Open Access

ARTICLE

Prolonged T_peak‐T_end interval is a risk factor for sudden cardiac death in adults with congenital heart disease

by

1 Department of Clinical and Experimental Cardiology, Heart Center, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands
2 Department of Cardiology, Universitair Ziekenhuis Leuven, Leuven, Belgium
3 Department of Cardiovascular Sciences, Katholieke Universiteit Leuven, Leuven, Belgium
4 Division of Cardiology, Peter Munk Cardiac Centre, Toronto Congenital Cardiac Centre for Adults, University of Toronto, Toronto, Ontario, Canada
5 Department of Clinical Epidemiology and Biostatistics, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands
6 Netherlands Heart Institute, Utrecht, the Netherlands

* Corresponding Author: Joris R. de Groot, Academic Medical Center, Department of Cardiology, PO‐Box 22700; 1100 DE Amsterdam. Email:

Congenital Heart Disease 2019, 14(6), 952-957. https://doi.org/10.1111/chd.12847

Abstract

Objective: Adult congenital heart disease (ACHD) patients are at risk of sudden cardiac death (SCD). However, methods for risk stratification are not yet well‐ defined. The T_peak‐T_end (TpTe) interval, a measure of dispersion of ventricular repolari‐ zation, is a risk factor for SCD in non‐ACHD patients. We aim to evaluate whether TpTe can be used in risk stratification for SCD in ACHD patients.
Design: From an international multicenter cohort of 25 790 ACHD patients, we iden‐ tified all SCD cases. Cases were matched to controls by age, gender, congenital de‐ fect, and (surgical) intervention.
Outcome Measures: TpTe was measured on a standard 12‐lead ECG. The maximum TpTe of all ECG leads (TpTe‐max), mean (TpTe‐mean), and TpTe dispersion (maximum minus minimum) were obtained. Odds ratios (OR) for SCD cases vs controls were calculated using conditional logistic regression analysis.
Results: ECGs were available for 147 cases (median age at death 33.5 years (quartiles 26.2, 48.7), 66% male) and 267 controls. The mean TpTe‐max was 97 ± 24 ms in cases vs 84 ± 17 ms in controls (P < .001); TpTe‐mean was 70 ± 16 vs 63 ± 10 ms (P < .001); and dispersion was 51 ± 22 ms vs 41 ± 16 ms (P = .02), respectively. Assessing each ECG lead separately, TpTe in lead aVR predicted SCD most accurately. TpTe in lead aVR was 71 ± 23 ms in cases vs 61 ± 13 ms in controls (P < .001). After adjusting for impaired ventricular function, heart failure symptoms, and prolonged QRS duration, the OR of SCD of TpTe in lead aVR at an optimal cutoff of 80 ms was 5.8 (95% CI 2.7‐12.4, P < .001).
Conclusions: The TpTe interval is associated with SCD in ACHD patients. Particularly, TpTe in lead aVR can be used as an independent risk factor for SCD in ACHD patients and may, therefore, add precision to current risk prediction models.

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