Brugada-like Electrocardiographic Pattern Research Articles

Reverse translational analysis of clinically reported, lamotrigine-induced cardiovascular adverse events using the halothane-anesthetized dogs.

Lamotrigine has been used for patients with epilepsy and/or bipolar disorder, overdose of which induced the hypotension, elevation of the atrial pacing threshold, cardiac conduction delay, wide complex tachycardia, cardiac arrest and Brugada-like electrocardiographic pattern. To clarify how lamotrigine induces those cardiovascular adverse events, we simultaneously assessed its cardiohemodynamic and electrophysiological effects using the halothane-anesthetized dogs (n = 4). Lamotrigine was intravenously administered in doses of 0.1, 1 and 10mg/kg/10min under the monitoring of cardiovascular variables, possibly providing subtherapeutic to supratherapeutic plasma concentrations. The low or middle dose of lamotrigine did not alter any of the variables. The high dose significantly delayed the intra-atrial and intra-ventricular conductions in addition to the prolongation of ventricular effective refractory period, whereas no significant change was detected in the other variables. Lamotrigine by itself has relatively wide safety margin for cardiohemodynamics, indicating that clinically reported hypotension may not be induced through its direct action on the resistance arterioles or capacitance venules. The electrophysiological effects suggested that lamotrigine can inhibit Na+ channel in the in situ hearts. This finding may partly explain the onset mechanism of lamotrigine-associated cardiac adverse events in the clinical cases. In addition, elevation of J wave was induced in half of the animals, suggesting that lamotrigine may have some potential to unmask Brugada electrocardiographic genotype in susceptible patients.

Two patients with COVID-19 and afever-induced Brugada-like electrocardiographic pattern.

Febrile states may unmask certain Brugada syndrome patients and precipitate ventricular arrhythmias. Here we describe two patients with COVID-19 who developed a fever-induced type 1 Brugada electrocardiographic pattern. Both patients did not show any ventricular arrhythmias during admission. These and previously published cases suggest that the threshold to run an ECG should be low in febrile patients with suspected COVID-19, because these patients are potentially at risk for developing proarrhythmic complications.

Transient Brugada-like ECG pattern incited by uncontrolled hypertension - a rare case report

Background: Brugada syndrome (BrS) is a rare form of channelopathy caused by mutation of SCN5A gene that encodes for sodium channel and is associated with increased risk of ventricular arrhythmia and sudden cardiac death. BrS has a characteristic electrocardiographic (ECG) pattern. Various stressors can induce Brugada-like pattern on ECG in the absence of BrS known as Brugada phenotype. Case Presentation: We report a case of a 28-year-old African-American male patient who presented to the emergency department with a chief complaint of atypical chest pain. He was noted to have an elevated blood pressure and a type 1 Brugada pattern on his 12-lead ECG. His ECG changed from type 1 to type 3 Brugada pattern upon controlling blood pressure, which indicated the presence of a Brugada phenocopy. Conclusion: It is important to recognize the underlying stressors that can lead to Brugada-like patterns on the ECG since these stressors are treatable without any sequel.

Brugada-Like Electrocardiographic Patterns Induced by Hyperkalemia

Brugada syndrome was described in 1992 as a new clinical and electrocardiographic syndrome involving susceptibility to ventricular arrhythmias and sudden cardiac death in patients with no obvious structural heart disease. Brugada syndrome is characterized by a hereditary anomaly in the sodium ion channel (mutation of the SCN5A gene) identified by a wide QRS associated with the ST-segment elevation and the T‑wave inversion in the right precordial leads. The Brugada-like electrocardiographic pattern can be caused by sodium channel-blocking drugs and electrolyte disorders. Hyperkalemia may produce multiple ECG abnormalities, including the ST-segment elevation and pseudomyocardial infarction with a resolution of these abnormalities after the correction of hyperkalemia. This article describes 8 cases of pseudoanteroseptal myocardial infarction in acute renal insufficiency with hyperkalemia. The ST-segment elevation related to hyperkalemia is resolved by the reduced serum potassium level. Clinicians should recognize that hyperkalemia is one of the etiologies of the Brugada-like electrocardiographic pattern.

Cocaine And Hyperkalemia Unmasked The Electrocardiogram (EKG) Pattern Of Brugada Syndrome

A very few case reports have indicated that hyperkalemia can induce a Brugada pattern in the electrocardiogram (EKG). On the other hand, very rare case reports have indicated that cocaine has precipitated life-threatening arrhythmias associated with development of Brugada syndrome. We present a 26-year old patient with hyperkalemia secondary to muscle damage and renal insufficiency after a reported large intake of cocaine. The electrocardiogram showed a Brugada pattern. These EKG changes disappeared directly after normalization of serum potassium. We concluded that cocaine and the hyperkalemia were probably the culprit causes of the Brugada-pattern EKG. Unfortunately, the provided data in this case appear to be incomplete; the patient was found unresponsive at home, and we do not exactly whether or not he developed a cardiac arrest secondary to a malignant arrhythmia before the arrival of the Emergency medical services. This case highlights the importance of recognizing cocaine and hyperkalemia as potentialtriggers of the acquired Brugada-like electrocardiographic pattern.

