Electrocardiographic diagnosis of Brugada syndrome: Medico-legal implications

Abstract Brugada syndrome is one of the main causes of sudden death in young adults without a structural heart disease. This is an electrical cardiac illness secondary to a mutation of SCN5A, a gene of chromosome 3 that encodes the cardiac sodium channel. The typical ECG pattern consists of a right bundle branch block pattern with an ST-segment elevation in leads V1 through V3. Two specific types of S-T-segment elevation, [ldquo ]coved[rdquo ] and [ldquo ]saddleback,[rdquo ] are observed in this syndrome. The coved shape of the ST-segment elevation is due to complete loss of action potential dome in epicardium but not endocardium; usually obscuring the downstroke of the R wave, resembling a giant J wave or right bundle branch block. The coved-type ST segment is arrhythmogenic and is associated with polymorphic VT and VF. The other type of ST-segment elevation, usually upward concave or [ldquo ]saddleback,[rdquo ] is due to partial loss (depression) of the action potential dome in the epicardium but not in the endocardium: under such conditions, dispersion of repolarization on the epicardial surface is minimal, so that there is no substrate for the development of polymorphic VT or VF. Transition between the 2 types of ST segment has been described in some Brugada syndrome patients. Therefore, every cardiologist should pay equal attention to both types of ST-segment elevation in patients with a diagnosis of the syndrome because pharmacologic interventions or pathophysiologic alterations may facilitate this transition and lead to development of polymorphic VT and VF. A recent study has shown a marked ST-segment elevation to a coved-type after intravenous administration of flecainide (a Class IC antiarrhythmic) in a Brugada patient with baseline saddleback-type ST-segment elevation. Consequently, an underestimation or failed recognition of these ECG patterns could cause negative repercussions on the management and treatment choices of patients at high risk for recurrence of lethal arrhythmias. In fact, transition from saddleback-type to coved-type may represent an important electrocardiographic factor in the development of lethal ventricular arrhythmias. It's well known that this disease causes sudden arrhythmic death with a high mortality, approximately 10% per year. Therefore, missed diagnosis or underestimation of patients with suspect ECG-patterns compatible with Brugada's syndrome and consequently a successive patient's sudden death, could lead to a legal trial. In this case, medico-legal consequences could be strictly connected to the diagnostic phase because wrong or missed diagnosis would mean wrong or failed clinical management of patients at risk for sudden death. In the legal field, misdiagnosis would mean an omission offense and a doctor could be charged of culpable homicide because of this omission. Conclusions: Two types of S-T-segment elevation, [ldquo ]coved[rdquo ] and [ldquo ]saddleback,[rdquo ] are observed in Brugada syndrome. Every cardiologist should be able to recognize these ECG patterns and should not underestimate the consequences. A correct diagnosis of a suspect ECG pattern would be of great importance to save the patient's life and to avoid medico-legal consequences.