the Brugada-type electrocardiogram (ECG) in a general population. BACKGROUND: The Brugada syndrome is characterized by evidence of right bundle branch block and ST segment elevation in the right precordial leads, as well as sudden death caused by ventricular fibrillation. However, the natural history of the Brugada-type ECG remains unclear. METHODS: We investigated 4,788 subjects (1,956 men and 2,832 women) who were <50 years old in 1958 and had undergone biennial health examinations, including electrocardiography, through 1999. The Brugada-type ECG was defined as a terminal r' wave in lead V(1) and ST segment elevation > or =0.1 mV in leads V(1) and V(2). Unexpected death was defined as sudden death or unexplained accidental death. RESULTS: There were a total of 32 Brugada-type ECG cases; the prevalence and incidence were 146.2 in 100,000 persons and 14.2 persons per 100,000 person-years, respectively. The incidence was nine times higher among men than women, and the average age at presentation was 45 +/- 10.5 years. The Brugada-type ECG appeared intermittently in most cases and was found in 26% of subjects who died unexpectedly. Cox survival analysis revealed that mortality from unexpected death was significantly higher in subjects with a Brugada-type ECG than in control subjects (p < 0.01). Unexpected deaths were more frequent among subjects with the Brugada-type ECG who had a history of syncope (p < 0.05). CONCLUSIONS: The Brugada-type ECG is not a very rare condition in the adult Japanese population. Subjects with a Brugada-type ECG have an increased risk of unexpected death.  (+info)

Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan. (66/664)

OBJECTIVES: We sought to study the prevalence and mortality of subjects exhibiting the Brugada-type electrocardiogram (ECG) in a community-based population in Japan. BACKGROUND: The Brugada syndrome has been associated with sudden death in subjects without structural heart disease. Hospital-based studies showed 11% to 38% annual fatal arrhythmic events in patients with the Brugada syndrome. METHODS: Prevalence and mortality of the Brugada-type ECG were studied in subjects who had ECGs during a health examination in Moriguchi, Osaka, Japan. Information about death and relocation from Moriguchi city was obtained prospectively. RESULTS: The Brugada-type ECG was found in 98 of 13,929 study subjects (0.70%, 95% confidence interval [CI]: 0.57% to 0.86%). The typical coved-type with an rsR' pattern in V(1) lead ("typical" Brugada-type) was found in 0.12% of subjects (95% CI: 0.07% to 0.20%). The prevalence for male subjects with the Brugada-type ECG (81%) was significantly higher than it was for those without (26%, p < 0.0001). In male subjects, the Brugada-type ECG was found in 2.14% (95% CI: 1.70% to 2.66%), and the "typical" Brugada-type was found in 0.38% (95% CI: 0.21% to 0.64%). After 2.6 +/- 0.3 years of follow-up, there was 1 death (1.0%, 95% CI: 0.03% to 5.6%) of a subject with the Brugada-type ECG, whereas there were 139 deaths (1.0%, 95% CI: 0.85% to 1.2%) of those without the Brugada-type ECG (p = 0.9943, log-rank test). CONCLUSIONS: A substantial number of the Brugada-type ECG were observed in subjects in a community-based population in Japan, especially in men. The total mortality of subjects with the Brugada-type ECG did not differ from the mortality of those without the Brugada-type ECG in a community-based population.  (+info)

His bundle electrogram in patients with acute myocardial infarction complicated by atrioventricular or intraventricular conduction disturbances. (67/664)

Seventy-two patients with acute myocardial infarction complicated by atrioventricular or bundle-branch block or a combination of both had His bundle electrogram studies performed during their stay in the coronary care unit. In 19 of the 72 patients a repeat His bundle electrogram was performed before discharge from hospital. These studies demonstrated that 30 of the 32 patients with atrioventricular block and narrow QRS complexes had a block above the origin othe His spike (proximal block). Eleven patients in this group had repeat His bundle electrograms performed before discharge and in 3 patients there was evidence of residual atrioventricular nodal dysfunction. Both the hospital and follow-up mortality in this group was low and there was no evidence to suggest that permanent pacing would benefit these patients. Of the 18 patients with bundle-branch block and a normal PR interval, 9 had prolongation of the HV interval, but there was no difference in mortality in patients with normal or prolonged HV intervals. Twenty-two patients with bundle-branch block also developed atrioventricular block. In 5 of these patients the site of the AV block was proximal and in 14 it was distal, while 3 patients had both proximal and distal block. The hospital mortality in those patients who progressed to second- or third-degree atrioventricular block was considerably higher than in those patients who remained in first-degree atrioventricular block.  (+info)

Left posterior hemiblock in acute myocardial infarction. (68/664)

