Brugada-like Pattern Research Articles

Role of telemedicine network provided by pharmacies to detect electrocardiographic changes deserving cardiological evaluation in young patients

Abstract Background cardiac arrhythmias affecting adolescents and young subjects are a wide-ranging problem. Often-such conditions, in addition to being highly varied and sometimes hard to diagnose, are largely silent and onset variably and suddenly, sometimes resulting in sudden cardiac death. Such individuals, being asymptomatics, usually do not undergo cardiological evaluation, as their condition may be misrecognized or not suspected until it manifests clinically. Thus, there is a need to develop cheap and easily accessible screening systems for patients that allow early identification of electrocardiographic (EKG) findings deserving evaluation by the cardiologist. Recently, pharmacies have proposed EKG screening programs for cardiac arrhythmias using a telematics network, enabling referral to the cardiology specialist and identification of patients worthy of further diagnostic investigations. Aim of the Study to assess validity, feasibility and usefulness of an electrocardiographic screening program for the prevention of cardiac sudden death in subjects < 18 years old with the support of a telemedicine service available in local pharmacies. Materials and Method we analyzed 12-lead electrocardiograms (ECGs) recorded by 4,500 country pharmacies in subjects with < 18 years old, evaluated and stored in one telemedicine platform provided by Health Telematic Network (HTN), in cooperation with a cardiology department hospital and a university. Results from April 2010 to January 2023, 266.381 subjects with < 18 years old underwent electrocardiographic examination in territorial pharmacies. Of them, 142.924 (53.65%) were men. In 440 subjects (0.16%) a first or a second-degree atrio-ventricular block were found. Moreover, in 94 (0.03%) of them a delta-wave in QRS complex was found, suggesting the presence of a Wolff-Parkinson-White syndrome. In 59 (0.022%), a ST segment with Brugada-like pattern was identified, whereas in 118 (0.04%) a long QT was detected. All subjects in which an electrocardiographic alteration was found were referred to outpatient cardiological visit for further diagnostic evaluations. Conclusion These data suggest the potential validity, feasibility and usefulness of an electrocardiographic screening program for the prevention of cardiac sudden death in subjects < 18 years old performed in territorial pharmacies. This could be a valuable strategy to noninvasively and easily identify those subjects who need further diagnostic investigations and to rule out conditions that, especially in a young and otherwise healthy population, could manifest dramatically and suddenly, often without the possibility of intervention.

Abstract 15641: Fever. The True Unmasker of My Disease

Introduction: The most common etiology of sudden cardiac death (SCD) from ventricular tachyarrhythmias (VTA) is an acute ischemic event from coronary artery disease (CAD; followed by genetic syndromes, including Brugada Syndrome (BS). The presentation of SCD with an ECG showing RBBB pattern with ST segment elevation (STSE) in leads V1-V3 in healthy patients and in the absence electrolyte imbalances, CAD, or structural heart disease is known as BS. It can be triggered by abundant meals, excessive alcohol intake, cocaine, local anesthetics, tricyclic antidepressants, lithium, propofol and fevers. Case Presentation: 29 y/o woman presenting with atypical chest pain, malaise, and a remote history of a syncopal episode. She denied family history of SCD. She was febrile to 100.4 o F, tachycardic, with regular heart sounds and no murmurs. Laboratory work up was normal. ECG from two years ago showed nonspecific interventricular conduction delay. ECG on admission showed STSE in anterior precordial leads which disappeared with resolution of her fever. Due to the Brugada-like pattern in her ECG and remote history of syncope, AICD placement was recommended. Flecainide challenge was not pursued, since the patient was amenable to AICD. Genetic counseling and testing were provided to her family members. Discussion: Most patients with BS are healthy adults between 30-40 y/o without significant medical history. A defect in the sodium channel SCN5A, results in a loss of homogeneity in the myocardial action potential. This mutant channel may be exaggerated when exposed to supraphysiologic temperatures, unmasking BS and elevating the risk of VTA and SCD. BS is carried through generations in an autosomal dominant fashion. Medical management alone is ineffective and not recommended. AICD is the only effective treatment for prevention of SCD. Conclusion: BS is an identifiable and preventable cause of death. In patients presenting with multiple syncopal episodes or aborted VTA’s, in the absence of significant cardiovascular history, and with known or equivocal family history of SCD, the diagnosis of BS must be considered. Health providers across all practice settings should have the skill of identifying its clinical and ECG presentation in order to decrease the rate of SCD.

