Differential Response of QTU Interval to Exercise, Isoproterenol, and Atrial Pacing in Patients with Congenital Long QT Syndrome

Sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and ventricular lachyarrhythmias in patients with congenital long QT syndrome. In this study, we performed exercise treadmill testing, isoproterenol infusion (1–2 μg/min), and right atrial pacing (cycle length 500 msec) in 11 patients with congenital long QT (LQT) syndrome (LQT group) and in 12 age- and sex-matched controls (control group). The responses of the corrected QT (QT_c; Bazett's method) interval and the TU wave complex tvere evaluated. The QT_c interval was prolonged from 482 ± 63 msec^1/2 to 548 ± 28 msec^1/2 by exercise in the LQT group (n = 11; P < 0.005), and this was associated with fusion of the T waves with enlarged U waves, whereas the QT_c interval did not increase with exercise in the control group (n = 12; 402 ± 19 msec^1/2 vs 409 ± 22 msec^1/2). The QT_c interval was also prolonged from 466 ± 50 msec^1/2 to 556 ± 33 msec^1/2 by isoproterenol in the LQT group (n = 7; P < 0.005) in association with morphological changes of the TU wave complex like those seen with exercise, whereas it was only slightly increased from 399 ± 10 msec^1/2 to 436 ± 13 msec^1/2 by isoproterenol in the control group (n = 77; P < 0.001). However, the QT_c interval did not increase with atrial pacing in the LQT group (n = 8; 476 ± 57 msec^1/2 vs 486 ± 59 msec^1/2), whereas it was slightly increased from 400 ± 21 msec^1/2 to 426 ± 18 msec^1/2 by atrial paring in (he control group (n = 8; P < 0.005). These results suggest that sympathetic stimulation plays an important role in the QTU prolongation and marked TU wave complex abnormalities in patients with congenital long QT syndrome.     

Is Dispersion of Ventricular Repolarization Rate Dependent?

QT dispersion has been adopted as a new index for the noninvasive assessment of the inhomogeneity of repolarization and has been evaluated in several clinical studies as an index of arrhythmia propensity. In most of these studies, indices of dispersion of repolarization were rate corrected by the Bazett formula calculating QT dispersion as QT_cmax-QT_cmin or JT dispersion as fT_cmax-fT_cmin, implying that dispersion of repolarization also changes with heart rate. This study aimed to determine in the electrically paced isolated heart whether dispersion of ventricular repolarization is rate dependent. Multiple (5–7) monophasic action potentials (MAPs) were recorded simultaneously from the epicardium and endocardium of both ventricles in 18 isolated Langendorff-perfused rabbit hearts. Hearts were paced from a right ventricular site at basic cycle lengths (CL) between 1,200 and 300 ms in 100-ms decrements. Action potential duration was measured at 90% repolarization (APD₉₀), and recovery time (RT) was defined as the sum of APD₉₀ and activation time in each of the simultaneous MAP recordings. The dispersion of APD₉₀ ond RT, respectively, were calculated as the maximal difference among all recordings. APD₉₀ and RT shortened continuously throughout the range of paced steady-state CLs from 1,200 to 300 ms. APD₉₀ was 197.6 ± 6.1 ms at a CL of 1,200 ms and decreased to 148.5 ± 2.5 ms at a CL of 300 ms (P < 0.0001). RT was 228.2 ± 6.2 ms at a CL of 1,000 ms and decreased to 175.9 ± 2.9 at a CL of 300 ms (P < 0.0001). In contrast, dispersion of APD₉₀ and RT did not change significantly. Dispersion of APD₉₀ was 24.8 ± 2.3 ms at a CL of 1,200 ms, 26.1 ± 1.9 msec at a CL of 1,000 ms, and 21.6 ± 2.1 at a CL of 300 ms (NS). Dispersion of RT was 29.7 ± 3.4 ms at a CL of 1,200 ms, 29.0 ± 3.0 ms at a CL of 1,000 ms, and 32.7 ± 3.2 ms at a CL of 300 ms (NS). In contrast to the duration of the QT interval, dispersion of ventricular repolarization does not change significantly with pacing induced changes in CL. Assuming that the rate-dependent behavior of action potential duration is similar between the rabbit and human heart, a rate correction of parameters of dispersion of repolarization is probably unnecessary.     

