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QTc Interval (qtc + interval)

Distribution by Scientific Domains

Medical Sciences	96%
Life Sciences	3%

Distribution within Medical Sciences

Cardiovascular Disease	33%
Anesthesia & Pain Management	12%
Pharmacology & Pharmaceutical Medicine	9%
Pediatrics	7%
12 Other Subdomains	30%

Selected Abstracts

Prognostic Significance of QTc Interval for Predicting Total, Cardiac, and Ischemic Heart Disease Mortality in Community-Based Cohort from Warsaw Pol-MONICA Population

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2000
Aleksandra Pytlak M.D.
Background: QT interval in resting electrocardiogram (ECC) is a sum of ventricular depolarization and repolarization time. Its prolongation is associated with a worse prognosis for survival due to a high incidence of severe ventricular arrhythmias. Methods: The random sample of the Warsaw Pol-MONICA population consisting of 2646 men and women, aged 35,64, screened in 1984, was followed-up until 1996. All deaths and their causes were registered based on death certificate diagnosis. QT interval was measured manually in three consecutive QRST complexes in each ECG and corrected using Bazett's formula (QT corrected: QTc). For statistical analyses the mean value of 3 QTc measurements were used. To assess the relationship between QTc and mortality, the Cox proportional hazards model with stepwise selection of variables was used. Results: Out of the screened sample, 459 persons died (309 men, 150 women), 226 due to cardiovascular diseases (CVD) (162 men, 64 women), and 81 due to ischemic heart disease (IHD) (59 men, 22 women). Both men and women who died were significantly older at baseline and had significantly longer mean QTc as compared to survivors (men: 457 ms vs 446 ms, P = 0.0001; women: 469 ms vs 459 ms, P = 0.001). Among men, after adjustment for confounding variables, mean QTc was significantly associated with total and CVD mortality, and in women, with CVD and IHD mortality. The risk of death rose with an increase in QTc duration. In men, with every increase in QTc by 20 ms, the risk of all causes of death rose by 11% (95% CI: 1.04,1.18), CVD death by 9% (95% Cl: 1.01,1.19), and IHD death by 11 % (95%: 0.97,1.28). In women, the risk of all-cause death increased by 9% (95% CI: 0.98,1.21), CVD death by 21% (95% Cl: 1.02,1.43), and IHD death by 41% (95% Cl: 1.08,1.85). Conclusion: QTc interval was significantly related to all cause, cardiovascular and ischemic heart disease. The risk of death increased with longer QTc duration. A.N.E. 2000;5(4):322,329 [source]

Effect of low-dose cisapride on gastric emptying and QTc interval in preterm infants

ACTA PAEDIATRICA, Issue 12 2000
C Costalos
The aim of the study was a prospective survey of the effects of low-dose cisapride on gastric emptying and QTc interval in very low birthweight infants. Twenty low birthweight infants were studied: mean (SD) gestation 30.5 (2.2) wk; birthweight 1320 (150)g. Gastric emptying was assessed ultrasonically in 15 of these infants, in a randomized blind crossover study, following 24-h low-dose oral cisapride administration (0.1 mg/kg given 8 hourly), or placebo. The QTc interval was also determined in all 20 infants following a 7-d course of cisapride or placebo. Conclusions: Cisapride significantly shortened both gastric emptying time and QTc interval (p < 0.05) compared to placebo. All infants completed the study without any apparent adverse effects. In conclusion, low-dose cisapride administration significantly improves gastric emptying without increasing the QTc interval. [source]

The effect of sertindole on QTD and TPTE

ACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2010
J. Nielsen
Nielsen J, Andersen MP, Graff C, Kanters JK, Hardahl T, Dybbro J, Struijk JJ, Meyer JM, Toft E. The effect of sertindole on QTD and TPTE. Objective:, Recent research suggests that other surrogate markers than QTc, including QTc dispersion and Tpeak-Tend, may better correlate with cardiac arrhythmia risk. While sertindole significantly prolongs the QTc interval, the effects on other markers of arrhythmia risk, such as QTc dispersion and Tpeak-Tend are unknown. Method:, Digital 12-lead ECG was recorded at baseline and at steady-state in 37 patients switched to sertindole. ECG was analysed for Fridericia-corrected QT duration (QTcF), QT dispersion and Tpeak-Tend. Results:, From a baseline QTcF of 407 ± 22 ms, mean QTcF prolongation during sertindole treatment was 20 ± 23 ms, P < 0.01. No effect on QTc dispersion was found (,1 ± 11 ms; P = 0.41). No increased duration of the Tpeak-Tend interval from baseline was found (+7 ± 21 ms; P = 0.05). Conclusion:, These findings might be related to the absence of confirmed Torsade de Pointes (TdP) cases related to sertindole exposure, despite sertindole's QTc prolonging effects. [source]

Torsade de pointes in a patient with complex medical and psychiatric conditions receiving low-dose quetiapine

ACTA PSYCHIATRICA SCANDINAVICA, Issue 4 2005
W. V. R. Vieweg
Objective:, Describe potential cardiac complications of low-dose quetiapine and other atypical antipsychotic drugs. Method:, We present a case report of a 45-year-old Black woman with multiple medical and psychiatric problems taking low-dose quetiapine. Results:, Coincident with a generalized seizure, the patient developed ,ventricular fibrillation'. She was countershocked with restoration of normal sinus rhythm. The initial electrocardiogram showed QT interval prolongation. Shortly thereafter, classical torsade de pointes appeared, lasted 10 min, and resolved spontaneously. Hypomagnesemia was present. A cardiac electrophysiologist was concerned that the very slow shortening of the prolonged QTc interval after magnesium replacement implicated quetiapine as a risk factor for QTc interval prolongation and torsade de pointes. A psychosomatic medicine consultant asserted that the fragmented medical and psychiatric care almost certainly contributed to the patient's medical problems. We discuss other cases of QT interval prolongation by newer antipsychotic drugs and previous reports by our group concerning the association of psychotropic drugs, QT interval prolongation, and torsade de pointes. Conclusion:, Atypical antipsychotic drug administration, when accompanied by risk factors, may contribute to cardiac arrhythmias including torsade de pointes. [source]

