Predictive factors of ventricular fibrillation triggered by pause-dependent torsades de pointes associated with acquired long QT interval: role of QT dispersion and left ventricular function

INTRODUCTION: Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause-dependent torsades de pointes are not understood. METHODS AND RESULTS: We evaluated 91 patients who fulfilled four criteria: (1) pause-dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 sec); (3) long-short initiation sequence; and (4) conditions known to induce pause-dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12-lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44% +/- 14% vs 65% +/- 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%; P < 0.0001), QT mean (591 +/- 73 msec vs 514 +/- 78 msec; P < 0.0001), QTc mean (563 +/- 76 msec vs 508 +/- 90 msec; P = 0.002), absolute QT dispersion (166 +/- 56 msec vs 84 +/- 49 msec; P < 0.0001), relative QT dispersion (9.9% +/- 3.5% vs 6.3% +/- 3.2%; P < 0.0001), absolute QTc dispersion (158 +/- 57 msec vs 81 +/- 44 msec; P < 0.0001), and relative QTc dispersion (9.9% +/- 3.6% vs 6.2% +/- 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF. CONCLUSION: Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.     

QT dispersion does not represent electrocardiographic interlead heterogeneity of ventricular repolarization

INTRODUCTION: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals. METHODS AND RESULTS: Seventy-eight normal subjects (47+/-16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38+/-15 years, 21 women), 72 dilated cardiomyopathy patients (DCM; 48+/-15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63+/-12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). QTd was 33.6+/-18.3, 47.0+/-19.3, 34.8+/-21.2, and 57.5+/-25.3 msec in normals, HCM, DCM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%+/-0.031%, 0.067%+/-0.067%, 0.112%+/-0.154%, and 0.186%+/-0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS, other P < 0.006). The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. CONCLUSION: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it.     

QT Dispersion and Mortality in the Elderly

Background: The prognostic value of QT interval dispersion measured from a standard 12‐lead electrocardiogram (ECG) in the general population is not well established. The purpose of the present study was primarily to assess the value of QT interval dispersion obtained from 12‐lead ECG in the prediction of total, cardiac, stroke, and cancer mortality in the elderly. Methods: A random population sample of community‐living elderly people (n = 330, age ≧; 65 years, mean 74 ±; 6 years) underwent a comprehensive clinical evaluation, laboratory tests, and 12‐lead ECG recordings. Results: By the end of the 10‐year follow‐up, 180 subjects (55%) had died and 150 (45%) were still alive. Heart rate corrected QT (QTc) dispersion had been longer in those who had died than in the survivors (75 ±; 32 ms vs 63 ±; 35 ms, P = 0.01). After adjustment for age and sex in the Cox proportional hazards model, prolonged QTc dispersion (≧; 70 msec) predicted all‐cause mortality (relative risk [RR] 1.38, 95% confidence interval [Cl] 1.02–1.86) and particularly stroke mortality (RR 2.7, 95% Cl 1.29–5.73), but not cardiac (RR 1.38, 95% Cl 0.87–2.18) or cancer (RR 1.51, 95% Cl 0.91–2.50) mortality. After adjustment for age, sex, body mass index, blood pressure, blood glucose and cholesterol concentrations, functional class, history of cerebrovascular disease, diabetes, smoking, previous myocardial infarction, angina pectoris, congestive heart failure, medication, left ventricular hypertrophy on ECG, presence of atrial fibrillation and R‐R interval, increased QTc dispersion still predicted stroke mortality (RR 3.21, 95% Cl 1.09–9.47), but not total mortality or mortality from other causes. The combination of increased QTc dispersion and left ventricular hypertrophy on ECG was a powerful independent predictor of stroke mortality in the present elderly population (RR 16.52, 95% Cl 3.37–80.89). QTcmin (the shortest QTc interval among the 12 leads of ECG) independently predicted total mortality (RR 1.0082, 95% Cl 1.0028–1.0136, P = 0.003), cardiac mortality (RR 1.0191, 95% Cl 1.0102–1.0281, P < 0.0001) and cancer mortality (RR 1.0162, 95% Cl 1.0049–1.0277, P = 0.005). Conclusions: Increased QTc dispersion yields independent information on the risk of dying from stroke among the elderly and its component, QTcmin, from the other causes of death. A.N.E. 2001; 6(3):183–192     