Cardiac repolarization properties during standardized exercise test as studied by QT,QT peak and terminated T-wave intervals

Summary. Changes in QT, QT peak (QT_p) and terminal T-wave, T_p–T_e (QT–QT_p) were studied in 11 apparently healthy subjects during and after a standardized exercise test. ECG was recorded at scalar lead positions. Averaged complexes were later analysed by computer for the different time intervals. QT and QT_p decreased in parallel with increasing heart rate with a ratio QT_p/QT of 0·80 ± 0.02 at rest and 0·74 ± 0·02 at maximal heart rate around 170. After exercise QT and QT_p prolonged disproportionately slower than heart rate, reaching the relation observed during exercise only 9·5 min post exercise. T_p–T_e was 75 ± 10 ms at rest and 65 ± 8 ms at maximal heart rate. The decrease was significant (P<0·001). The main part of the rate-associated shortening of the QT interval occurred in the QT_p interval where it was about six to seven times larger than in the T_p–T_e interval. In conclusion, QT and QT_p decreased similarly with heart rate during exercise. Post exercise there was an initial slower return of these intervals to the resting state than for heart rate. T_p–T_e changes were minimal.     

Ambulatory Assessment of the QT Interval in Patients with Hypertrophic Cardiomyopathy: Risk Stratification and Effect of Low Dose Amiodarone

This study aims to assess the dynamics of the QT interval in patients with hypertrophic cardiomyopathy (HCM). Three consecutive QT intervals and the preceding RR intervals were measured on 24-hour ambulatory electrocardiograms at 30-minute intervals in ten high risk patients with HCM (sudden cardiac death [SCD] and/or documented ventricular fibrillation), aged 29 ± 17 years, compared with ten age and sex matched low risk patients with HCM (no syncope, no adverse family history, and no ventricular tachycardia on Holter monitoring), and ten normal subjects. Another ten patients who were on amiodarone therapy (200-mg daily) were also studied. Patients witb intraventricular conduction defects were excluded. There were 4,424 pairs of QT intervals and their preceding RR intervals were measured in this study. A nonsignificant prolongation in the QT interval and a significant prolongation in QT_c values (Bazett's and Fridericia's formulas) were demonstrated in patients with HCM compared with normals. There were no significant differences in the QT and QT_c between high and low risk patients. The slope of regression line for the QT against RR interval was significantly different between normals and HCM (0.1583 ± 0.040 vs 0.2017 ± 0.043. P < 0.05), but not between high and low risk patients. Amiodarone significantly prolonged the QT and QT_c without significantly altering the slope of the regression line (0.2017 ± 0.043 vs 0.2099 ± 0.037, NS). Our findings support the observations that there is a prolonged QT interval in patients with HCM and that there is no significant use dependent effect of amiodarone on ventricular repolarization. In conclusion, ambulatory assessment of the QT interval provides an alternative method for the assessment of ventricular repolarization and for the assessment of use dependent effects of anti arrhythmic drugs on ventricular repolarization during normal daily activities. However, this method does not help in the identification of patients at high risk of SCD in HCM.     

