Minimum QT Intervals Research Articles

QT dispersion in premature beats produced by extrastimuli from the right atrium and right ventricle

The difference between the maximum and minimum QT interval measured from a 12-lead electrocardiogram was defined as an index of spatial inhomogeneous repolarization of the ventricular myocardium. The causal relationship between QT dispersion and incidence of ventricular arrhythmias has been pointed out in various heart diseases, but until now it was discussed mainly related to sinus rhythm. QT dispersion in extrasystole may be more important in the development of arrhythmias. We examined 5 cases (mean age 34 +/- 12 years) with a history of paroxysmal supraventricular tachycardia, who underwent electrophysiologic study. Both atrial and ventricular premature stimuli were given at a basic cycle length of 600 msec respectively. The QT interval and the ventricular activation time (VAT) (period from premature test stimulus to the summit of QRS) of the premature beats were measured in a simultaneously recorded 12-lead electrocardiogram. QT dispersion (the difference between the longest QT interval and the shortest QT interval) and VAT dispersion (the difference between the longest VAT and the shortest VAT) were measured. In atrial premature beats, there were no significant changes in the QT dispersion or VAT dispersion when the coupling interval of the premature beats was shortened. In the ventricular premature beats, however, both the QT dispersion and the VAT dispersion tended to increase with the shortening of the coupling interval. We concluded that only a short coupled ventricular premature beat induces greater QT and VAT dispersion. A ventricular couplet with short coupling interval may contribute to the development of ventricular tachyarrhythmias.

QT Dispersion as a Noninvasive Arrhythmiogenic Marker in Acute Myocardial Infarction

Backround: Prolongation of QT dispersion (QTD), defined as the difference between maximum and minimum QT intervals on surface ECG, has been proposed as a noninvasive arrythmogenic marker. The aim of this study was to estimate the value of QTD in identifing patients susceptible to ventricular fibrillation or ventricular tachycardia (VF/VT) after an acute myocardial infarction (AMI) and to evaluate the behavior of QTD in relation to the thrombolytic therapy.Methods: We studied 108 consecutive patients with AMI. All patients had a 12‐lead surface ECG recorded upon admission and a second ECG 24 hours later. QT interval was measured from the onset of Q to the end of T in each of 12 standard ECG leads. QTD was the difference between the longest and shortest values of QT. All QTD measurements were corrected for heart rate (QTcD) using QTc values according to Bazzet formula.Results: Fifteen patients (13.8%) developed VF/VT in the first week after AMI (group 1A) and 93 patients (86.2%) did not have VF/NT (group 1B). QTD and QTcD values were significantly greater in group 1A in comparison to group 1B on admission and 24 hours later. Sixty‐five patients (60%) received intravenous thrombolysis in the acute phase of AMI (group 2A) and 43 patients (40%) did not (group 2B). No significant difference in QTD and QTcD was observed in the first ECG on admission between the two groups. Conversely, QTD and QTcD were lower in group 2A patients in the second ECG 24 hours after admission.Conclusions: These results provide evidence that increased values of QTD are correlated well with occurrence of malignant ventricular arrhythmias after acute myocardial infarction while lower values associated with the thrombolytic therapy. A.N.E. 1999;4(1):35–38

Difference of QT Dispersion between Patients with Ischemic and Idiopathic Dilated Cardiomyopathy

Background and Objectives:QT dispersion (QTd is defined as the difference between the maximum and minimum QT interval in any of the 12 leads of the surface ECG. QTd has been shown to reflect regional variations in ventricular repolarization. Ischemic dilated cardiomyopathy (DCM may lead to more spatial and temporal dispersion in ventricular repolarization than idiopathic DCM. The purpose of this study was to determine the difference of QTd between patients who had ischemic and idiopathic DCM. Materials and Methods:The study population included 30 patients with ischemic DCM and 30 with idiopathic DCM. All standard 12-lead ECGs were examined prospectively by two observers who were unware of the patient's details. Results:QTd in ischemic DCM was significantly higher than that in idiopathic DCM (63±32 vs. 44 ±26 msec, p=0.012 and JTd in ischemic DCM was significantly higher than that in idiopathic DCM (48± 21 vs. 36±22 msec, p=0.036. Results did not change when Bazett's QTc and JTc was substituted for QT (QTcd:69±33 vs. 52±28 p=0.039 and JT (JTcd:56±21 vs. 41±25 p=0.043. Conclusion:Ischemic DCM has increased spatial inhomogeneity of repolarization probably due to more regional myocardial damages compared with idiopathic DCM. The value of QT dispersion as an easily accessible, non-invasive method in predicting the risk of life threatening arrhythmia and overall mortality in patients with dilated cardiomyopathy must be confirmed in prospective trials. (Korean Circulation J 1999;29(5 :492-497

Dynamic changes of QT dispersion as a predictor of myocardial ischemia on exercise testing in patients with angina pectoris.

