Twelve-lead ambulatory electrocardiographic monitoring in Brugada syndrome: Potential diagnostic and prognostic implications

Gray, Belinda; Kirby, Adrienne; Kabunga, Peter; Freedman, Ben; Yeates, Laura; Kanthan, A.; Medi, Caroline; Keech, Anthony; Semsarian, Christopher; Sy, Raymond W.

doi:10.1016/j.hrthm.2017.02.026

Cited by 45 publications

(37 citation statements)

References 35 publications

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“…According to the first explanation, patients who have spontaneous type‐I at presentation simply have it more often and therefore have higher risk of developing VF 12. After all, among patients with Brugada syndrome undergoing repeated ECGs or 12‐lead Holter recordings with continuous ST‐segment analysis, those with VF have longer time periods with ST‐segment elevation 13, 14…”

Section: Insights From the Present Study For The “Type‐i Paradox” Of mentioning

confidence: 99%

“…This second group could be larger than we think: If we compare the incidence of VF among patients who have spontaneous versus drug‐induced type I at presentation, a risk repeatedly reported as 1% versus 0.3% annual risk,5 by then assuming that VF events in the drug‐induced category occur only in patients who have “yet unrecognized” spontaneous type I, one may calculate that only 3 out of 10 patients with drug‐induced type I will ever develop a spontaneous type I. In studies performing repeated ECG or Holter recordings after a SCB test, only 29%2 to 35%13 are “caught” with a spontaneous type I. Clearly, this partition will depend on the frequency of ECG recordings done over time and needs to be better defined.…”

Section: Insights From the Present Study For The “Type‐i Paradox” Of mentioning

confidence: 99%

“…12 After all, among patients with Brugada syndrome undergoing repeated ECGs or 12-lead Holter recordings with continuous ST-segment analysis, those with VF have longer time periods with ST-segment elevation. 13,14 A second explanation for the "type-I paradox" could well be that patients with drug-induced type-I ECG consist of 2 subgroups: (1) patients presenting with a nondiagnostic ECG and a positive SCB test, who then develop a spontaneous type-I pattern at least once during follow-up; and (2) otherwise similar patients who never develop a spontaneous type-I ECG. This second group could be larger than we think: If we compare the incidence of VF among patients who have spontaneous versus drug-induced type I at presentation, a risk repeatedly reported as 1% versus 0.3% annual risk, 5 by then assuming that VF events in the drug-induced category occur only in patients who have "yet unrecognized" spontaneous type I, one may calculate that only 3 out of 10 patients with drug-induced type I will ever develop a spontaneous type I.…”

Section: Riskmentioning

confidence: 99%

See 2 more Smart Citations

Type‐I Paradox of Brugada Syndrome

Viskin

Hochstadt

Rosso

2018

JAHA

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Section: Insights From the Present Study For The “Type‐i Paradox” Of mentioning

confidence: 99%

Section: Insights From the Present Study For The “Type‐i Paradox” Of mentioning

confidence: 99%

Section: Riskmentioning

confidence: 99%

See 1 more Smart Citation

Type‐I Paradox of Brugada Syndrome

Viskin

Hochstadt

Rosso

2018

JAHA

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“…The ECG signature of BrS, an abnormal ST segment elevation in precordial leads, manifests intermittently (Veltmann et al, 2006). Circadian biases in the development of abnormal ST segment elevation (Gray et al, 2017), as well as in the initiation of VF (Matsuo et al, 1999), underscore the dynamic nature of BrS. Increased parasympathetic tone can also underlie the dynamic unmasking of the disease phenotype, which can be reverted by interventions that increase the sympathetic signals (Kasanuki et al, 1997).…”

Section: Stress Kinase Activity and The Brugada Syndromementioning

confidence: 99%

“Heart Oddity”: Intrinsically Reduced Excitability in the Right Ventricle Requires Compensation by Regionally Specific Stress Kinase Function

Warren

2020

Front. Physiol.

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The traditional view of ventricular excitation and conduction is an all-or-nothing response mediated by a regenerative activation of the inward sodium channel, which gives rise to an essentially constant conduction velocity (CV). However, whereas there is no obvious biological need to tune-up ventricular conduction, the principal molecular components determining CV, such as sodium channels, inward-rectifier potassium channels, and gap junctional channels, are known targets of the "stress" protein kinases PKA and calcium/calmodulin dependent protein kinase II (CaMKII), and are thus regulatable by signal pathways converging on these kinases. In this mini-review we will expose deficiencies and controversies in our current understanding of how ventricular conduction is regulated by stress kinases, with a special focus on the chamber-specific dimension in this regulation. In particular, we will highlight an odd property of cardiac physiology: uniform CV in ventricles requires co-existence of mutually opposing gradients in cardiac excitability and stress kinase function. While the biological advantage of this peculiar feature remains obscure, it is important to recognize the clinical implications of this phenomenon pertinent to inherited or acquired conduction diseases and therapeutic interventions modulating activity of PKA or CaMKII.

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“…This results in an increased diagnostic yield for BrS 31. A 12-lead Holter monitor with high precordial lead positions may then be used to assess for a dynamic spontaneous Brugada pattern over a 24-hour period for prognostic utility 32. Ideally, if performed beforehand, detection of a dynamic type 1 pattern may obviate the need for drug provocation testing.…”

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confidence: 99%

Evaluation After Sudden Death in the Young

Gray

Ackerman

Semsarian

et al. 2019

Circ: Arrhythmia and Electrophysiology

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Sudden cardiac death (SCD) is defined as a death occurring usually within an hour of onset of symptoms, arising from an underlying cardiac disease. SCD is a complication of a number of cardiovascular diseases, and is often unexpected. In individuals aged less than 35 years, unexplained SCD is the most common presentation. A significant proportion of SCD in the young (≤ 35 years, SCDY) events may be precipitated by underlying inherited cardiac conditions (ICCs), including both heritable cardiomyopathies and inherited arrhythmia syndromes (also known as cardiac channelopathies). Tragically, sudden death may be the first manifestation of the disease in a family and therefore clinical and genetic evaluation of surviving family members forms a key role in diagnosing the underlying ICC in the family. This is particularly relevant when considering that most ICCs are inherited in an autosomal dominant manner meaning that surviving family members have a 50% chance of inheriting the same disease substrate. This review will outline the underlying causes of SCDY and outline our universal approach to familial evaluation following a young person's sudden death.

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Twelve-lead ambulatory electrocardiographic monitoring in Brugada syndrome: Potential diagnostic and prognostic implications

Cited by 45 publications

References 35 publications

Type‐I Paradox of Brugada Syndrome

Type‐I Paradox of Brugada Syndrome

“Heart Oddity”: Intrinsically Reduced Excitability in the Right Ventricle Requires Compensation by Regionally Specific Stress Kinase Function

Evaluation After Sudden Death in the Young

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