Brugada-like electrocardiogram pattern in a young man taking a proton-pump inhibitor

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.

Brugada phenocopy induced by consumption of yellow oleander seeds – A case report

Brugada phenocopy is a brugada-like pattern in ECG seen in some diseases without an inherited channelopathy. The causes of brugada phenocopy are usually reversible. Once the reversible condition resolves, the ECG pattern disappears. There are many conditions that cause brugada phenocopy like myocardial infarction, hyperkalemia etc. Here we report a case of brugada phenocopy induced by consumption of yellow oleander seeds (T. Peruviana).

Transient Brugada-Like Electrocardiographic Pattern in a Patient With COVID-19

A 61-year-old man presented with fever, shortness of breath, and new chest pain. An electrocardiogram (ECG) revealed Brugada-like ECG pattern. Emergent coronary angiography demonstrated normal coronary arteries. He was subsequently diagnosed with COVID-19. After a few days he felt better and the ECG Brugada-like pattern resolved.

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.

Bupivacaine Toxicity Increases Transmural Dispersion of Repolarization, Developing of a Brugada-like Pattern and Ventricular Arrhythmias, Which is Reversed by Lipid Emulsion Administration. Study in an Experimental Porcine Model.

Unintentional administration of bupivacaine may be associated with electrocardiogram changes that promote the development cardiac arrhythmias. Ventricular repolarization markers (corrected QT, QT dispersion, Tpeak-Tend and Tpeak-Tend dispersion) are useful to predict cardiac arrhythmias. We aim to investigate the effects of bupivacaine on the transmural dispersion of repolarization and their reversion following intravenous lipid emulsion (ILE) administration. Fourteen pigs were anaesthetized with thiopental and sevoflurane and underwent tracheal intubation. After instrumentation, a 4mgkg-bolus of bupivacaine was administrated followed by an infusion of 100µgkg-1min-1. QT interval, QTc:QT corrected by heart rate, Tpeak-to-Tend interval and QT and Tpeak-to-Tend dispersion were determined in a sequential fashion: after bupivacaine (at 1min, 5min and 10min) and after ILE (1.5mLkg-1 over 1min followed by an infusion of 0.25mLkg-1min-1). Three additional animals received only ILE (control group). Bupivacaine significantly prolonged QT interval (∆:36%), QT dispersion (∆:68%), Tpeak-to-Tend (∆:163%) and Tpeak-to-Tend dispersion (∆:98%), from baseline to 10min. Dispersion of repolarization was related to lethal arrhythmias [three events, including asystole, sustained ventricular tachycardia (VT)] and repeated non-sustained VT (4/14, 28%). A Brugada-like-ECG pattern was visualized at V1-4 leads in 5/14 pigs (35%). ILE significantly decreased the alterations induced by bupivacaine, with the termination of VT within 10min. No ECG changes were observed in control group. Bupivacaine toxicity is associated with an increase of transmural dispersion of repolarization, the occurrence of a Brugada-like pattern and malignant VA. ILE reverses the changes in dispersion of repolarization, favouring the disappearance of the Brugada-like pattern and VT.

