Key result
Sinus rhythm activation maps in the infarct border zone predict arrhythmia inducibility in reentrant VT substrates.
Why the study?
Reentrant ventricular tachycardia mechanisms remain incompletely understood, and methods to assess inducibility using sinus rhythm parameters are needed.
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Sinus rhythm spatiotemporal activation profiles from substrate compilation maps can predict reentrant VT inducibility in a post-infarction canine model.
Introduction Reentrant ventricular tachycardia (VT) is an important clinical problem, with underlying biophysical mechanisms that remain incompletely understood. Substrate compilation maps were used to detect subtle spatial gradients and for assessing inducibility of sustained VT. Method/Results A subepicardial infarct was created via left anterior descending coronary artery (LAD) ligation in canine hearts. After 3–5 days, electrical activity was marked and mapped using a 312‐electrode array in 60 postinfarction hearts (30 noninducible for VT, 30 with sustained VT). Compilation maps were constructed by summing the N = 30 individual experiment maps of parameters from representative sinus rhythm (SR) and VT cycles. Gradients were determined by averaging multiarray data row‐by‐row, and by dividing 312‐grid sites into LAD‐proximate vs. apical‐lateral‐proximate halves. Prediction of VT induction was done using SR activation statistics. Compilation maps revealed that SR activation times were prolonged in inducible vs. non‐inducible experiments (means 21.64 vs. 13.58 msec, p < 0.001). SR activation means and standard deviations per experiment ( N = 312 sites) were predictive of reentrant VT inducibility (sensitivity = 28/30 or 93.3%, specificity = 26/30 or 86.7%). SR electrogram duration lengthened in inducible vs. non‐inducible VT experiments (36.54 vs. 32.40 msec, p < 0.001). VT electrogram duration averaged 34.70 msec, differing from both SR measurements ( p ≤ 0.003). Isthmus electrogram duration averaged 33.6 msec in SR vs. 40.6 msec in VT. The SR electrogram duration in VT inducible experiments exhibited a gradient with values increasing away from the LAD ( r 2 = 0.79, p < 0.001), perhaps resulting from decreasing blood perfusion. Conclusions Compilation maps provide insights into profiles of SR spatiotemporal activation, to predict arrhythmia inducibility in reentrant VT substrates.
Ciaccio et al. (2026) studied Reentrant ventricular tachycardia (n=60). Reentrant VT inducibility vs. Non-inducible VT was evaluated on Sinus rhythm activation times (p=<0.001). Sinus rhythm activation times were significantly prolonged in VT-inducible compared to non-inducible canine hearts (21.64 vs. 13.58 msec, p<0.001), predicting reentrant VT inducibility.
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