Article Text

67 Dynamic Characterisation of the Electrophysiological Substrate in Brugada Syndrome During Physiological Autonomic Stimulation
  1. Kevin Ming Wei Leong1,
  2. Fu Siong Ng1,
  3. Caroline Roney1,
  4. Phang Boon Lim2,
  5. Nicholas Simon Peters1,
  6. Amanda Varnava2,
  7. Prapa Kanagaratnam1
  1. 1NHLI, Imperial College London
  2. 2Imperial College Healthcare NHS Trust


Introduction Sudden death in Brugada Syndrome (BrS) is associated with rest, when parasympathetic tone predominates and/or sympathetic tone is diminished. Non-invasive electrocardiographical imaging (ECGi) allows electrophysiological properties to be studied outside the cardiac catheter laboratory. We tested the hypothesis that in BrS the electrophysiological response to autonomic stimulation can be measured with ECGi.

Methods Patients with ajmaline induced Type 1 Brugada ECG pattern and those with ventricular ectopy (as the control group) requiring electrophysiological studies were recruited. Anti-arrhythmic medications were stopped 5 days before the study, and echocardiography showed structurally normal hearts in all the participants.

CT-chest was performed with an ECGi vest to analyse reconstructed epicardial electrograms (EGMs) on a 3D geometry of the patient’s heart. Activation recovery interval (ARI), an action potential duration surrogate, of the epicardial EGM was taken from right and left apical, mid and basal regions of the ventricle from each individual and corrected for heart rate (cARI) at rest and during the various autonomic states of peak exertion, recovery (with exercise treadmill test) and postural change (with tilt table testing).

Results There were 4 patients in the BrS group (mean age 51 yrs; 4 males) and 4 patients in the control group (mean age 30; 2 males and 2 females). All patients were able to achieve their maximum target heart rate for age on treadmill, and all had completed the tilt table test with 1 in each group displaying evidence of orthostatic intolerance. Baseline cARI was not significantly different between groups (299 ± 17 msec vs 284 ± 18 msec; p=ns) (Table 1).

Abstract 67 Table 1

Whole heart corrected activation recovery intervals (cARI) values

There was appropriate shortening of cARI (299 ± 17 msec to 258 ± 22 msec; p = 0.006) from baseline to peak exertion, and prolongation on recovery (258 ± 22 msec to 296 ± 23 msec; p = 0.03) in the control group, but not in the BrS group. With upright tilt, a significant increase in cARI was noted in the control group by 5 and 20 min (p < 0.05). A smaller rise was seen in the BrS group with a significant rise noted later at 20 min (p = 0.04) (Figure 1).

Abstract 67 Figure 1

Changes in whole heart activation recovery intervals, corrected for heart rate (cARI), during exercise and tilt table testing

Conclusion This study shows how cARI during autonomic challenge is different for BrS patients. This could be the basis of an alternative approach to risk stratification.

  • Brugada Syndrome
  • Electrophysiology
  • Autonomic Stimulation

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