The difference between the maximum and minimum QT intervals on the standard 12-lead ECG (QT dispersion) may be a significant predictor of serious arrhythmias. Dynamic changes in QTd were determined during exercise-induced ischemia in 15 patients with effort angina (> or = 75% coronary stenosis) and 10 normal individuals. Treadmill exercise testing was performed according to Bruce's protocol and the rate-corrected QT dispersion (QTcd) was calculated using Bazett's formula. The resting QTcd before exercise was similar in the angina patients and the controls. After the first stage of exercise, QTcd was significantly increased in the angina patients (p = 0.035), while it remained near baseline in the controls. Five minutes after completing exercise, QTcd was significantly greater in the angina patients than in the controls (p = 0.011). Furthermore, QTcd values after the first stage of exercise were significantly correlated with the maximum ST depression observed on completing exercise in the angina patients (r = 0.714, p = 0.0028). Because QTd may represent the heterogeneity of ventricular repolarization, its significant exercise-induced increase in the angina patients suggests that myocardial ischemia caused repolarization disorders. The significant correlation between QTcd values after the first stage of exercise (before significant ST depression) and the maximum ST depression on completing exercise suggests that an increase in QTcd preceding ischemic ST depression may predict myocardial ischemia. In addition, even daily activities not causing significant ST changes may increase QTcd and the risk of serious arrhythmia in angina patients.

Significance of exercise QT dispersion in patients with coronary artery disease who do not have exercise-induced ischemic ST-segment changes.

The poor sensitivity and the poor predictive value of ST-segment depression have limited the usefulness of the exercise electrocardiogram (ECG) in the diagnosis and evaluation of coronary artery disease (CAD). The QT dispersion (QTD), recorded as the difference between maximal and minimal QT intervals on a 12-lead exercise ECG, is sensitive to myocardial ischemia and may improve the accuracy of exercise testing in patients with CAD who do not show an ST-segment depression. Exercise ECGs were analyzed in 50 subjects who had undergone coronary angiography for clinical indications. None of them showed an ST-segment depression during or after exercise: There were 25 patients with significant coronary artery stenosis and 25 without significant stenosis. The QTD measured before, immediately after, and 1 min after exercise was similar in the 2 groups. The QTD at 3 and 5 min after exercise was significantly greater in patients with CAD than in the controls, and the most marked difference in QTD was observed at 3 min after exercise. A QTD at 3 min after exercise of >60 ms had a sensitivity of 80% and specificity of 88% regarding the diagnosis of CAD. When a deltaQTD (post-exercise QTD minus QTD at rest) at 3 min after exercise of >0 ms was added to a QTD of >60 ms as a condition for positivity, the specificity increased to 96%. QTD measured at 3 min after exercise increases the accuracy of exercise testing in patients with CAD who do not show an ST-segment depression.

Relation between QT dispersion and slow intraventricular conduction in patients with acute anterior wall myocardial infarction