Prevalence and clinical relevance of corrected QT interval prolongation during methadone and buprenorphine treatment: a mortality assessment study

ADDICTION, Issue 6 2009
Katinka Anchersen
ABSTRACT Aims To determine the prevalence of corrected QT interval (QTc) prolongation among patients in opioid maintenance treatment (OMT) and to investigate mortality potentially attributable to QTc prolongation in the Norwegian OMT programme. Participants and setting Two hundred OMT patients in Oslo were recruited to the QTc assessment study between October 2006 and August 2007. The Norwegian register of all patients receiving OMT in Norway (January 1997,December 2003) and the national death certificate register were used to assess mortality. Mortality records were examined for the 90 deaths that had occurred among 2382 patients with 6450 total years in OMT. Design and measures The QTc interval was assessed by electrocardiography (ECG). All ECGs were examined by the same cardiologist, who was blind to patient history and medication. Mortality was calculated by cross-matching the OMT register and the national death certificate register: deaths that were possibly attributable to QTc prolongation were divided by the number of patient-years in OMT. Findings In the QTc assessment sample (n = 200), 173 patients (86.5%) received methadone and 27 (13.5%) received buprenorphine. In the methadone group, 4.6% (n = 8) had a QTc above 500 milliseconds; 15% (n = 26) had a QTc interval above 470 milliseconds; and 28.9% (n = 50) had a QTc above 450 milliseconds. All patients receiving buprenorphine (n = 27) had QTc results <450 milliseconds. A positive dose-dependent association was identified between QTc length and dose of methadone, and all patients with a QTc above 500 milliseconds were taking methadone doses of 120 mg or more. OMT patient mortality, where QTc prolongation could not be excluded as the cause of death, was 0.06/100 patient-years. Only one death among 3850 OMT initiations occurred within the first month of treatment. Conclusion Of the methadone patients, 4.6% had QTc intervals above 500 milliseconds. The maximum mortality attributable to QTc prolongation was low: 0.06 per 100 patient-years. [source]

Effects of adrenaline and potassium on QTc interval and QT dispersion in man

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2003
S. Lee
Abstract Background Hypoglycaemia alters cardiac repolarization acutely, with increases in rate-corrected QT (QTc) interval and QT dispersion (QTd) on the electrocardiogram (ECG); such changes are related to the counterregulatory sympatho-adrenal response. Adrenaline produces both QTc lengthening and a fall in plasma potassium (K+) when infused into healthy volunteers. Hypokalaemia prolongs cardiac repolarization independently however, and therefore our aim was to determine whether adrenaline-induced repolarization changes are mediated directly or through lowered plasma K+. Materials and methods Ten healthy males were studied on two occasions. At both visits they received similar l- adrenaline infusions but on one occasion potassium was also administered; infusion rates were adjusted to maintain circulating K+ at baseline. The QTc interval, QTd, peripheral physiological responses and plasma adrenaline and potassium concentrations were measured during both visits. Results The QTc interval and QTd increased both with and without potassium clamping. Without K+ replacement, mean (SE) QTc lengthened from 378 (5) ms to a final maximum value of 433 (10) ms, and QTd increased from 36 (5) ms to 69 (8) ms (both P < 0·001). During K+ replacement, QTc duration at baseline and study end was 385 (7) ms and 423 (11) ms, respectively (P < 0·001), and QTd 38 was (4) ms and 63 (5) ms (P = 0·001). Conclusions These data suggest that disturbed cardiac repolarization as a result of increases in circulating adrenaline occurs independently of extracellular potassium. A direct effect of adrenaline upon the myocardium appears the most likely mechanism. [source]

Automated mutation screening using dideoxy fingerprinting and capillary array electrophoresis

HUMAN MUTATION, Issue 5 2001
Lars Allan Larsen
Abstract The rapid progress in the isolation of genes associated with human disease has resulted in an increasing demand for mutation screening methods. The molecular diagnosis of the long QT syndrome (LQTS), a cardiac disorder characterized by prolongation of the QTc interval in the ECG, syncopes, and sudden death, requires mutation screening of all exons in at least five genes, encoding cardiac Na+ and K+ channel subunits. A method for automated dideoxy fingerprinting (ddF) using capillary array electrophoresis (CAE) was developed and the efficiency of the method was tested by analyzing 24 DNA samples with mutations in one of the genes KCNQ1 and KCNH2, which are involved in 50% of LQTS cases. One of these mutations, 362insQK in KCNQ1, is novel. The sensitivity was 100% using a single electrophoresis temperature of 18°C or 25°C. However, analysis of the samples in both the sense and anti-sense direction were required for high sensitivity. Analysis in a single direction resulted in a decrease of the sensitivity to 74% and 70%, respectively. The throughput of the ddF method, if performed with a 16 capillary CAE instrument, is 288 samples per seven hr if each sample is analyzed on both strands. Hum Mutat 18:451,457, 2001. © 2001 Wiley-Liss, Inc. [source]

Cardiovascular effects of high dose venlafaxine XL in patients with major depressive disorder

HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2007
Patrick Mbaya
Abstract Objective To assess cardiovascular safety profile of high dose Venlafaxine XL in patients with major depression. Method Effects of high dose venlafaxine (mean 346.15,mg;) on the cardiovascular system in 37 patients with major depressive disorder were evaluated: BP, ECG (PR, QT, QRSD and QTc intervals) and heart rate. Results 12.5% of patients developed hypertension after starting treatment with venlafaxine. There was an association between heart rate and the dose of venlafaxine although not statistically significant. There was no association between dose of venlafaxine and PR, QT, QRSD and QTc intervals. One patient on 300,mg who was hypertensive and on other medications that may prolong QTc, had mildly prolonged QTc. However this was not clinically significant. Conclusion This study of subjects on high dose venlafaxine (mean 346.15,mg; range 225,525,mg) did not demonstrate any clinical or statistically significant effects on electrocardiogram (ECG) parameters including PR, QT, QRSD and QTc interval. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Cyamemazine metabolites: effects on human cardiac ion channels in-vitro and on the QTc interval in guinea pigs

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2008
William Crumb
Monodesmethyl cyamemazine and cyamemazine sulfoxide, the two main metabolites of the antipsychotic and anxiolytic phenothiazine cyamemazine, were investigated for their effects on the human ether-à-go-go related gene (hERG) channel expressed in HEK 293 cells and on native INa, ICa, Ito, Isus or IK1 of human atrial myocytes. Additionally, cyamemazine metabolites were compared with terfenadine for their effects on the QT interval in anaesthetized guinea pigs. Monodesmethyl cyamemazine and cyamemazine sulfoxide reduced hERG current amplitude, with IC50 values of 0.70 and 1.53 ,M, respectively. By contrast, at a concentration of 1 ,M, cyamemazine metabolites failed to significantly affect INa, Ito, Isus or IK1 current amplitudes. Cyamemazine sulfoxide had no effect on ICa at 1 ,M, while at this concentration, monodesmethyl cyamemazine only slightly (17%), albeit significantly, inhibited ICa current. Finally, cyamemazine metabolites (5 mg kg,1 i.v.) were unable to significantly prolong QTc values in the guinea pig. Conversely, terfenadine (5 mg kg,1 i.v.) significantly increased QTc values. In conclusion, cyamemazine metabolite concentrations required to inhibit hERG current substantially exceed those necessary to achieve therapeutic activity of the parent compound in humans. Moreover, cyamemazine metabolites, in contrast to terfenadine, do not delay cardiac repolarization in the anaesthetized guinea pig. These non-clinical findings explain the excellent cardiac safety records of cyamemazine during its 30 years of extensive therapeutic use. [source]

The electrocardiographic and hemodynamic effect of metohexital and propofol with and without esmolol

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2006
R. Korpinen
Background:, Metohexital and propofol are short-acting induction agents, which have a tendency to prolong the QTc interval of the ECG. We studied whether this increase could be prevented by combining a beta-blocking agent, esmolol, with these drugs. Simultaneously, we studied the hemodynamic effects of these combinations. Methods:, In a randomized, double-blind study, 80 ASA I,II young adults were premedicated with oxycodone and atropin and allocated to one of four groups: propofol (P), propofol + esmolol (P + E), metohexital (E) or metohexital + esmolol (M + E). The doses were 2 mg/kg propofol/metohexital and 1 mg/kg esmolol. Alfentanil 15 µg/kg was used in all groups. The hemodynamic parameters were measured non-invasively and the electrocardiographic parameters using the signal processing method. Result:, The highest QTc values, which often exceeded the normal upper limit of 440 ms, were recorded at the baseline or immediately after the administration of the induction drugs. The intervals were significantly shorter if esmolol was co-administered with either propofol or metohexital. The heart rate increased in the group M and decreased in the group P + E but remained unchanged in the groups P and M + E. Systolic and diastolic arterial pressures decreased during the study in all groups, most prominently in group P + E. Conclusions:, During the anesthesia induction, the QTc interval was significantly shorter when esmolol was co-administered with either propofol or metohexital. The hemodynamic responses were properly controlled with the combination of metohexital and esmolol as well as with propofol alone, but the combination of propofol and esmolol tended to cause hemodynamic depression. [source]

Bilastine in allergic rhinoconjunctivitis and urticaria

ALLERGY, Issue 2010
C. Bachert
To cite this article: Bachert C, Kuna P, Zuberbier T. Bilastine in allergic rhinoconjunctivitis and urticaria. Allergy 2010; 65 (Suppl. 93): 1,13. Abstract Allergic rhinoconjunctivitis and urticaria are increasing in prevalence in many developed countries. The role of histamine in such conditions is well documented and clinical guidelines recommend non-sedating H1 -receptor antagonists as first-line treatment choices. Bilastine is a novel non-sedating histamine H1 -receptor antagonist developed for the treatment of allergic rhinoconjunctivitis and urticaria. The aim of this review is to critique the scientific evidence relating to the pharmacological properties of bilastine and the clinical evidence regarding its potential as an antihistamine. In vitro binding studies and investigations in animal tissue have demonstrated the high specificity of bilastine for H1 -receptors, and preclinical animal studies have also yielded promising results in terms of a reduction of histamine-mediated inflammatory effects, including capillary permeability and bronchospasm. In pharmacodynamic studies bilastine was found to down-regulate histamine-induced flare and wheal responses in healthy volunteers. Preclinical and clinical pharmacokinetic studies showed that bilastine has dose-dependent kinetics following oral administration. Excretion is almost exclusively via urine and faeces as unchanged drug. Early clinical trials have shown that bilastine has similar efficacy to other second-generation H1 -receptor antagonists such as cetirizine, desloratadine, fexofenadine and levocetirizine, in terms of reducing allergic symptoms. Clinical findings also indicate that bilastine has a rapid onset of action and a 20 mg single dose is effective throughout a 24-h period. Furthermore, bilastine has been associated with improved quality of life in allergic rhinoconjunctivitis and urticaria patients. Adverse effects have generally been minimal in these studies and doses up to twice those proposed did not exhibit differences in adverse events compared to placebo. Moreover, in vivo investigations have found no evidence of accumulation of bilastine in the central nervous system, and various studies have confirmed minimal effects on psychomotor performance in healthy volunteers administered up to four times the usual dose. Clinical studies have also found no effect of bilastine on the QTc interval and other ECG parameters, even at supratherapeutic dosages, confirming the good cardiac safety profile of this newer antihistamine. Given its pharmacodynamic profile, which appears to be similar to other second-generation H1 -receptor antagonists, and its favourable safety and tolerability, bilastine has the attributes of a potentially clinically useful non-sedating antihistamine. Larger clinical studies are now necessary to fully elucidate the clinical potential of this novel antihistamine. [source]