Effect of amiodarone on qt dispersion in the 12-lead standard electrocardiogram and its significance for subsequent arrhythmic events

Background and hypothesis: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization. The purpose of the present study was twofold: (1) to analyze the effect of amiodarone on QT dispersion measured in the 12-lead standard ECG, and (2) to examine the association between QT dispersion on amiodarone and subsequent arrhythmic events. Methods: To determine the effect of amiodarone on QT dispersion and its clinical significance for subsequent arrhythmic events, QT dispersion was measured in the 12-lead standard electrocardiogram (ECG) in 52 patients before and after administration of empiric amiodarone for ventricular tachyarrhythmias. Results: QT intervals increased from 401 ± 44 ms before amiodarone to 442 ± 53 ms after amiodarone therapy, and rate corrected QT intervals (QTc) increased from 452 ± 43 ms to 477 ± 37 ms, respectively (p<0.01). QT dispersion, QTc dispersion, and adjusted QTc dispersion, which take account of the number of leads measured, were not significantly different before and after initiation of amiodarone therapy (58 ± 24 ms vs. 61 ± 26 ms, 68 ± 29 vs. 66 ± 26 ms, and 22 ± 8 vs. 22 ± 8 ms, respectively, p = NS). During 31 ± 25 months follow-up after initiation of amiodarone therapy, arrhythmic events defined as sustained ventricular tachycardia, ventricular fibrillation, or sudden death occurred in 11 of 52 study patients (21%). QT dispersion, QTc dispersion, and adjusted QTc dispersion on amiodarone were not different between patients with and without arrhythmic events during follow-up (65 ± 14 vs. 59 ± 29 ms, 73 ± 15 vs. 64 ± 28 ms, and 25 ± 6 vs. 21 ± 8 ms, respectively, p=NS). Conclusions: We conclude that (1) amiodarone increases QT intervals and QTc intervals during sinus rhythm but does not significantly change measures of QT dispersion; and (2) QT dispersion measured in the 12-lead standard ECG after initiation of amiodarone therapy does not appear to be a useful marker for subsequent arrhythmic events.     

QT dispersion and late potentials during doxorubicin therapy for non-Hodgkin's lymphoma

OBJECTIVES: To investigate effects of doxorubicin therapy on cardiac electrophysiology, with special emphasis on QT dispersion and late potentials, in lymphoma patients. DESIGN: Prospective study. SETTING: University hospital. SUBJECTS: Twenty-eight adult non-Hodgkin's lymphoma patients who received doxorubicin to a cumulative dose of 400-500 mg m-2. MAIN OUTCOME MEASURES: Standard 12-lead electrocardiogram (ECG) and signal-averaged ECG (SAECG) recordings were performed at baseline and after cumulative doxorubicin doses of 200, 400 and 500 mg m-2. RESULTS: Heart rate-corrected QT interval (QTc) increased from 402 +/- 4 to 416 +/- 5 ms (P = 0.002) during the study period. QT dispersion (variability in QT interval duration amongst the different leads of the standard 12-lead ECG) increased from 24.1 +/- 2.5 to 35.0 +/- 2.8 ms (P = 0.041) and QTc dispersion increased from 26.5 +/- 2.5 to 39.0 +/- 3.5 ms (P = 0.039). Five patients (18%) developed QT dispersion exceeding 50 ms. In addition, two patients (7%) developed late potentials during doxorubicin therapy. The changes in QTc duration, QT dispersion and late potentials occurred independently of the impairment of left ventricular function. CONCLUSIONS: Prolongation of QTc, increased QT dispersion and development of late potentials are indicative of doxorubicin-induced abnormal ventricular depolarization and repolarization. QT dispersion and late potentials are both known to be associated with increased risk of serious ventricular dysrhythmias and sudden death in various cardiac diseases. Thus, follow-up of these parameters might also be useful in assessing the risk of late cardiovascular events in cancer patients treated with anthracyclines.     