Brugada-like ECG pattern induced by tricyclic antidepressants

We present the case report of a 57-year-old woman with severe monointoxication with dosulepine (Prothiaden) who developed a Brugada-like electrocardiographic pattern. In tricyclic antidepressants (TCAs) poisoning the Brugada-like pattern on electrocardiogram is a characteristic albeit rare manifestation of the frequently occurring conduction abnormalities in the myocardium and its recognition is imperative as it is associated with a higher degree of morbidity and mortality. An overview of the literature is given and recommendations concerning treatment of TCA-induced arrhythmias are provided. After successful treatment, the electrocardiogram in the patient normalized. However, 4 days after intoxication, the ajmaline test was positive (pharmacological induction of a type I Brugada-like pattern), but a subsequent one, repeated after 11 days, was reportedly normal, probably because of the slow clearance of dosulepine. This raises questions about the specificity of ajmaline testing for Brugada syndrome in patients taking dosulepine and perhaps other TCAs and neuroleptic agents.

Brugada-like Electrocardiographic Pattern Induced by Lamotrigine Toxicity

Brugada syndrome, a recognized cause of sudden cardiac death, is due to a defect of cardiac sodium channels. Many pharmotherapeutic agents induce an electrocardiographic (ECG) pattern that can be confused with Brugada syndrome in patients who may not have the disease. A 22-year-old Hispanic female presented for emergency evaluation with ataxia and alterations in consciousness. Her medical history was significant for temporal lobe epilepsy, treated with lamotrigine, a phenyltriazine agent known to block neuronal voltage-gated sodium channels. There was no family history of sudden cardiac death. Initial laboratory data, neuroimaging, and echocardiography were unremarkable. Her ECG on presentation was concerning for Brugada pattern. Because of the nonspecific ECG finding, the patient underwent procainamide challenge, which was initially felt to be positive. Serum lamotrigine level was subsequently reported in the toxic range at 20.4 μg/mL (therapeutic range, 1-4 μg/mL). Repeated procainamide challenge was performed with lamotrigine levels below the therapeutic range (0.2 μg/mL) and failed to show diagnostic ECG changes. Lamotrigine, at toxic levels, may lose specificity and exert an effect on cardiac sodium channels, a phenomenon that has not been previously described. Given previous reports of associations between the drug-induced Brugada ECG pattern and ventricular dysrhythmias, clinicians should be aware of this potential effect.

Hyperkalemia and cocaine induced dynamic Brugada-type electrocardiogram

Brugada syndrome is a well-defined clinical entity with the typical electrocardiographic changes in the right precordial leads (V1 and V2), attributed to mutation in SCN5A gene. Brugada-like electrocardiographic pattern can be replicated by sodium channel-blocking drugs and electrolyte abnormalities. We describe a 46-year-old individual, who presented with hyperkalemia secondary to muscle damage and renal insufficiency, after abusing cocaine. The electrocardiogram showed Brugada sign. The electrocardiogram changes disappeared after sodium bicarbonate administration and normalization of serum potassium. The case highlights the importance of recognizing cocaine and hyperkalemia, as potential triggers of the acquired Brugada sign.

Brugada-like electrocardiographic pattern and ventricular fibrillation in a patient with primary hyperparathyroidism

There are several causes for ST segment abnormalities in leads V1 to V3. Hypercalcaemia and Brugada syndrome are among them. Both are known to produce ventricular arrhythmia, albeit only rare cases have been reported with documented evidence of ventricular arrhythmias in association with a hypercalcaemic crisis but none when hypercalcaemic coexists with Brugada syndrome. We describe a patient with primary hyperparathyroidism who presented with ventricular fibrillation, and the ECG showed changes similar to Brugada syndrome. The provocation test with flecainide was conducted twice. This was positive, both before and after parathyroidectomy when serum calcium and parathormone levels had normalized. The patient was treated for hypercalcaemia and underwent parathyroidectomy. This is the first report of oral flecainide test unmasking the diagnostic coved Brugada ECG pattern in a patient with primary hyperparathyroidism and raising attention to hypercalcaemia as a potential trigger for life-threatening arrhythmia in Brugada syndrome.

Genetic and biophysical basis for bupivacaine-induced ST segment elevation and VT/VF. Anesthesia unmasked Brugada syndrome

Brugada syndrome is an inherited disease associated with sudden cardiac death. The electrocardiographic pattern associated with Brugada syndrome has been linked to the use of sodium channel blockers, including antiarrhythmics, trycyclics and anesthetics. We report a case of bupivacaine-induced Brugada syndrome, in which we investigated the genetic, biophysical and path physiological mechanism involved. The patient developed a Brugada-like electrocardiographic pattern twice under the influence of bupivacaine. The first occurrence was accompanied by ventricular tachycardia (VT) which subsided after withdrawal of the anesthetic. The VT was also observed during co-administration of diltiazem and isosorbide-5-mononitrate, agents thought to facilitate ST segment elevation in the Brugada syndrome. Genetic analysis revealed a missense mutation in the alpha subunit of the cardiac sodium channel, SCN5A. Biophysical analysis by whole-cell patch-clamping revealed a reduction in sodium current as a result of the mutation. The study of bupivacaine in the wedge model revealed use-dependent changes in conduction, heterogeneous loss of the action potential dome in RV epicardium and phase 2 re-entry when the preparations were pretreated with low concentrations of the calcium channel blocker verapamil. Our findings indicate that bupivacaine may induce the electrocardiographic and arrhythmic manifestations of the Brugada syndrome in silent carriers of SCN5A mutations. The data have important implications in the management of patients who develop ST segment elevation when under the influence of anesthetics such as bupivacaine.

A female case with Brugada-like electrocardiographic pattern unmasked by fever

[in Japanese]

Brugada-like electrocardiographic pattern induced by an episode of anemia

The mechanisms responsible for the undulating pattern of ST-segment elevations in the Brugada syndrome are still a matter of discussion. This report describes a young man with a Brugada-like electrocardiographic pattern. The specific ST-segment elevations were unmasked during an episode of anemia due to a duodenal ulcer.