Brugada syndrome is characterized by a typical electro-cardiographic pattern of ST segment elevation in the precordial leads, with or without right bundle branch block, malignant arrhythmias, and a structurally normal heart (Fig. 1).
It is certainly a challenge to risk stratify patients with Brugada syndrome. There have been many uncertainties which can only be clarified with further experience as more patients and families are being identified and followed for clinical outcome. Electrocardiographic criteria are used to try to risk stratify patients, but there is some disagreement on the criteria to be applied. Some of the conclusions are as follows. Symptomatic patients are at high risk. There is a consensus that symptomatic patients with documented ventricular fibrillation have close to a 50% chance of having another event within 5 years. If the patient experienced syncope, the recurrence rate is 20%. Individ uals with normal ECG at baseline and abnormal after antiarrhythmics have a good prognosis. This is the other side of the spectrum. Individuals that have the mutation but require an antiarrhythmic challenge to develop the abnormal electrocardiographic pattern probably also have a genetic background that is protecting them. A note of caution is required in this analysis; many of these are relatively young individuals, much younger than the symptomatic group. What will happen in the future remains unknown. Individuals with an electrocardiographic pattern that normalizes are at the same risk as patients with a consistent ECG abnormality. If the substrate for arrhythmias depends on the transmural voltage gradient, one might postulate that patients would develop reentrant arrhythmias more often with the ST segment elevation. It is of course possible the ST segment elevation appears just moments before the episode of ventricular fibrillation. More data and patients will be required to assess the risk of transient vs. continuous ST segment elevation.
Those with a coved-type ECG are at higher risk than saddleback type. Actually, our group does not accept a diagnosis of Brugada syndrome without a coved-type ECG either before or after sodium blocker drug challenge. Again, this may correspond to the severity of the defect that throws off the balance of currents during the early phases of the action potential, as previously discussed. Our current understanding of basic mechanisms is that the substrate for VT/VF is unlikely to be present when only a saddleback type of ST segment elevation is manifest, but more likely in the presence of a coved type. Consistent with this hypothesis is the clinical observation that saddleback ST segment elevation usually progresses to a coved type before VT/VF is observed.
The use of potent sodium channel blockers to diagnose patients at risk for Brugada syndrome has raised some controversy. There is a wide variety of medications used to unmask the disease. False negative results have been reported with procainamide and flecainide. False positive results have been reported with flecainide in patients with LQT3. The value of the antiarrhythmic challenge will be able to be ascertained once more people are tested and genotyped for mutations.
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