QT Duration and Dispersion in Patients with Anomalous Origins of Coronary Arteries

Background: Coronary artery anomalies have been reported to show various symptoms ranging from chest pain and dyspnea to cardio-respiratory arrest and sudden death. In this study, we attempted to assess the changes in QT interval duration and dispersion in anomalous origins of coronary arteries (AOCA).
Methods: Nineteen AOCA patients (mean age: 52 ± 11 years) and 30 healthy control subjects (mean age: 50 ± 12 years) were included in the study. Minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. The two groups were compared in terms of QT dispersion and QT duration.
Results: There was no difference between the two groups in terms of baseline demographic characteristics. Maximum corrected QT intervals (QTc max), minimum corrected QT intervals (QTc min), and corrected QT dispersion were higher in AOCA patients than controls (452 ± 38 vs 411 ± 25 ms [P = 0.0001], 402 ± 31 vs 383 ± 28 ms [P = 0.048], and 51 ± 30 vs 28 ± 12 ms [P = 0.001], respectively).
Conclusion: In the patients with anomalous origins of coronary arteries, QT dispersion that is an indicator of sudden cardiac death and arrhythmias frequency increased. QTc max, QTc min, and corrected QT dispersion are higher in patients with anomalous origin of the coronary artery than in control subjects.     

Acute effect of methylphenidate on QT interval duration and dispersion in children with attention deficit hyperactivity disorder

Among childhood psychiatric disorders, attention deficit hyperactivity disorder (ADHD) is of greatest interest to practitioners. Methylphenidate (MPH) is a drug that is widely used in the treatment of children in whom ADHD has been diagnosed. Although this treatment has been used for years, its effects on the heart remain the subject of debate. The QT interval comprises the ventricular activation and recovery periods as seen on electrocardiogram (ECG). The acute effect of MPH on QT interval dispersion is unknown. Researchers in the present study sought to investigate the acute effects of MPH on QT interval as seen on ECG. A total of 25 patients with ADHD (mean age, 9.4±2.1 y) who were treated with MPH were enrolled in the study. Twelve-lead derivation ECGs were taken before and 2 h after administration of 10 mg of MPH. Maximum QT interval, minimum QT interval, and interval durations were measured, and QT dispersion was calculated, for each ECG. QT dispersion measured after medication administration decreased significantly from 59.6±16.3 ms to 50.8±10.9 ms (P=.016); corrected QT dispersion decreased significantly from 70.9±17.6 ms to 61.3±13.3 ms (P=.011). Maximum QT interval duration decreased from 373.7±21.8 ms to 361.8±29.0 ms (P=.006); minimum QT interval duration rose from 317.0±23.3 ms to 322.3±21.6 ms (P=.312). In conclusion, the findings of this study show that MPH reduces QT dispersion during the acute period shortly after its administration.     

Late potentials and QT dispersion after high‐dose chemotherapy in patients with non‐Hodgkin lymphoma

The most common cardiotoxic effects of high‐dose cyclophosphamide (CY) are electrocardiographic changes and transient arrhythmias. Therefore, we prospectively assessed serial electrocardiogram (ECG) and signal‐averaged electrocardiogram (SAECG) recordings in 30 adult patients with non‐Hodgkin lymphoma (NHL) receiving high‐dose CY as part of high‐dose chemotherapy (HDT) regimen. All patients were treated with anthracyclines earlier. Heart‐rate‐corrected QT interval and QT dispersion (QTc and QTc dispersion) were measured from ECG. QRS duration and late potentials (LPs) were analysed from SAECG. Both ECG and SAECG were recorded 1 day (d) prior to HDT (d?7) at baseline, and 1 day (d?2), 7 days (d+7), 12 days (+12) and 3 months (m+3) after HDT. Stem cells were infused on day 0 (d0). Cardiac systolic and diastolic function were assessed on (d?7), (d+12) and (m+3) by radionuclide ventriculography. At baseline, four patients presented with LPs. Cardiac systolic function decreased significantly (53 ± 2; 49 ± 2%, P = 0·009 versus baseline), whilst no patient developed acute heart failure. QRS duration prolonged and RMS₄₀ reduced significantly versus baseline (104 ± 3; 107 ± 3 ms, P = 0·003; 41 ± 4; 38 ± 3 μV, P = 0·03), and six patients (21%) presented with LPs after CY treatment. Both QTc interval and QTc dispersion increased versus baseline (402 ± 5; 423 ± 5 ms, P<0·001; 32 ± 2; 44 ± 3 ms, P = 0·012), and six patients (20%) developed abnormal QT dispersion. In conclusion, high‐dose CY causes subclinical and transient electrical instability reflected by occurrence of LPs as well as increased QTc interval and QT dispersion. Thus, longer follow‐up is required to confirm the meaning of these adverse effects on cardiac function and quality of life.     

