Dynamics of the QT interval in patients with exercise-induced ventricular tachycardia in normal and abnormal hearts

doi:10.1016/0002-8703(93)90534-G

American Heart Journal

Volume 126, Issue 6, December 1993, Pages 1357-1363

https://doi.org/10.1016/0002-8703(93)90534-G Get rights and content

Abstract

Inhomogeneity of ventricular repolarization reflected in prolongation of the QT interval of the surface electrocardiogram can predispose patients to ventricular arrhythmia. This study examines whether an abnormality of QT adaptation to changes in heart rate is likely to be of importance in the pathogenesis of ventricular tachycardia (VT) in patients with and without underlying structural heart disease. The QT-R-R relationship during exercise was studied in 52 patients. Forty-two patients had VT associated with a “clinically normal” heart (idiopathic VT), of which 23 had no VT on exercise and 19 had exercise-induced VT. These patients were compared to 10 subjects with exercise-induced VT related to ischemic heart disease. The QT interval was measured manually from computer-averaged QRS complexes recorded at 1- to 3-minute intervals during treadmill exercise tests. An approximately linear association existed between the QT and R-R intervals within the range of heart rates observed. The slope of the QT-R-R relation was lower in patients with structural heart disease (0.23 ± 0.06) than in patients with normal hearts with (0.29 ± 0.12) and without (0.29 ± 0.12) exercise-induced VT (p < 0.05). The intercept of the regression line was higher in patients with structurally abnormal hearts (209.2 ± 55.3 msec) than in patients with idiopathic VT with (155.6 ± 49.7 msec) and without (157.7 ± 69.0 msec) exercise-induced VT (p < 0.02). The corrected QT (Bazett's formula) was similar in all three groups at rest, but was higher in patients with structurally abnormal hearts at peak exercise, 449.6 ± 28.0 versus 425.8 ± 27.4 msec (idiopathic VT, exercise induced) versus 427.3 ± 26.6 msec (idiopathic VT, not exercise induced) (p < 0.05). There was no statistically significant difference in any of these parameters between patients with and without exercise-induced VT in structurally normal hearts. The results suggest that rate adaptation of the QT interval is abnormal in patients with structural heart disease and may be involved in the pathogenesis of the VT. QT adaptation is normal in patients with idiopathic VT and exercise-induced arrhythmia in which the mechanism is less likely to be dependent on an abnormality of repolarization dynamics.

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Cited by (28)

