Ozcan Ozeke,
MD, Dursun
Aras, MD, Bilal Geyik,MD, Bulent Deveci, MD, Timur Selcuk, MD
Yuksek Ihtisas
Hospital,
Department of Cardiology, Ankara, Turkey
Address for
correspondence: Ozcan Ozeke, MD, Yuksek Ihtisas Hastanesi,
Kardiyoloji Klinigi, Sihhiye
06100 Ankara, Turkey. E mail:
ozcanozeke@hotmail.com
Abstract
ST-segment elevation
in Brugada syndrome is caused by a shift in the ionic current balance
and the creation of a voltage gradient between the epicardium and the
endocardium. This ionic mechanism have been shown to be
temperature dependent. We describe a 33-year-old man who presented with
fever with the dynamic electrocardiographic changes similar to the
Brugada syndrome. These electrocardiographic anomalies disappeared when
the temperature returned to normal.
Keywords: Brugada syndrome; Fever
Case Report
A 33-year-old
man with fever due to common cold was referred to our hospital with
suspicion of having an acute coronary syndrome. Three hours before
admission, the patient with complaints of fever, chills, sore
throat, was admitted to a local hospital, where the temperature was
38.7°C and his electrocardiogram showed characteristic Brugada
pattern with coved type ST-segment elevation in leads V1-V3 and
first-degree atrioventricular block (
Figure
1). He was diagnosed as having common cold and was
referred to our hospital because of his electrocardiographic changes
resembling acute coronary syndrome. He had no cardiac complaints and
did not have a history of syncope or a family history of sudden cardiac
death. On physical examination, the patient was dehydrated but alert.
In the emergency room, his temperature was 38.3°C, the blood
pressure was 120/70 mm Hg and the pulse was 88 per min. There was an
inflammation of the pharynx. No other abnormalities were found.
Hematological and biochemical tests including cardiac enzymes and
electrolytes were within normal limits and the chest X-ray was
unremarkable.The white blood cell count was 9600/cu mm. There was no
evidence of structural heart disease on echocardiographic examination.
Later that day, the patient’s temperature was 36.9°C
with antipyretics and electrocardiogram showed
saddle-back type ST-segment elevation in leads V1-V2 (
Figure 2A). Subsequently, drug
challenge test with propafenone was performed; the ST-segment
elevation changed from the saddle-back type (
Figure 2A) to the coved type (
Figure 2B). The next day, the
patient was afebrile and the incomplete right bundle branch block
disappeared on electrocardiogram, which showed only minimal ST-segment
elevation in V2 (
Figure 1B). An
electrophysilogical study was not performed because neither the patient
nor any of his family members had experienced any arrhytmic symptom or
sudden cardiac death, and medical follow up was decided. The
patient was recommended to came hospital for urgent therapy of fever
when a fever developed.
Figure 1. 12-lead
electrocardiogram shows incomplete right bundle branch block with coved
type ST-segment elevation in leads V1-V3, and first-degree
atrioventricular block at the condition of fever (
1A) and shows minimal ST-segment
elevation in V2 without the incomplete right bundle branch block at the
rest without fever (
1B).
Figure 2. 12-lead
electrocardiogram shows that the ST-segment elevation changed from the
saddle-back type (
2A) to the
coved type (
2B) with drug
challenge.
Discussion
Brugada
syndrome , first described as a new clinical entity by Pedro and Josep
Brugada in 1992, is an inherited cardiac disease causing
life-threatening ventricular tachyarrhythmias in patients with
structurally normal heart and a characteristic electrocardiogram
showing a pattern of right bundle branch block and ST segment elevation
in right precordial leads V1 to V3
1.
Wilde et al
2 reported 3
types of repolarization patterns as the ECG criteria for diagnosis of
Brugada Syndrome; type 1 ECG, a coved-type ST segment elevation of ≥ 2
mm; type 2 ECG, saddle-back type a J wave amplitude of ≥ 2
mm and gradually descending ST segment elevation remaining ≥ 1 mm above
baseline; and type 3 ECG, a coved-type or saddle-back type with
ST segment elevation of ≤ 2 mm.
In spite of
all the knowledge acquired over the last decade on this syndrome,
diagnosis and risk stratification can be difficult sometimes. The ECG
pattern may be dynamic over time and may include transient normalization
2. The pathophysiology of Brugada syndrome
is still under investigation. Insight from cellular electrophysiology
suggests that the ST-segment elevation is caused by a shift in
the ionic current balance and the creation of a voltage gradient, with
predominance of transient outward current in the epicardium over the
endocardium
3. The ionic
mechanism responsible for the Brugada syndrome have been shown to be
temperature dependent
4,5,6,7,8.
In the present case, the electrocardiographic anomalies were evident
when the fever was present and disappeared once the temperature
returned to normal. It is possible that an increase in temperature may
be the most important factor in the appearance of these
electrocardiographic changes. In consideration of its variability,
physicians should be aware of its often transient electrocardiographic
features and fever should be aggressively treated. Our present report
supports the effect of the body temperature in diagnosis and of on the
underlying ion channelopathy of Brugada syndrome .
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