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QT Duration (qt + duration)
Selected AbstractsThe effect of sertindole on QTD and TPTEACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2010J. 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] QT interval is prolonged but QT dispersion is maintained in patients with primary aldosteronismINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 3 2007T.-Y. Yang Summary The relationship between QT duration and its dispersion in patients with primary hyperaldosteronism is not clearly known. We studied 26 patients (nine males and 17 females) with primary hyperaldosteronism. The serum potassium levels were low (2.32 ± 0.52 mmol/l), did not correlate with serum renin or aldosterone levels, or aldosterone/renin ratio (ARR). The maximum QT intervals (QTmax) were prolonged (502 ± 62 ms), correlated well with ARRs (p = 0.005) and aldosterone levels (p = 0.019), but not to renin (p = 0.517) or potassium levels (p = 0.196). The QT dispersions (QTd) were small (60 ± 28.8 ms) and did not correlate with potassium, renin or aldosterone levels. QTmax but not QTd correlate with aldosterone levels in patients with primary aldosteronism. The maintenance of repolarisation homogeneity with relatively unchanged QT dispersion may contribute to our understanding of the clinical observation that ventricular tachydysrhythmia is rare among patients with primary aldosteronism. [source] The L-Type Ca2+ and KATP Channels May Contribute to Pacing-Induced Protection Against Anoxia-Reoxygenation in the Embryonic Heart ModelJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2008PHILIPPE BRUCHEZ M.D. Aims: The L-type Ca2+ channel, the sarcolemmal (sarcKATP), and mitochondrial KATP (mitoKATP) channels are involved in myocardial preconditioning. We aimed at determining to what extent these channels can also participate in pacing-induced cardioprotection. Methods: Hearts of 4-day-old chick embryos were paced in ovo during 12 hour using asynchronous intermittent ventricular stimulation at 110% of the intrinsic rate. Sham operated and paced hearts were then submitted in vitro to anoxia (30 minutes) and reoxygenation (60 minutes). These hearts were exposed to L-type Ca2+ channel agonist Bay-K-8644 (BAY-K) or blocker verapamil, nonselective KATP channel antagonist glibenclamide (GLIB), mitoKATP channel agonist diazoxide (DIAZO), or antagonist 5-hydroxydecanoate. Electrocardiogram, electromechanical delay (EMD) reflecting excitation-contraction (E-C) coupling, and contractility were determined. Results: Under normoxia, heart rate, QT duration, conduction, EMD, and ventricular shortening were similar in sham and paced hearts. During reoxygenation, arrhythmias ceased earlier and ventricular EMD recovered faster in paced hearts than in sham hearts. In sham hearts, BAY-K (but not verapamil), DIAZO (but not 5-hydroxydecanoate) or GLIB accelerated recovery of ventricular EMD, reproducing the pacing-induced protection. By contrast, none of these agents further ameliorated recovery of the paced hearts. Conclusion: The protective effect of chronic asynchronous pacing at near physiological rate on ventricular E-C coupling appears to be associated with subtle activation of L-type Ca2+ channel, inhibition of sarcKATP channel, and/or opening of mitoKATP channel. [source] QT Interval Variability and Adaptation to Heart Rate Changes in Patients with Long QT SyndromePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2009JAN N, MEC M.D. Background: Increased QT variability (QTV) has been reported in conditions associated with ventricular arrhythmias. Data on QTV in patients with congenital long QT syndrome (LQTS) are limited. Methods: Ambulatory electrocardiogram recordings were analyzed in 23 genotyped LQTS patients and in 16 healthy subjects (C). Short-term QTV was compared between C and LQTS. The dependence of QT duration on heart rate was evaluated with three different linear models, based either on the RR interval preceding the QT interval (RR0), the RR interval preceding RR0 (RR -1), or the average RR interval in the 60-second period before QT interval (mRR). Results: Short-term QTV was significantly higher in LQTS than in C subjects (14.94 ± 9.33 vs 7.31 ± 1.29 ms; P < 0.001). It was also higher in the non-LQT1 than in LQT1 patients (23.00 ± 9.05 vs 8.74 ± 1.56 ms; P < 0.001) and correlated positively with QTc in LQTS (r = 0.623, P < 0.002). In the C subjects, the linear model based on mRR predicted QT duration significantly better than models based on RR0 and RR -1. It also provided better fit than any nonlinear model based on RR0. This was also true for LQT1 patients. For non-LQT1 patients, all models provided poor prediction of QT interval. Conclusions: QTV is elevated in LQTS patients and is correlated with QTc in LQTS. Significant differences with respect to QTV exist among different genotypes. QT interval duration is strongly affected by noninstantaneous heart rate in both C and LQT1 subjects. These findings could improve formulas for QT interval correction and provide insight on