Predictive Value of QT Dispersion for Ventricular Tachyarrhythmias in Patients with Implantable Cardioverter Defibrillator

Background: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization as a potential substrate for ventricular arrhythmias. Methods: QT dispersion was measured in the standard 12-lead ECG in 51 patients at the time of implantation of a third generation implantable cardioverter defibrillator (ICD) with automatic electrogram storage capability for electrical events triggering device therapy. In addition, QT dispersion was measured in 100 age- and sex-matched healthy controls. All 5 1 study patients with ICD were prospectively followed to determine possible associations between QT dispersion at implant and subsequent spontaneous ICD shocks for ventricular tachyarrhythmias (VT). Results: Rate-corrected QT dispersion and adjusted QTc dispersion, which takes account of the number of leads measured, were significantly greater in ICD patients compared to controls (76 ± 25 ms vs 46 ± 11 ms, and 24 ± 7 ms vs 14 ± 3 ms respectively, P < 0.0 1). During 15 ± 8 months follow-up, ventricular tachyarrhythmias occurred in 23 (45%) of 51 ICD patients. QTc dispersion and adjusted QTc dispersion were not significantly different between ICD patients with ventricular tachyarrhythmias and ICD patients without ventricular tachyarrhythmias during follow-up (74 ± 19 ms versus 77 ± 29 ms, and 23 ± 6 ms vs 25 ± 8 ms respectively). Conclusion: Increased QT dispersion measured in the 12-lead standard ECG does not appear to be a useful marker for future arrhythmic events in a mixed patient population with ICD.     

The relative accuracies of ECG precordial lead waveforms derived from EASI leads and those acquired from paramedic applied standard leads

Accurate precordial electrode placement can be difficult in emergency situations leading either to loss of time or diminished accuracy. A possible solution is the quasi-orthogonal EASI lead system, with only five electrodes and easily defined landmarks to provide a derived 12-lead electrocardiogram (ECG). The purpose of this study was to test the hypothesis that precordial waveforms in EASI-derived ECGs have no greater deviation from those in gold standard ECGs, than do the precordial waveforms in paramedic acquired standard ECGs. Twenty paramedics applied the standard precordial electrodes employing the routine procedure. A certified ECG technician applied the 6 standard precordial electrodes in their correct gold standard positions, and the EASI electrodes. 12-lead ECGs were obtained from the paramedics' standard leads, and derived from the EASI leads, for comparison with the gold standard ECG. In each precordial lead recording, 6 computer-measured QRS-T waveform parameters were considered. Differences between deltaEASI-gold standard versus deltaparamedic-gold standard were calculated for every waveform in every lead resulting in 720 comparisons. EASI and paramedic results were "equally accurate" in 47%, the paramedic was more accurate in 31%, and EASI was more accurate in the remaining 22%. The differences from gold standard recording of precordial waveforms in ECGs derived from the EASI leads and those acquired via paramedic-applied standard electrodes are similar. The results suggest that the EASI lead system may provide an alternative to the standard ECG precordial leads to facilitate data acquisition and possibly save valuable time in emergency situations.     

QT interval change with age in an overtly healthy older population

Background: Prolonged QT interval on the surface electrocardiogram (ECG) is known to be associated with arrhythmias, coronary heart disease, and sudden cardiac death. Increased QT dispersion has also been related to arrhythymias which are more frequent in the elderly. Hypothesis: This study investigated the relationship between aging, QT interval, and QT dispersion. Methods: Normal resting ECGs were recorded from 96 healthy subjects (73 women, age range 40-102 years). No subject had symptoms or signs of heart disease and none was on medication affecting cardiac function. All had normal heart size on chest x-ray and normal electrolytes. Using a digitizing board, the RR and QT intervals were measured on each lead of each ECG, excluding only the leads in which the T wave was not visible. Mean RR, mean QT interval, and heart rate-adjusted QTc interval (standard Bazet's formula) were obtained from these measurements. Further, QT dispersion was calculated for each ECG as (1) the difference between the maximum and minimium QT interval, and (2) as the coefficient of variance of QT interval of all measurable leads. Results: A significant correlation between aging and prolonged QTc was noted in the total population (r = 0.43, p <0.05), as well as in men (r = 0.4, p <0.05) and women (r = 0.23, p<0.05) separately. There was no association between QT dispersion and increasing age regardless of the method of calculation (r= -0.04, r= -0.08 respectively, both NS). Conclusion: The rate-adjusted QT interval is prolonged with increasing age and may contribute to the increased risk of ventricular arrhythmias and cardiac mortality in elderly patients.     

