Reproducibility and automatic measurement of QT dispersion

This study investigated interobserver (two observers) and intrasubject(two measurements) reproducibility of QT dispersion from abnormalelectrocardiograms in patients with previous myocardial infarction,and compared a user-interactive with an automatic measurementsystem. Standard 12-lead electrocardiograms, recorded at 25mm. s^–1, were randomly chosen from 70 patients followingmyocardial infarction. These were scanned into a personal computer,and specially designed software skeletonized and joined eachimage. The images were then available for user-interactive (mouseand computer screen), or automatic measurements using a speciallydesigned algorithm. For all methods reproducibility of the RRinterval was excellent (mean absolute errors 3–4 ms, relativeerrors 0·3–0·5%). Reproducibility of themean QT interval was good; intrasubject error was 6 ms (relativeerror 1·4%), interobserver error was 7 ms (1·8%),and observers' vs automatic measurement errors were 10 and 11ms (2·5, 2·8%). However QTc dispersion measurementshad large errors for all methods; intrasubject error was 12ms (17·3%), interobserver error was 15 ms (22·1%),and observers' vs automatic measurement were errors 30 and 28ms (35·4, 31·9%). QT dispersion measurements relyon the most difficult to measure QT intervals, resulting ina problem of reproducibility. Any automatic system must notonly recognize common T wave morphologies, but also these moredifficult T waves, if it is to be useful for measuring QT dispersion.The poor reproducibility of QT dispersion limits its role asa useful clinical tool, particularly as a predictor of events.     

Rate-dependence of QT dispersion and the QT interval: comparison of atrial pacing and exercise testing

OBJECTIVES: The study was done to determine whether variables of QT dispersion from the 12-lead electrocardiogram (ECG) are dependent on heart rate. BACKGROUND: The dispersion of the QT interval is under evaluation as a risk marker in patients at risk for ventricular arrhythmias. Assuming that a similar rate correction is necessary as for the QT interval itself, investigators have frequently reported QTc-dispersion values utilizing the Bazett formula. It is not known whether there is a physiologic basis for such a rate correction in the human heart. METHODS: In 35 patients referred for evaluation of ventricular arrhythmias, digital 12-lead ECGs recorded at various heart rates during submaximal exercise testing and again during atrial pacing upon electrophysiologic testing were submitted to computerized interactive analysis of several ECG dispersion variables. RESULTS: Data from 11 patients were excluded due to incomplete high-quality analysis possible at all heart rates. From the remaining 24 patients, a total of 193 ECG recordings at various heart rates (ranging from 76 +/- 17 beats/min to 117 +/- 14 beats/min during atrial pacing and from 78 +/- 18 beats/min to 110 +/- 14 beats/min during exercise testing) were available. A highly significant linear relationship with heart rate was found for both the QT interval and the Q-to-T-peak interval. By contrast, standard QT interval dispersion (QTmax - QTmin), the T-peak-to-T-end interval, and the average area under the T wave did not change with increasing heart rates. CONCLUSIONS: Dispersion of the QT interval and other ECG variables of dispersion of ventricular repolarization are independent of heart rate. Therefore, it is not necessary to rate-correct these measurements.     

QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion

OBJECTIVE: To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function. DESIGN: A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment. SETTING: A regional cardiology centre and a university teaching hospital. PATIENTS: 25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function. MAIN OUTCOME MEASURES: QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion. RESULTS: All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01). CONCLUSIONS: QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade.     

Adjustment of QT dispersion assessed from 12 lead electrocardiograms for different numbers of analysed electrocardiographic leads: comparison of stability of different methods.