OC06_07 Prevalence, Treatment, and Control of Hypertension and/or Dyslipidemia in Korean Adults: Results From the Multinational Pan-Asia Dyslipidemia and Hypertension Diagnosis and Treatment Gap Assessment Study (PANDA)

Introduction: ECG in pre-participation screening in athletes is still debated. It is of relevant interest to have an automatic detection for this screening. 44’000 person a year are undergoing the screening at the age of 19 in Switzerland during Swiss Army conscription. Objectives: We hypothesize that is possible to perform automatic detection using the Seattle Criteria published for athlete screening based on a 10s 12-lead resting ECG. Methods: We performed a retrospective analysis of 274’468 digital standard 12-lead resting ECGs from military conscription acquired between 2008 and 2013. The Seattle Criteria were directly integrated into an automatic resting ECG measurement and interpretation software (ETM, SCHILLER AG) without any modification. Verification of proper implementation of the algorithm was done on the same dataset by visually and manually checking a randomly selected subset of abnormal (true positives) and normal ECGs (true negatives). The percentage of detection of any subtype as well as of the general finding ‘normal/abnormal ECG’ was calculated. Results: We found that the categories ‘Q-wave pathologies’, ‘ST-segment depressions’ and ‘Left axis deviations’ have a detection rate higher than 1%. All other Seattle Criteria detection rates were lower. ‘Brugada-like pattern’ and ‘Profound sinus bradycardia’ were not detected. The overall detection rate of 6.5% of abnormal ECGs is comparable to the found value of 4.5% (2) among elite athletes (false positive rate of 4.2%). Conclusion: It is possible to perform automatic detection abnormal ECG using the published Seattle Criteria. The 6.47% abnormal ECGs correspond to 2’850 male individuals per year which would warrant a more profound clinical, and/or electrophysiological and genetic investigation to confirm or exclude the presence of an acquired or familial cardiac disease. Disclosure of Interest: R. Abacherli Employee from: SCHILLER AG, Switzerland, R. Schmid Employee from: SCHILLER AG, Switzerland, K. Richard: None Declared, F. Frey: None Declared, J. Schmid: None Declared

All that looks like “Brugada” is not “Brugada”: Case series of Brugada phenocopy caused by hyponatremia

Brugada syndrome (BS), a life-threatening channelopathy associated with reduced inward sodium current due to dysfunctional sodium channels, is characterized by ST-segment elevation with downsloping “coved type” (type 1) or “saddle back” (type 2) pattern in V1–V3 precordial chest leads (1, 2). Brugada phenocopy, a term describing conditions inducing Brugada-like pattern of electrocardiogram (EKG) manifestations in patients without true BS, is an emerging condition (3). We describe a case series of Brugada phenocopy with hyponatremia.

Giant J-wave and Brugada-like pattern in a patient with severe hypothermia

We describe a patient with severe hypothermia, in whom the electrocardiogram showed giant J-waves, also known as Osborn waves, distinguishable in the inferior and anterolateral leads. Moreover, a Brugada-like pattern was also visible in leads V2 and V3. The presented case and ECG findings may contribute to the discussion about the pathophysiologic mechanism underlying Brugada syndrome and giant J-wave.

Type-1 Brugada-like ECG pattern induced by adrenal crisis

Type-1 Brugada-like ECG pattern induced by adrenal crisis

Catastrophic neurologic syndrome with dramatic ECG changes

Cerebrogenic ECG abnormalities, especially prominent T wave inversions and prolongation of the QT(U) interval, are well-described. Brady- and tachyarrhythmias, including polymorphic VT, have been also described in the setting of neurologic injury. We report an unusual case of a 22-year-old man who presented with idiopathic acute encephalopathy. His hospital course was complicated by persistent fevers, along with refractory seizures treated with propofol. Serial ECG findings included marked ventricular repolarization prolongation with bursts of torsade de pointes, diffuse ST elevations simulating extensive myocardial ischemia or infarction, as well as a Brugada-like pattern. To our knowledge, this case is the first reported with the combination of such findings in a patient with a catastrophic neurologic syndrome.

