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PubMed1998

QTc interval, and autonomic and somatic nerve function in diabetic neuropathy.

QTc intervals were measured using an electrocardiogram and other autonomic function tests, in 66 neuropathy patients with non-insulin-dependent diabetes mellitus (59.0 +/- 12.5 years; mean +/- SD). The change in R-R interval did not influence the QTc interval, as calculated by the equation: QTc = QT + (1000 - R-R)/7 (ms), compared with the conventional Bazett's equation which appeared to overcompensate in the case of a small R-R interval. The QTc interval in the diabetic patients was significantly longer than that in age-matched controls. The QTc interval showed an inverse correlation with the coefficient of variation of the R-R interval and skin blood flow at rest. However, no correlation was found between QTc interval and blood pressure change, change in heart rate on standing, or results of the sympathetic skin response. The QTc interval did not correlate significantly with motor or sensory nerve conduction parameters. We conclude that the QTc interval can be a simple and useful autonomic indicator for diabetic neuropathy relatively independent of other abnormalities of autonomic and somatic nervous system function.

Aged↗

PubMed2005

Effect of atenolol on QTc interval lengthening during hypoglycaemia in type 1 diabetes.

AIMS/HYPOTHESIS: Hypoglycaemia is associated with heart rate-corrected QT (QTc) interval lengthening on the ECG; this may be important in the pathogenesis of sudden overnight death in young people with diabetes. Since hypoglycaemic QTc lengthening appears to be mediated through the sympathoadrenal response, we tested the hypothesis that beta1-blockade will prevent these changes in type 1 diabetic patients and so provide a potential therapeutic intervention. METHODS: We studied eight type 1 diabetic adults without cardiovascular or renal complications. Similar hypoglycaemic clamp studies were performed on two occasions, at least 4 weeks apart, but immediately before one visit subjects received atenolol 100 mg daily for 7 days. Following a 60-min euglycaemic (5 mmol/l) period, blood glucose was lowered over 30 min to 2.5 mmol/l, and held for 60 min. High-resolution ECG was recorded at baseline and at 0, 30 and 60 min during each glycaemic plateau. QT interval was measured using a semiautomated tangent method and QTc was derived from QT using the Fridericia formula. RESULTS: Mean (SD) baseline QTc was similar at both visits: control 391 (30) ms, post-atenolol 386 (34) ms; (p=0.33). Without atenolol pretreatment, QTc lengthened during hypoglycaemia to a maximum of 448 (34) ms (p<0.001). On atenolol, QTc lengthening was significantly reduced (peak QTc 413 (27) ms; p=0.004 vs control visit). CONCLUSIONS/INTERPRETATION: Hypoglycaemic QTc lengthening is blunted by atenolol in patients with type 1 diabetes. Selective beta1-blockade may help prevent sudden death, if we can identify those at high risk.

Adrenergic beta-Antagonists↗

PubMed1996

Prolongation of QTc interval and autonomic nervous dysfunction in diabetic patients.

We have attempted to clarify the relationships of the QTc interval to alpha and beta sympathetic, as well as parasympathetic function tests including spectral analyses of the R-R interval and systolic blood pressure. The QTc intervals were estimated in 76 diabetic patients and 76 age-matched healthy controls whose R-R intervals were comparable to those of the diabetic patients. We also investigated the relationships of the QTc interval to various clinical features of diabetes mellitus and to autonomic function tests. The QTc interval in diabetic patients was significantly greater than that in healthy controls. The QTc intervals were unrelated to diabetic control, retinopathy and nephropathy, but were prolonged in patients with a long duration of diabetes as compared to those with a short disease duration. There were significant correlations between the QTc interval and orthostatic hypotension, R-R variation and the Valsalva maneuver. Significant correlations were observed between the QTc interval and both the low and the high frequency component of spectral analysis of the R-R interval, whereas no correlations were found with spectral analysis of systolic blood pressure. An abnormal QTc interval is an indicator of cardiac sympathetic and parasympathetic nervous dysfunction, but not vasomotor dysfunction.

Blood Glucose↗

PubMed2006

The effect of temperature on the QTc interval in the newborn infant receiving extracorporeal membrane oxygenation (ECMO).

