Inappropriate ICD Shocks Linked to Brugada Syndrome

Researchers at Academic Medical Center (AMC, Amsterdam, The Netherlands) conducted a study in 88 consecutive BrS patients (mean age 49 years; 47% men) who were screened at AMC and CardioCenter Ticino (Lugano, Switzerland) to see if they were suitable for an sICD. All patients underwent QRS/T-wave morphology analysis before and after ajmaline infusion. At baseline, 76% of the patients had a normal ECG, 19% had a type 3BrS-ECG, and 5% had a type 2 BrS-ECG.

The researchers found that morphology analysis failed in 24% of patients upon development of a type 1 ECG pattern during ajmaline testing, all due to more pronounced T-waves; all the patients had true morphology analysis at baseline. They concluded that as sICD arrhythmia discrimination is based on a comparison between a template acquired after implantation and a spontaneously occurring arrhythmia, it is susceptible to QRS-/T-wave over-sensing, and is a leading cause of inappropriate shocks by an sICD. The study was published on August 9, 2016, in the Journal of the American College of Cardiology (JACC).

“Sensing might be particularly difficult in Brugada syndrome patients because of the dynamic nature of the ECG morphology. These patients are accordingly at risk for inappropriate shocks,” concluded lead author Louise R.A. Olde Nordkamp, MD, PhD, of AMC, and colleagues. “We therefore recommend that in the presence of a type-1 Brugada Syndrome ECG after subcutaneous ICD implantation, for example during fever or during an additional ajmaline test, all three sensing vectors should be evaluated, and the best suitable sensing vector should be programmed.”

BrS is a genetic disease characterized by abnormal ECG findings and an increased risk of sudden cardiac death (SCD) due to ventricular fibrillation. Over time and during fever, the ECG of BrS patients may change from a type 3 or 2 Brugada ECG to type 1 Brugada ECG, which is characterized by prominent ST-T segment changes. Approximately 20% of BrS cases have been shown to be associated with mutations in a gene that encodes for a sodium ion channel in myocyte cell membranes.

Related Links:
Academic Medical Center
CardioCenter Ticino