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Volume 42, Issue 6, Pages 555-560 (November 2009)


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The prognostic value of the Tpeak-Tend interval in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction

Christian Haarmark, MDab, Peter R. Hansen, MD, PhDd, Esben Vedel-Larsen, MScEngab, Sune Haahr Pedersen, MDd, Claus Graff, MScEngc, Mads P. Andersen, MScEngc, Egon Toft, MD, PhDc, Fan Wang, MDab, Johannes J. Struijk, MScEng, PhDc, Jørgen K. Kanters, MDabdCorresponding Author Informationemail address

Received 26 April 2009 published online 30 July 2009.

Abstract 

Introduction

The Tpeak-Tend interval (TpTe) has been linked to increased arrhythmic risk. TpTe was investigated before and after primary percutaneous coronary intervention (pPCI) in patients with ST-segment elevation myocardial infarction (STEMI).

Method

Patients with first-time STEMI treated with pPCI were included (n = 101; mean age 62 years; range 39-89 years; 74% men). Digital electrocardiograms were taken pre- and post-PCI, respectively. Tpeak-Tend interval was measured in leads with limited ST-segment deviation. The primary end point was all-cause mortality during 22 ± 7 months (mean ± SD) of follow-up.

Results

Pre- and post-PCI TpTe were 104 milliseconds [98-109 milliseconds] and 106 milliseconds [99-112 milliseconds], respectively (mean [95% confidence interval], P = .59). A prolonged pre-PCI TpTe was associated with increased mortality (hazard ratio, 10.5 [1.7-20.4] for a cutoff value of 100 milliseconds). Uncorrected QT and heart rate–corrected QT intervals (Fridericia-corrected QT) were prolonged after PCI (QT: 401 vs 410 milliseconds, P = .022, and Fridericia-corrected QT: 430 vs 448 milliseconds, P < .0001).

Conclusion

In patients with STEMI undergoing pPCI, pre-PCI TpTe predicted subsequent all-cause mortality, and the QT interval was increased after the procedure.

a Laboratory of Experimental Cardiology, University of Copenhagen, Copenhagen, Denmark

b Danish National Research Foundation Centre for Cardiac Arrhythmia (DARC), Copenhagen, Denmark

c Department of Health Science and Technology, Aalborg University, Aalborg, Denmark

d Department of Cardiology P, Gentofte University Hospital, Hellerup, Denmark

Corresponding Author InformationCorresponding author. Laboratory of Experimental Cardiology, University of Copenhagen, Blegdamsvej 3C, DK-2200 Copenhagen N, Denmark.

 The study was supported by the Danish Heart Foundation, John and Tove Girotti's Foundation, Danish National Research Foundation, King Christian X' Foundation and Lægernes Forsikringsforening.

PII: S0022-0736(09)00254-4

doi:10.1016/j.jelectrocard.2009.06.009


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