Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5979585 | International Journal of Cardiology | 2010 | 4 Pages |
The prevalence of the Brugada-type ECG and its natural history are still unclear. The Brugada syndrome is usually identified by a characteristic Brugada-type ECG that consists of ST elevation of a coved type in the precordial leads V1 to V3 and ventricular fibrillation that can lead to sudden cardiac death, although affected individuals may have a normal ECG. Mutations in the cardiac sodium channel gene SCN5A, which encodes the alpha-subunit of the human cardiac voltage-dependent Na+ channel (Na(v)1.5), are identified in 15-30% of patients with Brugada syndrome. Most SCN5A mutations lead to a 'loss-of-function' phenotype, reducing the Na+ current during the early phases of the action potential. Several nongenetic factors have been mentioned in the literature as possible inductors of the ECG pattern resembling Brugada syndrome. As such, a Brugada-type ECG may appear in some patients during febrile states and in those who are under the influence of cocaine and pharmaceutical drugs that have a sodium channel-blocking effect. It has been also reported chest pain and ST elevation Brugada pattern during febrile states. We present a case of revelation of Brugada pattern in a 69-year-old Italian man during a febrile state associated with acute myocardial infarction. Also this report confirms that Brugada pattern should be considered as one of differential diagnoses when we examine the patients during a febrile state.