cellular mechanisms of QT adaptation. [source] Ventricular Dyssynchrony and Risk Markers of Ventricular Arrhythmias in Nonischemic Dilated Cardiomyopathy:PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003A Study with Phase Analysis of Angioscintigraphy FAUCHIER, L.,et al.: Ventricular Dyssynchrony and Risk Markers of Ventricular Arrhythmias in Nonischemic Dilated Cardiomyopathy: A Study with Phase Analysis of Angioscintigraphy.Biventricular pacing is a new form of treatment for patients with dilated cardiomyopathy and ventricular dyssynchrony. Limited information is available regarding the relationship between ventricular dyssynchrony and risk markers of ventricular arrhythmias in idiopathic dilated cardiomyopathy (IDC). In 103 patients with IDC, Fourier phase analysis of both ventricles was performed from equilibrium radionuclide angiography (ERNA). The difference between the mean phase of the LV and RV was a measure of interventricular dyssynchrony, and the standard deviations of the mean phases in each ventricle measured intraventricular dyssynchrony. There were no significant differences in inter- and intraventricular dyssynchrony between patients with versus without histories of sustained VT or VF, nonsustained VT, abnormal signal-averaged ECG, or induced sustained monomorphic VT. Dyssynchrony was not related to decreased heart rate variability (HRV). LV and interventricular dyssynchrony were weakly related to QT duration and QT dispersion. During a follow-up of27 ± 23 months, 21 patients had major adverse cardiac events (MACE), including 7 cardiac deaths, 11 progression of heart failure leading to cardiac transplantation, and 3 sustained VT/VF. The only independent predictors of MACE were an increased standard deviation of LV mean phase (P = 0.003), a decreased HRV (standard deviation of normal-to-normal intervals, P = 0.004), and histories of previous VT/VF (P = 0.03) or nonsustained VT (P = 0.04). In conclusion, left intraventricular dyssynchrony evaluated with ERNA was an independent predictor of MACE in IDC and was not related to usual risk markers of ventricular arrhythmias. This may have implications for resynchronization therapy and/or the use of implantable cardioverter defibrillators in IDC. (PACE 2003; 26[Pt. II]:352,356) [source] Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial InfarctionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001PAULUS KIRCHHOF KIRCHHOF P., et al.: Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial Infarction. QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2,3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%,15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 ± 7 vs 78 ± 1 ms, JT disp 80 ± 6 vs 79 ± 2 ms, mean ± SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction. [source] Steady-State versus Non-Steady-State QT-RR Relationships in 24-hour Holter RecordingsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000GILLES LANDE The aim of the present study was to investigate the QT-RR interval relationship in ambulatory ECG recordings with special emphasis on the physiological circumstances under which the QT-RR intervals follow a linear relation. Continuous ECG recordings make it possible to automatically measure QT duration in individual subjects under various physiological circumstances. However, identification of QT prolongation in Holter recordings is hampered by the rate dependence of QT duration. Comparison of QT duration and QT interval rate dependence between different individuals implies that the nature of the QT-RR relationship is defined in ambulatory ECG. Holter recordings were performed in healthy volunteers at baseline and after administration of dofetilide, a Class III antiarrhythmic drug. After dofetilide, beat-to-beat automated QT measurements on Holter tapes were compared with manually measured QT intervals on standard ECGs matched by time. The QT-RR relationship was analyzed at baseline in individual and group data during three different periods: 24-hour, daytime, and nighttime. Data were collected under steady-state or non-steady-state conditions of cycle length and fitted with various correction formulae. Our study demonstrated an excellent agreement between manually and automated measurements. The classic Bazett correction formula did not fit the QT-RR data points in individual or group data. When heart beats were selected for a steady rhythm during the preceding minute, QT-RR intervals fit a linear relationship during the day and night periods, but not during the 24-hour period in both individual and group data. In contrast, in the absence of beat selection, data fit a more complex curvilinear relationship irrespective of the period. Our study provides the basis for comparison of QT interval durations and QT-RR relationships between individuals and between groups of subjects. [source] Relationship between Genetic Variants in Myocardial Sodium and Potassium Channel Genes and QT Interval Duration in Diabetics: The Diabetes Heart StudyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009Allison 