The effects of halothane and sevoflurane on QT dispersion

QT dispersion is defined as the difference between QT (max) and QT (min) in the 12-lead surface ECG. It has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with arrhythmic events than in those without them. The aim of this study was to examine the effects of halothane and sevoflurane on QT and QTc dispersion during inhalational induction of anaesthesia. The effects on QT and QTc dispersion of halothane and sevoflurane have been investigated during induction of anaesthesia. Forty-six ASA (American Society of Anaesthesiologists) physical status I-II patients, aged 16-50 years, undergoing general anaesthesia were randomly allocated to receive either halothane or sevoflurane. The mean baseline values for QT and QTc dispersion were not significantly different between the two groups (P > 0.05). QT dispersion was increased with halothane compared with baseline values (50 +/- 16 ms vs. 29 +/- 9 ms, P < 0.01) and after sevoflurane compared with baseline (48 +/- 15 vs. 33 +/- 8 ms, P < 0.01). Also, QTc dispersion was increased with halothane compared with baseline values (48 +/- 13 ms vs. 31 +/- 9 ms, P < 0.001) and after sevoflurane compared with baseline (50 +/- 14 vs. 40 +/- 11 ms, P < 0.01). The QTc interval did not change by both sevoflurane (443 +/- 7 vs. 431 +/- 21 ms, P > 0.05) and halothane (419 +/- 33 vs. 431 +/- 19 ms, P > 0.05) compared with baseline. Both halothane and sevoflurane cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion. This may be relevant in the aetiology of arrhythmias in patients during anaesthesia with halothane or sevoflurane.     

Changes in QT dispersion magnitude during respiratory phases: role of maximum inspiration and expiration

There is still controversy about the reliability and prognostic value of QT interval dispersion because of interobserver and intraobserver variability. The authors aimed to study the effect of respiratory phases on QT dispersion. Sixty healthy volunteers (38 men, 22 women, mean age 25+/-3 years) from the medical staff comprised the study group. Electrocardiograms were recorded by the same technician with a rate of 50 mm/s during normal breathing, maximum inspiration and expiration. QT dispersion was defined as the difference between the maximal and minimal QT interval measurement occurring among any of the 12 leads. Corrected QT (QTc) interval was calculated according to Bazzet's formula. There were no significant differences between QTc max interval during maximum inspiration and expiration compared with those in normal breathing (409+/-20 ms vs 417+/-26 ms, p>0.05 and 412+/-18 vs 417+/-26 ms, p>0.05 respectively). QTc dispersion during maximum inspiration and expiration was significantly lower than that of normal breathing (36+/-8 ms vs 44+/-9 ms, p<0.003 and 32+/-7 vs 44+/-9 ms, p< 0.003, respectively). And the QTc dispersion during maximum expiration was also lower than that during maximum inspiration (p<0.01). QT dispersion magnitude is affected by the respiratory phases in healthy subjects and decreases during both maximum inspiration and expiration as compared with normal respiration.     

QT interval dispersion as a new marker of restenosis after percutaneous transluminal coronary angioplasty of isolated single-vessel coronary artery stenosis

BACKGROUND: There are no reliable non-invasive markers of restenosis after percutaneous transluminal coronary angioplasty (PTCA). The aim of our study was to measure changes in QT interval dispersion after PTCA and to determine whether restenosis subsequently affects QT interval dispersion. METHODS AND RESULTS: Fifty-six consecutive patients - 41 men and 15 women (mean age: 56.2 +/-8.3 years) - with isolated stenosis of the left anterior descending artery who underwent successful PTCA were studied. A symptom-limited treadmill exercise test was performed within 7 days after PTCA and then again before repeated angiography. Repeated coronary angiography revealed restenosis in 15 patients (26.8%) and no signs of significant stenosis in 41 patients (73.2%). QT interval dispersion in the group of patients with restenosis measured before exercise increased from baseline 34 +/- 7 to 49 +/- 15 ms after 6 months (p < 0.01) and QT interval dispersion measured immediately after exercise increased from baseline 38 +/- 4 to 68 +/- 21 ms after 6 months (p < 0.001). In contrast, patients without restenosis showed no significant changes in QT interval dispersion measured before (baseline: 34 +/- 9 ms; after 6 months 33 +/- 12 ms; p = NS) and immediately after exercise (baseline: 34 +/- 12 ms; after 6 months: 33 +/- 10; p = NS). When QT interval dispersion > or =60 ms (measured 6 months after PTCA procedure) was considered as a potential marker of restenosis, this indicator had very high sensitivity and specificity when measured immediately after exercise (80 and 95% respectively). CONCLUSIONS: QT interval dispersion significantly increases in the group of patients with documented restenosis and may be a simple, non-invasive marker of restenosis. However, further studies are needed to confirm this observation.     