Propofol Infusion Syndrome: A Case Report

Propofol is an ultra-short acting intravenous sedative/hypnotic agent commonly used for sedation in the intensive care unit (ICU) and operating room (OR). Up until recently, no severe systemic side effects were apparent but more recently severe and potentially lethal side effects have been sporadically reported and termed propofol-infusion syndrome (PRIS). Herein we describe a case of a 23 year s old previously healthy male admitted to the ICU secondary to trauma. Due to excessive agitation and failure of other agents, he was sedated on high dose propofol ( > 100 µ g/Kg/min) for several days. Following this he developed rhabdomyolysis, worsening renal failure, hyperkalemia, refractory acidosis, and eventually expired secondary to cardiovascular collapse. PRIS was attributed as the cause of death. Since its introduction in the 1980s propofol has been widely used for sedation in the ICU. PRIS has become an increasingly recognized phenomenon where propofol infusions have been used for prolonged periods of time. It is characterized by progressive rhabdomyolysis, renal failure, hyperkalemia, metabolic acidosis, Brugada-like pattern changes on ECG, cardiovascular collapse and finally death, all characteristics present in our patient. Several important risk factors for this condition exist such as prolonged propofol infusion, young age, head trauma, airway infection, increased catecholamine and glucocorticoid levels and malnutrition. The mechanism of PRIS remains incompletely understood but it is thought to be due to mitochondrial dysfunction with propofol serving to uncouple the respiratory chain; as such treatment involves stopping the medication and supportive care. In the vast majority of patients, propofol is safe with few side effects but given its potential for lethal complications heightened vigilance is required for its continued use. In particular, to minimize the potential for the development of PRIS, dose limitations and daily re-evaluation as to the necessity of its continued use are required. Further, PRIS must be considered when patients develop unexplained organ dysfunction with metabolic acidosis, increased creatinine phosphokinase and hemodynamic instability. Awareness of the early clinical manifestations of PRIS leading to prompt termination of propofol infusion and appropriate supportive care may improve its outcome if it does develop. doi: http://dx.doi.org/10.4021/jmc1269w

First clinical manifestation of Brugada syndrome during pregnancy

The role of hormonal changes during pregnancy in Brugada syndrome is unknown. Only rare case reports of Brugada syndrome during pregnancy have been published. In this article, we describe a patient with first clinical manifestation of Brugada syndrome during pregnancy. The definitive diagnosis could only be achieved by drug challenge with ajmaline after childbirth because the spontaneous typical Brugada-like pattern was absent. Elevated hormone levels during pregnancy may increase the risk for arrhythmias in particular cases.

Rhabdomyoma of the interventricular septum presenting as a Brugada phenocopy

Brugada syndrome is a channelopathy characterised electrocardiographically by distinctive coved ST-segment elevation in the right precordial leads and is associated with a predisposition for sudden death secondary to ventricular arrhythmias in otherwise healthy patients. Previously known as Brugada-like patterns, Brugada phenocopies include agents and conditions that mimic true Brugada syndrome, presenting with an acquired Brugada Type-1 ECG pattern. We describe the first reported case of a 17-month-old female with an asymptomatic rhabdomyoma of the interventricular septum that presented as a Brugada phenocopy.

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.

Dysrhythmias associated with cocaine overdose

Dysrhythmias associated with cocaine overdose

205 ST segment changes after external cardioversion using direct current shock: incidence, characteristics and predeictive factors

DC shock is commonly used for external cardioversion of cardiac arrhythmias. Incidence, characteristics and predictive factors of transient ST-segment changes after DC shock are poorly known. 91 consecutive pts referred for external cardioversion of atrial fibrillation (AFib) (61 men, 69 ± 10 yo) were prospectively included. Duration and amplitude of ST elevation or depression were quantified on12 lead-ECG immediately after the first DC shock. Correlations with DC shock characteristics clinical variables, underlying heart disease, echocardiographic parameters, biological parameters, medications, anesthesic drugs as well with morphological features were made. 18 and 20 pts underwent 200 J or 300 J monophasic and 53 pts 200 J biphasic DC shocks. Immediate success rate was 95%.We found an incidence of 48% for ST segment changes: 35% for ST elevation (0,81 ± 0,44 mV) and 13% for ST depression (0,2 ± 0,07 mV, p<0,0001). ST changes were essentially seen in the right precordial leads. Major ST elevation was observed in 27% which could sometimes display Brugada-like pattern. ST changes durations were similar for ST elevation and ST depression (60 ± 43 vs 50 ± 26 sec, p=ns) and were correlated to the amplitude of ST changes. ST changes did not induce significant cardiac events or alter immediate or late AFib recurrences. ST changes were not related to energy but ST elevation was significantly more often induced by monophasic (76% vs 6%, p<0,0001) and ST depression by biphasic DC shocks (26% vs 3%, p=0,01). Using multivariate analysis, independent predictors for ST elevation were the use of monophasic DC shocks, use of propofol and increased CRP, while a low ejection fraction and use of biphasic DC hocks were independent predictors of ST depression. ST segment changes after external cardioversion with DC shock are common, short living and do not seem to carry clinical significance. They are related to the monophasic or biphasic configuration of DC shock, to the use of propofol, to the ejection fraction and to an increased CRP. Direct membrane injury by electroporation is suspected.

