Abstract:
:The Brugada syndrome (BS) accounts for approximately 20% of cases of sudden cardiac death in patients with structurally normal hearts. The electrophysiologic basis for ST-segment elevation in the precordial electrocardiogram (ECG) leads that characterize the Brugada phenotype and its strong linkage to ventricular tachycardia (VT)/ventricular fibrillation is still a subject of controversy. Electrocardiographic manifestations of the syndrome have been attributed to one of two basic mechanisms: (1) conduction delay in the right ventricular (RV) epicardial-free wall in the region of the outflow tract or (2) premature repolarization of the RV epicardial action potential secondary to loss of the action potential dome. Signal-averaged ECG recordings have demonstrated late potentials that extend beyond the QRS complex in patients with the BS, especially in the anterior wall of the RV outflow tract. The basis for these epicardial late potentials remains a subject of interest among basic and clinical electrophysiologists. Endocardial late potentials in BS are even less well understood. We present a case of a patient with Brugada syndrome with a distinct endocardial late potential in the high ventricular septum coinciding with the ST-segment elevation. We discuss the possible mechanisms for this intracardiac finding and its clinical significance. We also review the effect of isoproterenol infusion on both the late potential and the surface ECG.
journal_name
J Electrocardioljournal_title
Journal of electrocardiologyauthors
Baez-Escudero JL,Shah DP,Weisberg IL,Beshai JF,Burke MCdoi
10.1016/j.jelectrocard.2010.07.008subject
Has Abstractpub_date
2010-09-01 00:00:00pages
459-62issue
5eissn
0022-0736issn
1532-8430pii
S0022-0736(10)00286-4journal_volume
43pub_type
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