Comparison of the effects of desflurane and sevoflurane on the QTc interval and QT dispersion

OBJECTIVE: The effects of desflurane and sevoflurane on QT interval and QT dispersion have been investigated in a prospective, double-blind, randomized study of patients undergoing noncardiac surgery. INTERVENTIONS: Sixty American Society of Anaesthesiologists physical status I-II adult patients were randomly assigned to two groups. Anaesthesia was induced with inhalation of desflurane (desflurane group) or sevoflurane (sevoflurane group) in increasing concentrations to 3 minimal alveolar concentration level. The maintenance of anaesthesia was provided with 2 minimal alveolar concentration agents in both groups until the end of the study. Electrocardiogram, heart rate and blood pressure were recorded as follows: before premedication, before induction, 1 and 3 min after the induction of anaesthesia, after the administration of vecuronium and after the tracheal intubation. The induction times and the complications were recorded. MEASUREMENTS AND RESULTS: The QTc interval was significantly more prolonged with desflurane than with sevoflurane at the first and third minute after the induction, and at the third minute after the administration of vecuronium. There were no significant differences in the QT dispersion between the two groups. Heart rate and blood pressure were found to be significantly higher in the desflurane group. CONCLUSION: The QTc interval was more prolonged with desflurane than sevoflurane, and QT dispersion was normal with both agents.     

长期运动诱导的心肌肥厚对QT离散度的影响

目的对长期运动左心室重量增加个体的QT离散度(QTd)进行分析。方法各入选26例长期运动个体和运动较少的正常个体,经二维超声心动图测量心室结构参数,记录同步12导联心电图测量QT离散度。结果长期运动的个体左心室重量明显大于运动少的个体(216±39kg对155±30kg;P<0.01);长期运动个体校正的QT离散度(QTcd)比运动少的个体明显减少(42±13ms对51±15ms,p<0.01)。左心室重量(LVM)与QT离散度和QTcd呈明显的负相关(r=-0.38,p=0.002和r=0.53,p=0.001)。结论运动诱导的心肌肥厚使QT离散度减小,反映了长期运动个体心肌复极化的稳定性。     

The effect of electroconvulsive therapy on QT dispersion

Electroconvulsive therapy (ECT) is used frequently in psychiatric practice and various electrocardiographic (ECG) changes have been described during ECT. QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. The aim of this study is to examine the effect of electroconvulsive therapy on QT dispersion. We studied 27 patients (age range 24-42 y, mean age 34 y, 11 men) without heart disease who were treated with ECT. Structural heart disease was eliminated with routine clinical examination and laboratory tests, echocardiography, and exercise treadmill test. QT interval and corrected QT (QTc) dispersion was measured on a 12-lead ECG before and just after ECT. QTc dispersion increased from 28.9 +/- 7.4 ms at baseline to 81.4 +/- 12.8 ms after the procedure (P < 0.0001). This result demonstrated that QTc dispersion increased significantly during ECT. This finding may explain that increased inhomogeneity of ventricular repolarization is associated with enhanced vulnerability to arrhythmias during ECT.     

The effects of perindopril on QT duration and dispersion in patients with coronary slow flow

Coronary slow flow (CSF) is characterized by delayed opacification of coronary arteries in the absence epicardial occlusive disease. QT duration and dispersion have been reported to be longer in patients with CSF. ACE inhibitors may improve CSF through positive effects on endothelial function. The study included 32 patients having CSF and 25 subjects having normal coronary arteries in coronary angiography. The patients were evaluated with 12-leads electrocardiography and echocardiography before and 3 months after treatment with perindopril. Compared to the control group, maximum corrected QT duration (QTcmax) (432.0 ± 28.9 vs. 407.0 ± 39.1 ms, p = 0.008) and QT dispersion (QTcD) (64.0 ± 16.5 vs. 37.3 ± 12.1 ms, p < 0.001), mitral inflow deceleration time (DT) (251.3 ± 49.4 vs. 218.8 ± 44.5 ms, p = 0.013), and isovolumetric relaxation time (IVRT) (115.8 ± 18.4 vs. 107.2 ± 22.9 ms, p < 0.001) were significantly longer and E/A ratio 0.85 ± 0.2 vs. 1.1 ± 0.3, p = 0.004) was lower in patients with CSF. QTcmax (to 407.0 ± 28.0 ms, p = 0.001), QTcD (to 44.5 ± 11.4 ms, p < 0.001), DT (to 221.6 ± 37.7 ms, p < 0.001) and IVRT (to 103.8 ± 16.1 ms, p < 0.001) were significantly decreased and E/A ratio (to 0.98 ± 0.3, p < 0.001) was significantly increased after treatment with perindopril. Coronary slow may be associated with prolonged QT interval and increased QT dispersion and impaired diastolic filling. Perindopril may be helpful in restoration of these findings.     