Brugada-like electrocardiogram pattern: how to stratify the risk for sudden cardiac death. Is sports activity contraindicated?

Brugada syndrome is associated with a considerable risk of sudden death in young and otherwise healthy adults. The syndrome is estimated to be responsible for at least 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts. The diagnosis of Brugada syndrome is based on peculiar electrocardiogram (ECG) abnormalities classified by the European Society of Cardiology in three types: type 1 (coved-type) is the diagnostic pattern; type 2 (saddle-back type); and type 3 are considered significant if there is a conversion to a type 1, spontaneously or during administration of class I A/C anti-arrhythmic drugs (flecainide, etc.). There is a general agreement about the high risk of sudden death in patients with previous cardiac arrest, for whom an implantable defibrillator (ICD) is recommended. In contrast, controversy exists on the correct clinical behaviour in individuals without a history of previous cardiac arrest. To stratify the risk in patients with type 1 pattern, three major factors have been suggested: typical ECG pattern in the basal state; a history of syncope; and inducible ventricular tachycardia/ventricular fibrillation during electrophysiological study (EPS). However, the indication and usefulness of an EPS is debatable. In patients with a type 2 or 3 pattern a pharmacological test is indicated in the presence of symptoms or of a familial history. With regard to sports eligibility, patients with a history of cardiac arrest should have an ICD and they can practise (low intensity) sport only after the implant of the device. Patients without documented cardiac arrest but at high risk (basal type 1 ECG pattern, syncope and/or positive EPS) should also have an ICD and they can practise (low intensity) sport only after the implant of the device. In patients at low risk (type 1 ECG pattern in the absence of symptoms, without family history and negative EPS) the behaviour regarding sport eligibility is not a matter of debate. In cases with type 2 or 3 pattern, in the absence of familial history and symptoms, a permissive behaviour should be assumed.

Brugada‐like ECG abnormalities during thioridazine overdose

A previously healthy 58-year-old woman was comatose when admitted to our emergency department. Physical evaluation showed muscular rigidity, opisthotonus, external-rotation of upper limbs in response to painful stimulation and neck stiffness. Arterial blood pressure (120/80 mmHg) and temperature (36.5 °C) were unremarkable. The ECG showed sinus rhythm with significant QT lengthening (Figure 1A). A CT scan of the brain and evaluation of spinal fluid were normal. The patient was intubated and mechanically ventilated. Figure 1 (A) Sinus rhythm with significant QT lengthening; (B) Brugada-like pattern; (C) Normal ECG A few hours after admission, we learnt that the patient's husband was being treated with haloperidol and risperidone. The ECG recorded the day after evolved into a Brugada-like pattern (Figure 1B). Over the next 72 h, both the ECG and the clinical abnormalities resolved (Figure 1C), and she was extubated on day 3. She denied deliberate ingestion of psychoactive drugs. Later we learned that the patient's husband was also receiving thioridazine. Thioridazine, measured by HPLC-UV and FL, in a blood sample drawn from the patient on day 4 was 1.48 µg ml−1 (therapeutic levels for our laboratory are up to 2 µg dl−1). No haloperidol or risperidone was detectable in the same sample. In the literature there are several reports of Brugada-like ECG abnormalities during tryciclic antidepressant intoxication [1, 2], but such abnormalities have not been reported during neuroleptic overdose.