OBJECTIVE: To explore the changes in the QTc interval during mild hypothermia in neonates receiving extracorporeal membrane oxygenation (ECMO). DESIGN: Twenty seven neonates (median gestation 40 weeks; range 33-41 weeks) enrolled in a pilot study of mild hypothermia were studied during the first five days of ECMO. The first group (N=7) were maintained at 37 degrees C throughout the study period. Subsequent groups (N=5) were cooled to 36 degrees C, 35 degrees C and 34 degrees C respectively for twenty four hours and the final group to 34 degrees C for forty eight hours before being rewarmed to 37 degrees C. Using a 24 h digital monitor, the QT and QTc intervals were recorded continuously during the cooling and rewarming period and validated using standard 12 lead electrocardiograms. Patients were carefully assessed clinically and routine biochemistry (including magnesium and calcium) laboratory tests measured pre ECMO and at timed intervals during cooling and rewarming. RESULTS: The mean difference between the continuous digital and 12 lead ECG values for QTc was -13.3 ms. During the first 24 h of cooling, the mean (95th centile) values for the digitally measured QTc interval at 37 degrees C=431(506) milliseconds (ms); 36 degrees C=459(521) ms; 35 degrees C=445(516) ms; 34 degrees C=465(531) ms; 34 degrees C for 48 h=466(521) ms. During this period overall QTc increased by 3.12 ms (95% confidence intervals 6.17 to 0.84; p=0.04) for each degree fall in body temperature. During rewarming, there was no significant relationship between QTc and temperature change. No serious arrhythmias were during cooling. Using univariate analysis, no relationship was found between QTc and electrolytes, heart rate and blood pressure. CONCLUSIONS: QTc shows significant variability in individuals, and only a small proportion of this can be explained by rectal temperature. Mild hypothermia was not associated with serious cardiac arrhythmias.

Body Temperature↗

PubMed2006

Repolarization morphology in adult LQT2 carriers with borderline prolonged QTc interval.

BACKGROUND: At least 50% of LQT2 carriers have borderline QTc (0.42-0.47 s), and they present a diagnostic difficulty to clinicians evaluating patients suspected of having long QT syndrome (LQTS). OBJECTIVES: Because QTc in this borderline range is nondiagnostic, the purpose of this study was to investigate whether analysis of phenotypic features of T-wave morphology could help identify LQT2 carriers with normal or near-normal QTc-interval duration. METHODS: Standard 12-lead ECGs recorded without beta-blockers from LQT2 carriers (n = 90, 33 +/- 14 years, 61% female) and noncarriers (n = 69, 38 +/- 17 years, 58% female) were digitized. The following parameters were automatically measured: RR interval, QT/QTc, QT apex, T-wave amplitude, ascending (alpha(L)) and descending slopes (alpha(R)) of the T wave, and T-wave symmetry. We used a linear logistic regression model to identify the most relevant parameters for separating LQT2 carriers from noncarriers, within the overall population and among patients without overt QTc prolongation (390 </= QTc </= 470). RESULTS: Logistic regression selected three parameters: QT, RR interval, and alpha(L) in all models. In the overall population, the model provided 92.7% sensitivity and 90.0% specificity. In the group of patients without beta-blockers and near-normal QTc interval, 92.0% sensitivity (n = 46) and 81.4% specificity (n = 49) were achieved by the model including alpha(L.) CONCLUSION: Abnormal T-wave morphology is a phenotypic expression of LQT2, and its quantification could be used to identify patients with suspected LQTS who do not have overt QTc prolongation (QTc >470).

Action Potentials↗

PubMed2004

A comparison of commonly used QT correction formulae: the effect of heart rate on the QTc of normal ECGs.