QT dynamics early after exercise as a predictor of mortality
2010, Heart Rhythm
Citation Excerpt :
Our work extends the existing literature on resting QT dynamics into the new area of stress QT dynamics. One prior work has explored the QT–RR relationship during exercise in patients with exercise-induced ventricular tachycardia compared with normal subjects.24 However, our results are the first, to our knowledge, to study the impact of stress QT dynamics on survival in an unselected group of patients undergoing stress tests.
Exercise and QT dynamics during ambulatory monitoring impact mortality in a variety of populations. Heart rate recovery (HRR) after exercise is a known strong predictor of mortality.
This study assessed the independent prognostic significance of the QT response to changing heart rate (QT dynamics) during recovery from exercise.
The cohort included patients referred for treadmill exercise stress testing over a 5-year period. Patients had to have at least 4 electrocardiographic tracings within 5 minutes of peak exercise. One had to be recorded 60 seconds into recovery to calculate the HRR. Linear regression of the QT–RR relation during recovery was used to predict the QT interval at cycle lengths of 500 and 600 ms (QT-500 and QT-600). Only studies with an R² ≥ 0.9 (72%) were retained. Optimal binary cut points were chosen. All-cause mortality was determined from either the Social Security Death Index or hospital records.
A total of 2,994 patients met inclusion criteria; 228 (7.6%) died during an average follow-up of 7.6 ± 1.9 years. Abnormal QT-500 (>316 ms) was the strongest univariate QT dynamics predictor in a Cox proportional hazards model (hazard ratio = 2.13, P <.001). It remained an independent predictor of mortality after adjustment for age, exercise capacity, medications, single photon emission computed tomography defects, and abnormal (<12 beats/min) HRR (hazard ratio = 1.46, P = .014).
An abnormal predicted QT interval at 500 ms (120 beats/min) during recovery from exercise independently predicts all-cause mortality. Because QT dynamics in recovery incorporate information on both repolarization and autonomic responsiveness, its role in risk prediction for sudden cardiac death should be further explored.
Lack of noninvasive markers of ventricular repolarization inhomogeneity in patients with idiopathic ventricular tachyarrhythmia
2001, Journal of Electrocardiology
Noninvasive markers reflecting repolarization inhomogeneity have been proposed to be useful indices for identifying patients at risk of ventricular arrhythmias based on organic heart disease. In this study, we clarify whether or not repolarization inhomogeneity markers are useful in patients with idiopathic ventricular tachycardia (VT). We investigated T-wave alternans (TWA) and corrected QT-interval dispersion (QTD) in 84 consecutive patients with idiopathic VT, 90 patients with VT associated with organic heart disease (organic VT), and 87 normal individuals. VT was defined as tachycardia lasting [ge ]5 consecutive ventricular ectopic beats at a rate of [ge ]120 beats/min. TWA was positive in 20 of 84 patients (24%) with idiopathic VT, 59 of 90 patients (66%) with organic VT, and 16 of 87 normal individuals (18%). The alternans voltage was 2.6 [plusmn] 3.1 [mu ] V in idiopathic VT patients, 5.6 [plusmn] 6.4 [mu ] V in organic VT patients, and 2.9 [plusmn] 5.7 [mu ] V in normal individuals. QTD were 53 [plusmn] 20 ms in idiopathic VT patients, 92 [plusmn] 20 ms in organic VT patients, 46 [plusmn] 18 ms in normal individuals, respectively. A positive TWA test result was seen more (P [lt ] .01) frequently, and QTD was longer (P [lt ] .01) in organic VT patients compared to normal individuals, whereas there was no difference between idiopathic VT patients and normal individuals. In addition, in patients with idiopathic VT, neither did any of these measurements differ between patients with sustained VT (lasting for [ge ]30 s) and those with nonsustained VT. Noninvasive markers of repolarization inhomogeneity, such as TWA and QTD, are not useful for identifying patients with idiopathic VT. Repolarization inhomogeneity may not affect to the pathogenesis of idiopathic VT.
QT interval and mortality from coronary artery disease
2000, Progress in Cardiovascular Diseases
