scholarly journals Hyperkalemia Induced Brugada Phenocopy: A Rare ECG Manifestation

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Muhammad Ameen ◽  
Ghulam Akbar ◽  
Naeem Abbas ◽  
Ghazi Mirrani

Brugada syndrome (BrS) is an inherited disorder of cardiac ion channels characterized by peculiar ECG findings predisposing individuals to ventricular arrhythmias, syncope, and sudden cardiac death (SCD). Various electrolyte disturbances and ion channels blocking drugs could also provoke BrS ECG findings without genetic BrS. Clinical differentiation and recognition are essential for guiding the legitimate action. Hyperkalemia is well known to cause a wide variety of ECG manifestations. Severe hyperkalemia can even cause life threatening ventricular arrhythmias and cardiac conduction abnormalities. Most common ECG findings include peaked tall T waves with short PR interval and wide QRS complex. Since it is very commonly encountered disorder, physicians need to be aware of even its rare ECG manifestations, which include ST segment elevation and Brugada pattern ECG (BrP). We are adding a case to the limited literature about hyperkalemia induced reversible Brugada pattern ECG changes.

2020 ◽  
pp. 17-20
Author(s):  
Michel de Lorgeril ◽  
Mikael Rabaeus

The Brugada syndrome (BrS) is an electrical heart disease with complex inheritance (some cases with SCN5A mutations), characterized by specific electrocardiogram (ECG) markers and high risk of associated lethal ventricular arrhythmias [1]. The ECG signature of BrS consists of right precordial ST-segment elevation (≥2 mm) followed by negative T waves [1]. It sometimes includes the findings of right bundle branch block (RBBB). In certain cases, the typical ECG pattern is present intermittently which creates a potential problem for reaching the diagnosis of BrS. Another problem in diagnosing BrS is the presence of so-called Brugada phenocopies (BrPs), i.e. an acquired Brugada-like ECG pattern that are visually identical and indistinguishable from true BrS [2]. This ECG pattern can be caused by other conditions including ischemia of the ventricular septum and/or right ventricle or by taking certain medications [2]. Proton-pump inhibitors (PPIs) are widely prescribed, often for prolonged use, and have been associated with electrolyte disturbances and cardiac arrhythmias [3,4]. We hereby present for the first time the case of a patient with an ECG suggestive of BrS while taking PPI; but no other medication known to cause BrS. The BrS ECG pattern disappeared a few months after stopping the medication.


2020 ◽  
Vol 25 (3) ◽  
pp. 226-231
Author(s):  
Daniel B. Munhoz ◽  
Luiz Sergio F. Carvalho ◽  
Frank N. C. Venancio ◽  
Osorio Luis Rangel de Almeida ◽  
Jose C. Quinaglia e Silva ◽  
...  

Background: Although there is strong evidence supporting the use of statin therapy after myocardial infarction (MI), some mechanistic gaps exist regarding the benefits of this therapy at the very onset of MI. Among the potential beneficial mechanisms, statins may improve myocardial electrical stability and reduce life-threatening ventricular arrhythmia, as reported in stable clinical conditions. This study was designed to evaluate whether this mechanism could also occur during the acute phase of MI. Methods: Consecutive patients with ST-segment elevation MI were treated without statin (n = 57) or with a simvastatin dose of 20 to 80 mg (n = 87) within the first 24 hours after MI symptom onset. Patients underwent digital electrocardiography within the first 24 hours and at the third and fifth days after MI. The QTC dispersion (QTcD) was measured both with and without the U waves. Results: Although QTcD values were equivalent between the groups at the first day (80.6 ± 36.0 vs 80.0 ± 32.1; P = 0.36), they were shorter among individuals using simvastatin than in those receiving no statins on the third (90.4 ± 38.6 vs 86.5 ± 36.9; P = .036) and fifth days (73.1 ± 31 vs 69.2 ± 32.6; P = .049). We obtained similar results when analyzing the QTcD duration including the U wave. All values were adjusted by an ANCOVA model after propensity-score matching. Conclusions: Statins administered within 24 hours of ST-segment elevation MI reduced QTc dispersion, which may potentially attenuate the substrate for life-threatening ventricular arrhythmias.


2019 ◽  
Vol 12 (7) ◽  
pp. e229829 ◽  
Author(s):  
Hassan Abbas ◽  
Sohaib Roomi ◽  
Waqas Ullah ◽  
Asrar Ahmad ◽  
Ganesh Gajanan

A prominent coved or saddle-shaped ST-segment elevation followed by T wave changes in V1-V3 and in the absence of other identifiable cause is termed as Brugada pattern. This pattern in the presence of documented ventricular arrhythmias or its symptoms (syncope, seizure) or significant family for sudden cardiac death or abovementioned ECG changes is called Brugada syndrome. Here we present a comprehensive literature review on the precipitation factors of Brugada syndrome/pattern by various stimuli, its presentation, associations, management and outcomes. We are also presenting a unique case of Brugada pattern where the patient’s Brugada pattern was unmasked at an extreme old age by infection.


