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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 90-92

Brugada syndrome presenting as atrial flutter with sick sinus syndrome


Department of Cardiology, Grant Medical College and Sir JJ Group of Hospitals, Mumbai, Maharashtra, India

Date of Submission04-Oct-2020
Date of Decision11-Dec-2020
Date of Acceptance05-Jan-2021
Date of Web Publication30-Mar-2021

Correspondence Address:
Rohit Rai
Department of Cardiology, Grant Medical College and Sir JJ Group of Hospitals, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_45_20

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  Abstract 


An incidentally diagnosed patient with Brugada syndrome was found to have atrial flutter on baseline electrocardiogram. He was DC (Direct current) cardioverted which revealed sick sinus syndrome. The patient was implanted with VVIR(Ventricular rate modulated pacing) pacemaker. Underlying sinus node dysfunction can be present in cases of Brugada syndrome with atrial flutter. The patient may require pacemaker insertion postcardioversion.

Keywords: Atrial flutter, Brugada syndrome, sick sinus syndrome


How to cite this article:
Rai R, Shaikh SS, Bansal NO. Brugada syndrome presenting as atrial flutter with sick sinus syndrome. Heart India 2021;9:90-2

How to cite this URL:
Rai R, Shaikh SS, Bansal NO. Brugada syndrome presenting as atrial flutter with sick sinus syndrome. Heart India [serial online] 2021 [cited 2021 Aug 1];9:90-2. Available from: https://www.heartindia.net/text.asp?2021/9/1/90/312486




  Introduction Top


Brugada syndrome was first described by Brugada and Brugada in 1992 on studying a group of eight patients with aborted sudden cardiac death.[1] Patients have a propensity of life-threatening ventricular arrhythmias and have ST elevation from V1–V3 with the right bundle branch block. Arrhythmogenic substrate is not only limited to ventricles but also involves the atria.[2] Spontaneous atrial arrhythmia's incidence varies from 6% to 38%, whereas inducible atrial arrhythmia's incidence varies from 3% to 100%.[3] The most common atrial arrhythmia found in Brugada syndrome is atrial fibrillation. A case series ranging from 38 to 542 patients in adults and 30–95 children with sinus node dysfunction has been reported. A case series of 487 patients with sick sinus syndrome has been reported by Hayashi et al., in 2010. Our case also had underlying sick sinus syndrome and presented as atrial flutter.


  Case Report Top


A 30-years-old male patient was apparently asymptomatic on admission. He had intermittent episodes of dizziness and syncope. He came with his son who was 6 years old admitted in the pediatrics department for syncope and was incidentally diagnosed with Brugada syndrome on electrocardiogram (ECG). On taking family history of the child, his father's brother had a history of sudden death during sleep, so his father's ECG was done and found out to have Brugada syndrome with atrial flutter [Figure 1]. The patient's COVID-19 report was negative. His hemoglobin was 14.7 mg/dl, white blood cell counts were 9100/mm3, creatinine was 1 mg/dl, sodium was 146 mEq/dl, potassium was 4.0 mEq/dl, calcium was 9.7 mEq/dl, FT3 was 2.9 pmol/L, FT4 was 0.8 pmol/L, and TSH was 1.5 mU/L. Atrial flutter can increase the risk of stroke. On echocardiography, his right atrium and right ventricle were dilated. He was taken for TEE which revealed no LA appendage clot. He was given anticoagulation with heparin for 2 days and DC cardioverted with 20 J shock with prophylactic temporary pacemaker in the right ventricle. After cardioversion, patient's ECG was showing bradycardia with a heart rate of 50/min with coved pattern of ST segment in V2–V3 and T wave inversion from V1 to V6, I, aVL suggestive of sick sinus syndrome [Figure 2]. Even after waiting for 5 days for spontaneous sinus rhythm, the patient had sick sinus syndrome on ECG. The patient had bradycardia with junctional rhythm when temporary pacemaker was switched off temporarily. Atropine test was done with 2 mg of atropine following which his heart rate increased to 96/min and developed coved-type Brugada pattern [Figure 3]. He had dizziness intermittently when his heart rate fell down and baseline pacing of temporary pacemaker was low. He was implanted VVIR pacemaker and successfully discharged.
Figure 1: Atrial flutter with Brugada syndrome

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Figure 2: Sick sinus syndrome

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Figure 3: Postatropine test coved pattern of Brugada syndrome

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  Discussion Top


In Brugada syndrome, enhanced duration of atrial action potential and increased intra-atrial conduction time may contribute to the genesis of atrial arrhythmias. An important cause of inappropriate discharge of implantable cardioverter-defibrillators (ICDs) in Brugada syndrome patients are atrial arrhythmias. Hence, it is recommended to implant dual-chamber ICDs and careful programming of single-chamber ICDs.[4] Previous life-threatening cardiac events are the most important predictor of atrial fibrillation in Brugada syndrome patients.[5] Our patient was asymptomatic and did not have any life-threatening cardiac event. Patients with spontaneous Brugada pattern on ECG and those with ICDs had greater incidence of atrial arrhythmias than those who manifest the pattern on drugs such as flecainide.[4] Our patient had spontaneous Brugada pattern on ECG.

Signal-averaged ECG is used to measure filtered p-wave duration to predict vulnerability of atrial fibrillation. In the study by Bordachar et al., signal-averaged p-wave duration was 143.2 ± 12.9 ms in Brugada syndrome patients and 129.6 ± 10.1 ms in controls.[4] Similarly, in the study by Osaka et al. also, the mean filtered p-wave duration was 143.7 ± 10.3 ms in Brugada syndrome patients and 122.3 ± 9.9 ms in controls.[6] In our case, p-wave was 144 ms.