急性心肌梗死经皮冠状动脉腔内成形术对QT离散度的影响

目的观察急性心肌梗死(AMI)患者成功的经皮冠状动脉腔内成形术(PTCA)后对QT离散度(QTd)的影响。方法选择32例AMI后成功的PTCA患者，分别记录术前1天、术后1天的心电图，测量QTd及校正的QTd(QTcd)，并与30例同期行冠状动脉造影结果正常者进行对照。结果AMI组行PTCA术前，QTd及QTcd均较对照组显著延长；PTCA术后QTd及QTcd均较术前显著缩短；而单纯行冠脉造影对QTd及QTcd无明显影响；冠状动脉造影及PTCA对心率亦无明显影响。结论AMI患者QTd及QTcd显著高于正常人，成功的PTCA可使QTd及QTcd明显缩短。     

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

Objective—To determine the normal values of QT and QTc dispersion and the effects of sinus arrhythmia on QT dispersion in healthy children.
Patients and setting—The study was carried out in a university hospital on 372 local schoolchildren (200 male, 172 female), aged seven to 18 years.
Methods—The QT and preceding RR intervals of at least one sinus beat were measured manually in a range of nine to 12 leads on standard 12 lead surface ECGs. The corrected QT interval was computed by the method of Bazett. Dispersion of QT and QTc were defined as (1) the difference between the maximum and minimum QT and QTc intervals occurring in any of the 12 leads (QTD and QTcD), (2) the standard deviation of the QT and QTc interval in the measurable leads (QT-SD and QTc-SD).
Results—There was no significant difference in QT, QTc, and RR dispersion between girls and boys. Overall 53% of children had sinus arrhythmia. Although QTD and QT-SD were not affected by sinus arrhythmia, both QTcD and QTc-SD were significantly greater in children with sinus arrhythmia than in those without (QTcD: 52.9 (17.4) v 40.9 (13.1); QTc-SD: 17.5 (5.9) v 13.2 (4.0); p < 0.001).
Conclusions—As calculation of QTc dispersion is affected by sinus arrhythmia, which is common in childhood, we suggest that QT dispersion should not be corrected for heart rate in children.

Keywords: QT dispersion;  heart rate;  children;  sinus arrhythmia     

氯沙坦对老年高血压病患者心室肥大和QTd的影响

目的　评价氯沙坦对老年原发性高血压病患者左心室肥大及 QT离散度 (QTd)的影响。方法　依据是否伴有左心室肥大 ,将 5 7例轻、中度高血压病患者分为两组 ,分别给予氯沙坦 5 0 mg/d,或氯沙坦 5 0 m g/d加双氢克尿噻12 .5 mg/d治疗 ,共 16～ 18周 ,比较两组治疗前后左心室大小 ,及 QTd改变 ,并分析 L VMI与 QTd的相关性。结果　治疗后高血压伴左心室肥大组 L VDd,IVST,PWT,L VMI比治疗前下降 (P<0 .0 5或 P<0 .0 1)。高血压伴左心室肥大组 QTd比不伴左心室肥大组大 (P<0 .0 1) ,治疗后则明显减小 (P<0 .0 1)。高血压伴左心室肥大组 L VMI与 QTd有较好的相关性。结论　氯沙坦或氯沙坦加双氢克尿噻能逆转老年高血压病患者的左心室肥大 ,并使 QTd相应减小。     

The effects of chronic carvedilol therapy on QT dispersion in patients with congestive heart failure.

BACKGROUND: Carvedilol therapy reduces mortality from sudden cardiac death and progressive pump failure in congestive heart failure (CHF). However, the effect(s) of carvedilol on ventricular repolarization characteristics is unclear. AIM: The aim of the study was to investigate the effects of chronic carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) in patients with CHF. METHOD: Nineteen patients (age 53+/-12 years; 16 male, three female) with CHF (eight ischemic, 11 non-ischemic dilated cardiomyopathy) were prospectively included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 3.125 mg bid and uptitrated biweekly to the maximum tolerated dose. From standard 12-lead electrocardiograms the maximum and minimum QT intervals (QTmax, QTmin), QTd, corrected QT intervals (QTcmax, QTcmin) and corrected QTd (QTcd) values were calculated at baseline, after the 2nd and the 16th month of carvedilol therapy. RESULTS: A significant reduction was noted in the QTd and QTcd values with carvedilol therapy after the 16th month (QTd: 81+/-22 ms vs. 40+/-4.3 ms P<0.001; QTcd: 91+/-25 ms vs. 51+/-7 ms P<0.001), but not after the 2nd month (P>0.05). The resting heart rate was also significantly reduced after a 16-month course of carvedilol therapy (78+/-13 bpm vs. 66+/-15 bpm, P<0.05). Carvedilol therapy did not alter QTmax and QTcmax intervals (P>0.05), however, QT min and QTcmin significantly increased with carvedilol at the 16th month (P<0.001 and P<0.01, respectively). CONCLUSION: Long-term carvedilol therapy was associated with a reduction in QTd, an effect that might contribute to the favorable effects of carvedilol in reducing sudden cardiac death in CHF.     

