scholarly journals Unmasking Brugada Syndrome with Oral Flecainide Provocation. A Case Series of Three Patients

Author(s):  
R. Singla ◽  
A. Udyavar ◽  
A. Gupta ◽  
A. Bade ◽  
K. Munde ◽  
...  

The present case series discuss three patients who had brugada type 2/ type 3 like ECG pattern that was converted to type 1 pattern with oral flecanide challenge test. Brugada syndrome is associated with a high incidence of sudden cardiac death,   typical ECG pattern being ST-segment elevation in the right precordial leads with T wave inversion. Pharmacological provocation should only be performed when the baseline ECG is not diagnostic of Brugada Syndrome. PR prolongation in the baseline ECG is also a contraindication because of the risk of inducing AV block. Drug challenge is performed under strict monitoring of BP and 12-lead ECG and facilities for cardio version and resuscitation are available. Atypical RBBB pattern/type 2/3 Brugada pattern on ECG in patients of syncope or family history of sudden cardiac arrest is commonly encountered by a cardiologist. This can be performed to provoke type 1 brugada pattern on ECG. Diagnosed cases of Brugada may be treated with ICD with proper indication if needed and thus prevent sudden cardiac death.

2021 ◽  
Vol 41 (5) ◽  
pp. 15-22
Author(s):  
L. Douglas Smith ◽  
Sarah Gast ◽  
Danielle F. Guy

Background Brugada syndrome is a genetic disorder of cardiac conduction that predisposes patients to spontaneous ventricular arrhythmia and sudden cardiac death. Although Brugada syndrome is one of the most common causes of sudden cardiac death, patients presenting with the syndrome often go misdiagnosed. This error has potentially fatal consequences for patients, who are at risk for sudden cardiac death without appropriate management. Objective To increase the critical care professional’s knowledge of Brugada syndrome through detailed description of the characteristic electrocardiographic findings, an algorithmic approach to electrocardiogram evaluation, and a case report of a patient with a previously missed diagnosis of Brugada syndrome. The essential concepts of epidemiology, pathophysiology, clinical presentation, risk stratification, and management are reviewed for critical care professionals who may encounter patients with the syndrome. Diagnosis Patients typically present with syncope or cardiac arrest and an abnormal electrocardiographic finding of ST-segment elevation in the precordial leads. The diagnosis of Brugada syndrome centers on identification of its electrocardiographic characteristics by critical care professionals who routinely evaluate electrocardiograms. Critical care professionals, especially nurses and advanced practice nurses, should be proficient in recognizing the electrocardiographic appearance of Brugada syndrome and initiating appropriate management. Interventions Management strategies include prevention of sudden cardiac death through lifestyle modification and placement of an implantable cardioverter-defibrillator. Critical care professionals should be aware of commonly used medications that may exacerbate ventricular arrhythmia and place patients at risk for sudden cardiac death. Conclusion Increased awareness of Brugada syndrome among critical care professionals can decrease patient morbidity and mortality.


2019 ◽  
Vol 41 (28) ◽  
pp. 2699-2706 ◽  
Author(s):  
Thomas Hadberg Lynge ◽  
Jesper Svane ◽  
Ulrik Pedersen-Bjergaard ◽  
Gunnar Gislason ◽  
Christian Torp-Pedersen ◽  
...  

Abstract Aims The aim of this study was to compare nationwide incidence rate (IR) of sudden cardiac death (SCD) in persons aged 1–49 years with and without diabetes mellitus (DM). Methods and results The study population consisted of all persons in Denmark aged 1–49 years in 2000–09, which equals 27.1 million person-years. All 14 294 deaths in the 10-year period were included. By using the highly descriptive Danish death certificates, 1698 cases of sudden and unexpected death were identified. Through review of autopsy reports, discharge summaries, and the Danish registries, we identified 1363 cases of SCD. The Danish Register of Medicinal Product Statistics was used to identify persons with type 1 DM and type 2 DM. Among the 14 294 decedents, there were 669 with DM, of which 118 suffered SCD (9% of all SCD), making SCD the leading cause of death among young persons with DM. Among those aged 1–35 years, the IR of SCD-DM was 21.9 per 100 000 person-years compared to 2.6 per 100 000 person-years among persons without DM [IR ratio 8.6, 95% confidence interval (CI) 5.8–28.6]. Within the age range 36–49 years, the IR among persons with DM was 119.8 per 100 000 person-years compared to 19.7 per 100 000 person-years among persons without DM (IR ratio 6.1, 95% CI 4.7–7.8). Conclusion We found that young persons with DM aged 1–35 years had >8-fold higher SCD IR compared to young persons without DM. Our study highlights the need for early cardiovascular risk monitoring and assessment in young persons with DM.