The corrected QT interval (QTc) is widely used in pharmaceutical studies and clinical practice. Bazett's QT correction formula is still the most popular, despite Simonson's warning in 1961 that it could not be recommended. Other QTc formulae, e.g. Fridericia, Framingham, and Hodges, are also used. This study compares these four formulae using 10,303 normal ECGs recorded from four US hospitals. QT intervals were measured by the same computer program on ECGs confirmed by physicians. The distributions of QTc based on Fridericia, Framingham, and Hodges formulae were similar but Bazett's was significantly wider. The global group QTc-heart rate (HR) correlation coefficients were calculated as Bazett 0.33, Fridericia 0.24, Framingham 0.26, and Hodges 0.11, with the uncorrected QT-HR correlation being 0.82. Overall by far, Hodges QTc is significantly less correlated with HR compared to the others. Certain subgroup correlations of gender and low, mid, or high HR show that one individual formula can out-perform the others, whereby automated selection of QT correction formula based on the patient's HR and gender could be implemented as another option in products. The upper normal limits of corrected QTc were determined by excluding the top 2% from the global distribution charts as follows: Bazett 483 ms, Fridericia 460 ms, Framingham 457 ms, and Hodges 457 ms. Whether for males and/or females, the middle range of HR from 60 to 99 bpm has similar upper normal limits of QTc for all formulae except Bazett. Numerous references recommend 420 to 440 ms as the threshold for reporting prolonged QTc when using Bazett's formula. Based on this database, 30% of apparently normal ECGs would be reported as having abnormal QT intervals for the 440 ms threshold, or 10% if 460 ms is chosen, compared to <2% for the other formulae. It was also noted that QT has a linear trend with HR but not with RR.

Adolescent↗

PubMed1986

Prediction of sudden death from QTc interval prolongation in patients with chronic ischemic heart disease.

Although prolongation of QTc interval has been shown to increase the risk of sudden death after recent myocardial infarction, no data exist on the relationship between sudden death and QTc duration in patients with chronic ischemic heart disease. Furthermore, it is not known whether patients with long QTc intervals (greater than or equal to 440 units) have more prevalent coronary risk factors. Thus 141 nonsurvivors (128 with coronary death and 13 with noncoronary death) representing the follow-up deaths of a cohort of 1157 medically treated patients with ischemic heart disease over a four-year period were compared to 141 consecutive long-term survivors of the same cohort. Thirty-one patients were excluded because of drug interactions, bundle-branch block or atrial fibrillation. QTc duration was calculated on the ECG immediately prior to angiography in 62 patients with sudden death, 36 with intermediate death, 13 with noncoronary death and 140 long-term survivors with chronic ischemic heart disease. In addition, in 64 nonsurvivors (58%) in whom more than one yearly follow-up ECG was available, QTc was calculated in the last ECG preceding death (mean of four months before death). These data were compared to those obtained in 140 long-term survivors at the time of last ECG (mean 48 months after enrollment). At the time of angiography, mean QTc intervals were similar in patients who later died of ischemic heart disease and in long-term survivors (423 +/- 35 vs 421 +/- 25 units). No difference in QTc duration was apparent among nonsurvivors with ischemic heart disease. All study patients were divided into normal and long QTc subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed1995

QTc behavior during treadmill exercise as a function of the underlying QT-heart rate relationship.

A mathematic description of the behavior of the Bazett-corrected QTc interval during exercise was developed from the underlying relationship between the unadjusted QT interval and heart rate in 94 normal men. Measurements were made from digitized precordial lead V5 complexes that were averaged by computer over 20-second periods at upright control (mean rate, 78 beats/min), during moderate exercise (mean rate, 125 beats/min), and at peak effort (mean rate, 162 beats/min), using a gently graded treadmill protocol that produces small heart rate increments between 2-minute stages. Although the group mean QTc interval increased during early exercise and decreased during higher exercise workloads, the mean unadjusted QT interval decreased throughout exercise in a strongly linear relationship with increasing heart rate: QT[ms] = 481 - 1.32HR, R2 = .99, where HR stands for heart rate. As a consequence of this linearity, the behavior of the QTc interval over a range of heart rates generally found during exercise could be modeled as a function of the slope (m) and intercept (b) of the observed relationship, since the Bazett relationship QTc = QT[ms]/R-R0.5 can, in this context, be rewritten simply as QTc = (481 - 1.32HR)/(60/HR)0.5, which reproduces the observed biphasic QTc interval behavior. Plots of the generalized equation QTc = (b - mHR)/(60/HR)0.5 allow theoretical exploration of QTc interval behavior that might result from varied disorders with different slopes (m) and intercepts (b), and these regression-based descriptors of the QT-heart rate relationship may provide useful, additional definitions of normal and abnormal QT interval behavior during exercise.