QTc interval and QTc dispersion during haemodiafiltration

NEPHROLOGY, Issue 6 2004
FULVIO FLOCCARI
SUMMARY: Background and Aim: Our aim was to evaluate QTc interval and QTc dispersion in 27 end-stage renal disease (ESRD) patients undergoing Acetate Free Biofiltration (AFB) in order to ascertain any correlations between the electrrocardiographic (ECG) parameters, serum Na+, K+, Ca++, Mg++ and intraerythrocytic Mg++ (Mg++e) concentrations. All measures were made at t0 (session beginning), t1 (first hour), t2 (second hour), t3 (third hour), and t4 (session end). Results: Blood pressure, heart rate, bodyweight and total ultrafiltration in the three dialysis sessions were constant. A significant progressive increase occurred in serum Ca++ during the sessions, while there was a significant diminution in serum K+. The pattern for Mg++ concentrations in serum and erythrocytes differed: in serum it decreased, whereas Mg++e increased. At t4, the QTc interval was reduced to a significant extent with respect to the baseline value. QTc dispersion significantly increased at t1 without there being significant variations at other times with respect to t0. At t2, t3 and t4, values promptly returned to baseline levels. QTc had a negative correlation with serum Ca++ levels at t4. In contrast, an inverse correlation was found between QTc dispersion and serum K+ at t1. No other correlations could be found between any other electrolytes, QTc interval or QTc dispersion. Conclusion: In conclusion, the decrease observed in the QTc interval at the end of an AFB session was inversely related to serum Ca++ concentrations. Moreover, an increase in QTc dispersion occurred during the first hour of the session, and was negatively correlated with serum K+. [source]

Exercise Does Not Increase QTcmax and QTcd in Diabetic Patients with Autonomic Neuropathy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2007
MEHMET YAZICI M.D.
Background:The purpose of this study was to examine the effects of exercise on maximum QTc interval (QTcmax) and QTc dispersion (QTcd) in diabetic patients without clinically evident heart disease. Methods: Seventy-six diabetic patients who had no coronary artery disease or hypertension (group I; mean age 48 ± 9 years old) and 40 healthy volunteers (group II; mean age 46 ± 13 years old) were enrolled in the study. Cases with clinically evident heart disease were excluded from the study. Resting 12-lead electrocardiogram (ECG) and maximal treadmill exercise test (according to Bruce protocol) were performed in all cases. The QTcmax interval was determined at rest (RQTcmax) and during peak exercise (PQTcmax). Also, the QTcd was measured at rest (RQTcd) and during peak exercise (PQTcd). Autonomic neuropathy was assessed by measuring the heart rate variability (HRV). Results: There was no significant difference between clinical characteristics of two groups. In group I, HRV parameters were significantly lower than group II. RQTcd, PQTcd, RQTcmax, and PQTcmax were significantly longer in group I (56 ± 16 vs 34 ± 11; P< 0.001, 62 ± 22 vs 40 ± 15; P < 0.001, respectively). In diabetic patients, there was no significant difference between RQTcmax and PQTcmax (428 ± 19 vs 420 ± 31; P > 0.05), and no significant difference was present between RQTcd and PQTcd (56 ± 16 vs 62 ± 22; P > 0.05, respectively). Conclusion: Exercise does not affect QTcd in patients with diabetes mellitus and without clinically evident heart disease. [source]

Relationship Between Abnormal Microvolt T-Wave Alternans and Poor Glycemic Control in Type 2 Diabetic Patients

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2007
GIULIO MOLON M.D.
Background:Abnormal microvolt T-wave alternans (TWA) predicts the risk of ventricular arrhythmias and sudden cardiac death. Although type 2 diabetes is associated with an increased risk of these events, there is a dearth of available data on microvolt TWA measurements in type 2 diabetic populations. Methods:We studied 59 consecutive type 2 diabetic outpatients without manifest cardiovascular disease (CVD) and 35 non-diabetic controls who were matched for age, sex, and blood pressure values. Microvolt TWA analysis was performed non-invasively using the CH-2000 system during a sub-maximal exercise with the patient sitting on a bicycle ergometer. Results:The frequency of abnormal TWA was significantly higher in diabetic patients than in controls (25.4 vs 5.7%; P < 0.01). Among diabetic patients, those with abnormal TWA (n = 15) had remarkably higher hemoglobin A1c (HbA1c) (8.1 ± 0.9 vs 7.1 ± 0.8%, P < 0.001) and slightly smaller time-domain heart rate variability parameters (i.e., RMSSD, root mean square of difference of successive R-R intervals) than those with normal TWA (n = 44). Gender, age, body mass index, lipids, blood pressure values, cigarette smoking, diabetes duration, microvascular complication status, QTc interval, and current use of medications did not significantly differ between the groups. In multivariate regression logistic analysis, HbA1c (OR 13.6, 95% CI 2.0,89.1; P = 0.0076) predicted abnormal TWA independent of RMSSD values and other potential confounders. Conclusions:Our findings suggest that abnormal TWA is a very common condition (,25%) among people with type 2 diabetes without manifest CVD and is closely correlated to glycemic control. [source]

