Brugada phenocopy secondary to hyperkalemia and hyponatremia in primary adrenal insufficiency

Amusina, Olga; Mehta, S.; Nelson, M. E.

doi:10.1002/emp2.12800

Cited by 5 publications

(6 citation statements)

References 14 publications

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“…A 63-year-old male was admitted for junctional rhythm requiring vasopressor support; another 26-year-old male was admitted for Brugada syndrome-like electrocardiogram elements. 14 , 15 A 40-year-old male had broad complex tachycardia, a cardiologic emergency that might not be related to ventricular tachycardia, but also to severe AD-associated hyperkalemia which, in this particular case, induced, as well, rapidly progressive muscle weakness to quadriparesis. 16 A woman in her 50s was admitted for cardiac tamponade as a consequence of AD.…”

Section: Resultsmentioning

confidence: 96%

Addison’s Disease: Diagnosis and Management Strategies

Cârșote¹,

Nistor²

2023

IJGM

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We aim to overview Addison’s disease (AD) with regard to current diagnosis and management. This is a narrative review of full-length articles published in English between January 2022 and December 2022 (including online ahead of print versions) in PubMed-indexed journals. We included original studies in living humans regardless of the level of statistical significance starting from the key search terms “Addison’s disease” or “primary adrenal insufficiency” in title or abstract. We excluded articles with secondary adrenal insufficiency. Briefly, 199 and 355 papers, respectively were identified; we manually checked each of them, excluded the duplicates, and then selected 129 based on their clinical relevance in order to address our 1-year analysis. We organized the data in different subsections covering all published aspects on the subject of AD. To our knowledge, this is the largest AD retrospective from 2022 on published data. A massive role of genetic diagnosis especially in pediatric cases is highlighted; the importance of both pediatric and adult awareness remains since unusual presentations continue to be described. COVID-19 infection is a strong player amid this third year of pandemic although we still not do have large cohorts in this particular matter as seen, for instance, in thyroid anomalies. In our opinion, the most important topic for research is immune checkpoint inhibitors, which cause a large panel of endocrine side effects, AD being one of them.

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Section: Resultsmentioning

confidence: 96%

Addison’s Disease: Diagnosis and Management Strategies

Cârșote¹,

Nistor²

2023

IJGM

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“…Hyponatremia has been clinically identified as a potential trigger for a BrS ECG pattern ( 10 – 14 ). We therefore perfused WT and Scn5a +/− hearts with a hyponatremic solution containing 120 mM Na + , comparable with the degree of hyponatremia recorded in case studies ( 10 – 14 ). Representative data in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Reducing extracellular sodium is another mechanism previously demonstrated to reduce ventricular CV in the Langendorff-perfused heart ( 8 , 17 ). Interestingly, hyponatremia has also been associated with unmasking a BrS ECG pattern in human patients ( 10 – 14 ). We therefore tested the hypothesis that hyponatremia exacerbates the conduction phenotype of Na v 1.5 LOF.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, numerous clinical case reports describe that a BrS ECG phenotype can be unmasked by hyponatremia ( 10 – 14 ). Although many of these studies report the phenomenon as a BrS “phenocopy” because of its transient nature (resolving upon recovery of serum sodium concentration), they nevertheless highlight the efficacy of hyponatremia as a substrate for electrophysiological conduction disturbance.…”

Section: Introductionmentioning

confidence: 99%

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Mannitol and hyponatremia regulate cardiac ventricular conduction in the context of sodium channel loss of function

Blair,

Wu,

Bain

et al. 2024

American Journal of Physiology-Heart and Circulatory Physiology

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Background: Scn5a heterozygous null (Scn5a+/-) mice have historically been used to investigate arrhythmogenic mechanisms of diseases such as Brugada Syndrome and Lev's disease. Previously, we demonstrated that reducing ephaptic coupling (EpC) in ex vivo hearts exacerbates pharmacological Nav1.5 loss of function (LOF). Whether this effect is consistent in a genetic Nav1.5 LOF model is yet to be determined. We hypothesized that loss of EpC would result in greater reduction in conduction velocity (CV) for the Scn5a+/- mouse relative to wild type (WT). Methods: In vivo ECGs and ex vivo optical maps were recorded from Langendorff-perfused Scn5a+/- and WT mouse hearts. EpC was reduced with perfusion of a hyponatremic solution, the clinically relevant osmotic agent mannitol, or a combination of the two. Results: Neither in vivo QRS duration nor ex vivo CV during normonatremia was significantly different between the two genotypes. In agreement with our hypothesis, we found that hyponatremia severely slowed CV and disrupted conduction for 4/5 Scn5a+/- mice, but 0/6 WT mice. Additionally, treatment with mannitol slowed CV to a greater extent in Scn5a+/- relative to WT hearts. Unexpectedly, treatment with mannitol during hyponatremia did not further slow CV in either genotype, but resolved the disrupted conduction observed in Scn5a+/- hearts. Similar results in guinea pig hearts suggest the effects of mannitol and hyponatremia are not species specific. Conclusion: Loss of EpC through either hyponatremia or mannitol alone results in slowed or disrupted conduction in a genetic model of Nav1.5 LOF. However, combination of these interventions attenuates conduction slowing.

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“…Changing his antihypertensive treatment and correcting the electrolyte disturbance improved the patient's ST-segment elevation [ 17 ]. On the other hand, it should be remembered that multiple electrolyte disturbances associated with primary adrenal insufficiency and hyponatremia due to excessive water and alcohol consumption may also present with BrP [ 18 , 19 ]. Even in all these scenarios, eliminating metabolic and electrolyte disorders resulted in the recovery of spontaneous ST-segment elevation.…”

Section: Discussionmentioning

confidence: 99%

Brugada Phenocopy Induced by Hypovolemic Hyponatremia

Yılmaz,

Özdemir

2023

Cureus

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Brugada syndrome (BrS) is a hereditary channelopathy caused by an autosomal dominant mutation in the cardiac sodium channel gene SCN5A alpha subunit. In individuals without structural heart disease, the risk of sudden cardiac death (SCD) increases in this channelopathy with ST-segment elevation in V1-3 precordials. Brugada phenocopy (BrP) is a condition in which transient ST-segment elevations are observed, mimicking BrS electrocardiographic changes, which can occur with electrolyte and metabolic disorder scenarios. In this study, we share a case of BrP that occurred due to hypovolemic hyponatremia and recovered spontaneously with the correction of electrolyte disturbance.

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Brugada phenocopy secondary to hyperkalemia and hyponatremia in primary adrenal insufficiency

Cited by 5 publications

References 14 publications

Addison’s Disease: Diagnosis and Management Strategies

Addison’s Disease: Diagnosis and Management Strategies

Mannitol and hyponatremia regulate cardiac ventricular conduction in the context of sodium channel loss of function

Brugada Phenocopy Induced by Hypovolemic Hyponatremia

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