Elsevier

Journal of Electrocardiology

Volume 41, Issue 6, November–December 2008, Pages 567-574
Journal of Electrocardiology

Tp-e/QT ratio as an index of arrhythmogenesis

https://doi.org/10.1016/j.jelectrocard.2008.07.016Get rights and content

Abstract

An increasing number of basic and clinical studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (Tp-e) may correspond to the transmural dispersion of repolarization and that amplification of the Tp-e interval is associated with malignant ventricular arrhythmias. In this review, we outline the utility of the Tp-e interval and the Tp-e/QT ratio as an electrocardiographic index of arrhythmogenesis for both congenital and acquired ion channel disease leading to ventricular arrhythmias. In healthy individuals, the Tp-e/QT ratio has a mean value of approximately 0.21 in the precordial leads and it remains relatively constant between the heart rates from 60 to 100 beats per minute. Interestingly, the Tp-e/QT ratio is significantly greater in the patients at risk for arrhythmic event such as those with long QT syndrome, Brugada syndrome, short QT syndrome, and also in patients with organic heart disease such as acute myocardial infarction. Functional reentry is the underlying mechanism for arrhythmogenesis associated with an increased Tp-e/QT ratio.

Introduction

Malignant ventricular arrhythmia culminating in to sudden cardiac death (SCD) is a leading cause of mortality in United States.1 Decades of advances in cardiac electrophysiology have significantly improved our understanding of pathophysiology of various disease processes leading to ventricular arrhythmias and also refined our diagnostic and risk stratifying tools. A myriad of sophisticated diagnostic indexes including but not limited to late potentials on SIGNAL averaged electrocardiogram (ECG), presence of T-wave alternans, decreased heart rate variability, and even invasive electrophysiologic testing have been employed and shown to be predictive of the risk of SCD in at risk population.2 Despite these advances, 12-lead body surface ECG remains the primary and the most commonly used cardiac diagnostic tool.

The T wave is the ECG manifestation of ventricular repolarization, and recent experimental evidences suggest that the interval from the peak to the end of the T wave (Tp-e interval) corresponds to the dispersion of ventricular repolarization.3, 4, 5 Amplification of dispersion of ventricular repolarization has long been known as a substrate for ventricular arrhythmias. Quite naturally then, the Tp-e interval can serve as a noninvasive index of arrhythmogenesis. In this review, we outline the cellular basis of and further demonstrate the applicability of the Tp-e interval and more precisely the Tp-e/QT ratio as a noninvasive arrhythmogenic index in different cardiac conditions associated with high risk of SCD.

Section snippets

Cellular basis of T wave and Tp-e interval

It is now well recognized that ventricular myocardium is electrically a heterogeneous structure, comprised of 3 distinct myocardial cell types—epicardial, endocardial, and midmyocardial M cells.6, 7 Although these cells are histologically similar, they have different electrophysiological properties. The M cells—Masonic Midmyocardial Moe cells—are located in subendocardial layer and characterized by the ability of their action potential to prolong more than that of epicardial or endocardial cell

Long QT syndrome

The congenitally long QT syndrome (LQTS) is an inherited channelopathy characterized by abnormally long QT interval on 12-lead ECG and an increased propensity to develop atypical polymorphic ventricular tachycardia called torsade de pointes (TdP) that can lead to sudden cardiac death.17, 18, 19, 20 It is genetically a heterogeneous disease and so far 500 different mutations in 10 different genes encoding various cardiac ion channels or membrane components have been identified as causing LQTS.5,

Brugada syndrome

Brugada syndrome was first recognized as an inherited channelopathy associated with a high risk of SCD in individuals with a structurally normal heart in 1992 and is characterized on ECG by ST-segment elevations in right precordial leads (V1-V3) followed by a negative T wave.35 Electrocardiographic signs of the Brugada syndrome can often be concealed and could be unmasked by potent sodium channel blockers. Similar to LQTS, the Brugada syndrome is also a genetically heterogeneous disease, and

Short QT syndrome

It is only recently that arrhythmic potential of abnormal abbreviation of ventricular repolarization has received significant attention.43 The Short QT syndrome, a mirror image disorder of LQTS, is characterized by abnormally short QT interval (<360 milliseconds) on ECG and an increased propensity of develop atrial and ventricular tachyarrhythmia and SCD.44, 45 As with other channelopathies, SQTS is also a genetically heterogeneous disease, and so far, mutations in 5 different genes encoding

Acute ST-segment elevation myocardial infarction

Acute ST-segment-elevation myocardial infarction (STEMI) is also associated with a very high incidence (20%-25%) of ventricular fibrillation and SCD at an early stage of the insult.48 We have previously shown that phase 2 reentry leading to R-on-T extrasystole, originating at the ischemic border, serves as a trigger for ventricular fibrillation in acute STEMI.49 As Tp-e interval (and TDR at cellular level) is significantly amplified in above described channelopathies with high risk of SCD, we

Tp-e interval and Tp-e/QT ratio as an index of arrhythmogenesis

Outlined evidence clearly suggests the applicability of Tp-e/QT ratio as a potentially important index of arrhythmogenesis, both under the conditions of short, normal and long QT interval, as well as in congenital and acquired channelopathies. Its potential applicability as an index of arrhythmogenesis for variety of other cardiac conditions like heart failure and hypertrophy still remains to be tested in future studies. All of the above disorders, although have diverse genotypic- phenotypic

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    Supported by the Sharpe-Strumia Research Foundation and the Albert M. Greenfield Foundation.

    1

    The authors have contributed equally to the work.

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