Electrocardiography↗

PubMed1997

Electrocardiographic QTC interval: short-term weight loss effects.

OBJECTIVE: Prolongation of the QTc interval is a risk-factor for ventricular arrhythmias and sudden death. There is a correlation between body mass index (BMI) and QTc, with longer intervals observed in obese subjects. Dieting and weight loss on selected diets are also associated with prolongation of the QTc interval, although the mechanisms and risk factors of this syndrome are not clearly established. The aim of the current investigation was to determine if short-term weight loss over seven days while living on a metabolic ward influences cardiac repolarization as indicated by QT interval duration. DESIGN AND SUBJECTS: The electrocardiogram QT, RR, and QTc (QT/RR(0.5)) intervals were assessed in 30 healthy obese (BMI > 27 kg/m2) men and women ingesting a balanced 1120 kcal/d formula diet (23% kcal as fat and 52 g protein/d). RESULTS: Weight loss (3.9 +/- 1.7 kg) over seven days had no measurable effect on the RR interval and there was a significant (P = 0.02) shortening of the QT interval (mean +/- s.d., 0.395 +/- 0.028-0.386 +/- 0.027 s) and borderline significant (P = 0.11) shortening of the QTc (0.411 +/- 0.028-0.404 +/- 0.025 s) interval. The QTc interval normalized in three subjects with prolonged baseline QTc (> 0.44 s). A statistically significant (P = 0.007) reduction in systolic blood pressure early in the course of weight loss (day 2) accompanied the electrocardiographic changes. CONCLUSION: These results fail to support the development of cardiac repolarization abnormalities in obese patients who ingest a nutritionally balanced low calorie diet over seven days. A significant reduction in QT interval duration and amelioration of abnormally prolonged baseline QTc intervals suggest improved cardiac repolarization with early weight loss.

Adult↗

PubMed2001

Prolonged QTc interval predicts mortality in patients with Type 1 diabetes mellitus.

AIMS: To evaluate prolonged QTc interval and QT dispersion as predictors of all-cause and cardiovascular mortality after adjustment for well-established risk factors in Type 1 diabetic patients. METHODS: From a cohort of all adult Type 1 diabetic patients, duration of diabetes >or= 5 years, attending the clinic in 1984 and followed in an observational study for 10 years (n = 939), all subjects with resting baseline electrocardiograms were identified (n = 697, 360 males). The QT length was measured and corrected for heart rate (QTc). Maximal QTc length (QTc max) and QT dispersion were determined. RESULTS: At baseline, 431 had normoalbuminuria (< 30 mg/24 h), 138 had microalbuminuria (30-299 mg/24 h) and 128 had macroalbuminuria (>or= 300 mg/24 h) of whom 66 (15%), 35 (25%) and 61 (48%) died during follow-up, respectively (26 (6%), 14 (10%), 21 (16%) from cardiovascular disease). QTc max. was 442 (1.2) ms (mean (SEM)) for survivors and 457 (3.7) in patients who died (P < 0.001). In a Cox proportional hazards model including baseline values of putative risk factors, independent predictors of death were QTc max (P = 0.03), age (P < 0.001), presence of hypertension (P = 0.001), male sex (P < 0.001), log urinary albumin excretion (P < 0.001), smoking (P = 0.04), log serum-creatinine (P < 0.001), height (P < 0.001), low social class (P = 0.04), whereas QT dispersion, heart rate, and HbA1c were not included. In the subgroup with macroalbuminuria, but not for all patients, QTc max was an independent risk factor for cardiovascular mortality. CONCLUSION: QTc prolongation, but not increased QT dispersion, is an independent marker of increased mortality in patients with Type 1 diabetes mellitus.

Adult↗

PubMed2000

QTc dispersion increases during hemodialysis with low-calcium dialysate.