In a case by Morimoto et al., autopsy of the patient with Brugada syndrome with sick sinus syndrome revealed replacement of sinus nodal cells with fatty tissue and prominent fibrosis.[7] Namdar et al. described a patient with hemochromatosis with Brugada syndrome with sick sinus syndrome.[8] Arrhythmias in Brugada syndrome and bradyarrhythmias are usually seen with SCN5A mutations. Long QT syndrome and lone atrial fibrillation have also been reported with SCN5A mutation. It encodes for alpha subunit of cardiac sodium channel (Nav1.5). Loss-of-function mutation creates a circuit for reentry in the ventricular myocardium and may also increase vagal activity, leading to the development of arrhythmias.[9] Takehara et al. also reported a case of Brugada syndrome with atrial standstill with SCN5A mutation.[10] Eckardt et al. also showed association between Brugada syndrome and supraventricular arrhythmias. They showed that, in patients with palpitations with Brugada syndrome, SVT should be considered and in patients with SVT with syncope or aborted sudden cardiac death Brugada syndrome should be considered.[3]

Sinus node function usually recovers after atrial flutter termination in patients without underlying cardiac disease. A case of atrial flutter for 25 years who regained sinus node function after ablation was reported by Palma et al.[11] However, in our case, sinus node function did not recover of termination of atrial flutter. Morita et al. also showed sinus node and AV node dysfunction by programmed electrical stimulation-induced ventricular fibrillation in Brugada syndrome patients.[12] Smits et al. showed an association between E161K mutation in Brugada syndrome with sick sinus syndrome.[13] Genetic analysis of our patient could not be done due to financial constraints.

Conclusion

Brugada syndrome can be associated with underlying sinus node dysfunction and pacemaker support should be used on aborting supraventricular arrhythmias.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical approval

Informed consent was obtained from the patient. Patient anonymity has been maintained.

Authors' contributions

Narendra O Bansal supervised the DC cardioversion, permanent pacemaker insertion, was involved in patient care and edited the manuscript. Rohit Rai performed the DC cardioversion, was involved in patient care and wrote the case report. Shakil S Shaikh performed the permanent pacemaker implantation, was involved in the patient care and edited the manuscript.



 
  References Top

1.
Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992;20:1391-6.  Back to cited text no. 1
    
2.
Yamada T, Watanabe I, Okumura Y, Takagi Y, Okubo K, Hashimoto K, et al. Atrial electrophysiological abnormality in patients with Brugada syndrome assessed by P-wave signal-averaged ECG and programmed atrial stimulation. Circ J 2006;70:1574-9.  Back to cited text no. 2
    
3.
Eckardt L, Kirchhof P, Loh P, Schulze-Bahr E, Johna R, Wichter T, et al. Brugada syndrome and supraventricular tachyarrhythmias: A novel association? J Cardiovasc Electrophysiol 2001;12:680-5.  Back to cited text no. 3
    
4.
Bordachar P, Reuter S, Garrigue S, Caï X, Hocini M, Jaïs P, et al. Incidence, clinical implications and prognosis of atrial arrhythmias in Brugada syndrome. Eur Heart J 2004;25:879-84.  Back to cited text no. 4
    
5.
Bigi MA, Aslani A, Shahrzad S. Clinical predictors of atrial fibrillation in Brugada syndrome. Europace 2007;9:947-50.  Back to cited text no. 5
    
6.
Osaka T, Yokoyama E, Yamazaki M, Ito A, Kodama I. Intraatrial conduction abnormalities in patients with Brugada-type ECG estimated by P wave triggered signal-averaged ECG. J Am Coll Cardiol 2002;39 Suppl 1:110.  Back to cited text no. 6
    
7.
Morimoto S, Uemura A, Hishida H. An autopsy case of Brugada syndrome with significant lesions in the sinus node. J Cardiovasc Electrophysiol 2005;16:345-7.  Back to cited text no. 7
    
8.
Namdar M, Rodriguez M, Brugada P. Haemochromatosis, sinus node dysfunction and Brugada syndrome – A ménage à trois of findings in one and the same patient: Coincidence or causality? Acta Cardiol 2012;67:249-51.  Back to cited text no. 8
    
9.
Risgaard B, Bundgaard H, Jabbari R, Haunsø S, Winkel BG, Tfelt-Hansen J. Pacemaker implantation in a patient with Brugada and sick sinus syndrome. World J Cardiol 2013;5:65.  Back to cited text no. 9
    
10.
Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, et al. A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill. J Intern Med 2004;255:137-42.  Back to cited text no. 10
    
11.
Palma EC, Vijayaraman P, Ferrick KJ, Gross JN, Kim SG, Fisher JD. Sinus node recovery after 25 years of atrial flutter. Pacing Clin Electrophysiol 2001;24:1295-6.  Back to cited text no. 11
    
12.
Morita H, Fukushima-Kusano K, Nagase S, Miyaji K, Hiramatsu S, Banba K, et al. Sinus node function in patients with Brugada-type ECG. Circ J 2004;68:473-6.  Back to cited text no. 12
    
13.
Smits JP, Koopmann TT, Wilders R, Veldkamp MW, Opthof T, Bhuiyan ZA, et al. A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families. J Mol Cell Cardiol 2005;38:969-81.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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