Journal Home
Search for

Volume 54, Issue 2, Pages 143-149 (7 July 2009)


View previous. 8 of 18 View next.

Giant T–U Waves Precede Torsades de Pointes in Long QT Syndrome: A Systematic Electrocardiographic Analysis in Patients With Acquired and Congenital QT Prolongation

Paulus Kirchhof, MD, Michael R. Franz, MD, PhDCorresponding Author Informationemail address, Abdennasser Bardai, MD, Arthur M. Wilde, MD

Received 25 November 2008; received in revised form 5 March 2009; accepted 10 March 2009.

Objectives

This study sought to identify electrocardiographic (ECG) criteria that are associated with initiation of torsades de pointes (TdP) in patients with acquired (a-) and congenital (c-) long QT syndrome (LQTS).

Background

Electrocardiographic criteria used as risk predictors for TdP commonly rely on a prolonged QT interval but rarely consider abnormal T–U waves.

Methods

We analyzed ECG recordings with TdP from 35 LQTS patients (15 c-LQTS and 20 a-LQTS) and compared them with premature ventricular complexes (PVCs) from 40 patients with normal QT intervals and with PVCs in 24 of the 35 LQTS patients not related to TdP.

Results

Abnormal T–U waves (6.2 ± 0.9 mm) directly preceded TdP in 34 of 35 LQTS patients and were larger than T-wave amplitude (2.8 ± 0.2 mm) in control patients and larger than the largest T–U-wave in LQTS without TdP (4.7 ± 0.8 mm). The TdP-initiating beat emerged from a T–U-wave in 27 of 35 LQTS patients and in none of 40 control patients. The QRS duration of the first TdP beat (175 ± 12 ms) was longer than in control PVCs (145 ± 4 ms) and in PVCs in LQTS patients not related to TdP (138 ± 22 ms). The QRS angle was less steep before TdP than in other PVCs (all p < 0.05).

Conclusions

Abnormal, giant T–U waves separate TdP initiation in LQTS patients from PVCs in other heart disease and from other PVCs in LQTS patients. These ECG analyses suggest that early afterdepolarizations initiate TdP and, if present, may help to identify an imminent risk for TdP.

 VA Medical Center/Georgetown University, Washington, DC

 Department of Cardiology and Angiology, University Hospital Münster, and IZKF Münster, Münster, Germany

 Heart Failure Research Centre, Department of Cardiology, Academic Medical Centre, Amsterdam, the Netherlands

Corresponding Author InformationReprint requests and correspondence: Dr. Michael R. Franz, VA Hospital, Cardiology, 50 Irving Street, NW, Washington, DC 40007

 This study was funded in part by Deutsche Forschungsgemeinschaft (DFG, Ki/713/1-1), by the German Ministry for Research and Education (BMBF, AFNET, 01Gi0204), and by Fondation LeDucq (Alliance Against Sudden Cardiac Death and ENAFRA). Dr. Kirchhof has received consulting fees or honoraria from 3M Medica, AstraZeneca, Bayer Healthcare, Boehringer Ingelheim, MEDA Pharma, Medtronic, Sanofi-Aventis, Siemens, Sorvier, and Takeda; and research grants from Cardiovascular Therapeutics, 3M Medica/MEDA Pharma, Medtronic, Omron, and St. Jude Medical. Drs. Kirchhof and Franz contributed equally to this work.

PII: S0735-1097(09)01291-1

doi:10.1016/j.jacc.2009.03.043


View previous. 8 of 18 View next.