Brugada-induced Severe Hyponatremia : Could it be lethal?

S.P. Mahaley ¹, Irnizarifka², C. Sukmagautama³, H. Arifianto²

¹General Practitioner

²Departement of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Sebelas Maret, Sebelas Maret University Hospital, Surakarta, Indonesia.

²Departement of Internal Medicine, Sebelas Maret University Hospital, Faculty of Medicine, Universitas Sebelas Maret, Indonesia.

 

Background: Brugada syndrome, first described in 1992, is a major cause of sudden cardiac death, syncope and ventricular tachyarrhythmia in people with no structural heart disease. Brugada syndrome usually manifests during adulthood, with a mean age of sudden death of 41±15 years old.

Case illustration: 58 years old male was admitted to RS UNS with fatigue for 3 days. Along with other physical and laboratory examinations, patient was diagnosed as having septic shock. As soon as transferred to high care unit, patient was having pulseless ventricular tachycardia but 3 minutes CPR was able to get him back with soporous condition. Laboratory showed severe hyponatremia (128 mEq/l) and baseline ECG evidenced type 1 Brugada. The 3% NaCl was administrated until his sodium level went up to 141 mEq/l. Patient’s condition was improved and brugada pattern ECG was back to normal. Patient was then discharged in good condition without any further cardiac events.

Discussion: Brugada syndrome is characterized electrocardiographically by ST segment elevation in the right precordial leads, followed by a negative T wave unrelated to ischemia, and prone to rapid polymorphic ventricular tachycardia capable of degenerating into ventricular fibrillation. The ECG pattern may be dynamic and is often concealed. Sodium channel blockers, drugs, electrolyte imbalances, fever and several other clinical circumstances are recognized inducers of a Brugada type 1 ECG in susceptible patients.

Conclusion: We have managed temporary but deadly type-1 Brugada Syndrome in septic patient through sodium level improvement. Brugada-induced severe hyponatremia did exist and might be lethal, thus accurate diagnosis must be done to generate definite treatment and convert ECG pattern to normal.

 

Keyword: brugada induced, severe hyponatremia, ventricular tachycardia

 

Role of Radiofrequency Ablation for Idiopathic Right Ventricular Outflow Tract Arrhythmias: a case report

S.P.I Nasruddin¹, Irnizarifka^1,2

¹Departement of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia.

²Departement of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Sebelas Maret, Sebelas Maret University Hospital, Surakarta, Indonesia.

 

Background: Premature Ventricular Contraction (PVC) is very common arrhythmia found in clinical practice. It may occur in healthy individual with no evidence of structural heart disease and most originate from right ventricular outflow tract (RVOT)¹. Idiopathic RVOT-PVC typically presents between the ages of 20 to 50 years and more frequent in women. When highly symptomatic or refractory to antiarrhythmic therapy, catheter ablation is recommended due to its > 95% success rate and a extremely low complication risk².

Case illustration: 27-year-old female came to outpatient clinic with chief complaint of recurrent palpitation. Frequent RVOT origin PVCs (unifocal, 50%) with coupling interval of 360 msec were obtained on Holter ECG monitor. Echocardiography did not evidence any structural heart diseases and revealed normal LVEF, whereas cardiac CT showed normal coronary arteries. Magnetic resonance imaging was done and revealed normal cardiac chamber, with no sign of arrhythmogenic right ventricular dysplasia or arrhytmogenic mitral valve prolapse. Verapamil was then initiated, but failed to improve her symptom and ECG. Electrophysiological study was finally done and showed unifocal RVOT-PVC with focal area at anteroseptal region. Radiofrequency ablation was performed (40 watts, 50⁰ celsius, 180 msec) without any complications. Evaluation showed normal sinus rhythm with no inducible PVC, and patient did not experience any more symptoms.

Conclusion: We have managed a young woman with frequent idiopathic RVOT-PVCs who are still symptomatic despite optimal anti-arrhythmic medication. Echocardiography, cardiac CT, and MRI showed no underlying structural heart disease and exclude arrhythmogenic right ventricular dysplasia. Timely decision to do radiofrequency ablation is particularly effective and safe to treat persistent and symptomatic idiopathic RVOT-PVC, with very low complication rate.

 

Keyword: radiofrequency catheter ablation, right ventricular outflow tract arrhythmia, premature ventricular contraction.

 

2:1 Atrioventricular Block : what can we learn from atropine effect?

Tridamayanti A ¹, Irnizarifka^1,2

¹Departement of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia.

²Departement of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Sebelas Maret, Sebelas Maret University Hospital, Surakarta, Indonesia.

 

Background: 2:1 atrioventricular block can occur in either AV node (AVN) or HIS-Purkinje System (HPS) and cannot be classified into type I or type II second-degree AV block because there is only one PR segment to be examined before the dropped-beat. On the other hand, it is essential to have two consecutive conducted P waves to differentiate between type I or type II second-degree AV block. Determining those types of atrioventricular or HPS block is very important as treatments are also unlike.

Case Illustration : 56 year old diabetic woman was admitted with chief complaint of chest pain since 15 hours beforehand, accompanied with diaphoresis and near syncope. Her resting ECG revealed 2:1 AV block, with PR interval was not prolonged (0.2 sec), and ST segments were not elevated. Cardiac enzyme proved diagnosis of NSTE-ACS and 2:1 AV block. In order to define the site of block, we performed atropine challenge test. After administration of 0.5 mg atropine, ECG revealed improvement of AV conduction ratio with 3:2 Wenckebach-like manners. It indicated the location of the block was at AV node.

Discussion: Fixed 2:1 AV block poses a diagnostic dilemma because it can be difficult to determine the site of block by the surface ECG alone. The AVN is richly innervated and highly responsive to both sympathetic and vagal stimuli, whereas HPS is influenced minimally by the autonomic nervous system. Atropine or exercise can improve AVN conduction because of sympathetic stimulation and/or parasympatholysis. Therefore, atropine administration can improve AVN conduction but worsen infranodal block due to sympathetic stimulation of the sinus node and AVN without changing the HPS refractoriness.

Conclusion: This case illustrates the importance of noninvasive atropine challenge test to confirm site of 2:1 atrioventricular block, thus will guide the definite therapy.

 

Keyword: 2:1 atrioventricular block, atropine challenge test, wenckebach, HIS-purkinje block