Background QT dispersion has been proposed as a simple, noninvasive measure for identifying patients at risk of postinfarction arrhythmia. It is assumed to reflect nonuniform ventricular repolarization, which, in turn, may result from regional differences in repolarization time as well as from localized activation delay. The aim of this study was to examine the relation between QT dispersion and intraventricular conduction abnormalities in patients with acute anterior wall myocardial infarction. Methods and Results Standard 12-lead electrocardiographic and 12-lead signal-averaged electrocardiographic recordings were performed in 25 patients with a first Q-wave anterior wall myocardial infarction. Measures calculated by using the 6 precordial (V 1 through V 6 ) leads for QT dispersion were (1) difference between maximum and minimum QT and QTc intervals and (2) standard deviation of QT and QTc intervals. Measures calculated from the signal-averaged electrocardiogram were (1) maximum filtered QRS duration; (2) mean; and (3) standard deviation of filtered QRS duration. No relation was found between any measure of filtered QRS duration and that of QT dispersion by using linear correlation analysis. Similarly, no significant association was demonstrated between the filtered QRS duration and corresponding QT interval measurements (total 131 leads). Conclusions The lack of correlation between signal-averaged electrocardiogram indexes of slow intraventricular conduction and electrocardiogram variables of QT dispersion suggests an independent predictive value for the 2 methods in identifying patients at risk of postinfarction arrhythmia. This suggestion is further supported by the finding that altered activation sequence is an unlikely mechanism of QT dispersion in patients with acute myocardial infarction, as indicated by the lack of association between the filtered QRS duration and corresponding QT interval measurements. (Am Heart J 1999;137:104-8.)

Increased QT dispersion in the absence of QT prolongation in patients with Behcet's disease and ventricular arrhythmias

In Behcet's disease, prominent clinical manifestations include involvement of mucocutaneous, ocular, gastrointestinal, respiratory, neurologic, urogenital, articular and cardiovascular systems. Patients with Behcet's disease have higher incidence of ventricular arrhythmia than healthy subjects. However there is a little information about the mechanism of ventricular arrhythmias in Behcet's disease. The aim of the study was to investigate whether dispersion of ventricular repolarisation was an arrhythmogenic mechanism. QT dispersion parameters were measured in 73 Behcet patients and QT dispersion was defined as the difference between the maximum and minimum QT interval in any of the 12 leads of surface electrocardiogram. Corrected QT dispersion for heart rate was calculated by Bazett's formula. The results were compared with the data from 51 matched controls without a history of cardiac disease. We found QT dispersion was greater in Behcet patients (58±12 vs. 37±8 ms, P=0.001) as was corrected QT dispersion (81±14 vs. 52±11 ms, P=0.001). There was no significant difference in minimum or maximum QT intervals between Behcet patients and controls ( P>0.05). We found a correlation between QT dispersion and grade of premature ventricular complexes ( r=0.7, P=0.002). Our findings suggest that increased dispersion of repolarisation may account for the development of ventricular arrhythmias in Behcet's disease.

Association of increased QT dispersion with coronary atherosclerosis in patients with aortic stenosis

To evaluate correlates between electrocardiographic QT dispersion and coronary atherosclerosis in patients with aortic stenosis before aortic valve replacement, 39 consecutive patients >40 years old with symptomatic aortic stenosis and coronary diameter narrowing ≥50% measured by digital angiographic study were included. An additional matched group with insignificant coronary lesions (<50%) consisted of 39 patients for comparisons. Matching by age, sex heart rate and incidence of chest pain resulted in two comparable groups with identical baseline characteristics. Preoperative transthoracic echocardiography and electrocardiograms were performed in all subjects. QT dispersion was defined as the difference between maximal and minimal QT interval measurements occurring among any of the 12 leads on a standard electrocardiogram. No subject had fewer than nine measurable leads. There were no significant differences of risk factors of coronary artery disease between the two groups. From a conditional multivariate logistic regression analysis, independent predictors of development of coronary artery disease in aortic stenosis were only QTc dispersion (odds ratio=1.255, P=0.01). A wide QTc dispersion (≥70 ins) correlated with the presence of angiographically significant coronary artery disease with a sensitivity and specificity of 72% and 79%. The positive accuracy of having significant coronary artery disease in the presence of QTc dispersion ≥70 ms was 78%. The negative predictive value was 74%. In conclusion, electrocardiographic QTc dispersion may provide important clinical information. A wide QTc dispersion in patients with aortic stenosis is associated with a high incidence of coronary artery disease. These findings warrant further investigation in a large trial.

Torsade de Pointes During Orthotopic Liver Transplantation

Torsade de Pointes During Orthotopic Liver Transplantation

Dispersion of QT and QTc interval in healthy children, and effects of sinus arrhythmia on QT dispersion

ObjectiveTo determine the normal values of QT and QTc dispersion and the effects of sinus arrhythmia on QT dispersion in healthy children.Patients and settingThe study was carried out in a...

