Indian Pacing Electrophysiol. J. 2003;3(3):184
Images in Electrophysiology
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Brugada-like Precordial ST Elevation on ECG by
Anterior Mediastinal Infective Mass Lesion
Yuji Nakazato, Takayasu Ohmura,
Issei Shimada, Hiroyuki Daida
Division of Cardiology,
Department of Internal Medicine, Juntendo University School of
Medicine, Tokyo, Japan.
Address for correspondence: Dr. Yuji Nakazato, MD, PhD, Division
of Cardiology, Department of Internal Medicine, Juntendo University
School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
E-mail: ynkzt@med.juntendo.ac.jp
Several causes are known to induce the right
precordial ST elevation mimicking Brugada syndrome. Right ventricular
outflow area is assumed to be responsible for such ECG changes. We
experienced a case of anterior mediastinal infective mass lesion with a
Brugada-like ECG.
A
52-year-old female, who has pulmonary stenosis and recurrent episodes
of right ventricular heart failure, complained of high fever, abdominal
discomfort, and edema. On physical examination, jugular vein dilation,
hepatomegaly, and facial and leg edema were noted. Leucocytosis was
also noted on blood examination. An ECG showed right ventricular
hypertrophy, incomplete right bundle branch block pattern and marked ST
elevation
on precordial leads mimicking Brugada syndrome. Magnetic resonance
imaging revealed an abnormal mass shadow located on the anterior
mediastinum
and compressing the right ventricle (Figure 1A). Trans-thoracic
echocardiography also showed the high echogenic mass lesion at the
anterior
side of right ventricle and the vicinity of pulmonary valve.
After
treatment with antibiotics, the mass lesion gradually shrunk.
Concomitantly,
the ST elevation disappeared with improvement of inflammatory markers
(Figure 1B). The symptoms suggesting right ventricular failure
were also ameliorated. The mechanism of Brugada-like ST elevation in
this patient was considered to be compression, by the abnormal
infective mass,
of the right ventricular outflow tract with/without focal pericardial
inflammation.
Figure 1 (A and B)
