Recurrent Ventricular Fibrillation Related to Hypokalemia in Early Repolarization Syndrome

Myojo, Takuya; Sato, Nobuyuki; Nimura, Asami; Matsuo, Aya; Taniguchi, Osamu; Nakamura, Hideki; Talib, Ahmed Karim; Naka, Sadahiro; Takeuchi, Toshiharu; Kawamura, Y.; Hasebe, Naoyuki

doi:10.1111/j.1540-8159.2012.03460.x

Cited by 20 publications

(9 citation statements)

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“…In the cases reported here, two of the three patients had hypokalemia, suggesting that hypokalemia, probably induced by corticosteroid therapy, may be closely related to VF episodes, because it is generally accepted that glucocorticoids reduce serum potassium concentration via their mineralocorticoid action. Moreover, in the cases of VF storm we have encountered, in early repolarization syndrome the rapid change in potassium concentration may have been related to the patients’ lethal arrhythmias [8], which would be compatible with the findings of Fujimoto et al [14]. …”

Section: Discussionsupporting

confidence: 82%

“…Steroids cause hypokalemia via their mineralocorticoid action, so hypokalemia is likely a key trigger of VF in J-wave syndromes, as in the case reported [1, 7, 8]. We have reported a case of early repolarization syndrome related to severe hypokalemia in a 66-year-old man [8]. On the other hand, stress, which may induce the release of intrinsic corticosteroids, is also a likely key triggering factor for VF.…”

Section: Introductionmentioning

confidence: 90%

“…There has been one case report of VF related to hypokalemia induced by steroid therapy in a patient with Brugada syndrome [7]. Steroids cause hypokalemia via their mineralocorticoid action, so hypokalemia is likely a key trigger of VF in J-wave syndromes, as in the case reported [1, 7, 8]. We have reported a case of early repolarization syndrome related to severe hypokalemia in a 66-year-old man [8].…”

Section: Introductionmentioning

confidence: 90%

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Three cases of corticosteroid therapy triggering ventricular fibrillation in J-wave syndromes

et al. 2013

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We describe three cases of J-wave syndrome in which ventricular fibrillation (VF) was probably induced by corticosteroid therapy. The patients involved were being treated with prednisolone for concomitant bronchial asthma. One of the three patients had only one episode of VF during her long follow-up period (14 years). Two patients had hypokalemia during their VF episodes. Corticosteroids have been shown to induce various types of arrhythmia and to modify cardiac potassium channels. We discuss the possible association between corticosteroid therapy and VF in J-wave syndrome based on the cases we have encountered.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 90%

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Three cases of corticosteroid therapy triggering ventricular fibrillation in J-wave syndromes

et al. 2013

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“…Hypokalemia is also associated with ES in structurally normal hearts and correction of hypokalemia can prevent the recurrent ventricular fibrillation (VF). 4, 5 However, because rapid and safe correction of serum potassium is often difficult, additional drug therapy is often necessary to manage the ES. Sympathetic blockade, while not always effective, is commonly used in the management of ES.…”

Section: Introductionmentioning

confidence: 99%

Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles

Maruyama

Chua

et al. 2014

Heart Rhythm

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BACKGROUND Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. OBJECTIVE To test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. METHODS Intracellular calcium (Cai) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. RESULTS Repeated episodes of electrically-induced VF at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+]o) (4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+]o, 9 of 10 hearts (90%) in 1.5 mmol/L [K+]o, and 7 of 7 hearts (100%) in 1.0 mmol/L [K+]o (P<0.001). Optical mapping showed isoproterenol and hypokalemia enhanced Cai transient duration (CaiTD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small conductance calcium activated potassium channel blocker (apamin) failed to prevent recurrent SVF. CONCLUSION Beta-adrenergic stimulation and concomitant hypokalemia could cause non-ischemic activation of IKATP, heterogeneous APD shortening and prolongation of CaiTD to provoke late phase 3 EAD, triggered activity and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.

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“…Neste âmbito, a identificação de subgrupos de maior risco constitui uma área de intensa investigação, admitindo-se que a elevação do ponto J possa ser um marcador de maior heterogeneidade transmural da repolarização ventricular, capaz de, na presença de fatores pró-arrítmicos ou triggers (alterações do tónus autonómico, hipocaliemia, dispersão da refratariedade ventricular ou potenciais tardios fragmentados) aumentar a vulnerabilidade para FV 14,15 . Apesar de se considerar que a grande maioria dos indivíduos com PRPr terá uma evolução benigna, particularmente se assintomáticos, sem documentação de arritmias ventriculares complexas e sem história familiar de MS 14 , são necessários estudos clínicos e experimentais que permitam contribuir para a compreensão dos mecanismos arritmogénicos relacionados com esta entidade, mantendo uma atitude clínica de precaução por forma a identificar os elementos a ter em conta numa estratégia de estratificação de risco adequada a esta população.…”

Section: Comentáriounclassified

Comentário a «Padrão de repolarização precoce e risco de morte arrítmica. Meta-análise»

Oliveira¹

2013

Revista Portuguesa de Cardiologia

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In Journal of the American College of Cardiology 2013; 61:645-50.Objectives: A meta-analysis was performed to determine the risk and incidence rate of arrhythmia death, cardiac death, and all-cause death in the general population with the early repolarization pattern (ERP).Background: The ERP has recently been associated with vulnerability to ventricular fibrillation in case-control studies. However, the prognostic significance of the ERP in the general population is controversial.Methods: Relevant studies published through July 31, 2012, were searched and identified in the MEDLINE and Embase databases. Studies that reported risk ratio estimates with 95% confidence intervals (CIs) for the associations of interest were included. Data were extracted, and summary estimates of association were obtained using a randomeffects model.Results: Of the 9 studies included, 3 studies reported on arrhythmia death (31,981 subjects, 1,108 incident cases during 726,741 person-years of follow-up), 6 studies reported on cardiac death (126,583 subjects, 10,010 incident cases during 2,054,674 person-years of followup), and 6 studies reported on all-cause death (112,443 subjects, 22,165 incident cases during 2,089,535 personyears of follow-up). The risk ratios of the ERP were 1.70 (95% CI: 1.19 to 2.42; p = 0.003) for arrhythmia death, 0.78 (95% CI: 0.27 to 2.25; p = 0.63) for cardiac death, and 1.06 (95% CI: 0.87 to 1.28; p = 0.57) for all-cause death. The estimated absolute risk differences of subjects with the ERP were 70 cases of arrhythmia death per 100,000 subjects per year. J-point elevation ≥ 0.1 mV in the inferior leads and notching configuration had an increased risk for arrhythmia death in subgroup studies.Conclusions: The ERP was associated with increased risk and a low to intermediate absolute incidence rate of arrhythmia death. Further study is needed to clarify which subgroups of subjects with the ERP are at higher risk for arrhythmia death.

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Recurrent Ventricular Fibrillation Related to Hypokalemia in Early Repolarization Syndrome

Cited by 20 publications

References 11 publications

Three cases of corticosteroid therapy triggering ventricular fibrillation in J-wave syndromes

Three cases of corticosteroid therapy triggering ventricular fibrillation in J-wave syndromes

Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles

Comentário a «Padrão de repolarização precoce e risco de morte arrítmica. Meta-análise»

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