Key result
ATP linked to VT acceleration in ~9% of episodes, predicted by shorter cycle lengths and ramp pacing.
Why the study?
Anti-tachycardia pacing can cause ventricular tachycardia acceleration or degeneration to ventricular fibrillation leading to ICD shocks, but predictors of this acceleration remain incompletely understood.
What are the predictors of ventricular tachycardia acceleration by anti-tachycardia pacing therapy in patients with structural heart disease and ICDs?
Observational (n=60)
Yes
What are the predictors of ventricular tachycardia acceleration by anti-tachycardia pacing therapy in patients with structural heart disease and ICDs?
In patients with ICDs, anti-tachycardia pacing can accelerate ventricular tachycardia, particularly in those with low ejection fraction, fast VTs (cycle length < 310 ms), and when using ramp pacing or multiple bursts.
BACKGROUND: Anti-tachycardia pacing therapy (ATP) has shown comparable efficacy to shock therapy in ventricular tachycardia (VT) termination with better quality of life. However, some ATPs may lead to VT acceleration or degeneration to ventricular fibrillation (VF), which will result in more ICD shocks. The aim of this study was to investigate the predictors of VT acceleration by ATP therapy in a real-life patient cohort. RESULTS: We retrospectively reviewed 448 monomorphic VT episodes that required ATP therapy in 60 patients with structural heart diseases implanted with ICD or CRTD. The clinical data of the patients and the episodes' details were evaluated. We found that patients with a higher ejection fraction (EF) were more likely to be cardioverted by ATP therapy (P: 0.024). VT acceleration was more frequent in patients with lower EF (mean 31.24 ± 4.08) compared with the non-accelerated patients with higher EF (mean 37.00 ± 9.4, P: 0.016). The percentage of accelerated episodes was 8.5%. VT episodes with a mean cycle length (CL) < 310 ms are more likely to accelerate (sensitivity 76.3%, specificity 67.7%, PPV value 45%, NPV 86%, and AUC 0.790). There was a statistically significant difference in the accelerated VT episodes as compared to non-accelerated episodes regarding the number of ATP bursts (mean 3.66 ± 2.22 vs. 1.76 ± 1.35, P: < 0.001), ramp (23.7% vs. 4.2%, P: < 0.001), scanning (55.3% vs. 31.3%, P: 0.003) and burst adaptive cycle length (mean 83.55 ± 2.92 vs. 84.64 ± 2.61, P: 0.016). In a multivariate analysis, the VT CL, number of ATP bursts and ramp pacing predicted VT acceleration by ATP therapy. CONCLUSIONS: Ventricular tachycardia in patients with low LV EF and fast VTs with a CL less than 310 ms were more likely to accelerate with ATP therapy. The number of ATP bursts and the use of ramp had a significant effect on VT acceleration. To avoid VT acceleration by ATP therapy, ramp pacing better be avoided, especially in fast VTs, and lesser number of bursts should be delivered.
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Awad et al. (2023) conducted an observational in Monomorphic ventricular tachycardia in patients with implantable cardioverter defibrillators (n=60). Anti-tachycardia pacing (ATP) vs. Non-accelerated VT episodes was evaluated on Ventricular tachycardia acceleration. Anti-tachycardia pacing therapy resulted in ventricular tachycardia acceleration in 8.5% of episodes, with shorter cycle length (<310 ms), higher number of bursts, and ramp pacing identified as significant predictors.
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