Effect of bisoprolol on QT dispersion in patients with congestive heart failure--the etiology-dependent response

AIMS: To evaluate the effect of beta1-selective blocker bisoprolol on the QT and QTc dispersion in patients with chronic heart failure and to compare the responses to bisoprolol in patients with different etiologies. METHODS AND RESULTS: Eighty-one patients with heart failure secondary to ischemic heart disease (n=47) or idiopathic dilated cardiomyopathy (n=34) were stratified by etiology and then randomly assigned to the bisoprolol and control group (no tablet) on top of the conventional treatment. QT dispersion was calculated by subtracting the shortest QT from the longest QT, in absolute value (Qtmax-Qtmin). It was also corrected with Bazett's formula (QTc dispersion). After 6 weeks of treatment, QT and QTc dispersion were significantly decreased in the bisoprolol group (QT dispersion: 66.5+/-13.4 ms vs. 49.1+/-16.8 ms for ischemic heart disease (P<0.01); 67.5+/-12.4 ms vs. 59.4+/-14.4 ms for dilated cardiomyopathy (P<0.05); QTc dispersion: 78.3+/-15.2 ms vs. 53.3+/-18.1 ms for ischemic heart disease (P<0.01); 79.1+/-14.2 ms vs. 69.0+/-17.9 ms for dilated cardiomyopathy (P<0.05)), but there was no significant decrease of QT and QTc dispersion in the control group. Linear regression analysis showed that patients with ischemic heart disease tend to have lower 6-week QT dispersion than patients with dilated cardiomyopathy (coefficient beta=-0.283, P=0.009) after controlling for their baseline values in the bisoprolol group. CONCLUSION: These findings suggested that bisoprolol reduces QT and QTc dispersion in patients with chronic heart failure, but the etiology of heart failure affects the response of patients to bisoprolol.     

Value of QT dispersion in the interpretation of treadmill exercise electrocardiograms of patients without exercise-induced chest pain or ST-segment depression

It has recently been reported that increased QT dispersion seen on standard 12-lead electrocardiograms (ECGs) reflects transient myocardial ischemia. The present study investigates whether increased QT dispersion induced by exercise is a useful indicator for detecting significant coronary stenosis in patients who do not have chest pain or significant ST-segment depression in response to exercise. We studied 135 consecutive patients (mean age +/- SD, 55 +/- 9 years; 97 men and 38 women) who complained of anginal chest pain and who did not have exercise-induced chest pain or significant ST-segment depression during treadmill exercise electrocardiography. Coronary angiography was performed in all of patients. Of the 135 patients, 97 had no significant coronary stenosis, 25 had 1-vessel coronary artery disease (CAD), and 13 had multivessel CAD. QT dispersion immediately after exercise was significantly greater in the group with significant coronary stenosis than without significant coronary stenosis (62 +/- 13 vs 40 +/- 14 ms, p <0.0001). When QT dispersion >/=60 ms immediately after exercise was considered a positive result, this indicator had a sensitivity of 74%, a specificity of 85%, and an accuracy of 81% for the diagnosis of significant coronary stenosis. In conclusion, we have shown that QT dispersion immediately after exercise is useful for detecting significant CAD in patients who do not have exercise-induced chest pain or significant ST-segment depression.     