Normal values for QT intervals in ECG during ramp exercise on bicycle

Summary. The relation between QT interval and heart rate during ramp exercise tests on a bicycle was investigated in 37 healthy individuals (21 women) without regular medication and with a normal thallium-201 exercise scintigram (mean age 52–9 ± 8–3, range 38–68). The test started at 20 W and the load increased by 10 W min^-1. A 12-lead ECG was recorded twice every min and mean complexes (during a 15 s period) were calculated by computer. At rest the QT interval (in s) corrected for heart rate (QT_C) for women and men was 0–408 ± 0–004 and 0–399 ± 0–005, respectively, P > 0–05). During exercise there was no difference in QT interval between women and men or between younger (<50 years) and older (> 50 years) individuals. A straight line was used to describe the relation between QT interval and heart rate (beats min^-1; QT = 0–459–12–3xlO^-4*HR). A 95% prediction interval around the regression line was determined using a non-parametric statistical method. When QT_C was calculated using Bazett's formula with a cut-off value of QT_c= 0–46, 19 individuals (11 women) had a prolonged QT interval during exercise. It is concluded that the relation between QT interval and heart rate can during exercise be described by a straight line for normal individuals. It is not valid to use Bazett's formula for correction of QT intervals during ramp exercise tests.     

Mutual Information Reveals Non-linear Relationships between Electrocardiographic Conduction or Repolarization Indices and Mechanical Dispersion by Speckle-Tracking Echocardiography in the General Population

Electrical inhomogeneities can lead to regional heterogeneity in left ventricular contraction. We investigated the correlation between electrocardiographic parameters of conduction and/or repolarization and myocardial longitudinal strain-derived parameters in a general population. Mean and dispersion (maximum–minimum) values were calculated for the electrocardiographic indices: QT interval, T_peak–T_end interval (Tpe), JT_peak interval (JTp), JT_end interval (JTe), QT_peak interval (QTp). Mechanical dispersion was assessed using the standard deviation (SD) of time-to-peak longitudinal strains (MD_SD) and the difference between the longest time and shortest time to peak strain (MD_delta) by speckle-tracking echocardiography. A total of 59 patients, 60 ± 12 y, were included. Tpe, Tpe/QT, Tpe/JTp and Tpe/JTe correlated well with MD_SD and MD_delta (r ≥ 0.43, p < 0.001). Mutual information revealed significant non-linear relationships between most of the electrocardiographic indices measured and mechanical dispersion. In conclusion, there is a moderate linear correlation between electrocardiographic indices reflecting repolarization heterogeneities and speckle tracking-assessed mechanical dispersion.     