Evidence for Electrical Remodeling of the Native Conduction System with Cardiac Resynchronization Therapy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007
CHARLES A. HENRIKSON M.D.
Background:Cardiac resynchronization therapy (CRT) improves hemodynamics and decreases heart failure symptoms. However, the potential of CRT to bring about electrical remodeling of the heart has not been investigated. Methods and Results:We studied 25 patients, of whom 17 had a nonischemic cardiomyopathy, and 8 had an ischemic cardiomyopathy; 16 had left bundle branch block (LBBB), 1 right bundle branch block (RBBB), and 8 nonspecific intraventricular conduction delay. During routine device clinic visits, patients with chronic biventricular pacing (>6 months) were reprogrammed to VVI 40 to allow for native conduction to resume. After 5 minutes of native rhythm, a surface electrocardiogram (ECG) was recorded, and then the previous device settings were restored. This ECG was compared to the preimplant ECG. Preimplant mean ejection fraction was 19% (range, 10%,35%), and follow-up mean ejection fraction was 35% (12.5%,65%). Mean time from implant to follow-up ECG was 14 months (range, 6,31). The QRS interval prior to CRT was 155 ± 29 ms, and shortened to 144 ± 31 ms (P = 0.0006), and the QRS axis shifted from ,1 ± 59 to ,26 ± 53 (P = 0.03). There was no significant change in PR or QTc interval, or in heart rate. Conclusion:CRT leads to a decrease in the surface QRS duration, without affecting other surface ECG parameters. The reduced electrical activation time may reflect changes in the specialized conduction system or in intramyocardial impulse transmission. [source]

Temporary Disturbances of the QT Interval Precede the Onset of Ventricular Tachyarrhythmias in Patients with Structural Heart Diseases

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2002
BJÖRN HENRIK DIEM
DIEM, B.H. et al.: Temporary Disturbances of the QT Interval Precede the Onset of Ventricular Tach-yarrhythmias in Patients with Structural Heart Diseases. An increase in sinus rate prior to ventricular tachyarrhythmias has been demonstrated in previous studies. There is no clear data available concerning changes in ventricular de- and repolarization prior to ventricular tachyarrhythmias, especially in patients with structural heart disease. Therefore, the aim of this study was to analyze the QT and QTc interval (Bazett's formula immediately before the onset of ventricular tachyarrhythmias in stored electrograms of patients with ICDs. The study analyzed 228 spontaneous ventricular tachyarrhythmia episodes in 52 patients (mean age 64 ± 10 years, 49 men, 3 women) and compared them with 146 electrograms of baseline rhythm recorded during regular ICD follow-up. Mean ventricular cycle length (CL), QT interval, and QTc were measured before the onset of ventricular tachyarrhythmia and during baseline rhythm. Prior to ventricular tachyarrhythmias onset, CL was significantly shorter than during baseline rhythm (714 ± 139 vs 828 ± 149 ms, P < 0.0001). By contrast, the QT interval (430 ± 67 ms) and QTc interval (518 ± 67 ms) were significantly prolonged before the onset of ventricular tachyarrhythmias as compared to baseline rhythm (QT 406 ± 67 ms, QTc 450 ± 61 ms; P < 0.0001). CL, QT, and QTc changes were independent of concomitant treatment with antiarrhythmic drugs. Ventricular tachyarrhythmias are preceded by a significant prolongation of the QT and QTc intervals. This phenomenon may represent a greater than normal disparity of repolarization recovery times possibly facilitating the development of ventricular tachyarrhythmias. [source]

Successful uses of magnesium sulfate for torsades de pointes in children with long QT syndrome

PEDIATRICS INTERNATIONAL, Issue 2 2006
KENJI HOSHINO
Abstract Background: Administration of magnesium sulfate (MgSO4) is an effective and safe treatment for torsades de pointes (TdP) associated with acquired long QT syndrome (LQTS) in adults. As for children, there are few reports focusing on it. The authors discuss the efficacy of MgSO4 for TdP in children with congenital and acquired LQTS. The authors also discuss the optimal administration dosage and serum magnesium (SMg) concentration during MgSO4 therapy. Methods: The authors studied seven consecutive LQTS children undergoing MgSO4 therapy for TdP. Of the seven children, five were congenital LQTS and two were acquired LQTS. A bolus injection of MgSO4 was given intravenously over 1,2 min followed by continuous infusion for the next 2,7 days. Results: Of the seven patients, six responded completely to the initial bolus. The bolus dosage was 5.9 ± 3.8 mg/kg (range, 2.3,12 mg/kg) in these six, and the other remaining one (neonate with congenital LQTS) required a total of 30 mg/kg until complete abolishment. The continuous infusion was given at rates of 0.3,1.0 mg/kg per h and patients did not show recurrence of TdP. The SMg concentration was 3.9 ± 1.0 mg/dL (2.9,5.4 mg/dL) immediately after bolus injection. The mean corrected QT (QTc) interval before and after bolus injection did not show significant difference. Conclusion: Intravenous infusion of MgSO4 was effective for TdP in children with LQTS, and MgSO4 abolished TdP without shortening the QTc interval. The optimal bolus dosage, infusion rates and SMg concentration were 3,12 mg/kg, 0.5,1.0 mg/kg per h and 3,5 mg/dL, respectively. [source]