OBJECTIVE--Normal electrocardiographic recordings were analysed to establish the influence of measurement of different numbers of electrocardiographic leads on the results of different formulas expressing QT dispersion and the effects of adjustment of QT dispersion obtained from a subset of an electrocardiogram to approximate to the true QT dispersion obtained from a complete electrocardiogram. SUBJECTS AND METHODS--Resting 12 lead electrocardiograms of 27 healthy people were investigated. In each lead, the QT interval was measured with a digitising board and QT dispersion was evaluated by three formulas: (A) the difference between the longest and the shortest QT interval among all leads; (B) the difference between the second longest and the second shortest QT interval; (C) SD of QT intervals in different leads. For each formula, the "true" dispersion was assessed from all measurable leads and then different combinations of leads were omitted. The mean relative differences between the QT dispersion with a given number of omitted leads and the "true" QT dispersion (mean relative errors) and the coefficients of variance of the results of QT dispersion obtained when omitting combinations of leads were compared for the different formulas. The procedure was repeated with an adjustment of each formula dividing its results by the square root of the number of measured leads. The same approach was used for the measurement of QT dispersion from the chest leads including a fourth formula (D) the SD of interlead differences weighted according to the distances between leads. For different formulas, the mean relative errors caused by omitting individual electrocardiographic leads were also assessed and the importance of individual leads for correct measurement of QT dispersion was investigated. RESULTS--The study found important differences between different formulas for assessment of QT dispersion with respect to compensation for missing measurements of QT interval. The standard max-min formula (A) performed poorly (mean relative errors of 6.1% to 18.5% for missing one to four leads) but was appropriately adjusted with the factor of 1/square root of n (n = number of measured leads). In a population of healthy people such an adjustment removed the systematic bias introduced by missing leads of the 12 lead electrocardiogram and significantly reduced the mean relative errors caused by the omission of several leads. The unadjusted SD was the optimum formula (C) for the analysis of 12 lead electrocardiograms, and the weighted standard deviation (D) was the optimum for the analysis of six lead chest electrocardiograms. The coefficients of variance of measurements of QT dispersion with different missing leads were very large (about 3 to 7 for one to four missing leads). Independently of the formula for measurement of QT dispersion, omission of different leads produced substantially different relative errors. In 12 lead electrocardiograms the largest relative errors (> 10%) were caused by omitting lead aVL or lead V1. CONCLUSIONS--Because of the large coefficients of variance, the concept of adjusting the QT dispersion for different numbers of electrocardiographic leads used in its assessment is difficult if not impossible to fulfil. Thus it is likely to be more appropriate to assess QT dispersion from standardised constant sets of electrocardiographic leads.     

QT dispersion: an electrocardiographic derivative of QT prolongation

BACKGROUND: QT dispersion has been considered a surrogate for heterogeneity of repolarization, leading to ventricular arrhythmias. METHODS: High-resolution 12-lead electrocardiograms were obtained in 15 patients with a history of ventricular tachycardia or ventricular fibrillation, 15 patients with congestive heart failure, 17 patients with a history of previous Q-wave myocardial infarction without heart failure, and 23 healthy control subjects. RESULTS: QTc dispersion was prolonged in all 3 patient groups compared with controls (71+/-22, 68 +/-31, 61+/-27 vs 44+/-17 msec, P =. 003), but no difference was seen between heart disease groups. QTc dispersion was strongly correlated with the QTc max (r = 0.73, P<.0001) but did not correlate with the QTc min (r = 0.04, P =.76). QTc dispersion also strongly correlated with the JTc max (r = 0.54, P<.0001) but did not correlate with JTc min (r = -0.007, P =.95). QTc dispersion correlated inversely with T-wave amplitude (r = -0.35, P =.003). When all 876 electrocardiographic signals were considered, a significant negative correlation was present between QTc duration and T-wave amplitude (r = -0.133, P =.0002). Logistic regression analysis failed to demonstrate any independent risk factors that predicted ventricular arrhythmias, including all measures of dispersion. CONCLUSIONS: The measurement of QT dispersion is strongly influenced by the maximum QT interval, as well as by changes in T-wave amplitude. QT "dispersion" may represent a summary of these changes that reflect the underlying myocardial process but does not represent an accurate quantitative measure of heterogeneity of refractoriness.     