BACKGROUND: The risk of ventricular arrhythmias is known to increase during hemodialysis (HD) treatment, but the cause of this phenomenon has remained unidentified. QT dispersion (= QTmax - QTmin) reflects heterogeneity of cardiac repolarization, and increased dispersion is known to predispose the heart to ventricular arrhythmias and sudden cardiac death. METHODS: We studied the effect of dialysate calcium concentration on cardiac electrical stability during HD treatment in 23 end-stage renal disease patients. Three HD treatments were applied with dialysate Ca++ concentrations of 1.25 mmol/L (dCa++1.25), 1.5 mmol/L (dCa++1.5), and 1.75 mmol/L (dCa++1.75). The QTc interval and QTc dispersion were measured before and after the three sessions. RESULTS: With the dCa++1.5 and dCa++1.75 dialyses, serum Ca++ increased and the QTc interval remained stable (dCa++1.5) or decreased (dCa++1.75), but no significant change was noted in QTc dispersion. With dCa++1.25 HD, serum Ca++ decreased (1.24 +/- 0.11 vs. 1.20 +/- 0.09 mmol/L, P < 0. 05), and both the QTc interval (403 +/- 27 vs. 419 +/- 33 ms, P < 0. 05) and QTc dispersion increased (38 +/- 19 vs. 49 +/- 18 ms, P < 0. 05). The change in the QTc interval correlated inversely with the change in serum Ca++ (r = -0.68, P < 0.0001). Except for serum Ca++ and plasma intact parathyroid hormone, predialysis and postdialysis values in other blood chemistry, blood pressure, heart rate, body weight, and total ultrafiltration were equal in the three dialysis sessions. CONCLUSION: This study is the first, to our knowledge, to demonstrate that HD increases QTc dispersion if a low-calcium (dCa++1.25) dialysate is used. This indicates that the use of low-calcium dialysate may predispose HD patients to ventricular arrhythmias and that perhaps it should be avoided, at least when treating patients with pre-existing cardiac disease.

Adult↗

PubMed1998

Usefulness of the QTc interval in predicting acute allograft rejection.

BACKGROUND: Endomyocardial biopsy (EMB) is the gold standard for detecting cardiac allograft rejection. However, EMB is invasive, costly, and unsuitable for frequent monitoring. Recent studies have shown that acute allograft rejection causes ventricular conduction disturbances. Therefore we tested the hypothesis that the electrocardiographic QTc interval correlates with the histopathologic degree of allograft rejection. METHODS: Between January 1994 and April 1997, 65 adult cardiac allograft recipients (mean age 52.1 +/- 1.7 years) were studied from transplantation until hospital discharge. During EMB, a 12-lead electrocardiogram was obtained. In grading acute allograft rejection, we used both the Texas Heart Institute (THI) scale and the International Society for Heart and Lung Transplantation (ISHLT) scale. 212 paired biopsy specimens and QTc intervals (mean 3.3 per patient) were obtained. We considered an increase of more than 10% of the QTc interval a rejection. RESULTS: Of the biopsy specimens 177 showed no or mild rejection (THI grade 0-5; ISHLT grade O-IIIA), and 35 showed moderate to severe rejection (THI grade 6-10; ISHLT IIIA-IV). The mean QTc interval was 449 +/- 2 msec for the first group and 517 +/- 11 msec for the second group (p = 0.0001). The correlation between the biopsy grades and the percentage of the changes in the QTc interval was r = 0.73 (p = 0.001). The QTc interval had a sensitivity of 86% (30/ 35) in predicting rejection and a specificity of 88% (1551177) in predicting the absence of rejection. CONCLUSIONS: Determination of the QTc interval is an accurate, noninvasive means of detecting acute cardiac rejection. Adoption of QTc testing may allow EMB to be used less frequently and more selectively.

Electrocardiography↗

PubMed1980

QTc intervals at discharge after acute myocardial infarction and long-term prognosis.

