Electrocardiographic Pattern Simulating Acute Myocardial Injury

Osher, Harold L.; Wolff, Louis

doi:10.1097/00000441-195322650-00011

Cited by 101 publications

(7 citation statements)

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“…The syndrome of sudden death with unexplained right precordial ECG abnormalities was described as early as the 1950s. 21 In the 1990s, Brugada and Brugada 22 described a cohort of patients that had no apparent structural heart disease, right ventricular ECG abnormalities, and a propensity to die suddenly. It is now recognized that idiopathic VF with right precordial ECG abnormalities is worldwide in distribution, with a high prevalence in Southeast Asia, 23,24 where it exhibits a striking male predominance (8:1), 23 distinct from that in Western cohorts.…”

Section: Brugada Syndromementioning

confidence: 99%

Molecular Basis of Arrhythmias

2005

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Abstract-The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias.

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Section: Brugada Syndromementioning

confidence: 99%

Molecular Basis of Arrhythmias

2005

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“…This variability of the ECG phenotype raises questions regarding the accuracy of diagnosis and the evaluation of the clinical course of patients in the absence of a genetic analysis. Since the initial report (Osher and Wolff, 1953), BS is now more frequently recognized and, recently, has been considered to be account for 20% of IVF (Viskin et al, 2000). Current reports also suggested that the ECG pattern has a frequency between 0.14 and 6.1% in asymptomatic (healthy) individuals (Furuhashi et al, 2001;Hermida et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Sodium channel gene (SCN5A) mutations in 44 index patients with Brugada syndrome: Different incidences in familial and sporadic disease

et al. 2003

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The Brugada syndrome (BS) is a distinct form of idiopathic ventricular fibrillation and may cause sudden cardiac death in healthy young individuals. In the surface ECG, BS can be recognized by an atypical right bundle branch block and ST-segment elevation in the right precordial leads. Mutations in the cardiac sodium channel gene SCN5A are only known to cause BS. In a multi-center effort, we have collected clinical data on 44 unrelated index patients and family members and performed a complete genetic analysis of SCN5A. In 37% the disease was familial, whereas in the majority it was sporadic (63%). Five novel SCN5A mutations (2602delC, resulting in: E867X; 2581_2582del TT: F861fs951X; 2673G>A: E1225K; 4435_4437delAAG: K1479del; and 5425C>A: S1812X) were found and were randomly located in SCN5A. Mutation frequencies (SCN5A+) differed significantly between familial (38%) and sporadic disease (0%) (p=0.001). Disease penetrance was complete in the SCN5A+ adult patients, but incomplete in SCN5A+ children (17%). Genetic testing of SCN5A is especially useful in familial disease to identify individuals at cardiac risk. In sporadic cases, however, a genetic basis and the value of mutation screening has to be further determined. These results are in line with a possibly genetic and clinical heterogeneity of BS.

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“…1,2 Patients are at risk for sudden cardiac death (SCD) due to ventricular fibrillation (VF). Since 1953, the ECG pattern similar to coved-type ST-segment elevation was reported as a normal variant in the healthy population or related to VF with structural abnormality, [3][4][5] but as a distinct disease entity, Brugada and Brugada 1 were the first to report 8 patients with VF, right bundle branch block, and ST-segment elevation on 12-lead ECG. Later, structural changes were reported in an explanted heart and by biopsy specimens in a small number of cases, 6,7 potentially opening up the discussion of who actually described this disease entity first.…”

mentioning

confidence: 99%