Prognostic value of exercise-induced QT dispersion in patients after acute myocardial infarction

BACKGROUND: Electrocardiographic exercise tests are widely recommended for patients before discharge after myocardial infarction, what justify the search for new variables which may improve their prognostic value. QT dispersion in 12 lead ECG reflects the heterogeneity of ventricular repolarisation. Increased QT dispersion is a noninvasive marker of ischaemia and electrical instability. AIM: Evaluation of the prognostic value of exercise-induced changes of QT dispersion in patients after an acute myocardial infarction. METHODS: Heart rate limited treadmill exercise test according to modified Bruce was performed 14+/-5 days after infarction in 77 patients (age 56+/-11,8 female). QT dispersion was measured at rest and on peak exercise. Patients were followed up for mean 88 months. RESULTS: QT dispersion was higher at peak exercise in those patients who died due to cardiovascular causes (n=8) or suffered from non-fatal myocardial infarction during follow-up (n=15), than in remaining group (71+/-20 vs 58+/-22 msec, p<0.01). At rest QT dispersion was similar in both groups (64+/-17 vs 66+/-20 msec, NS). CONCLUSIONS: The lack of an exercise-induced decrease in QT dispersion identifies a subgroup of patients after myocardial infarction with a poor long-term prognosis.     

Effects of oral L-arginine supplementation on exercise-induced QT dispersion and exercise tolerance in stable angina pectoris

We assessed the effects of L-arginine (an endogenous precursor of nitric oxide) on the magnitude of exercise-induced QT dispersion in patients with coronary artery disease. The study had a randomized double-blind cross-over design. Twenty-five patients with stable coronary artery disease underwent two separate exercise tests: after oral administration of L-arginine (6 g/24 h for 3 days) or placebo. Indications for cessation of exercise included: pulse limit, exhaustion, chest pain, ST segment depression >2 mm. We found that arginine significantly increased exercise duration from 604+/-146 to 647+/-159 s (P<0.03). However, it had no effect on the sum of exercise-induced ST segment depressions (1.9+/-2.3 and 2.4+/-3.3 on and off arginine, respectively, NS). Exercise shortened QT interval to a similar extent in patients treated with placebo or arginine. QT dispersion changed during exercise from 55+/-21 to 60+/-19 ms (NS) and from 60+/-21 to 53+/-17 ms (NS), respectively. We conclude that, in patients with coronary artery disease, oral supplementation of L-arginine does not affect exercise-induced changes in QT interval duration, QT dispersion or the magnitude of ST segment depression. However, it significantly increases exercise tolerance, most likely due to improved peripheral vasomotion. These results may be of clinical and therapeutic importance.     

Change with exercise in QT dispersion in infarct-related myocardium after angioplasty

BACKGROUND: The aim of this study was to evaluate the relationship between exercise-induced QT dispersion and condition of infarct-related myocardium including myocardial scar after angioplasty assessed with exercise perfusion single photon emission computed tomography (SPECT). METHODS: Exercise thallium-201 SPECT was performed 6 months after successful direct angioplasty in 67 male patients (60.6 +/- 11.5 years), who had Q wave infarction resulting from single vessel disease, and the number of perfusion defect areas (DS) was measured at rest and exercise together with QT (QTc) dispersion. RESULTS: In 52 patients with resting perfusion defects, the exercise-induced change in DS was correlated to the change in QT (or QTc) dispersion (r = -0.51 or r = -0.531, p < 0.0001). When the patients were grouped according to the patterns of transient perfusion defect, there were significant differences in DeltaQT dispersion and DeltaQTc dispersion among infarct-related three groups (reverse, fixed, and partial redistributions) and normal volunteers (DeltaQT dispersion; -5.7 +/- 12.7 ms in 13 patients with reverse redistribution, -16.3 +/- 13.1 ms in 30 patients with fixed redistribution, -28.9 +/- 29.5 ms in 9 patients with partial redistribution, and +3.4 +/- 20.9 ms in 12 normal volunteers, p = 0.0098; DeltaQTc dispersion; +18.2 +/- 20.8 ms, +1.4 +/- 16.7 ms, -15.4 +/- 30 ms, and +19 +/- 27.5 ms, p = 0.0017, respectively). DeltaQTc dispersion estimated the SPECT image patterns (p = 0.0002) with a sensitivity of 67.3%, a specificity of 83.7% and an accuracy of 78.2%. CONCLUSIONS: The change with exercise in QT dispersion may help detect the condition of infarct-related myocardium after angioplasty.     

QT peak dispersion, not QT dispersion, is a more useful diagnostic marker for detecting exercise-induced myocardial ischemia.

