Quarterly Focus Issue: Heart Rhythm Disorder
Clinical Research: Brugada Syndrome
Local Depolarization Abnormalities Are the Dominant Pathophysiologic Mechanism for Type 1 Electrocardiogram in Brugada Syndrome: A Study of Electrocardiograms, Vectorcardiograms, and Body Surface Potential Maps During Ajmaline Provocation

https://doi.org/10.1016/j.jacc.2009.11.033Get rights and content
Under an Elsevier user license
open archive

Objectives

We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing.

Background

BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization.

Methods

Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps.

Results

A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 ± 23 ms vs. 125 ± 14 ms, p < 0.01) and right terminal conduction delay (60 ± 11 ms vs. 53 ± 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 ± 8% vs. 8 ± 4%, p = NS), lower spatial QRS-T integrals (33 ± 12 mV·ms vs. 40 ± 16 mV·ms, p < 0.05), similar spatial QRS-T angles (92 ± 39° vs. 87 ± 31°, p = NS), similar Tpeak-Tendinterval (143 ± 36 ms vs. 138 ± 25 ms, p = NS), and similar Tpeak-Tenddispersion (47 ± 37 ms vs. 45 ± 27 ms, p = NS).

Conclusions

The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities.

Key Words

body surface potential mapping
Brugada syndrome
electrocardiography
sudden cardiac death
vectorcardiography

Abbreviations and Acronyms

BrS
Brugada syndrome
BSPM
body surface potential map
ECG
electrocardiogram
fQRSD
filtered QRS complex duration
LAS40
duration of low-amplitude signal (<40 μV) in the terminal part of the filtered QRS complex
LP
late potential
RMS40
root mean square value of voltage in the terminal 40 ms of the filtered QRS complex
RV
right ventricle/ventricular
SCN5a
gene that encodes the α-subunit of the cardiac sodium channel
VCG
vectorcardiogram
VT/VF
ventricular tachycardia/ventricular fibrillation

Cited by (0)

This study was funded by the Netherlands Heart Foundation(grants 2005T024to Dr. Postema and 2005B092to Dr. Linnenbank); Fondation Leducq Trans-Atlantic Network of Excellence, Preventing Sudden Death(grant 05-CVD-01to Dr. Wilde); Royal Netherlands Academy of Arts and Sciences(to Dr. Tan); and the Netherlands Organization for Scientific Research(grant ZonMW-VICI 918.86.616to Dr. Tan).