Determinant of QT Dispersion in Patients with Hypertrophic Cardiomyopathy

KAWASAKI, T., et al. : Determinant of QT Dispersion in Patients with Hypertrophic Cardiomyopathy. QT dispersion is thought to reflect a regional difference in repolarization process although QT interval is composed of depolarization and repolarization. This study was designed to investigate the effect of depolarization and repolarization on QT dispersion in hypertrophic cardiomyopathy. Standard 12-lead ECG was recorded in 70 hypertrophic cardiomyopathy patients with anteroseptal wall hypertrophy (HC-As), 8 patients with lateral wall hypertrophy (HC-L), 8 patients with diffuse hypertrophy (HC-D), and 46 normal controls. QRS, JTc, maximum and minimum QTc, and QTc dispersion were compared. The maximum QTc was greater in HC-As and HC-L than in the control; the minimum QTc was similar in all 3 groups; consequently, QTc dispersion was greater in HC-As and HC-L. In HC-D, the maximum QTc and the minimum QTc were greater than the control, which produced QTc dispersion similar to that in the control. JTc did not differ among 4 groups. In hypertrophic cardiomyopathy, both QTc and QRS duration were increased in the leads coinciding with the left ventricular portion of localized hypertrophy. We conclude that QTc dispersion depended on the heterogeneity of QRS duration or depolarization rather than repolarization, which in fact may be ascribed to the regionally different hypertrophy of the left ventricle in hypertrophic cardiomyopathy. (PACE 2003; 26[Pt. I]:819–826)     

Long QTc and Torsades de Pointes in Human Immunodeficiency Virus Disease

Three patients with human immunodeficiency virus (HIV) infection presented with QT_c prolongation (> 440 ms) and torsades de pointes. We sought to evaluate the etiology of the long QT syndrome in these patients without previously identified causes for QT_c prolongation, and determine the prevalence among patients with HIV infection. The three index patients underwent: (1) left stellate ganglion block; (2) β-blocker challenge; and (3) electrocardiographic stress testing. QT_c interval was measured before and after intervention. We undertook a retrospective analysis of prevalence of QT_c prolongation among all patients with computerized ECGs over a 6-month period at one institution and compared it to the prevalence in hospitalized patients with HIV disease. Thirty-four thousand one hundred eighty-one patients with computerized ECGs were screened for QT_c prolongation. Forty-two hospitalized patients with HIV disease had computerized ECG during the same 6-month period. In the three index patients, the QT_c failed to shorten with left stellate ganglion blockade, β-blocker challenge, or stress testing, suggesting an acquired form of the long QT syndrome in these patients with HIV disease. None had previously recognized acquired causes of QT_c prolongation. Mexiletine hydrochloride was useful in preventing recurrences of torsades de pointes. We observed a 7.0% prevalence of QT_c prolongation among all patients screened. Hospitalized patients with HIV disease (n = 42) during this same period, demonstrated an increased prevalence of QT_c prolongation (28.6%, P = 0.002). Patients with HIV disease have a significantly higher prevalence of QT_c prolongation than a general hospital-based population, may have an unrecognized acquired form of the long QT syndrome, and are at risk for torsades de pointes.     

Effects of intracoronary low-dose enalaprilat on ventricular repolarization dynamics after direct percutaneous intervention for acute myocardial infarction

Background: Data from animal models suggest that inhibition of angiotensin converting enzymes result in an increased ventricular electrical stability after reperfusion in acute myocardial infarction (MI). As electrical stability is largely dependent on ventricular repolarization, we sought to determine the impact of low-dose intracoronary (ic.) application of enalaprilat (EN) as an adjunct to direct primary coronary intervention (PCI) on QT dynamics in the acute phase of MI.
Methods: Twenty-two consecutive patients with a first acute MI who underwent successful direct PCI (TIMI 3 flow) were randomized to ic. EN (50 μg) or placebo/saline (PL), given immediately after reopening of the infarct vessel. On hospital admission, a 24-hour-Holter-electrocardiogram (ECG) was initiated. Slopes of the linear QT/RR regression were determined for the time intervals before reperfusion and after reperfusion.
Results: A total of 7 patients in the EN group and 8 patients in the PL group had valid ECG recordings for beat-to-beat QT analysis. Mean RR interval and mean QT interval were not significantly different between the EN and the PL groups both before and after PCI. There were also no significant differences regarding QT/RR slopes between EN and PL groups before PCI. After PCI, QT/RR slopes significantly decreased in the EN group (0.169 ± 0.04 to 0.121 ± 0.03; P < 0.01), whereas there were no significant alterations in the PL group (0.175 ± 0.04 to 0.171 ± 0.03; P = ns).
Conclusions: Intracoronary EN therapy as an adjunct to direct PCI significantly decreases QT/RR slopes, suggesting a normalization of the coupling between heart rate and repolarization by improving electrical restitution. Thus, our findings offer new insights into possible beneficial effects of ACE inhibition on cardiac electrical stability in acute MI.     

