
Electrocardiographic Transmural Dispersion of Repolarization in Patients with Inherited Short QT Syndrome
Author(s) -
Anttonen Olli,
Väänänen Heikki,
Junttila Juhani,
Huikuri Heikki V.,
Viitasalo Matti
Publication year - 2008
Publication title -
annals of noninvasive electrocardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.494
H-Index - 48
eISSN - 1542-474X
pISSN - 1082-720X
DOI - 10.1111/j.1542-474x.2008.00234.x
Subject(s) - short qt syndrome , medicine , cardiology , qt interval , repolarization , sudden cardiac death , j wave , long qt syndrome , electrophysiology
Background : Short QT syndrome (SQTS) carries an increased risk for sudden cardiac death. However, only a short QT interval does not express the risk of ventricular arrhythmias. Thus, additional evaluation of the repolarization abnormality in SQTS patients is essential. In experimental models of SQTS, increased transmural dispersion of repolarization (TDR) and its electrocardiographic counterpart T‐wave peak to T‐wave end interval (TPE) appeared critical for induction of polymorphic ventricular tachycardia (PMVT). In a clinical study with acquired long QT syndrome patients, TPE/QT ratio > 0.28 indicated arrhythmia risk. We hypothesized that the TPE/QT ratio would be greater in SQTS patients than in control subjects. Methods and Results : We compared the behavior of the electrocardiographic TDR in three seriously symptomatic SQTS patients of unknown genotype presenting baseline QTc values <320 ms and in nine healthy age‐matched control subjects. We determined QT and TPE intervals as well as TPE/QT ratio from 24‐hour ECG recordings using a computer‐assisted program. Diurnal average of TPE/QT ratio was 0.28 ± 0.03 in SQTS patients and 0.21 ± 0.02 in control subjects (P = 0.01). SQTS patients had also lesser capacity to change TPE intervals from steady‐state conditions to abrupt maximal values than control subjects. Conclusion : SQTS patients have increased and autonomically uncontrolled electrocardiographic TDR. According to experimental SQTS models, the present results may in part explain increased vulnerability of SQTS patients to ventricular arrhythmias.