Dispersion of QT Interval in Premature Ventricular Beats as a Marker of Susceptibility to Arrhythmic Events

Clinical observations indicate that increased QT interval dispersion in sinus beats may portend malignant ventricular arrhythmias and sudden cardiac death. The purpose of this study was to test the hypothesis that measures of QT dispersion in ventricular premature beats (QTd-V) may be also useful in identifying patients at high risk of arrhythmic events. In the group of 303 patients with ventricular premature beats on standard 12-lead ECG, the QTd-V was calculated as a difference between maximum and minimum QT interval in premature ventricular beats. During follow-up for 26 +/- 19 months the arrhythmic events (sustained ventricular tachycardia, ventricular fibrillation or sudden cardiac death) were noted in 42 patients. Patients with arrhythmic events had significantly (P < 0.005) greater values of QTd-V than those without arrhythmic events. Univariate predictors of arrhythmic events included QTd-V > or = 100 ms, left ventricular ejection fraction < 40%, QRS complex duration of ventricular premature beats > 150 ms, underlying heart disease and complete bundle branch block. Multivariate analysis using the Cox proportional hazard model showed that only QTd-V > or = 100 ms and ejection fraction < 40% were independent predictors of arrhythmic events. The results of this study indicate a significant relationship between QTd-V and the risk of arrhythmic events. The assessment of QTd-V may be useful for identifying patients with ventricular premature beats at high and low risk of subsequent arrhythmic events.

Agreement and Reproducibility of Automatic Versus Manual Measurement of QT Interval and QT Dispersion

To determine whether the automatic measurement of the QT interval is consistent with the manual measurement, this study evaluated the reproducibility and agreement of both methods in 70 normal subjects and 54 patients with hypertrophic cardiomyopathy. The mean, minimum, and maximum QT interval and QT dispersion were computed in a set of 6 consecutive electrocardiograms (3 in the supine and 3 in the standing position) obtained from each subject. The automatic method determined the T-wave end as the intersect of the least-squares-fit line around the tangent to the T-wave downslope with the isoelectric baseline. Manual measurements were obtained using a high-resolution digitizing board. QT dispersion was defined as the difference between the maximum and minimum QT interval and as standard deviations of the QT interval duration in all and precordial leads. In patients with hypertrophic cardiomyopathy, the absolute values of the QT interval and QT dispersion were significantly higher than those in normal subjects (p <0.0001). In both groups, the intrasubject variability of the QT interval was significantly lower with automatic than with manual measurement (p <0.05). The agreement between automatic and manual QT interval measurements was surprisingly poor, but it was better in patients with hypertrophic cardiomyopathy (r 2 = 0.46 to 0.67) than in normal subjects (r 2 = 0.10 to 0.25). In both groups, the reproducibility and agreement of both methods for QT dispersion were significantly poorer than for QT interval. Hence, the automatic QT interval measurements are more stable and reproducible than manual measurement, but the lack of agreement between manual and automatic measurement suggests that clinical experience gained with manual assessment cannot be applied blindly to data obtained from the automatic systems.

Exercise-induced changes in the QT interval duration and dispersion in patients with sudden cardiac death after myocardial infarction

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 Coronary Angioplasty on QT and JT Dispersion

Background:QT dispersion, reflecting inhomogenous ventricular repolarization, increases in myocardial ischemia. In addition, Many studies reported that prolonged QT dispersion reduced to normal after reperfusion treatment. We have carried out this study to evaluate the QT and JT dispersion before and after the angioplasty in patients with coronary artery diseases. Method and Materials:Seventy-two patients (55 men and 17 women: 18 acute myocardial infarction, 9 unstable angina and 45 stable angina who underwent percutaneous translu- minal coronary angioplasty were evaluated. Standard 12-lead electrocardiograms were recorded 24 hours before and 24 hours after angioplasty at a paper speed of 25 mm/sec. Results:There was no significant change in heart rate or the maximum or minimum QT interval after angioplasty. QT dispersion significantly decreased after angioplasty (p<0.05. And QTc dispersion (QTcd also similary reduced (p<0.01. JT dispersion (JTc and JTc dispersion (JTcd were not changed significantly. There were significant reduction in QTd and QTcd in the group of patients without acute myocardial infarction (p=0.005, 0.004, respectively but not in JTd and JTcd. However, in patients with acute myocardial infarction, all four dispersion were not reduced significantly. And in patients with multivessel angioplasty, there were significant reduction of QTd, QTcd, JTd and JTcd (p=0.016, 0.014, 0.036, 0.030, respectively. Conclusions:As changes in QT and JT dispersion reflect successful reperfusion by angioplasty, they can be accepted as promising test for assessing the effectiveness of angioplasty clinically. However the methodology still has several unresolved issues and larger, prospective clinical studies are needed. (Korean Circulation J 1998;28(8 :1280-1286