Increased heterogenity of ventricular repolarization in obese nonhypertensive children

Objective: Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on ventricular repolarization, excluding the influence of possible comorbidities. The QTc dispersion (QTc‐d), JTc dispersion (JTc‐d), and transmural dispersion of repolarization (TDR) have been suggested to be electrocardiographic indexes reflecting the physiological variability of regional ventricular repolarization. The aim of our study is to define the effects of obesity on the ventricular repolarization in obese children who have no other clinically appreciable cause of heart disease. Methods: The study involved 70 subjects (48 male, 22 female), with a mean age (± standard deviation) of 13 ± 2 years. A total of 35 individuals were obese (Group A: 24 male, 11 female, mean body mass index [BMI] of 38.2 ± 5.8 kg/m²), and 35 participants were healthy lean children (Group C: 24 male, 11 female, mean BMI of 22.3 ± 0.3 kg/m²). Heart rate; QRS duration; maximum and minimum QT interval; and QTc‐d, JTc‐d, and TDR measurement were performed. Results: Compared with the healthy control group, obese children presented increased values of the QTc‐d, JTc‐d, and TDR (31.1 ± 10.6 vs 46.2 ± 15.3 ms, P < 0.003; 29.8 ± 8.5 vs 40.1 ± 10.3 ms, P < 0.04; 83.2 ± 13.5 vs 100.7 ± 16.3 ms, P < 0.05). A statistically significant correlation was found between the values of QTc‐d, insulin serum concentration (r = 0.46, P = 0.04), and homeostasis model assessment of insulin resistance (r = 0.34, P = 0.03). Conclusions: Our data suggest that obese nonhypertensive children have an increased ventricular repolarization heterogeneity in relation to controls. (PACE 2010; 33:1533–1539)     

Transseptal left ventricular endocardial pacing reduces dispersion of ventricular repolarization

Background: Cardiac resynchronization therapy (CRT) may be proarrhythmic in some patients. This may be due to the effect of left ventricular (LV) epicardial pacing on ventricular repolarization. The purpose of this study was to evaluate the effect of endocardial versus epicardial LV biventricular pacing on surface electrocardiogram (ECG) parameters that are known markers of arrhythmogenic repolarization. Methods: ECG markers of repolarization (QT dispersion, QTD; T peak to end, T_peak‐end; T_peak‐end dispersion, T_peak‐endD; QTc) were retrospectively measured before and after CRT in seven patients with transseptal LV endocardial leads (TS group), 28 matched patients with coronary sinus (CS) LV leads (CS group), and eight patients with surgical LV epicardial leads (SUR group). All ECGs were scanned and analyzed using digital callipers. Results: Compared to the CS group, the TS group CRT was associated with a significant postpacing reduction in QTD (?45.2 ± 35.6 vs ?4.3 ± 43.6 ms, P = 0.03) and T_peak‐end (?24.2 ± 22.1 vs 3.4 ± 26.7 ms, P = 0.02). There was a nonsignificant post‐CRT reduction in both T_peak‐endD (?11.3 ± 31.0 vs 2.4 ± 28.9 ms, P = 0.27) and QTc (?50.0 ± 46.4 vs 4.4 ± 70.2 ms, P = 0.06) in the TS versus the CS group. In contrast, there were no differences between the SUR and CS groups in terms of the effect of CRT on these repolarization parameters. Conclusions: CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia. (PACE 2011; 34:1258–1266)     

