QT Peak Dispersion Research Articles

011 QT PEAK DISPERSION CORRELATED WITH LV SIZE AND MASS IN PATIENTS WITH CHRONIC HEART FAILURE, BUT NOT TO THE AMOUNT OF SCAR PRESENT

Introduction In middle aged men with a normal QT interval on a resting 12-lead ECG, increased QT peak dispersion is an independent risk factor for sudden cardiac death. QT peak prolongation is associated with left ventricular (LV) hypertrophy in hypertensive subjects, stroke survivors, and patients with suspected coronary artery disease. However, young footballers with LVH characterised by myocyte hypertrophy (with no fibrosis) do not have QT peak prolongation. We wondered if increased left ventricular mass and scar burden were associated with QT peak dispersion in patients with heart failure (HF). Methods 121 consecutive patients with chronic heart failure in sinus rhythm were studied. LV mass was determined on cardiac MRI. Scar mass was assessed using late gadolinium enhancement. The ECGs were analysed by a single observer who was blind to the results of the cardiac MRI and to clinical findings. QT peak (QTp) was measured from onset of the Q-wave to the peak of T-wave in every ECG lead of the 12-lead ECG, and heart rate corrected (QTpc) using Bazett9s formula. QTpc dispersion was defined as QTpc Max—QTpc Min. Results are presented as mean±SD, unless stated otherwise. Results 121 patients (17 female) were aged 66±10.9 years. LV ejection fraction was (EF) 36±11%, end-diastolic volume (EDV) 239±72 ml, end-systolic volume (ESV) 159±67 ml, LV mass 146±30.9 g, scar mass was 27±10 g and formed 19±7% of the LV mass. The QTpc dispersion was 76±40 ms. QTpc dispersion correlated with total LV mass (r=0.3, p=0.01) and size (EDV r=0.4, p=0.002; ESV 0.4, p=0.001). There was no correlation between QTpc dispersion and scar size, either expressed in absolute units or as a percentage of total LV mass. Conclusions QTpc dispersion correlated with the total LV mass and LV size. However, there was no correlation between QTpc dispersion and scar size as determined by cardiac MR with late gadolinium enhancement imaging.

Study of repolarization heterogeneity and electrocardiographic morphology with a modeling approach

Background Increase of heart repolarization heterogeneity has been linked to severe or even life-threatening arrhythmia like torsades de pointes and other forms of ventricular tachycardia. Although electrocardiography (ECG) still remains as the most convenient and cost-effective method of monitoring electrical activity of the heart, the link between ECG morphology and repolarization heterogeneity is not clear. Previous attempts of using QT interval dispersion from multiple leads to assess the heterogeneity changes were not successful either. Method The aim of this study is to use a cell-to-ECG model to study ECG morphology changes while varying transmural heterogeneity. The heterogeneity is simulated by increasing the difference of M cell Ikr block factors from either endocardial or epicardial cells. The model-simulated ECGs were processed and measured. The ECG parameters studied include QT interval dispersion of standard 12-lead ECG, QT peak dispersion, and T-peak to T-end interval (TpTe). An ECG vector magnitude signal based on 12-lead ECG was formed to estimate the global QT interval (vs lead-by-lead QT interval used for calculating QT dispersion) and also the global TpTe (TpTe_VM). Results The results based on the model simulation show that the TpTe_VM is highly correlated with transmural dispersion of repolarization (TDR), with a correlation coefficient of 0.97. The correlation coefficients of QT interval dispersion and QT peak dispersion with TDR are 0.44 and 0.80, respectively. Conclusion In conclusion, the cell-to-ECG model provides a unique way to study electrophysiology and to link physiologic factors to ECG morphology changes. The simulation results suggest that global TpTe can be a strong indicator of TDR.

QT peak dispersion, not QT dispersion, is a more useful diagnostic marker for detecting exercise-induced myocardial ischemia

The electrocardiographic indices of QT dispersion (QTd), QT peak dispersion (QTpd), and the principal component analysis ratio (PCAr) are related to the occurrence of fatal arrhythmia and are influenced by physical exercise. The purpose of this study was to investigate whether or not the QT parameters can be used as markers for exercise-induced myocardial ischemia. We measured these QT parameters at rest and at 3 minutes after exercise using exercise-stress thallium-201 scintigraphy (SPECT), compared with conventional ST segment changes in 161 patients with suspected or known coronary artery disease. The patients were classified into four groups (normal, redistribution, fixed defect, and redistribution with fixed defect) according to SPECT. At rest, QTd and PCAr were greater in the fixed defect and redistribution with fixed defect groups. PCAr, however, increased after exercise in the redistribution and redistribution with fixed defect groups. Although QTpd at rest was not significantly different among the four groups, it increased in the redistribution and redistribution with fixed defect groups after exercise (QTpd after exercise: normal, 36 +/- 16 ms vs. redistribution, 51 +/- 23 ms, redistribution with fixed defect, 53 +/- 19 ms; P<.05). For myocardial infarction reflected by fixed defect, QTd at rest was the most useful indicator, while QTpd after exercise was the most useful indicator for exercise-induced myocardial ischemia according to multiple logistic regression analysis with receiver operating characteristic curves. In addition, the change in PCAr by exercise was an independent predictor for exercise-induced ischemia. QTpd and PCAr could be useful indices for exercise-induced myocardial ischemia. Determining the QTpd of a patient after exercising can improve the diagnostic accuracy of ischemia in a routine clinical setting.