Is QT Dispersion Associated with Sudden Cardiac Death in Patients with Hypertrophic Cardiomyopathy?

QT dispersion is significantly greater in patients with hypertrophic cardiomyopathy (HCM) than that in healthy subjects. Few data exist regarding the prognostic value of QT dispersion in HCM. In this study, we retrospectively investigated the association between QT dispersion and sudden cardiac death in 46 patients with HCM (mean 33.1 ±; 15.5 years, 32 men). The case group consisted of 23 HCM patients who died suddenly, and the control group consisted of 23 HCM patients who survived uneventfully during follow‐up. Study patients were pair‐matched for age, gender, and maximum left ventricular wall thickness. QT dispersion (maximum minus minimum QT interval) was manually measured on early 12‐lead ECGs using a digitizing; board. An in‐house program was used for calculating QT interval, QT dispersion, JT interval, and JT dispersion (maximum minus minimum J point to T end interval). Patients in the case group tended to have shorter RR intervals than those in the control group (777 ±; 171 vs 856 ±; 192 ms, P = 0.08). Maximum corrected QT and JT intervals did not discriminate the case group from controls (489 ±; 29 vs 479 ±; 27 ms, P = NS; 375 ±; 36 vs 366 ±; 22 ms, P = NS, respectively). Greater QT dispersion and JT dispersion were found in the case group compared with controls (74 ±; 28 vs 59 ±; 21 ms, P = 0.02 and 76 ±; 32 vs 59 ±; 26 ms, P = 0.03, respectively). The measurements of maximum QT, JT, and T peak to T end intervals, precordial QT and JT dispersion, and T peak and T end dispersion were all comparable between the two groups (P = NS for all). No systematic changes in ECG measurements were found from late ECGs of the case group compared to those from early ECGs (P = NS). No correlation between maximum left ventricular wall thickness and QT dispersion, JT dispersion, maximum QTc or JTc intervals was observed (r < 0.29, P > 0.05 for all). Our results; show that increased QT dispersion and JT dispersion is weakly associated with sudden cardiac death in the selected patients with HCM. A.N.E. 2001; 6(3):209–215     

QT-interval prolongation in right precordial leads: an additional electrocardiographic hallmark of Brugada syndrome

OBJECTIVES: The aim of this study was to evaluate whether the occurrence of the Brugada Syndrome typical electrocardiogram (ECG) pattern (i.e., right bundle branch block, coved-type ST-segment elevation, and T-wave inversion in the right precordial leads) is characterized by a concomitant lengthening of QT intervals in the right precordial leads. BACKGROUND: It has been suggested that the typical ECG pattern of Brugada syndrome is due to a decreased net inward current during phase 1 of the action potential, which also leads to its prolongation in the right epicardium. METHODS: Thirty-two subjects (19 males) age 37 +/- 15 years with a suspicious baseline ECG, or who were relatives of Brugada syndrome patients, underwent 12-lead ECG before and after the administration of flecainide. RESULTS: The flecainide test was negative in 14 and positive in 18 subjects. After flecainide administration, the positive ECGs were characterized by a greater QT interval corrected for heart rate (QTc) prolongation in the right precordial leads than that in the negative ECGs (78.2 +/- 35.5 ms vs. 22.0 +/- 28.4 ms in V(1) and 107.1 +/- 43.8 ms vs. 26.7 +/- 30.1 ms in V(2); p < 0.01), whereas there was no difference in the QTc prolongation in the left precordial leads (55.2 +/- 25.3 ms vs. 35.1 +/- 28.1 ms in V(5) and 53.1 +/- 32.8 ms vs. 27.3 +/- 22.4 ms in V(6); p = NS). CONCLUSIONS: In accordance with the electrophysiological background, the typical ECG pattern of Brugada syndrome is also characterized by a considerable prolongation of the QT interval in right precordial leads.     