窦性心动过缓患者阿托品试验前后QTd变化

目的　探讨迷走神经对QT间期离散度的影响。方法　观察 12 2例窦性心动过缓者阿托品试验前后QTd和QTcd的变化。结果　注射阿托品后 3分钟内单纯窦性心动过缓组QTd和QTcd虽然缩短 ( 19.72± 12 .82ms对 2 5 .99± 10 .33ms ;17.5 4± 10 .18ms对 2 2 .84± 11.34ms) ,但无统计学差异 (P >0 .0 5 ) ;急性胆囊炎组明显缩短 ( 16 .6 6± 10 .0 0ms对2 8.89± 13.33ms ,P <0 .0 5 ;15 .0 9± 11.18ms对 2 4.35± 8.92ms ,P <0 .0 1) ;胆囊炎并缺血性心脏病组则显著延长 ( 6 6 .9± 14 .18ms对 2 9.78± 12 .5 4ms ;6 4.2 1± 15 .0 6ms对 2 6 .10± 10 .10ms ,P <0 .0 5 )。结论　提示迷走神经兴奋对缺血性心肌具有保护作用。     

Short-and Long-Term Reproducibility of QT, QTc, and QT Dispersion Measurement in Healthy Subjects

The study investigated interobserver and intrasubject reproducibility of QT interval duration and dispersion measured in standard 12-lead ECGs recorded at 25 mm/sec. Twenty-eight healthy volunteers were studied. Each undenvent four ECG recordings, which were performed 1, 7, and 30 days apart. Two independent observers analyzed each ECG record. In each lead with a distinguishable T wave pattern, the RR interval, Q-peak of T interval, and Q-end of T interval were measured using a digitizing board with a 0.1-mm resolution. From each recording the following measures were derived: the maximum, minimum, and mean QT interval; maximum, minimum, and mean heart rate corrected QT interval (QTc); QT and QTc dispersion (the difference between the maximum and minimum QT interval among the 12 leads); and adjusted QT and QTc dispersion (dispersion divided by the square root of the number of leads measured). The interobserver and short-term (1 day) and long-term (1 week and 1 month) reproducibility of individual indices was assessed by computing the relative errors and comparing them by a standard sign test. In addition, the distributions of maximum and minimum QTc values among electrocardiographicleads, and the differences between QT-end and QT-peak based measurements were investigated. The results showed that: (1) the measurement of the QT interval from standard ECG recordings is feasible and not operator dependent (interobserver relative error <4%); (2) the duration of the QT interval in healthy volunteers is stable and its short- and long-term reproducibility is high (intrasubject relative error < 6%); (3) parameters that characterize dispersion of the QT interval in the 12-lead ECG are highly nonreproducible, both between subsequent recording (relative error of 25%–35%) and between observers (relative errar 28%–33%), the reproducibility of QT dispersion is significantly lower than that of QT duration (P < 0.01); and (4) the duration of the entire QT interval correlates only weakly with the duration of the Q-peak of T interval.     

Recurrent Torsade de Pointes type ventricular tachycardia in intracranial hemorrhage

Two out of 72 cases of intracranial hemorrhage-induced polymorphous ventricular tachycardia with typical Torsade de Pointes morphology are presented. Bot patients had marked QT_c prolongation more than 550 ms. In one patient (QT_c: 669 ms) Torsade de Pointes degenerated into fatal ventricular fibrillation. Even though polymorphous Torsade de Pointes type ventricular tachycardia is rare during the clinical course of intracranial hemorrhage, attention should be given to the QT interval. QT_c prolongation more than 550 ms may carry a high risk of Torsade de Pointes type ventricular tachycardia and ventricular fibrillation.     