2015 ◽  
Vol 4 ◽  
pp. 77
Author(s):  
Saira Imran ◽  
Maxwell Afari ◽  
Ameya Hodarkar ◽  
Fady Y. Marmoush ◽  
Alice Y. Kim

<p>Brugada syndrome is an autosomal dominant disorder, characterized by electrocardiographic manifestations of a pseudo right bundle branch block and a distinctive ST segment elevation in the precordial leads, with a predisposition to ventricular arrhythmias and sudden cardiac arrest. Many medications and toxins have been reported to induce a Brugada pattern on electrocardiogram. We report a case of a patient who presented with chest pain and was found to have electrocardiographic manifestation of Brugada type II in the setting of cocaine use and chest pain.</p>


Author(s):  
Rod Partow-Navid ◽  
Narut Prasitlumkum ◽  
Ashish Mukherjee ◽  
Padmini Varadarajan ◽  
Ramdas G. Pai

AbstractST-segment elevation myocardial infarction (STEMI) is a life-threatening condition that requires emergent, complex, well-coordinated treatment. Although the primary goal of treatment is simple to describe—reperfusion as quickly as possible—the management process is complicated and is affected by multiple factors including location, patient, and practitioner characteristics. Hence, this narrative review will discuss the recommended management and treatment strategies of STEMI in the circumstances.


2020 ◽  
Vol 4 (2) ◽  
pp. 244-246
Author(s):  
Orhay Mirzapolos ◽  
Perry Marshall ◽  
April Brill

Introduction: Brugada syndrome is an arrhythmogenic disorder that is a known cause of sudden cardiac death. It is characterized by a pattern of ST segment elevation in the precordial leads on an electrocardiogram (EKG) due to a sodium channelopathy. Case Report: This case report highlights the case of a five-year-old female who presented to the emergency department with a febrile viral illness and had an EKG consistent with Brugada syndrome. Discussion: Fever is known to accentuate or unmask EKG changes associated with Brugada due to temperature sensitivity of the sodium channels. Conclusion: Febrile patients with Brugada are at particular risk for fatal ventricular arrhythmias and fevers should be treated aggressively by the emergency medicine provider. Emergency medicine providers should also consider admitting febrile patients with Brugada syndrome who do not have an automatic implantable cardioverter-defibrillator for cardiac monitoring.


1993 ◽  
Vol 18 (1) ◽  
pp. 63-79
Author(s):  
Sylvie Robichaud-Ekstrand

Many clinical factors influence the 1-year prognosis in myocardial infarction (MI) patients. The most important clinical determinants are the left ventricular dysfunction, myocardial ischemia, and complex ventricular arrhythmias. Some authors have found an independent prognostic value of complex ventricular arrhythmias, while others consider that ventricular arrhythmias predict future cardiac events only if associated with low ejection fractions. Other factors that have 1-year prognostic value are the following: a previous MI, a history of angina at least 3 months preceding the infarct, postmyocardial angina, and the criteria that indicate to the practitioner whether MI patients are medically ineligible for stress testing. There still remain controversies in regard to the predictive value of certain variables such as the site, type, and extension of the MI, the presence of complex ventricular arrhythmias, exercise-induced hypotension, ST segment elevation, and the electrical provocation of dangerous arrhythmias. Key words: cardiac rehabilitation, postinfarct mortality and morbidity, cardiac events predictors, postinfarct prognostic stratification


2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Nathalie Strutz-eebohm ◽  
Katja Steinke ◽  
Ulrike Henrion ◽  
Matthias Rohbeck ◽  
Karin Klingel ◽  
...  

In patients as well as in mouse models, enteroviral infections, especially Coxsackie group B viruses (CVB1-6), frequently induce ventricular arrhythmias and sudden cardiac death. The cardiac action potential requires proper function of cardiac ion channels. CVB3 alters Kv7.1 channel trafficking potentially leading to changes in action potentials and increasing likelihood of arrhythmias. Genetic variants of cardiac ion channels can cause changes in channel trafficking that may preserve from CVB3 modulations and present an evolutionary advantage. Here, we show that a common polymorphic Kv7.1 channel variant uses alternative trafficking pathways and may thus exert a benefit during CVB3 infections. Genetic and pharmacological disruption of a CVB3-stimulated Serum- and Glucocorticoid inducible Kinase 1 (SGK1) pathways blunts Kv7.1 channel dysfunctions. Our results suggest that escape from CVB3-induced SGK1-stimulation by genetic variation in Kv7.1 may be protective and inhibition of SGK1 may present a pharmacological approach to reduce the pro-arrhythmic risk associated with acute coxsackievirus infections.


Author(s):  
Borja Ibanez ◽  
Stefan James

ST-elevation myocardial infarction (STEMI) is a life-threatening conditioning caused by an abrup occlusion of an epicardial coronary artery. Reperfusion (ideally by primary angioplasty, and if not timely available by systemic fibrinolysis) massively improves survival in STEMI patients. Healthcare systems attending STEMI patients in the early phase are critical for a correct triage, reperfusion strategy selection and initial treatment. Besides reperfusion, coadjuvant therapies are critical to improve the success of management and in turn improves long-term mortality and morbidility associated with STEMI. The present chapter presents the state-of-art evidence guiding recommendations for treatment of STEMI with a special focus on the early phases of the process.


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