Computerized QT dispersion measurement and cardiovascular mortality in male veterans

We examined the prognostic value of computerized measurements of QT dispersion in 37,579 male veterans. The results of our study showed that QT dispersion is a poor independent predictor of cardiovascular mortality.     

QT dispersion in patients with different etiologies of left ventricular hypertrophy: the significance of QT dispersion in endurance athletes

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett's formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes' group (physiological LVH) and healthy subjects (P<0.05). The magnitude of QTcd was similar between athletes and the control group (P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant (P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.     

Effect of dofetilide on QT dispersion and the prognostic implications of changes in QT dispersion for patients with congestive heart failure

AIMS: Drug-induced changes in QT dispersion may be a way of detecting harmful repolarisation abnormalities for patients receiving antiarrhythmic drugs affecting ventricular repolarisation. METHODS AND RESULTS: In 463 congestive heart failure (CHF) patients enrolled in the Danish Investigations Of Arrhythmia and Mortality On Dofetilide-CHF (DIAMOND-CHF) study, both pre-treatment and on-treatment day 2-6 QT dispersion was available from standard 12-lead ECGs. Patients were randomised in a double-blind manner to receive either placebo or dofetilide, a new class III antiarrhythmic drug. During a median follow-up of 19 months (minimum 1 year), 179 patients (39%) died (135 patients from cardiac causes). Changes in QT dispersion did not predict all-cause or cardiac mortality for patients treated with dofetilide in multivariate survival analysis (Risk ratio: 1.02, 95% confidence interval: 0.97-1.08, P>0.4). This finding was independent of pre-treatment QT dispersion. Dofetilide caused a small QT dispersion increment of 8 ms, not different from the changes seen in the placebo group (3 ms). CONCLUSION: For patients with CHF and reduced left ventricular systolic function, changes in QT dispersion following treatment with dofetilide do not predict all-cause or cardiac mortality. The dofetilide-induced QT dispersion changes are small and comparable to those seen in placebo treated patients.     

Significance of QT dispersion in the long QT syndrome

The long QT syndrome (LQTS) has often been considered as a model to study the abnormalities of cardiac repolarization in humans because it represents a pure electrical disease with no evidence of cardiac structural abnormalities. The arrhythmogenic potential of prolonged ventricular repolarization has been extensively studied both in experimental models and at the clinical level in LQTS patients, and many studies pointed to the pathogenetic role of the dispersion of ventricular recovery times (i.e., dispersion of ventricular repolarization). In the last few years, a new critical knowledge has been achieved thanks to the molecular biology techniques that are unveiling the genetic bases of LQTS. Indeed, the understanding of the genes and mutations that may cause the LQTS opened the way to understanding the molecular determinants of the altered ventricular repolarization that can be found in LQTS patients. From the clinical standpoint, the traditional tools applied for the detection and quantification of the dispersion of ventricular repolarization (monophasic action potential, QT dispersion) showed their effectiveness but also their limitations. More recently, the availability of new algorithms and the development of powerful computerized supports allowed the evaluation of innovative techniques, which now represent possible attractive alternatives intended to quantify the degree of repolarization abnormalities in LQTS patients and possibly to noninvasively quantify the risk of cardiac events.     

Semiautomated QT interval measurement in electrocardiograms from a thorough QT study: comparison of the grouped and ungrouped superimposed median beat methods

IntroductionWe postulated that it may be easier to identify earliest Q onset and latest T offset when the median beats from 12 leads are separated vertically by 5 to 10 mm (ungrouped superimposed median beat [SMB] method) rather than when their baselines closely (but rarely perfectly) overlap (grouped SMB method).MethodsThree readers manually adjudicated annotations placed by an automated algorithm, using grouped (gSMB) and ungrouped (uSMB) methods in 2658 electrocardiograms (ECGs) recorded in 38 subjects in a crossover design thorough QT study at predose and 6 time points postdosing with placebo or moxifloxacin.ResultsPlacebo-subtracted, moxifloxacin-induced QTcF prolongation was comparable with both methods. Maximum QTcF prolongation was seen at 2 hours—10.5 milliseconds (90% confidence interval, 7.9-13.1 milliseconds) with gSMB and 12.9 milliseconds (90% confidence interval, 9.9-15.8 milliseconds) by uSMB. Both methods showed good agreement; mean QT was 4 milliseconds greater by uSMB. Interreader variability of absolute differences in QT measurements was 1 millisecond lower with the uSMB method (6.8 ± 5.7 milliseconds by gSMB and 5.9 ± 4.5 milliseconds by uSMB).ConclusionMean QT was 4 milliseconds longer, and interreader variability, 1 millisecond lower with uSMB. Otherwise, both methods were comparable and detected the moxifloxacin effect.     

