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|Title:||Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia|
|Citation:||Journal of Interventional Cardiac Electrophysiology, 2018; 51(1):13-24|
|Sachin Nayyar, Lauren Wilson, Anand Ganesan, Thomas Sullivan, Pawel Kuklik, Glenn Young, Prashanthan Sanders, Kurt C. Roberts-Thomson|
|Abstract:||Purpose: Protected channels of surviving myocytes in late postinfarction ventricular scar predispose to ventricular tachycardia (VT). However, only a few patients develop VT spontaneously. We studied differences in electric remodeling and protected channels in late postinfarction patients with and without spontaneous VT. Methods: Patients with ischemic cardiomyopathy (ICM) with recurrent sustained monomorphic VT (n = 22) were compared with stable ICM patients without spontaneous VT (control group; n = 5). Left ventricular mapping was performed with a 20-pole catheter. Detailed pace mapping was used to identify channels of protected conduction, and confirmed, when feasible, by entrainment. Anatomical and electrophysiological properties of VT channels and non-VT channels in VT patients and channels in controls were evaluated. Results: Seventy-three (median 3) VTs were inducible in VT patients compared to two (median 0) in controls. The VT channels in VT patients (n = 57, 3 ± 1 per patient) were lengthier (mean ± SEM 53 ± 5 vs. 33 ± 4 vs. 24 ± 8 mm), had longer S-QRS (73 ± 4 vs. 63 ± 3 vs. 44 ± 8 ms), longer conduction time (103 ± 13 vs. 33 ± 4 vs. 24 ± 8 ms), and slower conduction velocity (CV) (0.85 ± 0.21 vs. 1.39 ± 0.20 vs. 1.31 ± 0.41 m/s) than non-VT channels in VT patients (n = 183, 8 ± 6 per patient) (p ≤ 0.01) and channels in controls (n = 46, 9 ± 8 per patient) (p ≤ 0.01). Additionally, non-VT channels in VT patients had longer S-QRS (p = 0.02); however, they were similar in length, conduction time, and CV compared to channels in controls. Conclusions: Channels supporting VT are lengthier, with longer conduction times and slower CV compared to channels in patients without spontaneous VT. These observations may explain why some ICM patients have spontaneous VT and others do not.|
|Keywords:||Channels; ischemic cardiomyopathy; substrate; Ventricular tachycardia|
|Rights:||© Springer Science+Business Media, LLC, part of Springer Nature 2017|
|Appears in Collections:||Medicine publications|
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