scholarly journals Electrocardiographic Effects of Propofol versus Etomidate in Patients with Brugada Syndrome

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

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.


2019 ◽  
Vol 6 (7) ◽  
pp. 2598
Author(s):  
C. P. Karunadas ◽  
Cibu Mathew

Electrocardiography (ECG) patterns of ST-segment elevation in lead aVR with or without diffuse ST segment depression may predict either left main coronary artery or triple vessel stenosis. Here, we have presented the case of a 56-year-old female involving such an ECG pattern with ST-segment depression in more than eight leads and ST Segment elevation in lead aVR, however, showing stenosis of the mid-segment of the left circumflex artery (LCX). She was scheduled to undergo percutaneous coronary intervention with implantation of a drug-eluting stent with respect to mid LCX stenosis. The patient was asymptomatic post procedure and was discharged on beta blockers. To conclude, the ECG pattern of ST depression in multiple leads with ST-elevation in aVR lead can occur in LCX obstruction as well. 


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.


2019 ◽  
Vol 9 (8) ◽  
pp. 827-835 ◽  
Author(s):  
Rami Abu Fanne ◽  
Michael Kleiner Shochat ◽  
Avraham Shotan ◽  
Aharon Frimerman ◽  
Emad Maraga ◽  
...  

Background: Previous studies, published before the advent of primary reperfusion, described the electrocardiographic features of ST-segment elevation myocardial infarction (STEMI) caused by total diagonal artery occlusion, as demonstrated at pre-discharge coronary angiography. We aimed to assess the electrocardiographic and echocardiographic features in STEMI unequivocally attributed to a diagonal lesion in the era of primary coronary intervention. Methods: The electrocardiograms and echocardiograms of patients sustaining STEMI caused by diagonal artery involvement were compared with those of patients with STEMI attributed to proximal or mid left anterior descending artery (LAD) lesions. ST-segment deviations were measured at four different points in each lead and analyzed against TIMI flow and SNuH score. The electrocardiographic and echocardiographic features of each group were mapped. Results: In contrast to previous studies claiming an ever-present incidence of at least 1-mm ST-segment elevation in leads I and aVL with diagonal STEMI, we report 86% of any ST-elevation in leads I, aVL and V2 (64–71% for ST-elevation >1 mm). Both higher SNuH score and pre-intervention TIMI flow were associated with larger lateral ST-elevations (85.7% and 86.4–95.5%, respectively). Higher prevalence of ST-depression in the inferior leads reflecting reciprocal changes was observed in patients with diagonal-induced STEMI (57–76% vs. 24–51% in LAD obstructions, p <0.05). Conclusion: The most sensitive and predictive sign for acute ischemia was any degree of ST-deviation measured 1 mm beyond the J point. ST-elevations in I, aVL and V2, sparing V3-V5, strongly favor isolated diagonal lesion. Proximal LAD lesion lacking ST-segment elevations in leads I and aVL is primarily due to wraparound LAD anatomy.


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

2009 ◽  
Vol 2009 ◽  
pp. 1-3 ◽  
Author(s):  
John N. Makaryus ◽  
Jennifer Verbsky ◽  
Scott Schwarz ◽  
David Slotwiner

Since it was first described approximately 15 years ago, the Brugada Syndrome has spurred a significant quantity of interest in its underlying mechanism and physiology. The Brugada electrocardiographic pattern is characterized by right bundle branch block morphology and ST segment elevations in the right precordial leads with an absence of identifiable underlying structural heart disease. The syndrome is clinically significant since these patients are at a higher risk of developing malignant ventricular arrhythmias. One of the mechanisms behind the disorder involves mutations in specific myocardial sodium channels. Furthermore, these electrocardiographic changes appear to be temperature dependent. We present the case of a 35-year-old male who presented with intestinal Shigellosis and was also found to have Brugada-type electrocardiographic changes on ECG. The electrocardiographic changes that were present when the patient was admitted and febrile resolved following antibiotic therapy and defervescence.


2020 ◽  
Vol 23 (10) ◽  
pp. 704-706
Author(s):  
Tufan Çınar ◽  
Yavuz Karabağ ◽  
İbrahim Rencuzogullari ◽  
Metin Cağdaş

Coronary artery fistulas (CAFs) are described as abnormal communications between a coronary artery and cardiac chambers, or other vascular structures. The two types of CAFs are defined as type I (singular fistula) and type II (microfistulas). Even though various electrocardiographic changes have been previously described in CAF patients, coronary-artery microfistulas causing ST-segment elevation in diverse locations have not been reported. We describe a case report of an adult patient who presented with acute inferior myocardial infarction due to coronary-artery microfistulas. During the hospital stay, the patient re-experienced chest pain, and control electrocardiography revealed ST-segment elevation in the I and AVL leads along with reciprocal ST-segment depression in the inferior precordial leads. Although CAFs are clinically rare, they can have important clinical consequences. Microfistulas should be kept in mind as a cause of ST elevation myocardial infarction in some patients.