QT dispersion: an indication of arrhythmia risk in patients with long QT intervals

Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.     

QT dispersion: comparison between participants with Type 1 and 2 diabetes and association with microalbuminuria in diabetes

BACKGROUND AND AIMS: The interlead variation of QT duration in surface electrocardiogram [ECG; QT dispersion (QTd)] has been shown to predict mortality in both diabetic and general population. Diabetic cardiac autonomic neuropathy (CAN) is a common complication of diabetes, and it is also associated with worse prognosis among the diabetic population. In this study, we investigated the association between QTd duration and CAN, as well as other complications of diabetes in participants with Types 1 and 2 diabetes. METHODS: A total of 184 patients with either Type 1 (n=63) or 2 (n=121) diabetes, as well as 100 control participants, matched for age and sex with the diabetic individuals, were studied. QT and RR intervals were measured on 12 leads of resting ECG tracing. QTd was calculated semiautomatically using a computer program as the difference between the maximum and the minimum QT in any of the 12 leads. CAN was diagnosed when two out of the four classical tests were abnormal. RESULTS: QTd was not significantly different between controls and patients with either Type 1 or 2 diabetes. Age-adjusted QTd intervals were not significantly different between patients with Types 1 and 2 diabetes (P=.86). For both types of diabetes, no significant differences were found in QTd between patients with and without CAN. Multivariable linear regression analysis, after adjustment for a number of confounding factors, demonstrated a positive association between QTd and duration of diabetes (P=.02) in the group of the patients with Type 1 diabetes. In those with Type 2 diabetes, QTd was associated with age (P=.006) and presence of microalbuminuria (P=.001). In addition, no significant association was found with retinopathy or blood pressure levels. CONCLUSIONS: Age-adjusted QTd interval was not different between patients with Types 1 and 2 diabetes. CAN is not associated with QTd interval in both types of diabetes. Furthermore, microalbuminuria was found to be the strongest predictor of QTd in patients with Type 2 diabetes. Because long QTd interval predicts cardiac mortality in participants with diabetes, it is suggested that it may be a useful adjuvant index in the evaluation of cardiovascular risk in participants with Type 2 diabetes and microalbuminuria.     

Near infrared spectrometry for faecal fat measurement: comparison with conventional gravimetric and titrimetric methods.

This investigation was aimed at comparing a new method for measuring faecal fat excretion, carried out with a semi-automated instrument by using near infrared analysis (NIRA), with the traditional titrimetric (Van de Kamer) and gravimetric (Sobel) methods. Near infrared analysis faecal fat was assayed on the three day stool collection from 118 patients (68 chronic pancreatitis, 19 organic diseases of the gastrointestinal tract, 19 alcoholic liver disease, 12 functional gastrointestinal disorders). A strict linear correlation was found between NIRA and both the titrimetric (r = 0.928, p less than 0.0001) and the gravimetric (r = 0.971, p less than 0.0001) methods. On homogenised faeces, a mean coefficient of variation of 2.1 (SD 1.71)% was found. Before homogenisation (where a mean coefficient of variation of 7% was found) accurate results were obtained when the mean of five measurements was considered. In conclusion, the assay of faecal fat excretion by the near infrared reflessometry appears a simple, rapid and reliable method for measuring steatorrhoea.     

QT dispersion: an indication of arrhythmia risk in patients with long QT intervals.

Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.