2018 ◽  
Vol 7 (3) ◽  
pp. 199 ◽  
Author(s):  
Serge Sicouri ◽  
Charles Antzelevitch ◽  
◽  
◽  
◽  
...  

A number of antipsychotic and antidepressant drugs are known to increase the risk of ventricular arrhythmias and sudden cardiac death. Based largely on a concern over the development of life-threatening arrhythmias, a number of antipsychotic drugs have been temporarily or permanently withdrawn from the market or their use restricted. While many antidepressants and antipsychotics have been linked to QT prolongation and the development of torsade de pointes arrhythmias, some have been associated with a Brugada syndrome phenotype and the development of polymorphic ventricular arrhythmias. This article examines the arrhythmic liability of antipsychotic and antidepressant drugs capable of inducing long QT and/or Brugada syndrome phenotypes. The goal of this article is to provide an update on the ionic and cellular mechanisms thought to be involved in, and the genetic and environmental factors that predispose to, the development of cardiac arrhythmias and sudden cardiac death among patients taking antidepressant and antipsychotic drugs that are in clinical use.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Michael Papadakis ◽  
Carey Edwards ◽  
John C Rawlins ◽  
Sanjay Sharma

Risk stratification for sudden death in Brugada syndrome and hence indications for implantation of an internal cardioverter defibrillator are based on the presence of a spontaneous type 1 electrocardiogram (ECG) pattern, in association with unheralded syncope or documented polymorphic ventricular tachycardia. Increasingly, awareness of sudden death in the young and implementation of pre-participation screening programs in sport will identify young, asymptomatic patients with the Brugada phenotype. We evaluated the predictive accuracy of symptoms, particularly unheralded syncope in victims of sudden death from Brugada syndrome. Over the past 3 years we identified 22 victims of sudden cardiac death secondary to Brugada syndrome. The diagnosis was based on sudden death with normal findings at post mortem and the identification of the type 1 Brugada ECG pattern in first-degree relatives (spontaneous or following ajmaline provocation test). All relatives underwent 12-lead ECG, echocardiography, exercise testing, 24-hour Holter monitor and biochemical tests. Cardiac magnetic resonance imaging and coronary angiography were performed when appropriate. Of the victims dying from Brugada syndrome, 15 (68%) were male. The mean age of sudden death was 30 years (range 8 –56 years) and 95% died suddenly at rest or during sleep. We interviewed first-degree relatives and partners regarding prodromal symptoms or a history of epilepsy. Only 3 out of 22 victims (14%) had significant symptoms. Specifically, 2 individuals experienced unheralded syncope and 1 suffered nocturnal seizures. Only 14% had a family history of premature sudden cardiac death. Indeed we obtained 12-lead ECGs in 3 victims taken less than 6 months prior to sudden death, which failed to reveal the typical Brugada ECG phenotype. Our results indicate that the vast majority of individuals who die from Brugada syndrome in the UK are asymptomatic and raise concerns that the absence of symptoms does not necessarily mean low risk. Better understanding of the disorder and risk stratification protocols is necessary to permit genuine reassurance in asymptomatic individuals exhibiting the Brugada phenotype.


Author(s):  
Maria Cristina Pasqualetto ◽  
Andrea Corrado ◽  
Eleonora Secco ◽  
Fabio Graceffa ◽  
Fausto Rigo

Patients with COVID-19 pneumonia can develop heart problems and may also may be susceptible to proarrhythmia, virus-related issues such as fever, stress, electrolyte disturbance and adverse effects from the use of antiviral drugs. We report a transient Brugada-like ECG pattern without ongoing fever in a 57-year-old man, admitted with a diagnosis of COVID-19 pneumonia, who did not have syncope or a family history of sudden cardiac death.


Author(s):  
Guangchen Zou ◽  
Mukul Khanna ◽  
Saliha Zahid ◽  
Samir Dengle ◽  
Bhavna Matta ◽  
...  