Recovery time dispersion measured from 87-lead body surface potential mapping as a predictor of sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy

INTRODUCTION: The clinical usefulness of QT dispersion in 12-lead ECG has been controversial in identifying subjects at risk for sustained ventricular tachycardia (VT) in patients with idiopathic dilated cardiomyopathy (DCM). We hypothesized that increasing the spatial resolution of the ECG improves the accuracy of risk stratification. The purpose of this study was to test the ability of recovery time dispersion measured from 87-lead body surface potential mapping (BSPM) to identify patients at risk for sustained VT in idiopathic DCM. METHODS AND RESULTS: We obtained 87-lead BSPM and 12-lead ECG in 33 patients with idiopathic DCM (15 patients with a history of sustained VT [VT(+) group] and 18 patients without a history of sustained VT [VT(-) group]) and in 20 normal control subjects. We measured the corrected QT dispersion and corrected recovery time dispersion from 12-lead ECG (QTc-12 dispersion and RTc-12 dispersion, respectively) and 87-lead BSPM (QTc-87 dispersion and RTc-87 dispersion, respectively). Signal-averaged ECG also was recorded in 25 patients. Neither the QTc-12 nor QTc-87 dispersion discriminated between the VT(+) and VT(-) groups patients. The VT(+) group patients had a larger but insignificant RTc-12 dispersion than the VT(-) group patients. In contrast, the RTc-87 dispersion was significantly larger in the VT(+) group patients than in the VT(-) group patients (236 +/- 39 msec vs 184 +/- 28 msec, P < 0.001). Receiver operating curve analysis indicated that the RTc-87 dispersion was as good as late potentials in predicting susceptibility to sustained VT; its sensitivity, specificity, and negative predictive value were 73%, 76%, and 76%, respectively (cutoff value 200 msec). RTc-87 dispersion >200 msec combined with positive late potentials provide high sensitivity (92%) and high negative predictive value (88%) for sustained VT. CONCLUSION: The RTc-87 dispersion is a useful tool to identify subjects at risk for sustained VT in patients with idiopathic DCM.     

Comparison of EASI-derived 12-lead electrocardiograms versus paramedic-acquired 12-lead electrocardiograms using Mason-Likar limb lead configuration in patients with chest pain

INTRODUCTION: Monitoring or serial 12-lead electrocardiogram (ECG) recordings are the accepted requirement for prehospital data acquisition in patients with chest pain. The purpose of this study was to determine whether waveforms and clinical triage decision are similar in EASI-derived ECGs and paramedic-acquired 12-lead ECGs using Mason-Likar limb lead configuration when compared with standard 12-lead ECGs (stdECG). METHOD: Twenty patients with chest pain had a prehospital 12-lead ECG recorded in the ambulance, and paramedic-applied electrodes retained in place at hospital arrival. An ECG technician applied standard precordial and EASI electrodes in their correct positions. Twelve-lead ECGs were obtained from the paramedic-applied electrodes, using their Mason-Likar limb lead configuration, and derived from the EASI leads for comparison with the stdECG. Three computer-measured QRS-T waveform parameters were considered, and differences in waveform measurement between EASI and stdECG (EASIDeltastdECG) versus differences in waveform measurements between paramedic Mason-Likar and stdECG (PMLDeltastdECG) were calculated. Two physicians determined whether the EASI-derived or the paramedic Mason-Likar ECG contained information that would change their clinical triage decision from that indicated by the stdECG. RESULTS: EASIDeltastdECG and PMLDeltastdECG were identical in 28%, whereas EASIDeltastdECG was more than PMLDeltastdECG in 35%, and PMLDeltastdECG was accurate (both time) than EASIDeltastdECG in 37% (P = .62). The physicians were more likely to change the level of patient care based on the EASI-derived ECGs compared with the paramedic ECGs; however, this difference was not statistically significant (P = .27), but this may only be caused by the small study population. CONCLUSIONS: There are similar differences from stdECG waveforms in EASI-derived ECGs and those acquired via paramedic-applied precordial electrodes using Mason-Likar limb lead configuration. Either method can be used as a substitute for monitoring, but neither should be considered equivalent to the stdECG for diagnostic purposes.     

QT dispersion as a predictor of long-term mortality in patients with acute myocardial infarction and clinical evidence of heart failure.

