Author + information
- Received November 2, 2017
- Revision received January 25, 2018
- Accepted February 1, 2018
- Published online March 28, 2018.
- Gijsbert F.L. Kapel, MDa,
- Charlotte Brouwer, MDa,
- Zakaria Jalal, MDb,c,
- Frédéric Sacher, MD, PhDb,
- Jeroen Venlet, MDa,
- Martin J. Schalij, MD, PhDa,
- Jean-Benoît Thambo, MD, PhDc,
- Monique R.M. Jongbloed, MD, PhDa,
- Nico A. Blom, MD, PhDa,
- Marta de Riva, MDa and
- Katja Zeppenfeld, MD, PhDa,∗ ()
- aDepartment of Cardiology, Leiden University Medical Centre, Leiden, the Netherlands
- bElectrophysiology and Heart Modeling Institute, Bordeaux University Hospital, Bordeaux, France
- cDepartment of Paediatric and Adult Congenital Cardiology, Bordeaux University Hospital, Bordeaux, France
- ↵∗Address for correspondence:
Dr. Katja Zeppenfeld, Department of Cardiology, Leiden University Medical Centre, C5-P, PO Box 9600, 2300 RC Leiden, the Netherlands.
Objectives This study sought to evaluate the influence of slow conducting anatomic isthmuses (SCAI) as dominant ventricular tachycardia (VT) substrate on QRS duration.
Background QRS prolongation has been associated with VT in repaired tetralogy of Fallot.
Methods Seventy-eight repaired tetralogy of Fallot patients (age 37 ± 15 years, 52 male, QRS duration 153 ± 29 ms, 67 right bundle branch blocks [RBBB]) underwent programmed stimulation and electroanatomic activation mapping during sinus rhythm. Right ventricular (RV) surface, RV activation pattern, RV activation time, conduction velocity at AI, and remote RV sites were determined.
Results Twenty-four patients were inducible for VT (VT+); SCAI was present in 22 of 24 VT+ but only in 2 of 54 patients without inducible VT (VT−). Conduction velocity through AI was slower in VT+ patients (median of 0.3 (0.3–0.4) vs. 0.7 (0.6–0.9) m/s; p < 0.01) but conduction velocity in the remote RV did not differ between groups. In non-RBBB, QRS duration was similar in VT+ patients (n = 6) and VT− patients (n = 5), but RV activation within SCAI exceeded QRS offset in VT+ patients (37 ± 20 ms vs. –5 ± 9 ms, p < 0.01). In RBBB, both QRS duration and RV activation time were longer in VT+ patients (n = 18, 17 of 18 QRS > 150 ms) compared with VT− patients (n = 49, 27 of 49 QRS > 150 ms) (173 ± 22 ms vs. 156 ± 20 ms; p < 0.01; 141 ± 22 ms vs. 129 ± 21 ms; p = 0.04). In VT+ patients, QRS prolongation >150 ms (n = 17) was due to SCAI or blocked isthmus in 15 patients (88%) and 1 (6%). In contrast, in VT− patients, QRS prolongation >150 ms (n = 27) was due to enlarged RV or blocked isthmus in 10 patients (37%) and 8 (30%), but due to SCAI in only 1 (4%). After exclusion of a severely enlarged RV, a QRS duration >150 ms was highly predictive for SCAI/blocked AI (OR: 17; 95% CI: 3.3 to 84; p < 0.01).
Conclusions A narrow QRS interval does not exclude VT-related SCAI. In the presence of RBBB, SCAI further prolongs QRS duration. QRS duration >150 ms is highly suspicious for SCAI or isthmus block distinguishable by electroanatomic mapping.
The Department of Cardiology Leiden has received unrestricted research and fellowship grants from Edward Lifesciences, Boston Scientific, Medtronic and Biotronik. The Electrophysiology and Heart Modeling Institute has received financial support from the French government (grant ANR-10-IAHU-04). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received November 2, 2017.
- Revision received January 25, 2018.
- Accepted February 1, 2018.
- 2018 American College of Cardiology Foundation
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