2012 ◽  
Vol 140 (1-2) ◽  
pp. 84-90
Author(s):  
Vesna Bisenic ◽  
Sasa Hinic ◽  
Mirjana Krotin ◽  
Branislav Milovanovic ◽  
Jelena Saric ◽  
...  

Introduction. Brugada syndrome is an arrhythmogenic disease characterized by coved ST segment elevation and J point elevation of at least 2 mm in at least two of the right precordial ECG leads (V1-3) and ventricular arrhythmias, syncope, and sudden death. Risk stratifications of patients with Brugada electrocardiogram are being strongly debated. Case Outline. A 23-year-old man was admitted to the Coronary Care Unit of the Clinical Centre ?Bezanijska kosa? due to weakness, fatigue and chest discomfort. The patient suffered from fainting and palpitations. There was a family history of paternal sudden death at 36 years. Electrocardiogram showed a coved ST segment elevation of 4 mm in leads V1 and V2, recognised as spontaneous type 1 Brugada pattern. Laboratory investigations revealed normal serum cardiac troponin T and serum potassium, and absence of inflammation signs. Echocardiographic finding was normal, except for a mild enlargement of the right atrium and ventricle. The diagnosis of Brugada syndrome was made by Brugada-type 1 electrocardiogram and the family history of sudden death <45 years. The patient was considered as a high risk, because of pre-syncope and palpitations. He underwent ICD implantation (Medtronic MaximoVR7232Cx) using the standard procedure. After implantation, noninvasive electrophysiology study was done and demonstrated inducible VF that was interrupted with the second 35 J DC shock. The patient was discharged in stable condition with beta-blocker therapy. After a year of pacemaker check-ups, there were no either VT/ VF events or ICD therapy. Conclusion. Clinical presentation is the most important parameter in risk stratification of patients with Brugada electrocardiogram and Brugada syndrome.


2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Marko Perčić ◽  
Tea Friščić ◽  
Jasna Čerkez Habek ◽  
Dean Strinić ◽  
Ninoslav Rudman ◽  
...  

Changes of the ST segment are commonly used as predictors of the culprit vessel during an acute myocardial infarction. In case of combined ST elevation in both inferior and anterior leads, these changes can be due to a distal occlusion of a “wrapped” left anterior descending artery (LAD) or a two-vessel disease. Our case of anterior wall myocardial infarction with inferior ST elevation and anterior ST depression shows that electrocardiographic changes during acute myocardial infarction cannot always be explained by logical sequelae of the injury current, vessel anatomy, and their irrigation territory.


2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Aldino Satria Adhitya ◽  
Andika Sitepu ◽  
Zulfikri Mukhtar ◽  
Harris Hasan

Background: ST Elevation Myocardial Infarction (STEMI) may cause Major Cardiovascular Event (MACE). Revascularization needs to be done in all STEMI patients to restore coronary blood flow, hence saving myocardial perfusion. ST Segment Depression (STSD) in reciprocal ECG lead is associated with poor prognosis in STEMI patients receiving fibrinolytic therapy. The main purpose of this study is to evaluate MACE in STEMI patients receiving fibrinolytic therapy using resolution in STSD. Methods: This cohort prospective study with 60 subjects of STEMI patients which are evaluated for MACE (death, heart failure, and rehospitalization) within 30 days after myocardial infarction. Resolution in STSD is defined as resolution ≥ 50% STSD in reciprocal leads within 90 minutes after fibrinolytic therapy.Results: Bivariate analysis showed that Ejection fraction (EF) <40% with OR 8,32 (2,11-32,74), p=0,001; smoking with OR 4,17 (1,05-16,57), p=0,034; Anterior STEMI with OR 3,94 (1,11-13,90), p= 0,027; Creatinine > 1,97 mg/dl with OR 3,69 (1,18-11,55), p= 0,022; complete outpatient medication with OR 5,23 (1,61-17,01), p= 0,004; fragmented QRS with OR 5,23 (1,61-17,01), p= 0,001; resolution in STSD with OR 26,35 (5,16-134, 40), p=<0,001; resolution in ST Segment Elevation with OR 10,5 (2,97-37,24), p=<0,001; are proven to be determining factor for MACE within 30 days. Multivariate analysis showed that among those determining factors for MACE, resolution in STSD on reciprocal leads is evidently the most dominant factor for predicting MACE within 30 days in STEMI patients receiving fibrinolytic therapy [OR 11.47 (1.14-115.10), p=0.038].Conclusion: There is significant difference in MACE within 30 days after myocardial infarction (MI) between patients with and without resolution in STSD. The subjects without resolution in STSD showed higher MACE incidence. Resolution in STSD is evidently an independent predictor for MACE within 30 days after myocardial infarction in STEMI patients.Keywords: Resolution in STSD, MACE, STEMI, Fibrinolytic


Sign in / Sign up

Export Citation Format

Share Document