A comparison of the effect on QT interval between thiamylal and propofol during anaesthetic induction,

ANAESTHESIA, Issue 7 2010
U. Higashijima
Summary The aim of this study was to determine the effect of thiamylal and propofol on heart rate-corrected QT (QTc) interval during anaesthetic induction. We studied 50 patients undergoing lumbar spine surgery. Patients were administered 3 ,g.kg,1 fentanyl and were randomly allocated to receive 5 mg.kg,1 thiamylal or 1.5 mg.kg,1 propofol as an induction agent. Tracheal intubation was performed after vecuronium administration. Heart rate, mean arterial pressure, bispectral index score, and 12-lead electrocardiogram were recorded at the following time points: just before (T1) and 2 min after (T2) fentanyl administration; 2 min after anaesthetic administration (T3); 2.5 min after vecuronium injection (T4); and 2 min after intubation (T5). Thiamylal prolonged (p < 0.0001), but propofol shortened (p < 0.0001), the QTc interval. [source]

Influence of promethazine on cardiac repolarisation: a double-blind, midazolam-controlled study

ANAESTHESIA, Issue 6 2009
R. Owczuk
Summary Drugs used in anaesthesia may provoke torsadogenic changes in cardiac repolarisation. The aim of this study was to assess the effect of promethazine on the parameters of ventricular repolarisation: QTc interval and transmural dispersion of repolarisation. Forty patients were randomly allocated to receive promethazine (25 mg) or midazolam (2.5 mg). Changes in the ECG and arterial blood pressure were recorded. Correction of QT interval was calculated using Bazett's formula and Fridericia's correction; transmural dispersion of repolarisation was determined as Tpeak,Tend time. Significant prolongation of QT interval, corrected with both formulae, was detected in patients receiving promethazine, while no change in the QTc value was observed in the midazolam group. There were no significant differences in Tpeak,Tend time either between or within the groups. In conclusion, promethazine induces significant QTc prolongation but the lack of influence on transmural dispersion of repolarisation makes the risk of its torsadogenic action very low. [source]

The effect of esmolol on the QTc interval during induction of anaesthesia in patients with coronary artery disease

ANAESTHESIA, Issue 3 2009
F. Erdil
Summary The aim of this study was to evaluate whether esmolol has an effect on QT interval during induction of anaesthesia using etomidate and fentanyl in patients with known coronary artery disease. Sixty patients were prospectively randomised to either a control group or the esmolol group. Esmolol was administered as a bolus 1 mg.kg,1, followed by a continuous infusion at 250 ,g.kg,1min,1. All patients received etomidate 0.3 mg.kg,1 and fentanyl 15 ,g.kg,1. The ECG was recorded prior to induction of anaesthesia (T0), 5 min following the start of drug infusions (T1), 1 min following etomidate (T2), 3 min following vecuronium (T3), 30 s (T4), 2 min (T5) and 4 min (T6) after intubation. In the esmolol group, QTc interval was significantly shorter at T1, T2 and T4 compared to the control group (p < 0.05). In conclusion, QTc interval increased following tracheal intubation during induction of anaesthesia using etomidate and fentanyl. An infusion of Esmolol attenuated the QTc interval prolongation associated with tracheal intubation. [source]

Familial Aggregation and Heritability of Electrocardiographic Intervals and Heart Rate in a Rural Chinese Population

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009
Jianping Li M.D., Ph.D.
Background: Estimates of the genetic influences on electrocardiographic (ECG) parameters are inconsistent in previous reports, and no such studies have been performed in China. So we estimated genetic contributions to PR and QRS intervals and the rate-adjusted QT interval (Bazett's QTc) in a Chinese rural population. Methods: A total of 2909 subjects from 847 families were enrolled in the current study. Genetic contributions to ECG parameters were estimated in two ways: correlation coefficients among family members (father-mother, parent-offspring, first sibling-other sibling) and the heritability of each of the ECG parameters. Results: Our results showed significant correlations among family members on theses parameters: the correlation coefficients for PR interval, QRS duration, QTc interval, and HR, between parent-sibling, and sibling-sibling were 0.17 and 0.13, 0.18 and 0.23, 0.22 and 0.28, 0.19 and 0.18, respectively. The heritability for PR interval, QRS duration, QTc interval, and HR were estimated as 0.34, 0.43, 0.40, and 0.34, respectively. Conclusion: Genetic factors, together with the environmental and other cofactors contribute no more than 60% to the variance of the ECG intervals, supporting the concept that multiple factors, including gene-gene and gene-environment interactions could influence ECG interval phenotypes, and genetic factors play a major role. [source]

Short QT Interval: A Novel Predictor of Androgen Abuse in Strength Trained Athletes

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009
Mohammad Ali Babaee Bigi M.D.
Objectives: To find the relationship between anabolic androgenic steroids (AAS) using and QT interval in athletes. Methods: Between January 1, 2005 and May 31, 2007, we examined QTc interval duration in 165 consecutive male professional bodybuilders [age: 32.1 ± 4.6 years]. Of these, 79 were AAS users. The control group included 90 sedentary age and gender matched subjects [none of them were AAS users]. Results: The QTc interval of AAS abusing bodybuilders was significantly shorter compared with QTc interval in AAS-free bodybuilders and control group. Short QTc interval (,380 ms) was an independent predictor of AAS abusing in the multivariate analysis. Conclusions: To the best of our knowledge, there is no published report regarding electrocardiographic diagnosis and screening of AAS abusing athletes. In the present study, we present an easy and applicable method to screen and diagnose AAS abusing among professional bodybuilders. In the presence of QTc interval , 380 ms in a bodybuilder, one would predict AAS abusing with 83% sensitivity and 88% specificity. [source]

