Prolonged Tpeak-to-Tend Interval on the Resting ECG Is Associated With Increased Risk of Sudden Cardiac Death

Background— Early studies indicate that prolongation of the interval between the peak and the end of the T wave (Tpeak to Tend [TpTe]) on the 12-lead ECG is a marker of ventricular arrhythmogenesis. However, community-based studies have not been conducted. Methods and Results— TpTe and other ECG predictors were evaluated in the ongoing Oregon Sudden Unexpected Death Study based in the Portland, Oregon, metropolitan area using a case-control design. Cases of sudden cardiac death (SCD) (n=353; mean age, 66.6 years; 95% CI, 65.1 to 68.1 years; 67% men) were compared with living controls with coronary artery disease (n=342; mean age, 64.7 years; 95% CI, 63.4 to 66.0 years; 69% men) from the same region. Analysis of TpTe and selected ECG intervals was limited to sinus rhythm 12-lead ECGs. For cases, these were obtained before and unrelated to SCD. Independent-samples t tests and multiple logistic regression were used. Mean TpTe was significantly greater in cases (89.4 ms; 95% CI, 87.7 to 91.2 ms; P<0.0001) than in controls (76.1 ms; 95% CI, 74.8 to 77.4 ms). The other ECG intervals (corrected QT interval [QTc], QRS duration [QRSD], and TpTe/QT ratio) also were significantly prolonged among cases versus controls (P⩽0.01). TpTe remained a significant predictor of SCD after adjusting for age, sex, QTc, QRSD, and left ventricular function. Odds of SCD increased more with a 1-SD increase in TpTe (12 ms) among subjects with prolonged QRSD (odds ratio, 3.49; 95% CI, 2.06 to 5.91) than with a 1-SD increase in TpTe among subjects with normal QRSD (odds ratio, 1.96; 95% CI, 1.65 to 2.32). TpTe remained significantly associated with SCD in subjects with normal QTc. Conclusions— Prolongation of the TpTe interval measured in lead V5 was independently associated with SCD, with particular utility when the QTc was normal or not measurable because of prolonged QRSD.

[1]  Mark E. Anderson,et al.  Sudden Cardiac Death Prediction and Prevention: Report From a National Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop , 2010, Circulation.

[2]  K. Reinier,et al.  Factors Associated With Pulseless Electric Activity Versus Ventricular Fibrillation: The Oregon Sudden Unexpected Death Study , 2010, Circulation.

[3]  S. Chugh Early identification of risk factors for sudden cardiac death , 2010, Nature Reviews Cardiology.

[4]  K. Reinier,et al.  Women have a lower prevalence of structural heart disease as a precursor to sudden cardiac arrest: The Ore-SUDS (Oregon Sudden Unexpected Death Study). , 2009, Journal of the American College of Cardiology.

[5]  Esben Vedel-Larsen,et al.  The prognostic value of the Tpeak-Tend interval in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. , 2009, Journal of electrocardiology.

[6]  Dawn Peters,et al.  Determinants of Prolonged QT Interval and Their Contribution to Sudden Death Risk in Coronary Artery Disease: The Oregon Sudden Unexpected Death Study , 2009, Circulation.

[7]  Ruben Coronel,et al.  Repolarization Gradients in the Intact Heart , 2009, Circulation. Arrhythmia and electrophysiology.

[8]  K. Reinier,et al.  Physical activity as a trigger of sudden cardiac arrest: the Oregon Sudden Unexpected Death Study. , 2009, International journal of cardiology.

[9]  K. Reinier,et al.  Epidemiology of sudden cardiac death: clinical and research implications. , 2008, Progress in cardiovascular diseases.

[10]  G. Yan,et al.  T(p-e)/QT ratio as an index of arrhythmogenesis. , 2008, Journal of electrocardiology.

[11]  C. Callaway,et al.  Regional variation in out-of-hospital cardiac arrest incidence and outcome. , 2008, JAMA.

