© 2002 European Society of Cardiology
QT duration and dispersion response to exercise in coronary artery disease patients with and without myocardial infarction
IIIrd Department of Cardiology, Silesian Medical School Zio
owa Street 47, 40635 Katowice, Poland
* Corresponding author. Tel.: +48-32-2523930; fax: +48-32-2523930
Received February 15, 1999; Revised November 21, 2001; Accepted January 19, 2002
 |
1. Background |
|---|
 Top 1. Background 2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
QT interval prolongation during exercise has been reported in patients with coronary artery disease (CAD), mainly in those after myocardial infarction (MI). Much less is known about the behaviour of the spatial dispersion of QT. CAD-patients with three vessel disease had increased precordial SD-QT>30 ms in the resting ECG. This criterion was proposed to diagnose a critical stenosis of the left main coronary artery. Patients after MI also had increased QTc dispersion in resting ECG; however, its behaviour in response to exercise remains unclear.
This study deals with the changes in measures of ventricular repolarisation induced by exercise, and later in the recovery period, in patients after myocardial infarction (MI) and in those with uncomplicated coronary artery disease (CAD).
|
2. Material and methods |
|---|
|
Top1. Background2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
The 58 patients (12 females, 46 males, mean age 53±8 years [range 33–67]) were examined if they had angiographically proven CAD (>50% stenosis of the epicardial coronary arteries). There were 33 patients (pts) who had MI in the past (group PMI). The remaining 25 pts without a history of MI (group CAD) presented clinically with stable exertional angina.
All patients were in sinus rhythm without an arrhythmia or conduction disturbances at resting ECGs. The only medications allowed were aspirin and beta-blockers (all subjects). Patients receiving other drugs, especially those which are known to influence ventricular repolarisation, were not included. The purpose of the study and the methods used was explained to each patient and informed consent was obtained.
An echocardiographic examination (Hewlett-Packard Sonos 1500, USA) was performed in each patient in order to obtain left ventricular diastolic diameter (LVEDD, cm), left ventricular ejection fraction (LVEF, %) and left ventricular mass index (LVMI, g/m2). Only LVEF was slightly, but significantly lower in post-MI patients (55.2±10.4%) as compared to CAD-pts (63.3±11.0, P<0.01). There were no patients with LVEF<35%. Other echocardiographic measures were comparable in both groups.
A symptom-limited exercise treadmill test was performed on each subject in the mid-morning after a light breakfast. The Bruce protocol was used. Twelve-lead ECG recordings were obtained at rest (REST), immediately after the exercise (EXE) and after 6 min of recovery (REC). The QT interval was measured in each suitable lead from the beginning of the QRS complex to the point at which the T-wave crosses the isoelectric line. In all ECG recordings, the QT interval was suitable to determine at least eight leads. All measurements were performed by one of the co-authors in a blinded order. Measurements were repeated in 3–5 consecutive cycles and corrected to the duration of the preceding RR interval using the Bazett formula (corrected QT, QTc). The mean for each lead was calculated. The following parameters were drawn for further analysis: the maximum QTc interval (maxQTc, ms), the difference between the longest and the shortest QT interval (QT dispersion, dispQT, ms) and the standard deviation (S.D.) of all measured QT intervals over the suitable leads (SD-QT, ms). Other clinical and ECG variables were also drawn for comparison.
In order to analyse the dynamic changes of the measures of ventricular repolarisation the maxQTc, dispQTc and SD-QTc were expressed as the ratios between the exercise and resting values, as well as the recovery values to the exercise ones. The changes of maxQTc above 5% of resting values, as well as the changes of dispQTc and SD-QTc above 20% were considered significant.
The statistical comparisons were performed using the Student's t-test for unpaired or paired data. A linear regression and Fisher's exact test were used as appropriate. All statistics were performed using the commercial package CSS-Statistica (Statsoft Corp., Tulsa, USA). A P-value <0.05 was considered significant.
|
3. Results |
|---|
|
Top1. Background2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
The results of exercise testing parameters are presented in Table 1. Means of the analysed parameters of ventricular repolarisation did not allow us to distinguish between both groups at rest, immediately after the exercise and after 6 min of recovery. In both groups, the maxQTc at EXE was significantly longer than at REST. During recovery, the maxQTc shortened and achieved the values comparable to the initial ones in the PMI-group, while it was still prolonged in the CAD-group. Dispersion of repolarisation, represented by dispQT and SD-QT, significantly increased in response to the exercise and normalised at REC in the PMI-pts. In the CAD-group, the dispQT and SD-QT did not change significantly. This contrasts with a significantly greater sum of ST depression and DP at EXE in the CAD-group.
|
In approximately half of the patients in both groups, the maxQTc was not prolonged by more than 5% of the resting values, which was considered as a lack of significant change. Simultaneously, the QT dispersion increased significantly (by more than 20% of initial values) in approximately 70% of the PMI-pts, but only in approximately 40% of the CAD-group (Fisher's exact test, P=0.0228). After 6 min of recovery, a significant reduction in exercise-induced SD-QT was more frequently observed in the PMI-pts (61%), as compared to 36% of the CAD-group (Fisher's exact test, P=0.0554).
