Background Early studies indicate that prolongation of the interval between the peak and 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 had sudden cardiac death (SCD), and were compared to living controls with coronary artery disease (CAD) from the same region. Analysis of TpTe and selected ECG intervals was limited to sinus rhythm 12-lead ECGs; for cases, these were obtained prior to and unrelated to SCD. Independent-samples t tests and multiple logistic regression were used. Mean TpTe was significantly greater in cases [89.4 (87.7 – 91.2) ms, p <0.0001; n=353, 66.6 (65.1 – 68.1) yr, 67% male] vs. controls [76.1 (74.8 – 77.4) ms; n=342, 64.7 (63.4 – 66.0) yr, 69% male)]. The other ECG intervals [Corrected QT interval (QTc), QRS duration (QRSD), and TpTe/QT ratio) were also significantly prolonged among cases vs. controls (p≤0.01). TpTe remained a significant predictor of SCD after adjusting for age, gender, QTc, QRSD and left ventricular function. Odds of SCD increased more with a one standard deviation increase in TpTe (12 ms) among subjects with prolonged QRSD [OR 3.49, 95% CI (2.06-5.91)] than with a one SD increase in TpTe among subjects with normal QRSD [OR1.96, 95% CI (1.65-2.32)]. 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 due to prolonged QRSD.

Background-In a recent cohort study, prolongation of the corrected QT interval (QTc) was associated with an independent increased risk of sudden cardiac death (SCD). We evaluated determinants of prolonged QTc and the relationship of prolonged QTc to SCD risk among patients with coronary artery disease in the general population. Methods and Results-A case-control design was used. Cases were SCD patients with coronary artery disease among a metropolitan area of 1 000 000 residents (2002 to 2006); controls were area residents with coronary artery disease but no history of SCD. All cases were required to have an ECG suitable for QTc analysis before and unrelated to the occurrence of SCD. A total of 373 cases and 309 controls met criteria for analysis. Mean QTc was significantly longer in cases than in controls (450Ϯ45 versus 433Ϯ37 ms; PϽ0.0001). In a multivariate model, gender, diabetes mellitus, and QTc-prolonging drugs were significant determinants of QTc prolongation in controls. In a logistic regression model predicting SCD, diabetes mellitus (odds ratio, 1.97; 95% confidence interval, 1.32 to 2.96) and use of QTc-prolonging drugs (odds ratio, 2.90; 95% confidence interval, 1.92 to 4.37) were significant predictors of SCD among subjects with normal or borderline QTc. However, abnormally prolonged QTc in the absence of diabetes and QT-prolonging medications was the strongest predictor of SCD (odds ratio, 5.53; 95% confidence interval, 3.20 to 9.57). Conclusions-Diabetes mellitus and QTc-affecting drugs determined QTc prolongation and were predictors of SCD in coronary artery disease. However, idiopathic abnormal QTc prolongation was associated with 5-fold increased odds of SCD. A continued search for novel determinants of QTc prolongation such as genomic factors is likely to enhance risk stratification for SCD in coronary artery disease. (Circulation. 2009;119:663-670.)

Background Sudden cardiac death (SCD) is a leading cause of death in the US, but the relative public health burden is unknown. We estimated the burden of premature death from SCD and compared it to other diseases. Methods and Results Analyses were based on the following data sources (using most recent sources that provided appropriately stratified data): 1) Leading causes of death among men and women from 2009 US death certificate reporting; 2) Individual cancer mortality rates from 2008 death certificate reporting from the CDC’s National Program of Cancer Registries; 3) County, state and national population data for 2009 from the US Census Bureau; 4) SCD rates from the Oregon Sudden Unexpected Death Study (SUDS) population-based surveillance study of SCD between 2002 and 2004. Cases were identified from multiple sources in a prospectively designed surveillance program. Incidence, counts and years of potential life lost (YPLL) for SCD and other major diseases were compared. The age-adjusted national incidence of SCD was 60 per 100,000 population (95% confidence interval = 54 – 66 per 100,000). The burden of premature death for men (2.04 million YPLL; 95% uncertainty interval 1.86 – 2.23 million) and women (1.29 million YPLL; 95% uncertainty interval 1.13 – 1.45 million) was greater for SCD than all individual cancers and most other leading causes of death. Conclusions The societal burden of SCD is high relative to other major causes of death. Improved epidemiologic surveillance of SCD and other forms of cardiovascular disease is necessary to evaluate and improve prevention and treatment.