QTc intervals were measured retrospectively in 46.3 survivors of AMI with a mean age of 65 years. The measurement was made one at discharge from hospital. Patients with anterior infarcts had significantly longer QTc intervals than those with inferior or uncertain infact localization. A weak but significant correlation was found between S-GOT maximum and QTc interval. Patients with ventricular arrhythmias in the CCU had longer QTc intervals. Patients with a poor long-term prognosis had significantly shorter QTc intervals. This finding was explained by digitalis therapy. Among patients without bundle branch block, digitalis and quinidine, those below 66 years of age who died within the first six months tended to have longer QTc intervals than the survivors. It is concluded that measurements of QTc interval at discharge have no long-term predictive value. This factor may, however, have some bearing on the short-term prognosis in younger patients without therapy which affects the QTc interval.

Adult↗

PubMed2005

Investigation of the effects of physiological and vasodilation-induced autonomic activation on the QTc Interval in healthy male subjects.

AIMS: Drug-induced prolongation of the QTc interval is an important marker for potential proarrhythmic action. Prolongation of the QTc interval results from alteration of the ionic currents that regulate cardiac repolarisation. Such effects may result from direct drug action or alternatively they could also occur indirectly by drug-induced modulation of autonomic tone, which is known to regulate cardiac repolarization. This study examined the effects of physiological and drug-induced autonomic activation on heart rate, QT and QTc intervals. METHODS: We studied 29 healthy male subjects aged 18-30 years. Electrocardiographs were recorded before and during autonomic activation induced by mental activation, standing, exercise and glyceryl trinitrate (GTN) (0.5 mg sublingual)-induced vasodilation in the presence and absence of beta-blockade (atenolol 100 mg daily for 4 days). QT intervals were measured manually by electronic callipers and corrected using the Fridericia formula. RESULTS: Heart rates were significantly increased during mental arithmetic, standing, exercise and GTN and this effect was significantly attenuated by atenolol, except for mental activation. QTc intervals were significantly reduced on standing and exercise and this was significantly attenuated by atenolol during exercise. In contrast, GTN increased QTc intervals (Delta = 5.7 ms, confidence interval +/- 3.2 ms, P < 0.005) and this was not attenuated by atenolol. CONCLUSIONS: Alteration in QTc intervals may result from physiological manoeuvres and vasodilation, interventions known to induce autonomic activation. We suggest that QTc prolongation due to GTN is indirectly mediated and unlikely to carry any proarrhythmic effect. Understanding whether drug-induced QTc prolongation is directly or indirectly mediated may be important to determine any potential proarrhythmic risk.

Adolescent↗

PubMed2006

QTc dispersion and P-wave dispersion during migraine attacks.

The aim of this study was to investigate increase of QTc dispersion and P-wave dispersion during migraine attacks. Fifty-five patients (16-65 years of age, 49 women, six men) with migraine were included in our study. Heart rate, QTc interval, maximum and minimum QTc interval, QTc dispersion, maximum and minimum P-wave duration and P-wave dispersion were measured from 12-lead ECG recording during migraine attacks and pain-free periods. ECGs were transferred to a personal computer via a scanner and then used for magnification of x400 by Adobe Photoshop software. Maximum QTc interval (454 +/- 24 ms vs. 429 +/- 23 ms, P < 0.001), QTc interval (443 +/- 26 ms vs. 408 +/- 22 ms, P < 0.001) and QTc dispersion (63 +/- 18 ms vs. 43 +/- 14 ms, P < 0.001) were found significantly higher during migraine attacks compared with pain-free periods. Maximum P-wave duration (107 +/- 11 ms vs. 100 +/- 11 ms, P < 0.001) and P-wave dispersion (45 +/- 13 ms vs. 35 +/- 13 ms, P < 0.001) were found higher during migraine attacks than pain-free periods. We concluded that migraine attacks are associated with increased QTc and P-wave dispersion compared with pain-free periods.

Adult↗

PubMed2001

The clinical significance of QTc dispersion measurement for risk of syncope in patients with aortic stenosis.

