Abstract
Hypokalemia accentuates the electrocardiographic (ECG) pattern of Brugada syndrome. We report two patients with Brugada syndrome and hypokalemia‐induced lethal events. Despite concealing the typical ECG pattern with normalization of serum potassium levels, late potentials were persistently detected by signal‐averaged ECG, even at the 18‐month follow‐up. An implantable cardioverter defibrillator was inserted to prevent sudden cardiac death.
Ann Noninvasive Electrocardiol 2011;16(1):104–106
Keywords: Brugada syndrome, hypokalemia, late potential
Low potassium levels are associated with Brugada syndrome and the occurrence of ventricular arrhythmia. 1 , 2 However, no studies have shown late potentials (LPs) detected by signal‐averaged electrocardiography (ECG) after restoring serum potassium levels in patients with Brugada syndrome.
CASE 1
A 50‐year‐old man was being transported following syncope. In the ambulance, he experienced ventricular fibrillation (VF), which was successfully treated with direct current shock. His body temperature was 37.0°C and chest x‐ray and echocardiogram were normal. Blood chemistry showed hypokalemia (2.6 mEq/L). The 12‐lead ECG on admission showed an ECG aspect compatible with pattern of Brugada in precordial leads (Fig. 1A). The Brugada ECG was normalized with restoration of serum potassium (3.6 mEq/L, Fig. 1B). No further arrhythmic events occurred during hospitalization. Cardiac catheterization revealed no significant stenosis in the coronary arteries. During the electrophysiological study, VF was reproducibly induced by programmed stimuli from the right ventricle. An intravenous pilsicainide (50 mg) test exaggerated the ECG pattern of Brugada syndrome (Fig. 1C). An implantable cardioverter defibrillator (ICD) was implanted to prevent sudden cardiac death.
Figure 1.
ECG patterns of two patients with Brugada syndrome and hypokalemia‐induced lethal events. (A) A 12‐lead ECG of Case‐1 on admission showed an ECG aspect compatible with pattern of Brugada. (B) Normalization of the ECG upon restoration of serum potassium levels. (C) An intravenous pilsicainide (50 mg) test reproduced the ECG pattern of Brugada syndrome. (D) A 12‐lead ECG of Case‐2 at Emergency Room revealed complete right bundle branch block with a coved‐type ST‐segment elevation in precordial leads. (E) Normalization of the ST‐segment elevation upon restoration of serum potassium, even in the presence of high fever.
CASE 2
A 53‐year‐old man who suffered sudden cardiopulmonary arrest was referred to our hospital for cardiopulmonary resuscitation. His body temperature was 39.2°C. Laboratory evaluation revealed leukocytosis (16,400 mm3), elevated C‐reactive protein (8.85 mg/dL), and hypokalemia (3.0 mEq/L). Echocardiography showed normal wall motion of the left ventricle. Chest x‐ray and computed tomography (CT) scan confirmed pneumonia. The 12‐lead ECG revealed complete right bundle branch block with a coved‐type ST‐segment elevation in precordial leads (Fig. 1D). An intravenous infusion of potassium and intravenous administration of antibiotics were initiated. Serum potassium was 3.9 mEq/L on day 2, with normalization of coved ST elevation, irrespective of marked febrile state (Fig. 1E). No significant stenosis was observed in the coronary arteries. VF was reproducibly induced by programmed stimuli from the right ventricle. An ICD was inserted to prevent sudden death.
LPs BY SIGNAL‐AVERAGED ECG
The LPs were analyzed using a signal‐averaged ECG System (FCP7541, Fukuda Denshi Co., Tokyo, Japan). Three parameters were assessed via a computer algorithm: (1) the filtered QRS duration; (2) the root mean square voltage of the terminal 40 ms in the filtered QRS complex (RMS40); and (3) the duration of low‐amplitude signals <40 μV in the terminal filtered QRS complex (LAS40). LPs were considered abnormal when two criteria (RMS40 < 20 μV and LAS40 > 38 ms) were met. 3 Despite the normalization of serum potassium level, LPs were persistently abnormal in both patients before discharge and even at the 18‐month follow‐up (Table 1).
Table 1.
Serum Potassium Levels and LPs (by Signal‐Averaged Electrocardiogram) of Two Cases Presenting with Brugada Syndrome and Hypokalemia‐Induced Lethal Events
| Case‐1 | Case‐2 | |||
|---|---|---|---|---|
| Before Discharge | After 18 Months | Before Discharge | After 18 Months | |
| Serum potassium level (mEq/L) | 4.0 | 4.4 | 4.2 | 3.9 |
| fQRS (ms) | 117 | 119 | 194 | 175 |
| RMS40 (μV) | 13.3 | 13.8 | 2.4 | 5.5 |
| LAS40 (ms) | 41 | 40 | 136 | 116 |
fQRS = the filtered QRS duration; LAS40= the duration of low‐amplitude signals <40 μV in the terminal filtered QRS complex; RMS40= the root mean square voltage of the terminal 40 ms in the filtered QRS complex.
DISCUSSION
In both cases, hypokalemia was clearly associated with Brugada syndrome and the occurrence of lethal events. We implanted an ICD because latent conduction delay was evident even when typical ECG patterns were masked. Abnormal LP values were persistently observed at the 18‐month follow‐up, irrespective of serum potassium levels.
The ECG features of Brugada syndrome are often concealed but can be unmasked or modulated by many factors. 4 , 5 , 6 , 7 Hypokalemia is also known to be associated with Brugada syndrome and occurrence of the polymorphic ventricular tachyarrhythmia. 1 , 2 In consistence with previous case reports, the Brugada ECG pattern was observed when the serum potassium levels were 2.6 mEq/L (Case 1) and 3.0 mEq/L (Case 2), respectively. A febrile state also accentuates the Brugada ECG pattern and precipitates VF. 6 Case 2 exhibited a coved‐type Brugada ECG pattern with hypokalemia and high body temperature. The characteristic ST‐segment elevation was normalized with intravenous potassium infusion, even in the presence of high fever. In both cases, hypokalemia was mainly related to a Brugada ECG pattern. The cause of hypokalemia was not known and these patients had no prior drug use, and urinary potassium excretion levels and blood endocrine activity were also within the normal range.
A majority of spontaneous type 1 Brugada syndrome with a history of life‐threatening events have demonstrated LPs. 3 , 8 Multivariate analyses revealed that the presence of LPs is an independent predictor of sudden death. LPs have also been observed in a high percentage of Brugada syndrome patients with induced VF. 9 Conduction delays, especially at the right ventricular outflow track, produce LPs in Brugada syndrome. 9 Despite the restoration of serum potassium level, LPs were persistently abnormal even at the long‐term follow‐up. Ventricular tissue abnormality may exist irrespective of serum potassium levels in both patients.
CONCLUSION
Although the role of hypokalemia in Brugada syndrome is not so clear and has been rarely described, in the cases presented here, LPs were obvious even at the 18‐month follow‐up. These cases provided further evidence of risk for the future in Brugada syndrome associated with hypokalemia. ICD implantation should be considered to prevent sudden cardiac death in these patients.
Acknowledgments
Acknowledgment: This work was supported by a Grant‐in‐Aid from the Global COE Program of the Japan Society for the Promotion of Science.
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