Abstract

A 56-year-old woman with well-documented Chagas disease was found to have a spontaneous type 1 electrocardiographic (ECG) pattern of Brugada syndrome. It is most likely that this characteristic ST-segment elevation is an unusual manifestation of the pathological changes in Chagas disease. This ECG pattern has been found with other cardiac pathology and has been reported to be induced in patients with Chagas disease.

Case report

A 56-year-old woman with Chagas disease presented with syncopal episodes, sometimes preceded by palpitations. The diagnosis of Chagas disease was confirmed by positive immunofluorescence and haemaglutination tests to Trypanosoma cruzi . Her electrocardiogram (ECG) showed a spontaneous type 1 ECG pattern of the Brugada syndrome (BrS) ( Figure  1 ) that was not related to antiarrhythmic drug administration or febrile illness. This ECG pattern was not constant and sometimes reverted to a type 2 saddleback pattern. A Holter monitor showed 1376 premature ventricular contractions/24 h including ventricular triplets. She had invasive electrophysiological testing with no induction of sustained ventricular tachycardia or ventricular fibrillation. The only cardiac abnormality documented by echocardiogram and magnetic resonance imaging (MRI) was an apical left ventricular aneurysm. Implantation of an implantable cardioverter defibrillator was advised but was not approved by the insurance company.

Electrocardiogram shows maximal ST-segment elevation in right precordial leads compatible to the type 1 Brugada pattern.
Figure 1

Electrocardiogram shows maximal ST-segment elevation in right precordial leads compatible to the type 1 Brugada pattern.

Discussion

We describe the unique case of a patient with well-documented Chagas disease affecting the heart who had the typical ST-segment elevation consistent with the Brugada syndrome (BrS). 1 It is most likely that the pathological changes of Chagas disease are responsible for the Brugada ECG pattern. Although the original report by Brugada indicated that there was no cardiac structural abnormality, there is now adequate documentation of cardiac fibrosis, particularly in the right ventricular (RV) outflow tract of patients with the BrS. There are morphological and clinical similarities of Chagas disease and RV cardiomyopathy. It is important to note that in 1982, before the BrS was first reported, Chiale et al.2 showed that ajmaline provoked a type 1 ECG pattern and short-coupled ventricular premature beats as in the BrS in 7 of 101 patients in the early stages of Chagas disease. Ajmaline did not provoke this ECG pattern in normal controls. This provides evidence that the type 1 Brugada ECG can be observed in patients with Chagas disease. Chiale et al. speculated that the ajmaline test could be used as a detector of myocardial damage in Chagas disease. The observation that there was no RV outflow tract abnormality by two-dimensional echocardiogram or MRI in this patient does not exclude this possibility. In a recent publication, Postema et al.3 concluded that the BrS ECG can be due to localized depolarization abnormalities and conduction delay in the RV. Hoogendijk et al.4 speculated that structural discontinuities in the RV subepicardium can cause excitation failure and activation delay by current-to-load mismatch and can cause the Brugada ECG pattern.

It is unlikely that the Brugada ECG pattern in this patient is due to a rare association of two diseases in the same individual. Genetic testing for mutations in SCN5A was not performed. Since only 15–20% of the patients with the syndrome have a genetic abnormality, negative genetic tests would not exclude the diagnosis of the BrS.

Conclusion

This is a unique observation of the Brugada ECG in a patient with Chagas disease. It has been well documented that ajmaline can provoke a type 1 Brugada pattern in patients with Chagas disease. In addition, since this ECG pattern can be present with cardiac pathology in other diseases such as arrhythmogenic RV cardiomyopathy, it appears most likely that this characteristic ST-segment elevation is an unusual manifestation of the underlying cardiac pathology of Chagas disease.

Conflict of interest: none declared.

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