Electrocardiographic J wave of hypercalcemia

Sridharan, Marandapalli R.; Horan, Leo G.

doi:10.1016/0002-9149(84)90273-x

Cited by 90 publications

(43 citation statements)

References 3 publications

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“…Importantly, confounding factor or factors that could account for the ECG abnormality or syncope should be carefully excluded, including atypical right bundle-branch block, left ventricular hypertrophy, early repolarization, acute pericarditis, acute myocardial ischemia or infarction, pulmonary embolism, Prinzmetal angina, 21 dissecting aortic aneurysm, 22 various central and autonomic nervous system abnormalities, 23,24 Duchenne muscular dystrophy, 25 thiamin deficiency, 26 hyperkalemia, 22,27,28 hypercalcemia, 29,30 arrhythmogenic right ventricular dysplasia/cardiomyopathy, 31,32 pectus excavatum, 33 hypothermia, 34,35 and mechanical compression of the right ventricular outflow tract (RVOT) as occurs in mediastinal tumor 36 or hemopericardium. 37 Of note, a Brugada-like ECG can occasionally appear for a brief period or for a period of several hours after directcurrent cardioversion; it is not known whether these patients are gene carriers for Brugada syndrome.…”

Section: Diagnostic Criteria and Recommendationsmentioning

confidence: 99%

Brugada Syndrome: Report of the Second Consensus Conference

Antzelevitch

Brugada²,

Borggrefe³

et al. 2005

Circulation

1,651

818

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Abstract-Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, ␣-adrenergic agonists, ␤-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo-and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred.

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Section: Diagnostic Criteria and Recommendationsmentioning

confidence: 99%

Brugada Syndrome: Report of the Second Consensus Conference

Antzelevitch

Brugada²,

Borggrefe³

et al. 2005

Circulation

1,651

818

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“…4, 5 More recently, the presence of prominent J waves has been identified as a marker for a substrate capable of generating life-threatening ventricular arrhythmias. 6 In humans, the J wave more commonly appears as a J point elevation, with part of the J wave buried inside the QRS.…”

Section: Introductionmentioning

confidence: 99%

J-wave syndromes: Brugada and early repolarization syndromes

2015

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A prominent J wave is encountered in a number of life-threatening cardiac arrhythmia syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes. BrS and ERS differ with respect to the magnitude and lead location of abnormal J waves and are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. Despite two decades of intensive research, risk stratification and the approach to therapy of these two inherited cardiac arrhythmia syndromes are still undergoing rapid evolution. Our objective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular and genetic mechanisms underlying these two fascinating syndromes that have captured the interest and attention of the cardiology community in recent years.

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“…1 Also referred to as the Osborn wave, the J wave or elevated J point has been described in the ECG of animals and humans for over six decades, 2 since Osborn's observation in the early 1950s. 3 In humans, the appearance of a prominent J wave in the ECG is considered pathognomonic of hypothermia, 4-6 hypercalcemia 7,8 and more recently as a marker for a substrate capable of generating life-threatening ventricular arrhythmias. 9 A distinct J wave has been described in subjects completely recovered from hypothermia 10,11 or those predisposed to idiopathic ventricular fibrillation (IVF), but is otherwise rarely observed in humans under normal conditions.…”

Section: Evolution Of the J Wave Syndromesmentioning

confidence: 99%

J Wave Syndromes as a Cause of Sudden Arrhythmic Death

Antzelevitch

2013

Cardiogenetics

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Accentuated J waves have been associated with idiopathic ventricular tachycardia and fibrillation (VT/VF) for nearly three decades. Prominent J waves characterize both Brugada and early repolarization syndromes leading to their designation as J wave syndromes. An early repolarization (ER) pattern, characterized by J point elevation, slurring of the terminal part of the QRS and ST segment elevation was considered to be a totally benign electrocardiographic manifestation until a decade ago. Recent casecontrol and population-based association studies have advanced evidence that an ER pattern in the inferior or infero-lateral leads is associated with increased risk for life-threatening arrhythmias, named early repolarization syndrome (ERS). ERS and Brugada syndrome (BrS) share similar electrocardiogram features, clinical outcomes, risk factors as well as a common arrhythmic platform related to amplification of I_to-mediated J waves. Although BrS and ERS differ with respect to the magnitude and lead location of abnormal J wave manifestation, they are thought to represent a continuous spectrum of phenotypic expression, termed J wave syndromes. A classification scheme for ERS has been proposed: type 1, displaying an ER pattern predominantly in the lateral precordial leads, is considered to be largely benign; type 2, displaying an ER pattern predominantly in inferior or infero-lateral leads, is associated with a higher level of risk; whereas type 3, displaying an ER pattern globally in inferior, lateral and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with VF storms

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Electrocardiographic J wave of hypercalcemia

Cited by 90 publications

References 3 publications

Brugada Syndrome: Report of the Second Consensus Conference

Brugada Syndrome: Report of the Second Consensus Conference

J-wave syndromes: Brugada and early repolarization syndromes

J Wave Syndromes as a Cause of Sudden Arrhythmic Death

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