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] Methodology of QT-Interval Measurement in the Modular ECG Analysis System (MEANS)ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2009Jan A. Kors Ph.D. Background: QT prolongation as can be induced by drugs, signals the risk of life-threatening arrhythmias. The methodology of QT measurement in the modular ECG analysis system (MEANS) is described. Methods: In the simultaneously recorded leads of the standard 12-lead electrocardiogram (ECG), the QRS complexes are detected by a spatial velocity function. They are typed as dominant or nondominant, and a representative complex per lead is obtained by averaging over the dominant complexes. QRS onset and T end are determined by a template technique, and QT is measured. MEANS performance was evaluated on the 125 ECGs of the common standards for quantitative electrocardiography (CSE) multilead database, of which the waveform boundaries have been released. Results: MEANS detected correctly all 1445 complexes of the CSE library, with one false-positive detection due to a sudden baseline jump. All dominant complexes were correctly typed. The average of the differences between MEANS and reference was less than 2 ms (=1 sample) for both QRS onset and T end, and 2.1 ms for QT duration. The standard deviation of the differences was 3.8, 8.4, and 10.4 ms, respectively. Conclusions: A standard deviation of 10.4 ms for QT measurement seems large when related to the regulatory requirement that a prolongation as small as 5 ms should be detected. However, QT variabilities as encountered in different individuals will be larger than when measured in one individual during pharmacological intervention. Finally, if the U wave is part of the total repolarization, then T and U form a continuum and the end of T becomes questionable. [source] ECG Evaluation of Ventricular Properties: The Importance of Cardiac Cycle LengthANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2009Fabrice Extramiana M.D., Ph.D. Ventricular repolarization properties are dependent on cardiac cycle length. The aim of this article is to emphasize the importance of taking into account heart rate influences on QT duration but also on current and future T-wave morphology parameters. The relationship between QT interval duration and RR interval is a fundamental property of the myocardium that is impaired by the presence of channelopathies such as the LQTS or SQTS, but also by the presence of a cardiomyopathy. Assessing this property is also important when the individual QT/RR relationship is used for individual QT correction in the setting of evaluation of drugs' effect on QT duration. T-wave descriptors such as the relative weight of the terminal part of the T-wave, the amplitude of T-wave apex and Principal Component Analysis parameters are also dependent on heart rate. Assessing ventricular repolarisation ECG parameters at different heart rates avoids the need for difficult rate-correction and helps to better understand and characterize ventricular repolarisation properties. [source] Dynamics of Ventricular Repolarization in Patients with Dilated Cardiomyopathy Versus Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2005Jose Luis Alonso M.D. Background: Patients with impaired left ventricular function have a high risk of developing ventricular arrhythmias and sudden death. Among different markers of risk, the prolongation and regional heterogeneity of repolarization are of increasing interest. However, there are limited data regarding feasibility of analyzing repolarization parameters and their dynamics in 24-hour Holter ECG recordings. Methods: Dynamic behavior of repolarization parameters was studied with a new automatic algorithm in digital 24-hour Holter recordings of 60 healthy subjects and 55 patients with idiopathic dilated cardiomyopathy (IDC). Repolarization parameters included the mean value of QT and QTc durations, QT dispersion, and peaks of QT duration and QT dispersion above prespecified thresholds. Results: In comparison to healthy subjects, patients with IDC had lower heart rate variability, longer mean QT and QTc durations, higher content of QTc peaks >500 ms, longer QT dispersion and its standard deviation, and a higher content of peaks >100 ms of QT dispersion (P < 0.01 for all comparisons). These repolarization parameters were significantly higher in IDC patients after adjustment for age, sex, and heart rate variability. The parameters of repolarization dynamics correlated with SDNN in healthy subjects but not in dilated cardiomyopathy patients. Conclusions: The automatic assessment of repolarization parameters in 24-hour digital ECG recordings is feasible and differentiates dilated cardiomyopathy patients from healthy subjects. Patients with dilated cardiomyopathy have increased QT duration, QT dispersion, and increased variability of QT dispersion reflecting variations in T-wave morphology, the factors which might predispose them to the development of arrhythmic events. 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