Email this article Antitachycardic Therapy of ICD in Patients with Multiple Morphologies of Monomorphous Ventricular Tachycardia Refractory to Therapy
- Authors: Goncharik D.B.1, Barsukevich V.C.1, Plashchinskaya L.I.1, Zakhareuski M.A.1
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Affiliations:
- Republican Scientific and Practical Centre "Cardiology"
- Issue: Vol 2, No 4 (2022)
- Pages: 43-54
- Section: Case reports
- URL: https://journals.rcsi.science/cardar/article/view/132571
- DOI: https://doi.org/10.17816/cardar112248
- ID: 132571
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Fig. 1. ICD detects VT with a cycle of 330 ms (a), delivers a series of ATP pacing (b), whereas the analysis of the ICD endogram indicates effective pacing, with post-pacing interval of 420 ms. ATP has entered a VT cycle which is at a distance of (420–330)/2 = 45 ms from the ICD stimulation electrode. However, VT persists at the same rate
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Fig. 2. Owing to the lack of effect of ATP pacing, the ICD delivers a discharge and stops VT
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Fig. 3. Summary of the detected and arrested VT episodes. The total duration from the onset of the paroxysm to its arrest was 1 min 27 s. The episode of SM-VT with HR of 182–188 bpm was detected by ICD. To stop the ICD-detected VT, three attempts were made to arrest VT using ATP, starting from a cycle of 88% of the detected VT cycle. Thus, for the VT cycle of 330 ms, the first sequence of ATP Burst-1 is plotted with a cycle of 330 × 0.88 = 290 ms. The imposition was effective, and there were no signs of loss of capture. ATP “entered a VT cycle” but did not stop VT and was not effective. As VT persists, the ICD delivers the next series of cycles 10 ms shorter, i.e. 280 ms and then 270 ms. The duration of the post-stimulation interval (return cycle 1 of VT) ranged from 410 to 420 ms, which indicated the effective imposition of ATP pacing and the absence of loss of capture. However, this cycle of ATP pacing was too long to induce VT arrest (by creating a blockade in both directions of the VT reentry chain). Owing to the lack of VT arrest, the ICD delivered a discharge and stopped VT
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Fig. 4. SM-VT induced during EEPS of two main morphologies
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Fig. 5. a — Typical burst pacing from the right ventricular (RV) lead (88% of the SM-VT cycle). After ATP termination, VT continues with the same cycle of 365 ms. b — Typical burst pacing from the RV lead (83% of the SM-VT cycle). VT changed slightly the morphology and continues with the same cycle of 365 ms. c — “Aggressive” antitachycardic burst pacing from the RV lead (approximately 55% of the SM-VT cycle of 200 ms) with no effect. VT was maintained with the same cycle. d — “Aggressive” antitachycardiac burst pacing from the RV lead with a very short interval on the verge of an effective ventricular refractory period (approximately 52% of the SM-VT cycle of 190 ms). At the end of ATP stimulation, VT accelerates to 280–290 bpm and transforms into polymorphic VT (short fragment), with spontaneous arrest
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Pic. 6. a — ATP pacing with an insufficiently short pacing cycle produces blockade in one direction but does not achieve blockade in the antegrade propagating reentry wave. S1 stimulation “enters the VT cycle” (VT entrainment), but does not stop VT. b — S1 pacing “enters the VT cycle” and given the short interval, achieves blockade of impulse propagation in both directions (stops VT)
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Fig. 7. After entering the reentry cycle, the application of the S2 pacing with a sufficiently short coupling interval “closes” the impulse propagation in both directions (due to the entry of vulnerable VT isthmus into the tissue refractoriness period)
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