BACKGROUND: The electrocardiographic indices of QT dispersion (QTd), QT peak dispersion (QTpd), and the principal component analysis ratio (PCAr) are related to the occurrence of fatal arrhythmia and are influenced by physical exercise. OBJECTIVE: The purpose of this study was to investigate whether or not the QT parameters can be used as markers for exercise-induced myocardial ischemia. METHODS: We measured these QT parameters at rest and at 3 minutes after exercise using exercise-stress thallium-201 scintigraphy (SPECT), compared with conventional ST segment changes in 161 patients with suspected or known coronary artery disease. The patients were classified into four groups (normal, redistribution, fixed defect, and redistribution with fixed defect) according to SPECT. RESULTS: At rest, QTd and PCAr were greater in the fixed defect and redistribution with fixed defect groups. PCAr, however, increased after exercise in the redistribution and redistribution with fixed defect groups. Although QTpd at rest was not significantly different among the four groups, it increased in the redistribution and redistribution with fixed defect groups after exercise (QTpd after exercise: normal, 36 +/- 16 ms vs. redistribution, 51 +/- 23 ms, redistribution with fixed defect, 53 +/- 19 ms; P<.05). For myocardial infarction reflected by fixed defect, QTd at rest was the most useful indicator, while QTpd after exercise was the most useful indicator for exercise-induced myocardial ischemia according to multiple logistic regression analysis with receiver operating characteristic curves. In addition, the change in PCAr by exercise was an independent predictor for exercise-induced ischemia. CONCLUSIONS: QTpd and PCAr could be useful indices for exercise-induced myocardial ischemia. Determining the QTpd of a patient after exercising can improve the diagnostic accuracy of ischemia in a routine clinical setting.     

Exercise-induced QTc-interval changes for predicting improvement in regional blood flow in ischemic myocardium and cardiac output after coronary angioplasty in patients with right bundle-branch block

BACKGROUND: We have previously shown that QT-interval changes are more useful than ST-T changes in evaluating the severity of exercise-induced myocardial ischemia in patients with right bundle-branch block (RBBB). HYPOTHESIS: The purpose of this study was to evaluate whether the improvement in regional myocardial blood flow (RMBF) in ischemic areas and cardiac output after percutaneous transluminal coronary angioplasty (PTCA) can be predicted by exercise-induced QT-interval changes prior to PTCA. METHODS: The RMBF and cardiac output were quantified with nitrogen-13 ammonia positron emission tomography at rest and during exercise in 20 patients with RBBB and ischemic heart disease before and 6 months after PTCA, and in 9 healthy volunteers. RESULTS: Before PTCA, exercise-induced prolongation by < 20 ms or shortening of the Bazett-corrected QT (QTc) interval (454 +/- 38 to 451 +/- 41 ms, p = NS) was observed in 13 patients (Group 1) and prolongation by > or = 20 ms (429 +/- 44 to 466 +/- 50 ms, p < 0.002) was observed in 7 (Group 2). The number of regions of exercise-induced ischemia was significantly greater in Group 2 than in Group 1 (4.0 +/- 1.2 vs. 2.1 +/- 1.2, p < 0.01). The RMBF in regions of exercise-induced ischemia and cardiac output at rest was not significantly different between Groups 1 and 2, whereas during exercise both the parameters were significantly lower in Group 2 than in Group 1 (both p < 0.05). After successful PTCA, RMBF both at rest and during exercise improved significantly in Group 1 (0.67 +/- 0.04 to 0.71 +/- 0.06 ml/min/g, 0.74 +/- 0.05 to 0.84 +/- 0.08 ml/min/g; both p < 0.0001), but did not improve significantly in Group 2 (0.63 +/- 0.05 to 0.65 +/- 0.07 ml/min/g, 0.65 +/- 0.04 to 0.69 +/- 0.11 ml/ min/g; both p = NS). Cardiac output during exercise improved significantly in Group 1 (6.4 +/- 0.7 to 7.4 +/- 0.9 l/min; p < 0.002) but not in Group 2 (5.7 +/- 0.6 to 5.9 +/- 0.6 l/min; p = NS). CONCLUSIONS: Our results suggest that the marked prolongation of the QTc interval induced by pre-PTCA exercise may predict a lack of improvement in RMBF in ischemic areas and cardiac output after PTCA in patients with RBBB and ischemic heart disease.     

Exaggerated QT prolongation after cardioversion of atrial fibrillation.