OBJECTIVES: (1) To evaluate the clinical usefulness of QTc dispersion determination in aortic stenosis and (2) to compare the effects of QTc dispersion on the occurrence risk of syncope in aortic stenosis. BACKGROUND: QT interval dispersion has long been known to be a marker of dispersion of ventricular repolarization and, hence, electrical instability. Additionally, it has been shown that these patients have a propensity to ventricular tachyarrhythmic syncope. METHODS: The study included 86 patients with aortic stenosis who underwent left-heart catheterization and coronary angiography during investigation of syncope, as well as 30 control subjects. The patients were characterized with regards to the presence or absence of a history of syncope and the severity of aortic stenosis (the degree of peak transvalvular gradient). In addition, QT dispersion measurements were corrected for heart rate according to Bazett's formula and both were measured. RESULTS: QTc dispersion was greater in patients with aortic stenosis than in the control subjects (60 +/- 13 msec vs 38 +/- 12 msec, P < 0.001). Similarly, QTc dispersion was greater in the patients with a history of syncope than in the patients with no history of syncope (68 +/- 12 msec vs 53 +/- 10 msec, P < 0.001). In addition, QTc dispersion values were greater in the patients with a high transvalvular gradient than in the patients with a low transvalvular gradient (65 +/- 12 msec vs 50 +/- 9 msec, P < 0.001). Multivariate logistic regression analysis showed that only an increased QTc dispersion had significant value for the risk of syncope in aortic stenosis. CONCLUSIONS: An increased QTc dispersion increases the occurrence risk for syncope in aortic stenosis. These results suggest that high values of QTc dispersion are a sensitive noninvasive marker for determining the risk for syncope in aortic stenosis.

Adult↗

PubMed2001

Effects of cisapride on QTc interval in term neonates.

BACKGROUND: Cisapride administration for 48 hours has been shown to increase heart rate corrected QT (QTc) interval in preterm neonates. Accumulation of the drug because of liver enzyme immaturity has been suggested to be the reason. If this is correct, a longer survey of QTc interval should disclose an increase even in term neonates. OBJECTIVE: A prospective survey of the effects of cisapride on QTc interval in term neonates administered cisapride. SETTING: Neonatal Unit of the University Hospital of Dijon, France. DESIGN: QTc interval was determined just before and 48 hours, seven days, and 15 days after the start of treatment. SUBJECTS: Twenty one term newborn infants (mean gestational age 39.3 weeks) given the recommended dose of cisapride (0.2 mg/kg, four times a day). RESULTS: Administration of cisapride caused a significant increase in QTc interval (p < 0. 01). The mean value increased from 0.397 before treatment to 0.418 after 48 hours, 0.431 by day 7, and 0.447 by day 15. A QTc interval exceeding 0.450 was found in six neonates: three at 48 hours, one at day 7, and two at day 15. In two infants, withdrawal of the drug was associated with normalisation of the QTc interval. CONCLUSIONS: These results support the hypothesis of cisapride accumulation in newborns due to enzymatic immaturity and indicate that QTc interval should be monitored in neonates receiving this drug.

Analysis of Variance↗

PubMed1998

Effect of hemodialysis on the dispersion of the QTc interval.

The QTc dispersion reflects the underlying regional heterogeneity of the recovery of the ventricular excitability, thereby it is considered as a novel marker of risk of ventricular arrhythmias. Because a higher incidence of ventricular arrhythmias is described during and after hemodialysis, the aim of this study has been to evaluate the QTc dispersion before and after uncomplicated hemodialysis session. Twenty chronic uremics without heart failure, ischemic heart disease or dialysis hypotension were selected. The QTc dispersion was determined as the difference between the longer and the shorter QTc interval measured on a 12-lead electrocardiogram. Following the hemodialysis session, the QTc dispersion increased from 30 +/- 9 to 54 +/- 17 ms (p < 0.001) associated with the expected reduction of potassium and magnesium and with the increase of extracellular calcium concentration. However, no correlation has been observed between the QTc dispersion increase and the degree of the intradialytic changes of plasma electrolytes, blood pressure or body weight. In summary, the hemodialysis treatment per se does induce an increase of the QTc dispersion, likely due to the rapid changes of electrolyte plasma concentrations. This can potentially contribute to the arrhythmogenic effect of the hemodialysis procedure, reflecting an enhanced regional heterogeneity of ventricular repolarization. The clinical importance of the increase of QTc dispersion as risk factor of ventricular arrhythmias, particularly in hemodialyzed patients suffering from ischemic or hypertrophic heart diseases, should be the matter of further investigations.

Adult↗