BACKGROUND: QT interval dispersion is a marker of inhomogeneous ventricular repolarization, and therefore has the potential to predict re-entry arrhythmias. Following acute myocardial infarction, increased QT dispersion has been associated with a higher risk of ventricular arrhythmias. However, whether or not QT dispersion predicts prognosis post-acute myocardial infarction is not clear. We addressed this issue by analysing the AIREX study registry. METHODS: AIREX was a follow-up study of 603 post-acute myocardial infarction patients who exhibited clinical signs of heart failure and were randomly allocated to ramipril or placebo. An interpretable 12-lead ECG obtained between day 0 and day 9 after the index infarction (median time 2 days) was available in 501 patients. We examined whether QT dispersion was a predictor of all-cause mortality in the AIREX study registry (mean follow-up 6 years). RESULTS: QT dispersion measurements were significantly increased in patients who subsequently died (QT dispersion: 92.0 +/- 38.5 ms vs 82.7 +/- 34.3 ins. P=0.005; rate corrected QT dispersion: 105.7 +/- 42.7 ms vs 93.1 +/- 35.9 ms, P<0.001). Univariate analysis showed that QT dispersion as a predictor of all-cause mortality risk (QT dispersion: hazard ratio per l0 ms 1.05, [95% CI 1.02 to 1.09]. P= 0.004; rate corrected QT dispersion: 1-07 [1.03 to 1.10], P<0.001): an increase of 10 ms added a 5-7%, relative risk of death. QT dispersion remained an independent predictor of all-cause mortality risk on multivariate analysis (QT dispersion: 1.05 [1.01 to 1.09], P=0.027; rate corrected QT dispersion: 1.05 [1.01 to 1.09]. P=0.022). CONCLUSION: QT dispersion. measured from Li routine 12-lead ECG following acute myocardial infarction complicated by heart failure provides independent information regarding the probability of long-term survival. However. the low sensitivity of this electrocardiographic marker limits its usefulness for risk stratification if used in isolation.     

An Evaluation of the Impact of Gender and Age on QT Dispersion in Healthy Subjects

Objectives: To determine if gender, age, and gender per age category, have an impact on QT and QTc dispersion in healthy volunteers. Methods: This study was undertaken in 150 patients (50 per age group, 75 males, 75 females). The age groups included young (20–40 years), middle‐aged (41–69 years) and elderly (> 70 years) subjects. The QT intervals on a 12 lead ECG were determined and Bazett's formula was used to derive the QTc intervals. The QT and QTc dispersion were determined by subtracting the shortest QTc interval from the longest on each 12‐lead recording. Results: Males had higher QT dispersion than females (50 ± 22 vs 42 ± 18 ms, P = 0.017) but QTc dispersion was not significantly changed. No significant differences were seen among the different age categories for QT or QTc dispersion. In elderly subjects, males had higher QT and QTc dispersion than females (54 ± 23 vs 42 ±15 ms, P = 0.039 and 63 ± 23.7 vs 48 ± 21 ms, P = 0.032, respectively). Conclusions: When evaluating the effect of gender in different age categories, elderly males have significantly greater QT and QTc dispersion than elderly female subjects. No other gender differences were noted for QT or QTc dispersion in the other two age categories. When evaluating a population of healthy volunteers, regardless of age, gender has an impact on QT dispersion but no significant interaction with QTc dispersion. Evaluating age without dividing the data by gender yields no significant differences in QT or QTc dispersion. A.N.E. 2001;6(2):129–133     

Interobserver Reproducibility of QT Interval Measurement and QT Dispersion in Patients After Acute Myocardial Infarction