Fifteen cases of left posterior hemiblock associated with acute myocardial infaction were studied. In 5 cases the left posterior hemiblock was the only intraventricular conduction defect, while in the other 10 cases it was associated with complete right bundle-branch block. Left posterior hemiblock proved to be an early complication, appearing within a few hours from the onset of the acute episode, and an ominous sign, since hospital mortality rate was 87 per cent. Cause of death was mainly pump failure. In most of these cases ther was electrocardiographic evidence of infarction involving both anterior and inferior ventricular walls. Infarction of most or all of the ventricular septum was a common finding in the cases examined anatomically. Histologically, acute changes involving mainly the posterior septal and midseptal fibres were observed in 6 of the 8 cases studied. On the basis of these findings and of other published findings an alternative physiopathological mechanism for so-called left posterior hemiblock is proposed.  (+info)

Familial, isolated, complete right bundle-branch block. (69/664)

An electrocardiographic study of the families of two children with isolated complete right bundle-branch block is presented. Several cases of classical complete right bundle-branch block were disclosed (17/69 and 3/22 respectively) in three generations of the two families. Personal interviews and parish registers showed that the two families were related, being descendants 8 generations back from a glass-blower who has emigrated to Sweden in the eighteenth century. It is concluded that complete right bundle-branch block can be an autosomal, genetic anomaly which is inherited dominantly but with reduced penetrance and/or expressivity.  (+info)

Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. (70/664)

BACKGROUND: In patients with syncope and bundle branch block (BBB), syncope is suspected to be attributable to a paroxysmal atrioventricular (AV) block, but little is known of its mechanism when electrophysiological study is negative. METHODS AND RESULTS: We applied an implantable loop recorder in 52 patients with BBB and negative conventional workup. During a follow-up of 3 to 15 months, syncope recurred in 22 patients (42%), the event being documented in 19 patients after a median of 48 days. The most frequent finding, recorded in 17 patients, was one or more prolonged asystolic pause mainly attributable to AV block; the remaining 2 patients had normal sinus rhythm or sinus tachycardia. The onset of the bradycardic episodes was always sudden but was sometimes preceded by ventricular premature beats. The median duration of the arrhythmic event was 47 seconds. An additional 3 patients developed nonsyncopal persistent III-degree AV block, and 2 patients had presyncope attributable to AV block with asystole. No patients suffered injury attributable to syncopal relapse. CONCLUSIONS: In patients with BBB and negative electrophysiological study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolonged asystolic pauses, mainly attributable to sudden-onset paroxysmal AV block.  (+info)

Assessing the risk of sudden cardiac death. (71/664)

Detection of a major risk factor for sudden death in an otherwise asymptomatic person often raises major difficulties in management, particularly where the only treatment available is invasive, such as the implantable defibrillator. Recent guidelines have described the appropriate use of this technology, but often difficulty remains. This is particularly the case where the condition is newly recognised and its natural history not yet extensively described. A 63 year old man, whose condition was diagnosed as Brugada syndrome, in whom this problem is illustrated is described.  (+info)

New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives. (72/664)

AIMS: Sudden unexplained death syndrome occurs in previously healthy South-east Asian young adults without any structural cause of death. The common electrocardiographic (ECG) change in sudden unexplained death syndrome survivors is right bundle branch block and ST elevations in leads V(1) to V(3), which are similar to the ECG pattern in the Brugada syndrome (Brugada sign). It is difficult to diagnose the Brugada sign with the 12-lead ECG in sudden unexplained death syndrome survivors and their family members because the ECG could be transiently normalized. We proposed using the higher intercostal space V(1) to V(3) lead ECG, together with procainamide to detect the Brugada sign. METHODS AND RESULTS: Among 20 ventricular fibrillation cardiac arrest patients, 13 sudden unexplained death syndrome survivors and their relatives (n=88) were studied using the single standard 12-lead ECG and the new six higher intercostal space V(1) to V(3) lead ECG (-V(1) to -V(3) and -2V(1) to -2V(3)). Ten sudden unexplained death syndrome survivors and relatives (n=48) who had a normalized ECG were also infused with procainamide (10 mg x kg(-1)i.v.) to unmask the Brugada sign and both ECG methods were recorded. Forty healthy individuals and 13 spouses served as the control group. Prior to the procainamide infusion, the Brugada sign could be detected in nine sudden unexplained death syndrome survivors (69.2%) and three (3.4%) relatives with the standard ECG and in 12 (92.3%) and nine (10.2%) with the new six-lead ECG. After the procainamide infusion, the Brugada sign could be demonstrated in seven sudden unexplained death syndrome survivors (70%) and seven (14.6%) relatives with the standard ECG and in nine (90%) (P=0.26) and 23 (47.9%) (P=0.0004) with the new six-lead ECG, respectively. All the controls were negative for the Brugada sign. CONCLUSIONS: Our data suggest that the new higher intercostal space lead ECG, with or without the procainamide test is helpful in detecting the Brugada sign in sudden unexplained death syndrome survivors and their relatives.  (+info)