Impact of QT Variables on Clinical Outcome of Genotyped Hypertrophic Cardiomyopathy

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009
Katsuharu Uchiyama M.D.
Background: Although QT variables such as its interval and/or dispersion can be clinical markers of ventricular tachyarrhythmia, few data exist regarding the role of QT variables in genotyped hypertrophic cardiomyopathy (HCM). Therefore, we analyzed QT variables in genotyped subjects with or without left ventricular hypertrophy (LVH). Methods: QT variables were analyzed in 111 mutation and 43 non-mutation carriers who were divided into three groups: A, those without ECG abnormalities and echocardiographically determined LVH (wall thickness ,13 mm); B, those with ECG abnormalities but LVH; and C, those with ECG abnormalities and LVH. We also examined clinical outcome of enrolled patients. Results: Maximal LV wall thickness in group C (19.0 ± 4.3 mm, mean ±SD) was significantly greater than that in group A (9.2 ± 1.8) and group B (10.4 ± 1.8). Under these conditions, maximum QTc interval and QT dispersion were significantly longer in group C than those in group A (438 ± 38 ms vs 406 ± 30 and 64 ± 31 vs 44 ± 18, respectively; P < 0.05). QTc interval and QT dispersion in group B (436 ± 50 and 64 ± 22 ms) were also significantly greater than those in group A. During follow-up periods, four sudden cardiac deaths and one ventricular fibrillation were observed in group C, and two nonlethal ventricular tachyarrhythmias were observed in group B. Conclusions: Patients with HCM-related gene mutation accompanying any ECG abnormalities frequently exhibited impaired QT variables even without LVH. We suggest that careful observation should be considered for those genotyped subjects. [source]

Relationship between Genetic Variants in Myocardial Sodium and Potassium Channel Genes and QT Interval Duration in Diabetics: The Diabetes Heart Study

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009
Allison B. Lehtinen Ph.D.
Background: Genetic variants in myocardial sodium and potassium channel genes are associated with prolonged QT interval and increased risk of sudden death. It is unclear whether these genetic variants remain relevant in subjects with underlying conditions such as diabetes that are associated with prolonged QT interval. Methods: We tested single nucleotide polymorphisms (SNPs) in five candidate genes for association with QT interval in a family-based study of subjects with type 2 diabetes mellitus (T2DM). Thirty-six previously reported SNPs were genotyped in KCNQ1, HERG, SCN5A, KCNE1, and KCNE2 in 901 European Americans from 366 families. The heart rate-corrected (QTc) durations were determined using the Marquette 12SL program. Associations between the QTc interval and the genotypes were evaluated using SOLAR adjusting for age, gender, T2DM status, and body mass index. Results: Within KCNQ1 there was weak evidence for association between the minor allele of IVS12 +14T>C and increased QTc (P = 0.02). The minor allele of rs2236609 in KCNE1 trended toward significance with longer QTc (P = 0.06), while the minor allele of rs1805123 in HERG trended toward significance with shorter QTc (P = 0.07). However, no statistically significant associations were observed between the remaining SNPs and QTc variation. Conclusions: We found weak evidence of association between three previously reported SNPs and QTc interval duration. While it appears as though genetic variants in previously identified candidate genes may be associated with QT duration in subjects with diabetes, the clinical implications of these associations in diabetic subjects at high risk for sudden death remain to be determined. [source]

Electrocardiographic Alterations during Hyperinsulinemic Hypoglycemia in Healthy Subjects

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2008
Tomi Laitinen M.D.
Background: We evaluated the arrhythmogenic potential of hypoglycemia by studying electrocardiographic (ECG) changes in response to hyperinsulinemic hypoglycemia and associated sympathoadrenal counterregulatory responses in healthy subjects. Methods: The study population consisted of 18 subjects, aged 30,40 years. Five-minute ECG recordings and blood samplings were performed at baseline and during the euglycemic and hypoglycemic hyperinsulinemic clamp studies. PR, QT, and QTc intervals of electrocardiogram and ECG morphology were assessed from signal-averaged ECG. Results: Although cardiac beat interval remained unchanged, PR interval decreased (P < 0.01) and QTc interval (P < 0.001) increased in response to hyperinsulinemic hypoglycemia. Concomitant morphological alterations consisted of slight increases in R-wave amplitude and area (P < 0.01 for both), significant decreases in T-wave amplitude and area (P < 0.001 for both), and moderate ST depression (P < 0.001). Counterregulatory norepinephrine response correlated with amplification of the R wave (r =,0.620, P < 0.05) and epinephrine response correlated with flattening of the T wave (r =,0.508, P < 0.05). Conclusions: Hyperinsulinemic hypoglycemia with consequent sympathetic humoral activation is associated with several ECG alterations in atrioventricular conduction, ventricular depolarization, and ventricular repolarization. Such alterations in cardiac electrical function may be of importance in provoking severe arrhythmias and "dead-in-bed" syndrome in diabetic patients with unrecognized hypoglycemic episodes. [source]

An Evaluation of the Impact of Oral Magnesium Lactate on the Corrected QT Interval of Patients Receiving Sotalol or Dofetilide to Prevent Atrial or Ventricular Tachyarrhythmia Recurrence