OBJECTIVES: The purpose of this study was to test the hypothesis that the extent of drug-induced QT prolongation by dofetilide is greater in sinus rhythm (SR) after cardioversion compared with during atrial fibrillation (AF). BACKGROUND: Anecdotes suggest that when action potential-prolonging antiarrhythmic drugs are used for AF, excessive QT prolongation and torsades de pointes (TdP) often occur shortly after sinus rhythm is restored. METHODS: QT was measured in nine patients with AF who received two identical infusions of dofetilide: 1) before elective direct current cardioversion and 2) within 24 h of restoration of SR. RESULTS: During AF, dofetilide did not prolong QT (baseline: 368 +/- 48 ms vs. drug: 391 +/- 60, p = NS) whereas during SR, QT was prolonged from 405 +/- 55 to 470 +/- 67 ms (p < 0.01). In four patients (group I), the SR dofetilide infusion was terminated early because QT prolonged to >500 ms, and one patient developed asymptomatic nonsustained TdP. The remaining five patients (group II) received the entire dose during SR. Although deltaQT was greater in group I during SR (91 +/- 22 vs. 45 +/- 25 ms, p < 0.05), plasma dofetilide concentrations during SR were similar in the two groups (2.72 +/- 0.96 vs. 2.77 +/- 0.25 ng/ml), and in AF (2.76 +/- 1.22 ng/ml). DeltaQT in SR correlated inversely with baseline SR heart rate (r = -0.69, p < 0.05), and QT dispersion developing during the infusion (r = 0.79, p < 0.01). CONCLUSIONS: Shortly after restoration of SR, there was increased sensitivity to QT prolongation by this I(Kr)-specific blocker. Slower heart rates after cardioversion and QT dispersion during treatment appear to be important predictors of this response.     

女性运动试验前后QT离散度变化对冠心病诊断的价值

探讨女性病人运动试验前、后ＱＴ离散度（ＱＴｄ）的变化和其对冠心病诊断的价值。对临床上以胸痛为主诉的８４例女性病人,先后行运动试验和冠状动脉造影检查,并测量运动试验前、后体表１２导联心电图ＱＴｄ。结果：在冠心病病人中,无论运动试验阳性还是阴性,运动试验后ＱＴｄ明显大于运动试验前,差异有显著性（５３．５９±１６．９３ｍｓｖｓ３２．０５±１４．１８ｍｓ,Ｐ＜０．０１）;在非冠心病病人中运动试验前、后ＱＴｄ无显著性差异（３０．９８±１２．００ｍｓｖｓ２９．２７±１２．３３ｍｓ,Ｐ＞０．０５）。以运动试验后即刻和运动试验前ＱＴｄ的差值≥２０ｍｓ作为指标,诊断冠心病的敏感性为８７．１８％、特异性为８０．００％、准确性为８３．３３％。结果提示运动试验与ＱＴｄ相结合可提高对女性冠心病诊断的敏感性、特异性和准确性。     

QT dispersion and early arrhythmic risk in acute myocardial infarction

BACKGROUND: This study sought to find out QT dispersion in healthy individuals and patients of acute myocardial infarction and to find correlation, if any, between QT dispersion and the incidence of ventricular arrhythmias in acute myocardial infarction. METHODS AND RESULTS: QT dispersion was calculated from a 12-lead electrocardiogram in 100 patients of acute myocardial infarction admitted in intensive coronary care unit and 100 age- and sex-matched healthy individuals. In patients of acute myocardial infarction, QT dispersion was calculated on admission, 24 hours after admission and at the time of discharge from intensive coronary care unit. Average QT dispersion in acute myocardial infarction was found to be significantly higher on admission (76.4 +/- 18.3 ms), 24 hours after admission (62.88 +/- 17.52 ms) and at the time of discharge from intensive coronary care unit (51.79 +/- 16.79 ms) than in healthy individuals (29.76 +/- 6.06 ms; p<0.05). QT dispersion was found to be significantly increased in patients of acute myocardial infarction with ventricular arrhythmias (82.06 +/- 16.86 ms) than in those without (66.75 +/- 16.28 ms; p<0.01). Patients of acute myocardial infarction with ventricular tachycardia or ventricular fibrillation had significantly increased QT dispersion (96.25 +/- 15.97 ms) than those who had only ventricular premature beats (80 +/- 15.04 ms; p<0.01). QT dispersion was found to be significantly greater in patients with anterior wall acute myocardial infarction (79.80 +/- 18.19 ms) than in those with inferior wall acute myocardial infarction (71.9 +/- 17.48 ms; p<0.05). At the time of discharge from intensive coronary care unit no statistically significant difference was found in QT dispersion in those who received thrombolysis (51.58 +/- 16.05 ms) and those who did not (48.18 +/- 14.68 ms; p>0.05). QT dispersion was found to be significantly higher in those who died (88.66 +/- 15.97 ms) than in those who survived (74.23 +/- 17.91 ms; p<0.05). QT dispersion was significantly higher in ventricular arrhythmic deaths (97.14 +/- 17.04 ms) than those who had non-arrhythmiac deaths (81.25 +/- 11.25 ms; p<0.05). CONCLUSIONS: Interlead QT variation and its measure as QT dispersion challenges our current approach to the electrocardiographic assessment of arrhythmic risk. QT dispersion may provide a potentially simple, cheap, non-invasive method of measuring underlying dispersion of ventricular excitability.     