QT dispersion in sarcoidosis

STUDY OBJECTIVES: QT dispersion (QTd) is the maximal interlead difference in QT interval on surface 12-lead ECG. An increase in QTd is found in various cardiac diseases. Sarcoidosis augments inhomogeneity in ventricular repolarization by sarcoid granuloma, which significantly correlates with ventricular fibrillation. Changes in QTd in the course of sarcoidosis have not been investigated previously. DESIGN: The study included 35 patients with systemic sarcoidosis. The diagnosis of systemic sarcoidosis was made by biopsy. Thallium scintigraphy was performed in all patients with systemic sarcoidosis. Cardiac sarcoidosis was diagnosed in 16 patients based on abnormal thallium scintigraphy and normal coronary arteriography results. QTd, corrected QTd (cQTd), maximum QT (QTmax), maximum corrected QT (cQTmax), minimum QT, and minimum corrected QT intervals were measured. Twenty-four healthy subjects represented the control group for QT interval analysis. MEASUREMENTS AND RESULTS: In the cardiac sarcoidosis group, mean QTd (+/- SD) was significantly greater than in the noncardiac sarcoidosis group and control group (49.50 +/- 10.86 ms, 28.14 +/- 11.02 ms, and 27.08 +/- 10.41 ms, respectively; p < 0.001). cQTd was significantly greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group and control group (53.17 +/- 10.44 ms, 30.61 +/- 10.94 ms, and 29.01 +/- 10.52 ms, respectively; p < 0.001). QTmax (440 +/- 15.01 ms, 409 +/- 14.86 ms, and 410 +/- 13.21 ms; p < 0.001) and cQTmax (449 +/- 16.31 ms, 417 +/- 12.51 ms, and 418 +/- 11.76, respectively; p < 0.001) were also significantly greater in patients with cardiac sarcoidosis. In a limited follow-up group (11 cardiac and 9 noncardiac sarcoidosis patients), the incidence of premature ventricular contraction (PVC) on ECG was greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group (36% and 0%, respectively; p < 0.05). A medium correlation existed between QTd and PVC (r = 0.331, p < 0.05). CONCLUSIONS: QTd, cQTd, QTmax, and cQTmax are prolonged in patients with cardiac sarcoidosis compared to the patients with noncardiac sarcoidosis and control subjects. The incidence of PVC on ECG was greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group.     

Measurement and interpretation of QT dispersion

QT dispersion was proposed as an index of the spatial inhomogeneity of ventricular recovery times. The results of studies that found significant correlation between dispersion of ventricular recovery times measured with monophasic action potentials and QT dispersion were interpreted as proof of the direct link between QT dispersion and the dispersion of ventricular recovery times. Later it was shown that QT dispersion is not a direct reflection of the spatial variation of the recovery times and cannot be used for quantification of this variation. The interlead variability of the QT intervals is a result of different projections of the spatial T-wave loop into the various electrocardiographic leads. The reliability of both manual and automatic measurement of QT dispersion is low and is often of the order of the differences of Qt dispersion between different patient groups. The measurement reliability is influenced by intrinsic factors (e.g., amplitude of the T wave) and extrinsic factors (e.g., noise, paper speed of recording, instruments for manual measurements, and type of algorithm and interalgorithmic settings for automatic measurement). There is very little to choose between the different indices of expression of QT dispersion, as well as between the different lead configurations used for its measurement. QT dispersion is not simply a result of measurement error, but a crude measure of abnormalities during the whole course of repolarization. Only grossly prolonged QT dispersion (e.g., > or =100 ms), must be interpreted simply as a sign of the abnormal course of the repolarization, and inferences about the actual dispersion of the ventricular recovery times should not be made. Newer concepts of assessment of the morphology of the T wave are already emerging and will probably be of higher clinical value.