Reduction in QT dispersion and ventricular arrhythmias by ischaemic preconditioning in anaesthetized, normotensive and spontaneously hypertensive rats

QT dispersion is a marker for dispersion of ventricular repolarization and electrical instability of the heart. However, QT dispersion remains undocumented in both normotensive rats (NTRs) and spontaneously hypertensive rats (SHRs), in particular in conditions of myocardial ischaemia/reperfusion (isch./rep.) and ischaemic preconditioning (IP). Therefore, we assessed the effects of IP on the dynamic change of QT and QTc dispersion during isch./rep., and on isch.- and rep.-induced ventricular arrhythmias in both NTRs and SHRs. Isch. and rep. were produced by occlusion and release of a snare around the left coronary artery in all rats. The effect of IP (three cycles of 3 min coronary artery occlusion and 5 min rep.) on myocardial repolarization and on development of isch.- and rep.-induced ventricular arrhythmias was studied in 12 NTRs and 12 SHRs. Another 12 NTRs or 12 SHRs were subjected to 10 min of isch. followed by 10 min rep. without IP. SHRs have significantly longer QT- and QTc-intervals as well as QT and QTc dispersion before isch. compared to NTRs. Myocardial isch. and early rep. largely increased QT and QTc dispersion in both NTRs and SHRs and resulted in a high incidence of isch.- and rep.-induced ventricular tachycardia (VT) and fibrillation (VF). IP significantly reduced QT and QTc dispersion in SHRs before isch., and remarkably reduced the elevation of QT and QTc dispersion during a prolonged period of isch. and rep. in all rats. This protective effect on electrophysiology of IP was associated with an antiarrhythmic effect against both isch.- and rep.-induced ventricular arrhythmias in NTRs and SHRs. Our data indicate that: 1) SHRs have a significantly higher baseline dispersion of ventricular repolarization than NTRs; 2) IP provides protection against ventricular arrhythmias in SHRs; 3) the increasing QT dispersion provoked by myocardial isch. and rep. is associated with a high incidence of isch.- and rep.-induced ventricular arrhythmias and; 4) the reduction of QT dispersion by IP may be involved in its protective effect against isch.- and rep.-induced arrhythmias in both NTRs and SHRs.     

Correlation of Heart Rate Variability Parameters and QT Interval in Patients After PTCA of Infarct Related Coronary Artery as an Indicator of Improved Autonomic Regulation

The purpose of this study was to determine if PTCA of the infarct related coronary artery (IRA) in the late phase of myocardial infarction (MI) can improve autonomic regulation of sinus rhythm and electrical stability of the myocardium measured by heart rate variability (HRV), QT, QTc, and its dispersion (QTd) and if any correlation exists among these measures. The study was performed in 25 patients (21 male, age: 50 ± 9 years, EF: 52%± 11%) in the late phase of MI (2.5 ± 1.5 months). HRV parameters were calculated automatically. QT, QTc, and QTd were measured manually from a 12-lead surface ECG (50 mm/s). All measurements were made before and 3–5 days after PTCA. Day and night parameters of HRV were sampled over two periods: 2 pm to 10 pm (day) and 10 pm to 6 am (night). Parameters of HRV measured from whole recordings were significantly higher after successful PTCA: SDRR (116 31 vs 128 ± 38 ms), SD (55 ± 17 vs 62 ± 22 ms), rMSSD (30 ± 13 vs 36 ± 14 ms) and HF (246 ± 103 vs 417 ± 224 ms2). Significant differences were found during daytime for SD, rMSSD, and HF, and during nighttime for SDRR, SDANN. QT interval duration, QT corrected to the heart rate, and QT dispersion were significantly lower after PTCA (QTd: 54 ± 15 vs 39 ± 12 ms). There was no correlation between HRV and QT values before PTCA. High correlations were found after the procedure, particularly between QTd and nighttime HRV. Conclusions: PTCA of IRA in the late phase of MI enhances sympathovagal regulation of the cardiac rhythm and the electrical stability of the heart, which may be prognostically important.     

Effect of epirubicin-based chemotherapy and dexrazoxane supplementation on QT dispersion in non-Hodgkin lymphoma patients

BACKGROUND AND OBJECTIVE: Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. METHODS: Twenty untreated patients, 相似文献