Background: The study evaluated interobserver differences in the classification of the T-U wave repolarization pattern, and their influence on the numerical values of manual measurements of QT interval duration and dispersion in standard predischarge 12-lead ECGs recorded in survivors after acute myocardial infarction. Methods: Thirty ECGs recorded at 25 mm/s were measured by six independent observers. The observers used an adopted scheme to classify the repolarization pattern into 1 of 7 categories, based on the appearance of the T wave, and/or the presence of the U wave, and the various extent of fusion between these. In each lead with measurable QRST(U) pattern, the RR, QJ, QT-end, QT-nadir (i.e., interval between Q onset and the nadir or transition between T and U wave) and QU interval were measured, when applicable. Based on these measurements, the mean RR interval, the maximum, minimum, and mean QJ interval, QT-end and/or QT-nadir interval, and QU interval, the difference between the maximum and minimum QT interval (QT dispersion [QTD]), and the coefficient of variation of QT intervals was derived for each recording. The agreement of an individual observer with other observers in the selection of a given repolarization pattern were investigated by an agreement index, and the general reproducibility of repolarization pattern classification was evaluated by the reproducibility index. The interobserver agreement of numerical measurements was assessed by relative errors. To assess the general interobserver reproducibility of a given numerical measurement, the coefficient of variance of the values provided by all observers was computed for each ECG. Statistical comparison of these coefficients was performed using a standard sign test. Results: The results demonstrated the existence of remarkable differences in the selection of classification patterns of repolarization among the observers. More importantly, these differences were mainly related to the presence of more complex patterns of repolarization and contributed to poor interobserver reproducibility of QTD parameters in all 12 leads and in the precordial leads (relative error of 31%–35% and 34%–43%, respectively) as compared with the interobserver reproducibility of both QT and QU interval duration measurements (relative error of 3%–6%, P < 0.01). This observation was not explained by differences in the numerical order between QT interval duration and QTD, as the reproducibility of the QJ interval (i.e., interval of the same numerical order as QTD was significantly better (relative error of 7.5%–13%, P < 0.01) than that of QTD. Conclusions: Poor interobserver reproducibility of QT dispersion related to the presence of complex repolarization patterns may explain, to some extent, a spectrum of QT dispersion values reported in different clinical studies and may limit the clinical utility in this parameter.     

Ventricular activation and recovery measured in electrocardiographic limb leads correlate with measurements from specific areas in body surface mapping.

AIMS: Dispersion of ventricular depolarization-repolarization in 12-lead electrocardiograms (ECGs) has been reported to provide noninvasive information on arrhythmogenicity. However, there are two methods to calculate the dispersion from ECGs including and excluding limb leads. The aim of this study was to examine whether temporal parameters from limb leads represent activation and repolarization of a particular part of the body surface. METHODS AND RESULTS: We compared the temporal parameters of activation time (AT), activation-recovery interval (ARI), and recovery time (RT) from limb leads of ECGs with those from an 87-lead body surface maps. The study population consisted of 50 normal subjects (25 men and 25 women, 19.4 +/- 1.6 years). The temporal parameters in leads I, II, and III were highly (r > 0.9) correlated with those in unipolar leads over the left lateral, left lower, and right lower chest, respectively. The temporal parameters in leads aVR, aVL, and aVF showed a significant correlation (r > 0.8) with those in unipolar leads over the right upper, left upper, and lower anterior chest, respectively. The mean AT, ARI, and RT from each limb lead of ECG were almost the same as those of unipolar leads over the corresponding areas of the body surface. CONCLUSIONS: These findings suggest that ATs, ARIs, and RTs from limb leads may represent those from unipolar leads of particular areas over the body surface in normal subjects. The temporal parameters from limb leads of ECGs may provide information on activation and repolarization as well as the precordial leads of ECGs.     

Circadian and Gender Effects on Repolarization in Healthy Adults: A Study Using Harmonic Regression Analysis

Background: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT‐dispersion and T‐wave peak to T‐wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization. Methods: Forty healthy adults (20 women), age 35–67 years old, with normal EKGs, echocardiograms, stress tests, and tilt‐table tests were analyzed during a 27‐hour hospital stay. EKGs were done at eight different time points. QT‐intervals, QT‐dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant. Results: The composite QT‐interval was longer in women than in men (416 ± 17 msec vs 411 ± 20 msec, respectively, P = 0.006). The QT‐dispersion among all leads was greater in men than women (37 ± 13 msec vs 30 ± 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT‐dispersion had a significant circadian variation, primarily in men. In men, the maximum QT‐dispersion occurred at 6 AM (45 ± 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads. Conclusions: A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT‐dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed. Ann Noninvasive Electrocardiol 2010;15(1):3–10     

