Late potential at the high ventricular septal level in a patient with Brugada: possible mechanisms and clinical implications.

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 Electrocardiol

authors

Baez-Escudero JL,Shah DP,Weisberg IL,Beshai JF,Burke MC

doi

10.1016/j.jelectrocard.2010.07.008

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

459-62

issue

5

eissn

0022-0736

issn

1532-8430

pii

S0022-0736(10)00286-4

journal_volume

43

pub_type

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