Dr. Hudzik, Dr. Szkodzinski, Prof. Polonski: During medical training, students and residents are being taught a quintessential maxim of clinical medicine—“When you hear hoofbeats, think of horses, not zebras”. Common diseases are what physicians should expect to encounter. Unfortunately, in a world of horses, the hoofbeats of zebras too often go unrecognized or misdiagnosed. The diagnosis of Brugada syndrome may be difficult and somewhat tricky, given that a wide spectrum of diseases can be associated with ST-segment elevation . These include: acute myocardial infarction, variant angina, pericarditis, myocarditis, early repolarization syndrome, and aortic dissection. Brugada-type ECG changes may be also elicited by other conditions: 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, such as antidysrhythmics, anesthetics, and tricyclic antidepressants (although the clinical meaning and the risk of dysrhythmias induced by this pattern are unknown) . A differential diagnosis is at times difficult, particularly when the degree of ST-segment elevation is relatively small . Gu et al.  examined 820 patients with suspected STEMI and found 19 patients with conditions mimicking STEMI (final diagnosis other than acute myocardial infarction). They report one patient (5%) with a primary diagnosis of STEMI who was finally diagnosed with a Brugada syndrome, and an ICD was implanted. Similar cases have been reported previously [8, 9].
Timely institution of reperfusion therapy is essential in the treatment of STEMI [10, 11]. Therefore, available time most often does not allow for a solid differential diagnosis. We should be especially vigilant in the settings of suspected STEMI and normal coronary arteries on coronary angiography.
Meanwhile, ECG changes are the hallmark of the Brugada syndrome, which consist of (a) an electrocardiographic pattern with a static or transient ST-segment elevation (Table 1); (b) a structurally normal heart and (c) a predisposition toward ventricular tachyarrhythmias leading to syncope or SCD [12, 13]. The diagnosis of Brugada syndrome can be made if a type 1 ECG pattern occurs spontaneously or after pharmacological provocative tests . When type 2 or 3 patterns are observed, a conversion to type 1 pattern must occur during sodium channel blocker (e.g., procainamide, ajmaline, flecainide) administration to make a diagnosis of Brugada syndrome. The diagnosis of Brugada syndrome can be made if type 1 ECG pattern is accompanied by at least one of the following clinical situation :
documented polymorphic VT,
inducible ventricular dysrhythmias during electrophysiological study (EPS),
family history of SCD at <45 years of age
ECG type 1 pattern in other family members.
A proper diagnosis is crucial given the life-threatening nature of the disease. Up to 27% of patients with a Brugada syndrome are at risk of developing ventricular tachycardia/fibrillation or SCD. ICD placement is currently the only treatment of proven efficacy for the management of the Brugada syndrome.
It is prudent to search for a Brugada syndrome when classical ECG findings are absent, but the patient has symptoms of dysrhythmia and normal coronary arteries.