Determinants of precordial QT dispersion in normal subjects

Dispersion of precordial QT intervals has been attributed to delay in the recovery process in the myocardium under the exploring electrode, a local effect. However, the phenomenon also could be explained by different projections of the heart vector, in which case the 12-lead electrocardiogram (ECG) derived from the heart vector would show similar dispersion that could not be local in nature because the electrical activity of the heart is represented by a single dipole. Using an analog device that switched between the two, conventional and derived ECGs were obtained from 129 normal subjects. Measured as the difference between the longest and shortest precordial QT intervals, QT dispersion from the derived ECGs (mean ± SD, 40 ± 20 ms) was nearly identical in magnitude to that from the standard ECGs (41 ± 18 ms, P = NS). Further analysis of the derived ECGs revealed nonuniform distributions of both the maximal and minimal QT intervals across the precordial leads. In addition, a weak correlation was found between the QT interval and the T wave amplitude in the two precordial leads with the lowest T-wave amplitudes ( r = −0.303 in V1, P = .001, and r = 0.253 in V6, P = .005). While findings in patients with disease or with abnormal ECGs may differ and require separate examination, these data suggest that the observed magnitude of precordial QT dispersion in normal subjects can be explained by differences in precordial projection of the end of the T wave rather than by local effect.

Relationship between QT dispersion and the incidence of early ventricular arrhythmias in patients with acute myocardial infarction

There is controversy about the influence of QT dispersion on the incidence of early ventricular arrhythmias in patients with acute myocardial infarction (AMI). The QT and QTc dispersion (QTd, QTcd) between two groups of patients with AMI were compared: 39 patients with early sustained ventricular tachycardia or ventricular fibrillation (VT/VF) and 40 patients without such arrhythmias. QTd and QTcd were calculated from the admission and predischarge ECG, expressed as the difference between the maximum and minimum QT and QTc interval in 12 leads. The coefficient of variability was also calculated (VQT, VQTc). Groups did not differ significantly in age, incidence of previous infarction, Killip class, electrolyte status, infarct location, expected and final ECG infarct size, enzymatic infarct size, thrombolytic treatment and reperfusion rate, i.e., in variables that could influence the VT/VF occurrence. On admission, patients with VT/VF had significantly greater QTd (77±23 vs 53±27 ms, P<0.001) and QTcd (90±29 vs 62±28 ms, P<0.001); VQT and VQTc were also significantly higher. Although similar differences existed on predischarge ECG, they were smaller. The results indicate that QT dispersion varies during the illness, and that measurements of QT dispersion could be helpful in predicting serious ventricular arrhythmias.

Value of QT dispersion in the interpretation of exercise stress test in women.

Exercise testing in women is associated with a high incidence of false-positive ECG changes and should be combined with an imaging study. The QT dispersion (QTD), recorded as the difference between maximum and minimum QT intervals on a 12-lead ECG, is sensitive to myocardial ischemia and may improve the accuracy of exercise testing in women. Exercise ECGs were analyzed in 64 women who had undergone exercise ECG and coronary angiography for clinical indications: 20 patients with normal exercise stress test and nonsignificant (< or = 50% diameter narrowing of a major epicardial coronary artery) coronary artery disease (CAD) on angiography (true-negative; TN group), 20 patients with positive exercise stress tests (> or = 1 mm ST-segment depression or reversible perfusion defects) and significant CAD (true-positive; TP group), and 24 patients with positive exercise stress tests but no significant CAD (false-positive; FP group). The exercise QTD was 45+/-15 ms in TN, 80+/-23 ms in TP (P<.0001 versus TP), and 41+/-14 ms in FP (P=NS versus TN and <.0001 versus TP) groups. A stress QTD of > 60 ms had a sensitivity of 70% and specificity of 95% for the diagnosis of significant CAD compared with 55% (P<.05) and 63% (P<.01), respectively, for > or = 1 mm ST-segment depression during stress. When QTD of > 60 ms was added to ST-segment depression as a condition for positive test, the specificity increased to 100%. Exercise QTD is an easily measurable ECG variable that significantly increases the accuracy of exercise testing in women.

Influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and clinical outcome

Increased QT dispersion, defined as the difference between the maximum and minimum QT interval on the standard 12-lead electrocardiogram, is assumed to reflect regional inhomogeneity of ventricular repolarization and has been shown to be associated with an increased risk of arrhythmic events. The purpose of the present study is to examine the influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and to evaluate the predictive value of QT dispersion after amiodarone therapy for further arrhythmic events. ECG's were obtained in 47 patients 1–2 days before and 6–8 weeks after amiodarone was started. All patients had coronary artery disease with a mean EF of 34±14%. The QT interval was measured in each lead of a digitized ECG displayed on a high resolution monitor (250 mm s −1). Amiodarone therapy resulted in a significant increase in the maximal QT c interval (476±44 to 505±44 ms, p<0.001). However, measurement of QT dispersion (70±34 vs 73±29 ms) and Qtc dispersion (78±37 vs 77±31 ms) revealed no significant difference before and after amiodarone. During a one year follow-up period 26 patients were free of arrhythmic events and 7 patients developed further arrhythmic events. The remaining 14 patients were excluded from the one year follow-up analysis because of drug discontinuation ( n=8), death due to heart failure ( n=1), medical intervention ( n=3) and incomplete follow-up ( n=2). No measure of QT dispersion was predictive of recurrent arrhythmic events during treatment with amiodarone. Conclusion: Treatment with amiodarone results in significant QT prolongation without altering QT dispersion. Measurements of QT dispersion were not predictive of amiodarone efficacy in this patient population.

QT Dispersion as a Marker of Risk in Patients Awaiting Heart Transplantation

Objectives. The objectives of this study were to determine whether a signal-averaged electrocardiogram (SAECG) or measurement of interlead variability of QT intervals on an electrocardiogram (ECG) obtained at the time of wait-listing could provide prognostic value with respect to cardiac death during the waiting period.Background. Because heart transplantation is a life-saving but limited resource, there remains an urgent need to identify those patients at greatest risk of dying while awaiting heart transplantation as part of the strategy to optimize the allocation of donor organs to those in greatest need. This study was undertaken to prospectively identify clinical, ECG or SAECG variables that might predict mortality during the waiting period.Methods. Of 108 consecutive patients referred for heart transplant evaluation, 80 were placed on a waiting list, at which time a standard 12-lead ECG and a SAECG were recorded. In this cohort of 80 patients, QT dispersion was characterized from the 12-lead ECG as either the maximal–minimal QT interval (QTDISP) or as the coefficient of variation of all QT intervals (QTCV).Results. During the 25-month follow-up period (mean time on waiting list, 201 days), the mortality rate was 27%/year, divided equally between heart failure and sudden deaths. No clinical variable identified at entry predicted mortality. QTDISP and QTCV were strong mortality predictors, with a 4.1-fold increase in mortality in patients with QTDISP >140 ms compared with those patients with QTDISP ≤140 ms (95% CI 1.1 to 14.9), whereas a QTCV ≥9% also predicted a 4.1-fold increased risk of death (95% CI 1.4 to 11.8). Although 88% of all SAECGs were abnormal, no patient with a normal SAECG died suddenly during the waiting period.Conclusions. Indexes of QT dispersion provide a means of stratifying a patient’s risk of dying while awaiting heart transplantation and may help to establish priority on a heart transplant waiting list.(J Am Coll Cardiol 1997;29:1576–84)

Effect of coronary angioplasty on precordial QT dispersion

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 ± 9 ms, immediately after PTCA 23 ± 14 ms (p < 0.001), and late after PTCA 29 ± 18 ms (p < 0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 ± 40 vs 391 ± 39 ms; p < 0.02) and then remained stable late after PTCA (376 ± 36 ms, p = NS vs immedately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 ± 15 ms [p < 0.01] vs 25 ± 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 ± 13 ms [p < 0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.