QT dispersion in patients with Takayasu arteritis

This study was designed to test the hypothesis that myocardial involvement exists in patients with Takayasu arteritis and is associated with increased QT dispersion, which is a marker of repolarization inhomogeneity. Twenty-one consecutive patients with Takayasu arteritis and no significant coronary artery disease were included. Twelve-lead electrocardiogram and exercise-induced thallium-201 myocardial scintigraphy were performed in all patients. Ten of 21 patients (48%) had abnormal findings on scintigraphy. Patients were divided into two groups by the presence (group P, n = 10) or absence (group N, n = 11) of exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities, including permanent defects in three, reversible defects in four, and slow washout in three. The QT dispersion at rest was significantly greater in group P than that in group N (54 +/- 12 vs 40 +/- 8 msec, p < 0.005). The QTc dispersion at rest was also significantly greater in group P than in group N (59 +/- 15 vs 43 +/- 11 msec, p < 0.01). In patients with Takayasu arteritis, myocardial involvement suggested by exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities is not rare, even when no significant coronary stenosis is present on angiography. Increased baseline QT dispersion was associated with scintigraphic abnormalities and may be a useful marker of myocardial involvement in patients with Takayasu arteritis.     

Exercise-induced repolarization changes in patients with stable coronary artery disease

Exercise is a classic trigger of ventricular arrhythmias in the setting of coronary artery disease (CAD). The aim of this study was to examine the changes of novel indexes of repolarization in patients with stable CAD who underwent exercise stress testing. Sixty-seven consecutive patients (mean age 62 ± 9 years, 60 men) who underwent treadmill exercise stress testing according to the Bruce protocol and completed the test without evidence of ischemia were enrolled. Baseline clinical and demographic characteristics were recorded, and indexes of repolarization such as corrected QT (QTc) interval, T peak-to-end (Tpe) interval, and Tpe/QT ratio were assessed at baseline and at peak exercise. A similar group of control subjects without CAD (n = 68, mean age 60 ± 11 years, 52 men) were also studied. All participants successfully completed the test. In the patient group, the QTc interval significantly increased from baseline to peak exercise (median 385 ms [25th percentile 357 ms, 75th percentile 407 ms] vs 418 ms [381 ms, 447 ms], p <0.001). The Tpe interval and the Tpe/QT ratio were also significantly increased at peak exercise (42 ms [36 ms, 60 ms] vs 78 ms [60 ms, 84 ms], p <0.001; and 0.17 [0.14, 0.22] vs 0.21 [0.16, 0.25], p = 0.015). In the control group, the QTc interval did not change significantly, the Tpe interval decreased at peak exercise (62 ms [41 ms, 80 ms] vs 48 ms [40 ms, 78 ms], p = 0.05), and the Tpe/QT ratio did not show a significant change (0.18 [0.12, 0.22] vs 0.16 [1.14, 0.21], p = 0.39). In patients with stable CAD and normal treadmill exercise stress test results, the QTc interval, the Tpe interval, and the Tpe/QT ratio increased during exercise. In conclusion, it is reasonable to assume that despite the absence of inducible ischemia, the spatial dispersion of repolarization is increased during exercise, exposing these patients to increased arrhythmic risk.     

