Prolonged right ventricular ejection delay identifies high risk patients and gender differences in Brugada syndrome

Background and purpose:
Right ventricular (RV) conduction delay has been suggested as an underlying pathophysiological mechanism in Brugada syndrome (BS). In this cross-sectional study we non-invasively assessed the valueof echocardiographic markers reflecting ventricular ejection delay in identifying BS patients at risk for life-threatening arrhythmic events. Furthermore, because male BS patients demonstrate a more malignant clinical phenotype, we sought to
assess differences in ejection delays between both genders.
Methods:
124 BS patients (57.3% males) and 62 controls (CTR) (48.4% males)
were included. Using Tissue Velocity Imaging, the ejection delay, determined as
the time from QRS onset to the onset of the sustained systolic contraction, was
measured for both RV free wall (RVED) and lateral LV wall (LVED). From these
parameters, the interventricular ejection delay between both walls (IVED) was calculated.
Results:
BS patients had longer RVED’s and IVED’s compared to the CTR. BS
patients with a previous history of syncope or spontaneous ventricular arrhythmia showed the longest RVED’s and IVED’s. Male BS patients demonstrated longer RVED’s and IVED’s than females. Male BS patients with malignant events had the longest delays. No significant differences regarding LVED were observed between BS patients and CTR.
Conclusions:
We demonstrated that a previous history of malignant events was
associated with longer RVED’s. Our findings supported the RV conduction delay
mechanism behind BS and demonstrated for the first time that the predominant
malignant male Brugada phenotype might also be the result of a more delayed
RV conduction in males