Electrophysiologic Effects of Endothelin Receptor–A Blockade in Patients with Coronary Artery Disease

Selective endothelin receptor-A antagonists are a promising new treatment in patients with heart failure and/or pulmonary hypertension. Animal studies have suggested that these agents may have additional cardiac electrophysiologic actions, however, no data exist in man. We examined the effects of acute endothelin receptor-A blockade on the sinus node, the atrioventricular node and on the ventricular myocardium, in patients with single-vessel coronary artery disease and preserved left ventricular function. The selective endothelin receptor-A antagonist BQ-123 was administered by the intracoronary route, in order to achieve maximum local cardiac effects.After endothelin receptor-A blockade, QT interval increased from 373 ± 30 msec (mean ± SD) to 395 ± 20 msec (p < 0.01) and QTc interval increased from 394 ± 36 msec to 421 ± 28 msec (p < 0.01). QT-dispersion, calculated from 12-lead ECG, decreased from 40 ± 18 msec to 24 ± 8 msec (p < 0.01) and QTc-dispersion decreased from 44 ± 20 msec to 26 ± 9 msec (p < 0.05). These changes were evident only after infusion in the left, but not in the right coronary artery. No effect was found on the sinus node, the atrioventricular node, or the ventricular effective refractory periods.We conclude that selective endothelin receptor A blockade lengthens ventricular repolarization and decreases its inhomogeneity. Further studies are needed to evaluate possible antiarrhythmic actions of this class of agent.     

QT dispersion, T-wave projection, and heterogeneity of repolarization in patients with coronary artery disease

The clinically useful prognostic value of precordial QT dispersion in patients with heart disease is generally attributed to its measurement of regional heterogeneity of ventricular repolarization. However, when repolarization is abnormal, differences in measured QT intervals might result simply from variation in projection of the T-wave loop. To provide insight into the mechanism of QT dispersion, we used an analog device to transform conventional 12-lead electrocardiograms (ECGs) of 78 patients to derived 12-lead ECGs based on the heart vector. Because the electrical activity of the heart is represented by a single dipole, all QT dispersion in the transformed ECGs results from variation in projection of the T-wave loop and cannot be due to local heterogeneity of repolarization. Measured as the difference between the longest and shortest precordial QT intervals, QT dispersion in the derived ECGs, with no local heterogeneity of repolarization, was 53 +/- 49 ms (mean +/- SD). QT dispersion in these derived ECGs was similar in magnitude to that measured from the original standard 12-lead ECGs in these patients (49 +/- 23 ms, p = NS). Therefore, the precordial QT dispersion measured from standard ECGs of patients with coronary artery disease can be explained by interlead variation in precordial projection of the T-wave loop. Although regional heterogeneity might still contribute to precordial repolarization findings and to prognosis, this is not required to explain the QT dispersion observed in patients with coronary artery disease. Therefore, QT interval dispersion is not equivalent to heterogeneity of repolarization.     

Global T-wave inversion: limited QT dispersion despite QTc prolongation--a correlate of benignity in patients with strikingly abnormal electrocardiograms.

BACKGROUND: The global T-inversion (GTI) electrocardiogram (ECG) is strikingly abnormal with major QTc prolongation, but with a surprisingly good prognosis by Kaplan-Meier curve. This contrasts with most significant QTc prolongations. HYPOTHESIS: This study was undertaken to ascertain QT interval dispersion (QTd) in global T wave inversion, a clinically benign long QTc ECG. METHODS: Longest and shortest QT intervals in all 12 leads in 35 consecutive patients with GTI were determined by two mutually blinded observers. QTd was determined by subtraction (maximum-minimum) and QTc was calculated using the Bazett formula. RESULTS: There was a 2:1 female preponderance QTc was prolonged and equal for men (0.471) and women (0.469). Observer variability of under 2% permitted averaging of QT measurements. Composite mean QTd was 55 ms. The literature revealed a range of QTd in normal subjects of 39 to 59 ms (mostly 49 to 59 ms). Patient series with abnormal QTd were well above this level. CONCLUSION: Despite a strikingly abnormal ECG with marked QTc prolongation, QT dispersion was limited in global T inversion, consistent with its previously demonstrated benignity.