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2006
Brian F. McBride Pharm.D.
Background: Intravenous magnesium reduces the QTc interval of patients receiving ibutilide. Whether oral magnesium can reduce the QTc interval associated with oral sotalol and dofetilide is not known. This study was undertaken to evaluate the impact of oral magnesium on the QTc interval and whether an inherent intracellular magnesium deficiency exists among patients with arrhythmias. Methods: Participants receiving sotalol or dofetilide for atrial or ventricular arrhythmias were randomized to receive magnesium l -lactate (504 mg elemental magnesium daily, Niche Pharmaceuticals, Roanoke, TX) or placebo for 48 hours. A 12-lead electrocardiogram (ECG) was obtained at baseline, 3 hours, and 51 hours after dosing to correspond to the Tmax after oral ingestion. The QTc interval was measured from the ECGs and compared between groups. Intracellular magnesium concentrations were determined by energy-dispersive x-ray analysis at baseline and 51 hours after dosing (Intracellular Diagnostics, Inc., Foster City, CA). Results: The QTc interval reductions from baseline were greater in the magnesium group than placebo at 3 and 51 hours (P = 0.015 and P < 0.001, respectively). Sixty-three percent of patients (regardless of experimental group) had baseline intracellular magnesium concentrations below the normal reference range of 33.9,41.9 mEq/IU, with an average level of 32.6 ± 2.2 mEq/IU. Conclusions: Oral magnesium l -lactate raises intracellular magnesium concentrations and lowers the QTc interval of patients receiving sotalol or dofetilide. [source]

QT Dispersion and Mortality in the Elderly

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

Prognostic Significance of QTc Interval for Predicting Total, Cardiac, and Ischemic Heart Disease Mortality in Community-Based Cohort from Warsaw Pol-MONICA Population

A prospective open-label treatment trial of ziprasidone monotherapy in children and adolescents with bipolar disorder

BIPOLAR DISORDERS, Issue 8 2007
Joseph Biederman
Objective:, To assess the effectiveness and tolerability of ziprasidone for treating pediatric mania. Methods:, This was an eight-week, open-label, prospective study of ziprasidone monotherapy (57.3 ± 33.9 mg/day) in 21 bipolar youth [manic, mixed, or bipolar not otherwise specified (NOS); 6,17 years old]. Assessments included the Young Mania Rating Scale (YMRS), Clinical Global Impressions-Improvement scale (CGI-I), and Brief Psychiatric Rating Scale (BPRS). Adverse events were assessed through spontaneous self-reports, vital signs, weight monitoring, and laboratory analysis. Results:, Fourteen of the 21 youth (67%) completed the study. Ziprasidone treatment was associated with clinically and statistically significant improvement in mean YMRS scores (,10.8 ± 8.4, p < 0.0001) and 57% had a CGI-I ,2 at endpoint. Ziprasidone was well tolerated with no statistically significant increase in body weight (0.6 ± 0.4 kg, p = 0.2) or QTc interval (,3.7 ± 4.7, p = 0.5). Conclusions:, Open-label ziprasidone treatment was associated with a significant short-term improvement of symptoms of pediatric bipolar disorder. Future placebo-controlled, double-blind studies are warranted. [source]

Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjects

BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 3 2008
Ruth Dixon
WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Drugs that inhibit the human cardiac delayed rectifier potassium current may lead to prolongation of the cardiac QT interval and are associated with a fatal, polymorphic, ventricular tachycardia known as torsades de pointes. , Lamotrigine is indicated in the treatment of epilepsy and the prevention of mood episodes in patients with bipolar disorder. , Lamotrigine inhibits the human cardiac delayed rectifier potassium current in vitro, and it has been hypothesized that QT prolongation may contribute to the risk of sudden unexpected death in epilepsy patients. WHAT THIS STUDY ADDS , This is the first reported thorough QT/QTc study with lamotrigine conducted to International Conference on Harmonization guidelines. , The mean QTc interval was not prolonged by lamotrigine in healthy subjects, as assessed by the standard heart rate correction methods (Fridericia's and Bazett's). , The in vitro inhibition of the delayed rectifier potassium current does not translate into an effect on QT in man. AIM To characterize the effects of lamotrigine on QT interval in healthy subjects. METHODS Healthy subjects received a single oral dose of moxifloxacin (400 mg) or placebo in crossover design, followed by a dose-escalating regimen of lamotrigine (n = 76) over a 77-day period, or matched placebo (n = 76). Blood samples were taken for determination of moxifloxacin and lamotrigine concentrations and digital 12-lead ECGs were recorded. The relationships between individual QT values and respective individual moxifloxacin or lamotrigine concentrations were explored using population pharmacokinetic,pharmacodynamic (PK,PD) modelling. RESULTS Moxifloxacin was associated with a maximum mean increase from baseline in QTcF of 14.81 ms [90% confidence interval (CI) 13.50, 16.11] 2.5 h after dosing. Steady-state exposure to lamotrigine (50, 150 or 200 mg b.d.) was not associated with an increase in QTc interval. Small reductions in QTcF (maximum mean difference from placebo ,7.48 ms, 90% CI ,10.49, ,4.46) and small increases in heart rate (maximum mean difference from placebo 5.94 bpm, 90% CI 3.81, 8.06) were observed with lamotrigine 200 mg b.d. vs. placebo. No effect of lamotrigine on QRS duration or blood pressure was observed. No outliers with QTcF > 450 ms, or with an increase from baseline of >60 ms were observed in the lamotrigine group. PK,PD modelling indicated statistically significant decreases in individually corrected QT intervals for lamotrigine and statistically significant increases in individually corrected QT intervals for moxifloxacin over the concentration ranges studied. CONCLUSIONS Therapeutic doses of lamotrigine (50,200 mg b.d.) were not associated with QT prolongation in healthy subjects. [source]