Diurnal variation of the P-wave dispersion in chronic ischemic heart diseases

OBJECTIVE: Electrocardiographic indices like maximum P-wave duration (P(max)) and P-wave dispersion (PD) can be used to detect patients with atrial conduction disorders, myocardial ischemia and those at risk for atrial fibrillation. Considering the diurnal variation of ischemia in patients with significant coronary lesions, this study was designed to investigate the diurnal variation of eventual atrial conduction abnormalities. METHODS: Forty-eight patients (31 male) with typical angina were grouped according to coronary angiography results as group 1 - 70% or more luminal reduction in at least one of the coronary arteries (n=28), and group 2 - normal coronary arteries (n=20). The difference between the P(max) and minimum P-wave durations (P(min)) is designated as PD. The diurnal P(max), P(min) and PD values were compared between and within the groups. RESULTS: The morning P(max) value of group 1 was significantly higher than the value of group 2 (112+/-1 vs. 102+/-1 ms, P<0.001). The morning PD of group 1 was significantly higher than that of group 2 (54+/-9 vs. 48+/-1 ms, P<0.05). The morning P(max) of group 1 (112+/-1 ms) was significantly higher than its afternoon (102+/-9 ms) and night (102+/-1 ms) values (P<0.001). The morning PD of group 1 (54+/-9 ms) was higher than the afternoon (40+/-10 ms) and night (43+/-9 ms) PD (P<0.001). No significant difference was observed between the P(max), P(min) and PD values in group 2 (P>0.05). CONCLUSION: This study demonstrated that coronary heart disease patients have higher morning P(max) and PD values that may be important regarding prediction of timing and treatment of atrial conduction disorders in myocardial ischemia.     

Lack of electrocardiographic changes in women with polycystic ovary syndrome

OBJECTIVE: The aim of the present study was to investigate the potential alterations in electrocardiographic (ECG) pattern in patients with polycystic ovary syndrome (PCOS). PATIENTS: Fifty PCOS patients and 50 age- and body mass index-matched healthy women were studied. METHODS: We assessed hormonal and metabolic pattern, and performed ECG analysis for evaluating PQ interval, QRS duration, minimum and maximum QT interval corrected for heart rate (QT(c)min and QT(c)max, respectively), corrected QT dispersion (QT(c)d), corrected J point/T-wave interval (JTend(c)), corrected JTmax interval (JTmax(c)), and corrected Tmax-end interval (Tmax-end(c)). RESULTS: QT(c)min (399 +/- 21 vs. 396 +/- 25 ms, P = 0.51); QT(c) max (445 +/- 25 vs. 443 +/- 27 ms, P = 0.70); and QT(c)d (46 +/- 13 vs. 47 +/- 15 ms, P = 0.72); JTend(c) (337 +/- 14 vs. 336 +/- 16 ms(1/2), P = 0.74); and JTmax(c) (256 +/- 22 vs. 258 +/- 21 ms(1/2), P = 0.64); Tmax-end(c) (81 +/- 18 vs. 78 +/- 19 ms(1/2), P = 0.42) were not significantly different between PCOS and healthy women. CONCLUSION: Despite profound differences in hormonal and metabolic pattern, our data demonstrate no significant difference in ECG pattern in PCOS compared to healthy controls.     

Role of alpha1-blockade in congenital long QT syndrome: investigation by exercise stress test.