[12]  Charles Antzelevitch,et al.  Role of spatial dispersion of repolarization in inherited and acquired sudden cardiac death syndromes. , 2007, American journal of physiology. Heart and circulatory physiology.

[13]  Li Zhang,et al.  Does Tpeak-Tend provide an index of transmural dispersion of repolarization? , 2007, Heart rhythm.

[14]  Michael Glikson,et al.  The morphology of the QT interval predicts torsade de pointes during acquired bradyarrhythmias. , 2007, Journal of the American College of Cardiology.

[15]  P. Kowey,et al.  Blinded validation of the isolated arterially perfused rabbit ventricular wedge in preclinical assessment of drug-induced proarrhythmias. , 2006, Heart rhythm.

[16]  K. Reinier,et al.  Incidence of sudden cardiac arrest is higher in areas of low socioeconomic status: a prospective two year study in a large United States community. , 2006, Resuscitation.

[17]  Charles Antzelevitch,et al.  Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome. , 2006, Journal of the American College of Cardiology.

[18]  Karen L. Gunson,et al.  Population-based analysis of sudden cardiac death with and without left ventricular systolic dysfunction: two-year findings from the Oregon Sudden Unexpected Death Study. , 2006, Journal of the American College of Cardiology.

[19]  A. Hofman,et al.  Prolonged QTc interval and risk of sudden cardiac death in a population of older adults. , 2006, Journal of the American College of Cardiology.

[20]  Mohamud Daya,et al.  Current burden of sudden cardiac death: multiple source surveillance versus retrospective death certificate-based review in a large U.S. community. , 2004, Journal of the American College of Cardiology.

[21]  Taku Asano,et al.  Transmural dispersion of repolarization and ventricular tachyarrhythmias. , 2004, Journal of electrocardiology.

[22]  H. Mabuchi,et al.  T wave peak-to-end interval and QT dispersion in acquired long QT syndrome: a new index for arrhythmogenicity. , 2003, Clinical science.

[23]  K. Hayashi,et al.  T‐peak to T‐end interval may be a better predictor of high‐risk patients with hypertrophic cardiomyopathy associated with a cardiac troponin i mutation than qt dispersion , 2002, Clinical cardiology.

[24]  C. Antzelevitch,et al.  Cellular Basis for Complex T Waves and Arrhythmic Activity Following Combined IKr and IKs Block , 2001, Journal of cardiovascular electrophysiology.

[25]  P Taggart,et al.  Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia. , 2001, Cardiovascular research.

[26]  M. Radomski,et al.  The Terminal Portion of the T Wave: A New Electrocardiographic Marker of Risk of Ventricular Arrhythmias , 2000, Pacing and clinical electrophysiology : PACE.

[27]  CHARLES ANTZELEVITCH,et al.  The M Cell: , 1999, Journal of cardiovascular electrophysiology.

[28]  C Antzelevitch,et al.  Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. , 1998, Circulation.

[29]  H. Bazett,et al.  AN ANALYSIS OF THE TIME‐RELATIONS OF ELECTROCARDIOGRAMS. , 1997 .

[30]  H V Huikuri,et al.  Dispersion of QT interval in patients with and without susceptibility to ventricular tachyarrhythmias after previous myocardial infarction. , 1995, Journal of the American College of Cardiology.

[31]  G. Gintant,et al.  Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells. , 1991, Circulation research.

[32]  C Antzelevitch,et al.  A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell. , 1991, Circulation research.

[33]  D. Corrado,et al.  Sudden death as the first manifestation of coronary artery disease in young people (less than or equal to 35 years). , 1988, European heart journal.

[34]  D. Corrado,et al.  Sudden death as the first manifestation of coronary artery disease in young people (≤ 35 years) , 1988 .

[35]  Fred S Apple,et al.  Etiology of sudden death in the community: results of anatomical, metabolic, and genetic evaluation. , 2010, American heart journal.

[36]  C Antzelevitch,et al.  Cellular basis for QT dispersion. , 1998, Journal of electrocardiology.