Abnormalities in the QT interval can be divided into 3 types, prolongation of the QT interval, increases in the dispersion of the QT interval, and abnormalities in the heart rate dependent behavior of the QT interval. Abnormalities may be found in short or long-term recordings. Prolongation of the QT interval may reflect factors associated with an adverse prognosis in coronary disease and may in itself be arrhythmogenic. The data to date suggest that there is an association between adverse prognosis and QT interval prolongation in coronary disease, both before and after acute myocardial infarctions. This relationship is weak, however, and is not clinically useful. The data as to whether increased QT dispersion postmyocardial infarction relates to adverse prognosis is weak because there is no convincing evidence yet. If there is a relationship it is weak. Abnormalities in the rate dependent behavior of the QT interval are widely found, but as no large scale prospective study with mortality as an endpoint has yet been undertaken the significance of rate dependent abnormalities is uncertain. The widespread introduction of beat-to-beat QT analysis of 24 hour Holter tapes may take QT intervalology into the realm of clinical practice. Copyright © 2000 by W.B. Saunders Company
Progress in Cardiovascular Diseases, Vol. 42, No. 5 (March/April), 2000: pp 359-384
Exercise-induced changes in the QT interval duration and dispersion in patients with sudden cardiac death after myocardial infarction
1998, International Journal of Cardiology
Background: Prolongation of the QT interval and increased QT dispersion have been proposed to be associated with arrhythmic risk after myocardial infarction. However, controversy remains regarding the prognostic value of ventricular repolarization abnormalities in the risk stratification of patients surviving acute myocardial infarction. Hypothesis and objective: The QT interval is sensitive to myocardial ischaemia, and exercise-induced ischaemia may change the QT interval regionally, resulting in increased QT dispersion. This study examined whether there are abnormalities of ventricular repolarization during exercise and whether assessment of the exercise-induced changes in QT interval duration and dispersion would be able to differentiate patients at high risk from those at low risk of sudden cardiac death after myocardial infarction. Methods: Twenty-six post-myocardial infarction patients (mean age 54.5±8.9 years, 22 men) were retrospectively studied. Thirteen patients who died suddenly (SCD patients) during a follow-up of 39±6 months were compared to 13 patients who remained event-free, i.e. no ventricular tachyarrhythmias, no reinfarction, no by-pass (MI survivors). The two groups were pair-matched for age, gender, site of infarction, left ventricular ejection fraction and use of beta blocker. A further 13 patients with chest pain, normal coronary arteriograms and negative exercise test results were studied as controls. They were age and gender matched with the post-infarction patients. A 12-lead exercise ECG was recorded from each patient before, during and after exercise. QT and RR interval were measured on the exercise ECGs at each stage and QT dispersion was defined as the difference between the maximum and minimum QT intervals across the 12-lead ECG. Results: There were no significant differences in RR, QT and QTc (Bazett's and Fridericia's correction) intervals, or QT dispersion between any groups before exercise. A significant difference in QT and QT dispersion was found at peak exercise between post-infarction patients and controls (P=0.03 and P=0.0001, respectively), but no difference was observed between SCD patients and MI survivors. The maximum QTc at peak exercise was longer in SCD patients compared with MI survivors (P=0.02) and a maximum QTc>440 ms (Bazett's correction) was common in SCD patients but not in MI survivors or controls (62%, 15%, 15%, P=0.01). The differences in QT, QTc or QT dispersion observed at peak exercise were no longer significant after exercise. Conclusions: Exercise-induced prolongation of the QTc interval differentiates patients at high risk of sudden cardiac death from those at low risk, whereas exercise-induced changes in QT dispersion failed to identify patients at high risk of sudden cardiac death after myocardial infarction.
Effect of exercise-induced ischemia on QT interval dispersion
1998, American Heart Journal
An increased spatial dispersion of ventricular repolarization duration (QT dispersion) is associated with an increased vulnerability to arrhythmias. This study was designed to examine the effect of exercise on QT dispersion in ischemic heart disease (IHD). QT dispersion, corrected QT dispersion, and percentage change in uncorrected and corrected QT dispersion between rest and peak exercise were examined in 14 members of a control group, 17 patients with IHD, and 14 patients with IHD who were receiving β-blockers (IHD-B). All subjects had undergone a standard Bruce protocol exercise test, and QT intervals were measured at rest and peak exercise with a digitizing tablet interfaced to a personal computer. QT dispersion at rest was