Left ventricular hypertrophy increases transepicardial dispersion of repolarisation in hypertensive patients: a differential effect on QTpeak and QTend dispersion.

Ventricular arrhythmias in left ventricular hypertrophy (LVH) are related to regional electrical heterogeneity. The significance of noninvasive electrocardiographic indices of electrical heterogeneity in LVH has not been established. The aim of the study was to investigate changes in the Tpeak-Tend interval (an index of transmural dispersion of repolarisation) in addition to other traditional electrocardiographic indices of electrical dispersion in patients with hypertensive LVH. Consecutive patients were screened for the presence of hypertensive echocardiographic LVH and compared with a control group. LVH was identified as left ventricular mass > 134 g m-2 in men and > 110 g m-2 in women. Twelve-lead ECGs were analysed in respect of various indices of electrical dispersion. Left ventricular mass was greater in the LVH than in the control group (174 +/- 39 vs. 101 +/- 18 g m-2, P < 0.0001). The Tpeak-Tend interval was not affected by LVH. The main effect of LVH was an increase in QTpeak dispersion (40 +/- 13 vs. 53 +/- 21 ms, P < 0.05), which resulted from an increase in the maximum QTpeak interval (337 +/- 24 vs. 358 +/- 30 ms, P < 0.04), without any change in the minimum QTpeak interval. There was a significant correlation between the left ventricular mass index and QTpeak dispersion (r = 0.40; P < 0.01). In contrast, LVH did not exert any effect on QTend dispersion (65 +/- 21 vs. 65 +/- 16 ms, ns), because LVH increased both the maximum QTend interval (430 +/- 30 vs. 449 +/- 28 ms, P < 0.05) and the minimum QTend interval (365 +/- 29 vs. 384 +/- 27 ms, P < 0.04). Hypertensive LVH exerts a differential effect on QTpeak and QTend interval dispersion. The most likely explanation is that these changes reflect a nonuniform prolongation of action potential duration across the epicardium, leading to an increase in transepicardial dispersion of repolarisation.

Effects of cardiovascular autonomic function tests on QT dispersion in the 12-lead electrocardiogram of healthy patients

Changes in autonomic tone modulate QT interval duration. How cardiovascular autonomic reflexes affect QT dispersion, a suggested marker of arrhythmia risk, is not well established. We studied 10 healthy young adult volunteer men during quiet and deep breathing, the Valsalva maneuver, sustained handgrip, hyperventilation, the cold pressor test, and mental stress. An automated method was used for measurement of QT-peak and QT-end intervals, and QT dispersion was defined as maximum-minimum of the measured intervals. QT-peak dispersion was greater on deep expiration than deep inspiration (49 ± 20 ms vs 37 ± 14 ms, P <.05). QT-end dispersion decreased in the tachycardia phase of the Valsalva maneuver (45 ± 23 ms vs 35 ± 21 ms, P <.05), but QT dispersion did not change during the other interventions. Rapid cardiovascular autonomic reflex adjustment does not change QT dispersion in healthy young adult men. However, large intrathoracic volume and intrathoracic pressure changes during forced respiratory movements might confound QT dispersion measurements.

Dispersion of the QTend, QTpeak and Tpeak‐Tend Interval: Comparison of Reproducibility in Normal Subjects and Patients with Hypertrophic Cardiomyopathy

BackgroundProlonged QT interval and QT dispersion have been reported to be associated with arrhythmogenesis in patients with cardiac disorders. However, the use of QT dispersion for risk stratification is limited by its low reproducibility. Recently, measurement of the interval between the peak and the end of the T wave (Tp‐Te interval) has been suggested for detection of repolarization abnormalities, but its clinical utility has not been studied in a systematic fashion.MethodsThis study assessed the intrasubject reproducibility of automatic measurements of QTend, QTpeak, and Tp‐Te interval dispersion in 71 normal subjects and 37 patients with hypertrophic Cardiomyopathy (HC). A set of 20 ECGs (10 in supine and 10 in standing position) was evaluated in each subject. Measurements were performed automatically using an advanced commercial computer system.ResultsHC patients showed significantly higher values of QTtend, QTpeak, Tp‐Te intervals, and QTend, QTpeak dispersion compared to normal subjects (42 ± 20 vs 20 ± 12 ms and 45 ± 24 vs 33 ± 12 ms, respectively; P &lt; 0.04), but no significant difference was observed in Tp‐Te dispersion between both groups (32 ± 16 vs 29 ± 8 ms; NS). The reproducibility of QTend, QTpeak, and Tp‐Te dispersion, expressed as coefficients of variation, was poor in both groups (14%‐28% in normal subjects and 18% to 37% in HC patients).ConclusionDespite higher values of QTend, QTpeakTp‐Te intervals and QTend, QTpeak dispersion in HC patients than in normal subjects, Tp‐Te dispersion was similar in both groups. The reproducibility of QTend, QTpeak, and Tp‐Te dispersion was low. Automatic measurement of Tp‐Tp dispersion failed to differentiate normal subjects and HC patients.

QT dispersion as a risk factor for sudden cardiac death and fatal myocardial infarction in a coronary risk population.

OBJECTIVE: To test in a prospective study the hypothesis that increased QT dispersion in resting 12-lead ECG is a predictor of sudden cardiac death. DESIGN: A nested case-control study during...