Beta-blockade is widely reported to reduce the incidence of syncope in 75-80% of patients with congenital long QT syndrome (LQTS). However, despite full-dose beta-blockade, 20-25% of patients continue to have syncopal episodes and remain at high risk for sudden cardiac death. In some patients refractory to beta-blockade, the recurrence of arrhythmias is successfully prevented by left stellate ganglionectomy, and also by labetalol, a nonselective beta-blockade with alpha1-blocking action. These observations suggest that not only beta-adrenoceptors, but also alpha1-adrenoceptors, play an important pathogenic role, especially under sympathetic stimulation, in LQTS. The clinical effects of alpha1-blockade in congenital LQTS were investigated in 8 patients with familial or sporadic LQTS. Two measurements of the QT interval were taken, from the QRS onset to the T wave offset (QT) and from the QRS onset to the peak of the T wave (QTp). Using the Bruce protocol, an exercise test was performed after administration of beta-blockade alone and again after administration of alpha1-blockade. The following were compared: (1) Bazzet-corrected QT (QTc) and QTp (QTpc) intervals in the supine and standing position before exercise and in the early recovery phase after exercise; and (2) the slopes (reflecting the dynamic change in the QT interval during exercise) of the QT interval to heart rate were obtained from the linear regression during the exercise test. In the supine position before exercise, there was no change in the QTc before or after the addition of alpha1-blockade (498+/-23 vs 486+/-23 ms [NS]). However, in the upright position before exercise and in the early recovery phase after exercise, QTc was significantly shortened from 523+/-21 to 483+/-22ms (p<0.01), and from 521+/-30 to 490+/-39ms (p<0.01), respectively, by alpha1-blockade. The QTpc was unchanged in any situation. Consequently, QTc-QTpc was significantly shortened by alpha1-blockade in the upright position before exercise and in the early recovery phase after exercise (131+/-36 to 105+/-37ms (p<0.05), and 132+/-29 to 102+/-31 ms (p<0.01), respectively). The slopes of the QT interval-heart rate relation by linear regression became significantly steeper from -2.23+/-0.38 to -2.93+/-0.76 (p<0.01) with the addition of alpha1-blockade. The findings suggest that the addition of alpha1-blockade attenuated the exercise-induced prolongation of the QT interval and that the rate adaptation of the QT interval to heart rate during exercise was improved. This indicates that additional treatment with alpha1-blockade may be beneficial to prevent cardiac events in LQTS patients in whom ventricular arrhythmia is resistant to beta-blockade.     

Use of autonomic maneuvers to probe phenotype/genotype discordance in congenital long QT syndrome

Patients with congenital long QT syndrome due to potassium channel mutations (LQT1 and LQT2) may elude diagnosis due to normal electrocardiographic findings at rest, yet remain at risk of sudden death during bradycardia or sympathetic stimulation. To test the hypothesis that autonomic maneuvers can unmask long QT syndrome in genetically abnormal subjects with a normal phenotype (QTc < or =450 ms), we exposed 13 controls (33 +/- 9 years; 5 men), 5 patients with LQT1 (32 +/- 12 years; 3 men), and 5 patients with LQT2 (30 +/- 11 years; 5 men) to phenylephrine bolus, exercise, and epinephrine infusion. The QT interval was measured at baseline and after each intervention. A substantial overlap was found in QTc among the groups at baseline and after phenylephrine. In contrast, QTc was significantly and consistently longer in subjects with LQT1 compared with controls during and after exercise (492 +/- 40 vs 407 +/- 14 ms, p <0.0001, at peak exercise; 498 +/- 30 vs 399 +/- 20 ms, p <0.0001, at 1 minute into recovery) or epinephrine (623 +/- 51 vs 499 +/- 51 ms, p <0.001, at peak epinephrine; 604 +/- 36 vs 507 +/- 54 ms, p <0.01, at 1 minute into recovery) but not in subjects with LQT2. In conclusion, sympathetic stimulation can reveal the LQT1 phenotype even in subjects with normal baseline electrocardiographic findings.     

Cold effect on qt dispersion in healthy subjects

Thirty-one healthy subjects, aged 35 +/- 6 (21 to 48) years, were included in the study to evaluate the effect of ice water immersion on QT dispersion. There was no difference in the age between females (n = 11) and males (n = 20). Baseline, stress (at the end of ice water immersion, 4 degrees C, for 3 minutes) and recovery 12-lead electrocardiograms (ECGs) were recorded on each subject. During the test, a significant variability developed in both the QT dispersion (52 +/- 17, 68 +/- 25 and 59 +/- 21 ms; p = 0.015) and the corrected QT dispersion (56 +/- 17, 76 +/- 27 and 64 +/- 23 ms; p = 0.005), but not in the heart rate (74 +/- 11, 76 +/- 9, and 74 +/- 9 bpm, respectively; p = 0.447). There was no inter-sex difference in the baseline heart rate or QT dispersion, or in their response to ice water immersion. Age significantly correlated with the variation of QT dispersion to ice water immersion (r = 0.380, p = 0.035). With 37 years of age as a separation point, the variation of QT dispersion to ice water immersion was more obvious in the older group (28 +/- 22 vs. 10 +/- 19 ms, p = 0.023). In conclusion, cold may increase QT dispersion in healthy subjects, with a more obvious effect in the older ones.