markedly increased in the IHD group compared with that in the control and IHD-B groups, respectively (corrected QT dispersion in milliseconds), 74 ± 7, 40 ± 4, 49 ± 5, p < 0.03). The corrected QT dispersion at peak exercise was greater in the IHD group compared with that in the control group (57 ± 5 vs 26 ± 3 msec, p < 0.03). The percentage change in QT dispersion with exercise was significantly higher in the IHD group (52% ± 5%) compared with that in both the control group (28% ± 4%, p < 0.002) and the IHD-B group (30% ± 3%, p < 0.01). A larger mean QT dispersion at peak exercise and an increased percentage change in QT dispersion with exercise may help explain the increased susceptibility of the IHD group for arrhythmias. The cardioprotective action of β-blockers may be explained by their blunting effect on exercise-related changes in QT dispersion. (Am Heart J 1998;135:88-92.)
QT interval-heart rate relation during exercise in normal men and women: Definition by linear regression analysis
1996, Journal of the American College of Cardiology
Objectives. This study sought to develop a regression-based method for characterization of QT interval behavior during exercise and to define the noral range of the resulting “dynamic” measures of repolarization during submaximal treadmill testing in men and women.
Background. The Bazett-corrected QT (QTc) interval during exercise has been used as a market for ischemic disease, arrhythmogenic substrate and the long QT syndrome. However, recent studies indicate that the QTc interval is nonlinear with respect to heart rate during exercise, making the end-exercise QTc interval dependent on peak work load achieved. In contrast, the unadjusted QT interval measured from QkS onset to T wave offset (QTo) and from QRS onset to T wave peak (QTm) appears to vary linearly with heart rate during gently graded effort.
Methods. The QT interval relation to heart rate and cycle length was examined by linear regression in 50 normal men (mean age 48 years) and 30 normal women (mean age 51 years), all of whom had normal rest electrocardiograms. The QTo and QTm measurements were made from digitized lead V₅ complexes averaged by computer over 20-s periods, at upright control and after seven 2-min stages of the Cornell modification of the Bruce treadmill protocol (work load equivalent to Bruce stage 3).
Results. For each subject, regression of QTo (ms) versus heart rate (beats/min) resulted in a slope (reflecting the “dynamic” change in QTo during effort), an adjusted intercept (reflecting QTo extrapolated to a heart rate 60 beats/min) and a significant correlation coefficient (r) value. Under these conditions, mean ± SD (5th to 95th percentile) values for men were −1.45 ± 0.34 ms/beat per min (−0.90, “less dynamic” to −1.96, “more dynamic”) for the slope; 403 ± 21 ms (365 to 431) for the adjusted intercept; and −0.93 ± 0.06 (−0.81 to −0.99) for r. Values for women were more dynamic, with a mean slope of −1.74 ± 0.32 ms/beat per min (−1.23 to −2.18, p < 0.0005 vs. men) and higher adjusted intercept of 426 ± 23 ms (392 to 462, p < 0.0001 vs. men) at similar strength of correlation (r = −0.95 ± 0.06). Corresponding normal data were also tabulated for QTm behavior and QT-RR interval behavior during exercise.
Conclusions. These data provide a “dynamic” definition of normal and abnormal repolarization and describe normal limits for the linear relations of the QTo and QTm intervals with respect to heart rate and cycle length during submaximal exercise in normal men and women.

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Dynamics of the QT interval in patients with exercise-induced ventricular tachycardia in normal and abnormal hearts

Abstract

J Am Coll Cardiol

Am J Cardiol

J Am Coll Cardiol

Am J Cardiol

Am Heart J

Am Heart J

Am Heart J

Am J Cardiol

Am Heart J

Influence of cycle length upon refractory period of auricles, ventricules and AV node in the dog

Am J Physiol

An analysis of the time relations of electrocardiograms

Heart

QT interval prolongation as predictor of sudden death in patients with myocardial infarction

Circulation

Delayed repolarisation (QT or QU prolongation) and malignant ventricular arrhythmias

Mod Con Cardiovasc Dis

Congenital deaf mutism, prolonged QT interval, syncopal attacks and sudden death

N Engl J Med

Influence of heart rate and inhibition of autonomic tone on the QT interval

Circulation

Relationship between QT interval duration and exercise-induced ventricular arrhythmias

Eur Heart J

Long QT syndrome: evidence for two kinds of QT prolongation

Br Heart J

Paroxysmal ventricular tachycardia: a clinical classification

Br Heart J

Ventricular tachycardia unassociated with coronary artery disease

Prog Cardiol