In post-MI patients, significant correlations were observed between maxQTc achieved at exercise and LVEF, LVEDD or LVMI (Pearsons’ R –0.38, 0.35 and 0.37, respectively, P<0.05), but not at rest or during the recovery. In contrast, in CAD-pts significant relationships were observed for QTdisp or SDQT and LVEF irrespective of the exercise-testing period (Pearsons’ r between –0.49 and –0.59, P<0.01).
|
4. Discussion |
|---|
|
Top1. Background2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
The results of our study indicate that the behaviour of QT interval duration and dispersion differs in patients with CAD with and without previous MI. The maxQTc duration increased in both groups. This change is already a well-recognised behaviour in patients with coronary artery disease [1]. The measures of QT dispersion increased only in post-MI patients immediately after exercise, despite a smaller workload achieved and the severity of ischaemia observed. This suggests that other factors influence QT dispersion in post-MI patients. A recent study by Ikonomidis et al. [2] showed that an increase in QT dispersion by more than 30% during dobutamine stress predicts the presence of viable myocardium in patients with old MI. In our study, the QT dispersion was relatively small, as indicated by a mean value of 53 ms. This may indicate that the majority of patients examined had a viable myocardium, since a resting QT dispersion <65 ms was found to correlate with a reduction in total wall motion score of the left ventricle at peak stress during dobutamine infusion [2]. A relatively preserved left ventricular function may be another explanation for the small values of QT dispersion measures. Previous data has shown that, in patients with ventricular dysfunction or heart failure, these measures are increased and correlate with a poor survival [3,4]. There were, however, no relations between QT dispersion and left ventricular function measures in our study, while QT duration at EXE related positively to left ventricular dilation and mass and negatively with ejection fraction. The lack of correlation of QT dispersion with the measures of left ventricular function has been reported previously [2,5].
In patients with uncomplicated CAD we did not observed the increase in QT dispersion after exercise. This might be explained by the effects of beta-blockers used by the patients in our study [6].
We have used exercise testing to assess the changes in QT duration and dispersion. This approach may have several limitations, coming mainly from errors with the manual QT measurements and with the use of the Bazett formula [7]. Keeping this in mind, we decided to overcome these limitations by considering the significant changes of either parameter if at least 10% change in QT duration or 20% in QT dispersion were observed.
|
5. Conclusion |
|---|
|
Top1. Background2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
The QTc-interval prolongation and QT-dispersion increase in response to the exercise are greater in CAD-patients with a remote myocardial infarction. The behaviour of the measures of ventricular repolarisation are significantly related to left ventricular function.
|
References |
|---|
|
Top1. Background2. Material and methods3. Results4. Discussion5. ConclusionReferences |
|---|
- Surawicz B., Knoebel S.B. Long QT: good, bad or indifferent? J Am Coll Cardiol (1984) 4:398–413.[Abstract]
- Ikonomidis I., Athanassopoulos G., Karatasakis G., et al. Dispersion of ventricular repolarization is determined by the presence of myocardial viability in patients with old myocardial infarction. Eur Heart J (2000) 21:446–456.
[Abstract/Free Full Text] - Fu G.S., Meissner A., Simon R. Repolarisation dispersion and sudden death in patients with impaired left ventricular function. Eur Heart J (1997) 18:281–289.
[Abstract/Free Full Text] - Barr C.S., Mass A., Freeman M., et al. QT dispersion and sudden unexpected death in chronic heart failure. Lancet (1994) 343:327–329.[CrossRef][Web of Science][Medline]
- Perkiömäki J.S., Koistinen J.M., Yli-Mäyry I.S., Huikuri H.V. Dispersion of QT interval in patients with and without susceptibility to ventricular tachyarrhythmias after previous myocardial infarction. J Am Coll Cardiol (1997) 30:1331–1338.[Abstract]
- Day C.P., McComb J.M., Mathews J., et al. Reduction in QT dispersion by sotalol following myocardial infarction. Eur Heart J (1991) 12:423–427.
[Abstract/Free Full Text] - Macfarlane P.W. Measurement of QT dispersion. Heart (1998) 80:421–423.
[Free Full Text]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||