(Tpeak - Tend)/QRS and (Tpeak - Tend)/(QT × QRS): novel markers for predicting arrhythmic risk in the Brugada syndrome.

  title={(Tpeak - Tend)/QRS and (Tpeak - Tend)/(QT × QRS): novel markers for predicting arrhythmic risk in the Brugada syndrome.},
  author={Gary Tse},
  journal={Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
  volume={19 4},
  • G. Tse
  • Published 2017
  • Medicine
  • Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
I read the recent paper by Zumhagen et al . with great interest, who demonstrated that the interval from the peak to the end of the electrocardiographic T wave (Tpeak − Tend) and (Tpeak − Tend)/QT ratio, were strong risk markers for Brugada patients with life-threatening ventricular arrhythmias.1 These ratios reflect the transmural dispersion of repolarization (TDR), increases in which can lead to unidirectional conduction block and reentry. … 
Novel arrhythmic risk markers incorporating QRS dispersion: QRSd × (Tpeak − Tend)/QRS and QRSd × (Tpeak − Tend)/(QT × QRS)
  • G. Tse, B. Yan
  • Medicine
  • Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc
  • 2017
Two novel indices are proposed that may have a higher accuracy in risk stratification and have the potential of having superior predictive values than ventricular repolarization markers such as QTc, QTd, T peak − Tend, or (Tpeak − Tend)/QT ratio. Expand
Meta-analysis of Tpeak-Tend and Tpeak-Tend/QT ratio for risk stratification in congenital long QT syndrome.
This meta-analysis showed that Tpeak-Tend interval is significant higher in individuals who are at elevated risk of adverse events in congenital LQTS, offering incremental value for risk stratification. Expand
Electrophysiological mechanisms of long and short QT syndromes
The molecular determinants of the AP duration and the causes of long and short QT syndromes (LQTS and SQTS) are explored and a discussion on strategies for the future rational design of anti-arrhythmic agents is discussed. Expand
T-Wave Indices and Atherosclerosis
This review provides a comprehensive overview on how Tpeak-Tend is altered in different atherosclerotic conditions such as hypertension, stable coronary artery disease, acute coronary obstruction, and coronary slow flow as well as inflammatory diseases affecting the arterial tree. Expand
High risk electrocardiographic markers in Brugada syndrome
Specific ECG markers based on depolarization and/or repolarization that have been associated with an increased risk of arrhythmic events in patients with BrS are highlighted. Expand
Present Status of Brugada Syndrome: JACC State-of-the-Art Review.
The Brugada syndrome is an inherited disorder associated with risk of ventricular fibrillation and sudden cardiac death in a structurally normal heart and in approximately 30% of patients, a genetic variant may be implicated in causation after a comprehensive analysis. Expand
Variability in local action potential durations, dispersion of repolarization and wavelength restitution in aged wild-type and Scn5a+/− mouse hearts modeling human Brugada syndrome
This letter attempts to provide a brief overview to illustrate the importance of understanding the limitations of experimental methods and the need to appraise experimental data. Expand
Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts
Hypercalcemia treatment exerted anti-arrhythmic effects during hyperkalemia, reducing the proportion of hearts showing VT to 1 of 7 hearts, and epicardial VERPs without further altering the remaining parameters, returning VERP/latency ratio to normokalemic values and also decreased the critical intervals. Expand
Brugada syndrome: A comprehensive review of pathophysiological mechanisms and risk stratification strategies
Evidence from computational modelling, pre-clinical and clinical studies illustrates that molecular abnormalities found in BrS lead to alterations in excitation wavelength (λ), which ultimately elevates arrhythmic risk. Expand
Tachycardia-bradycardia syndrome: Electrophysiological mechanisms and future therapeutic approaches (Review)
The aim of this article is to review the different ion channels involved in TBS, examine the three-way relationship between ion channel dysfunction, tachycardia and bradycardia in T BS and to consider its current and future therapies. Expand


Tpeak-Tend interval and Tpeak-Tend/QT ratio in patients with Brugada syndrome.
Assessment of the Tpeak-Tend intervals or the TpTe/QT ratio in lead V1 is potentially useful as a non-invasive risk marker for BrS patients with life-threatening arrhythmias. Expand
A new biomarker--index of cardiac electrophysiological balance (iCEB)--plays an important role in drug-induced cardiac arrhythmias: beyond QT-prolongation and Torsades de Pointes (TdPs).
The data from 7 reference drugs of known pro-arrhythmic effects suggests that this non-invasive iCEB predicts potential risk of drug-induced CAs beyond long QT and TdP, and is more useful than the current biomarkers (i.e. transmural dispersion and instability) in predicting potential risks for drug- induced non-TdP-like VT/VF. Expand
Prolonged QRS duration in lead V2 and risk of life-threatening ventricular Arrhythmia in patients with Brugada syndrome.
Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome. Expand
Cardiac dynamics: Alternans and arrhythmogenesis
The mechanisms that generate cardiac repolarization alternans are reviewed and a discussion on how alternans generate arrhythmias in a number of clinical scenarios is discussed, followed by an outline of future therapeutic targets for anti‐arrhythmic therapy. Expand