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

Heart Rhythm ◽  
2006 ◽  
Vol 3 (9) ◽  
pp. 1074-1078 ◽  
Author(s):  
Kevin Vernooy ◽  
Serge Sicouri ◽  
Robert Dumaine ◽  
Kui Hong ◽  
Antonio Oliva ◽  
...  
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.


2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Jagadeesh K. Kalavakunta ◽  
Vishwaroop Bantu ◽  
Hemasri Tokala ◽  
Mihas Kodenchery

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads.Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias.Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.


2020 ◽  
Vol 132 (3) ◽  
pp. 440-451 ◽  
Author(s):  
Panagiotis Flamée ◽  
Varnavas Varnavas ◽  
Wendy Dewals ◽  
Hugo Carvalho ◽  
Wilfried Cools ◽  
...  

Abstract Background Brugada Syndrome is an inherited arrhythmogenic disease, characterized by the typical coved type ST-segment elevation in the right precordial leads from V1 through V3. The BrugadaDrugs.org Advisory Board recommends avoiding administration of propofol in patients with Brugada Syndrome. Since prospective studies are lacking, it was the purpose of this study to assess the electrocardiographic effects of propofol and etomidate on the ST- and QRS-segments. In this trial, it was hypothesized that administration of propofol or etomidate in bolus for induction of anesthesia, in patients with Brugada Syndrome, do not clinically affect the ST- and QRS-segments and do not induce arrhythmias. Methods In this prospective, double-blinded trial, 98 patients with established Brugada syndrome were randomized to receive propofol (2 to 3 mg/kg-1) or etomidate (0.2 to 0.3 mg/kg-1) for induction of anesthesia. The primary endpoints were the changes of the ST- and QRS-segment, and the occurrence of new arrhythmias upon induction of anesthesia. Results The analysis included 80 patients: 43 were administered propofol and 37 etomidate. None of the patients had a ST elevation greater than or equal to 0.2 mV, one in each group had a ST elevation of 0.15 mV. An ST depression up to −0.15mV was observed eleven times with propofol and five with etomidate. A QRS-prolongation of 25% upon induction was seen in one patient with propofol and three with etomidate. This trial failed to establish any evidence to suggest that changes in either group differed, with most percentiles being zero (median [25th, 75th], 0 [0, 0] vs. 0 [0, 0]). Finally, no new arrhythmias occurred perioperatively in both groups. Conclusions In this trial, there does not appear to be a significant difference in electrocardiographic changes in patients with Brugada syndrome when propofol versus etomidate were administered for induction of anesthesia. This study did not investigate electrocardiographic changes related to propofol used as an infusion for maintenance of anesthesia, so future studies would be warranted before conclusions about safety of propofol infusions in patients with Brugada syndrome can be determined. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New


2011 ◽  
Vol 27 (Supplement) ◽  
pp. JAAC_3 ◽  
Author(s):  
Hisaki Makimoto ◽  
Eiichiro Nakagawa ◽  
Hiroshi Takaki ◽  
Yuko Yamada ◽  
Hideo Okamura ◽  
...  

2019 ◽  
Vol 20 (9) ◽  
pp. 2123 ◽  
Author(s):  
Sendfeld ◽  
Selga ◽  
Scornik ◽  
Pérez ◽  
Mills ◽  
...  

Brugada syndrome is an inherited, rare cardiac arrhythmogenic disease, associated with sudden cardiac death. It accounts for up to 20% of sudden deaths in patients without structural cardiac abnormalities. The majority of mutations involve the cardiac sodium channel gene SCN5A and give rise to classical abnormal electrocardiogram with ST segment elevation in the right precordial leads V1 to V3 and a predisposition to ventricular fibrillation. The pathophysiological mechanisms of Brugada syndrome have been investigated using model systems including transgenic mice, canine heart preparations, and expression systems to study different SCN5A mutations. These models have a number of limitations. The recent development of pluripotent stem cell technology creates an opportunity to study cardiomyocytes derived from patients and healthy individuals. To date, only a few studies have been done using Brugada syndrome patient-specific iPS-CM, which have provided novel insights into the mechanisms and pathophysiology of Brugada syndrome. This review provides an evaluation of the strengths and limitations of each of these model systems and summarizes the key mechanisms that have been identified to date.


Circulation ◽  
2005 ◽  
Vol 111 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Lars Eckardt ◽  
Vincent Probst ◽  
Jeroen P.P. Smits ◽  
Eric Schulze Bahr ◽  
Christian Wolpert ◽  
...  

2019 ◽  
Vol 58 (21) ◽  
pp. 3099-3102
Author(s):  
Akihito Ideishi ◽  
Masahiro Ogawa ◽  
Yoshihisa Nagata ◽  
Yoshiaki Idemoto ◽  
Tomo Komaki ◽  
...  

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