Abstract Background Pharmacologic challenge test is often used to diagnose Brugada syndrome (BrS) when spontaneous ECGs do not show type I Brugada pattern but reported sensitivity varies. The role of exercise stress test in diagnosing Brugada syndrome is not well-established. Case Summary A patient had a type I Brugada pattern ECG during the recovery phase of exercise stress test but had a negative procainamide challenge test. He had a loop recorder implanted and later survived a ventricular fibrillation (VF) arrest provoked by COVID-19. ECG on arrival showed type 1 Brugada pattern. He was discharged after implantable cardioverter-defibrillator (ICD) implantation. He later underwent genetic testing and was found to be heterozygous for c.844C>G (p.Arg282Gly) mutation in the SCN5A gene. Discussion Type 1 Brugada pattern ECG may be unmasked by ST segment augmentation during recovery from exercise. Exercise stress test may play a role in diagnosis of Brugada syndrome when suspicion for Brugada syndrome remains after a negative procainamide challenge test or if the patient has exercise related symptoms. COVID-19 can unmask BrS and trigger a VF cardiac arrest.


2005 ◽  
Vol 33 (2) ◽  
pp. 266-270 ◽  
Author(s):  
B. Bigwood ◽  
D. Galler ◽  
N. Amir ◽  
W. Smith

The Brugada syndrome, a pro-arrhythmogenic repolarization abnormality, is becoming increasingly recognised as a cause of collapse and sudden cardiac death3. We report a case of a 48-year-old man with a tricyclic overdose and a delayed presentation of the Brugada pattern in the ICU. This case raises the need for clinicians to be aware of the Brugada pattern and those patients potentially at risk.


Author(s):  
Monterrubio-Villar Jesús ◽  
Llinares-Moya David

Brugada phenocopies (BrP) are clinical entities that present with an ECG pattern identical to either the type 1 or type 2 Brugada pattern without true congenital Brugada syndrome. This ECG pattern is associated with an identifiable condition and normalizes upon resolution or treatment of the underlying cause. We present a case of a 54-year-old man with extreme metabolic acidosis, hyperkalaemia and a Brugada type 1 ECG pattern in the setting of a suicidal methanol (MeOH) poisoning. Upon correction of these metabolic derangements with bicarbonate infusions and continuous veno-venous haemodiafiltration (CVVH), the Brugada type 1 ECG pattern normalized. Unfortunately, the patient developed signs of cerebral herniation followed by brain death and died on the first day of ICU admission.


2007 ◽  
Vol 30 (4) ◽  
pp. 50
Author(s):  
M. A. Nault ◽  
A. Baranchuk ◽  
C. S. Simpson ◽  
D. P. Redfearn ◽  
H. Abdollah

Sudden cardiac death (SCD) in healthy young men was first recognized in 1917. Combined with an electrocardiographic (ECG) abnormality reported in 1953, the resulting syndrome would by 1996 eventually be recognized worldwide as Brugada Syndrome (BrS). There is evidence that “labeling” (i.e. the process of naming a disease state or ascribing a diagnosis) alters perceptions, awareness and behaviours in medicine. Our objective was to determine whether naming a cluster of signs and symptoms as a specific syndrome raised attention given to a previously recognized though poorly defined condition as evidenced through an increase in publications. We hypothesized that naming BrS resulted in such a “labeling” stimulus. A systematic review of the Pubmed database of indexed journals was performed to identify references to BrS between 1950 and 2006. Search terms were: “Brugada Syndrome”; “Sudden Cardiac Death AND Right Bundle Branch Block”; “Bangungot” (Filipino); “Bangungut” (Filipino); “Pok kuri” (Japanese); “Lai tai” (Thai); “Sudden Unexplained Death Syndrome”; and “SUNDS”. Publications identified after 1996 by search strategies other than “Brugada Syndrome” were omitted to avoid double counting. The search resulted in 1,042 citations. Of these, 208 occurred after 1996 and were omitted, leaving a total of 834 citations to be analyzed. Between 1950 and 1993 a total of 32 publications met the above search criteria. Thereafter, publication rate on this topic increased exponentially from 16 articles in 1994-1995 to 290 in 2005-2006. Though numerous articles recognized either RBBB-like ECG pattern, ST segment elevation or SCD in otherwise healthy young men, it was not until publication of the 1992 Brugada and Brugada paper that the coexistence of these two conditions was recognized as a syndrome. Rising interest, as identified by publication frequency, preceded the naming of this syndrome by 4 years. This finding suggests that factors other than labeling have also contributed to the publication history of BrS. Osher H, Wolff L. Electrocardiographic pattern simulating acute myocardial injury. Am J Med Sci 1953; 226:541-5. Brugada P, Brugada J. Right bundle branch block, persisting ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992; 20:1391-6. Yan G-X, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996; 93:372-9.


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