When you hear hoofbeats, think of horses and zebras: a 58-year-old man with chest pain and palpitations
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Case presentation and primary diagnosis
Dr. Hudzik, Dr. Szkodzinski: We presumed that positive troponin and CK-MB were associated with the reported palpitations with a rapid heart rate, which could have resulted from a sustained ventricular tachycardia, which, in turn, could have led to the increase in serum cardiac markers. We ruled out myocarditis as the cause of the presented symptoms, given the negative inflammatory markers, preserved left ventricular systolic function, no pericardial effusion, the dynamics of ECG changes and no prior history of infection or febrile state. Therefore, we did not perform contrast-enhanced magnetic resonance imaging to exclude myocarditis .
Given the diagnosis, ventricular dysrhythmia and a positive TWA, the patient underwent a successful placement of an implantable cardioverter-defibrillator (ICD). The patient was discharged and remained well during 6-month follow-up.
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.
Electrocardiographic types of ST-segment elevation in leads V1–V3 in Brugada syndrome
J-point or ST-segment elevation >2 mm at its peak followed by a negative T-wave (cove-type appearance)
J-point amplitude >2 mm giving rise to a downsloping ST-segment elevation ≥1 mm above baseline (“saddle back” appearance)
J-point amplitude >2 mm giving rise to a downsloping ST-segment elevation <1 mm above baseline (“saddle back” appearance)
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.
Conflict of interest
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