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Repolarization Heterogeneity (repolarization + heterogeneity)

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Medical Sciences100%

Selected Abstracts

Validation of ECG Indices of Ventricular Repolarization Heterogeneity: A Computer Simulation Study

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2005
BART HOOFT VAN HUYSDUYNEN M.D.
Introduction: Repolarization heterogeneity (RH) is functionally linked to dispersion in refractoriness and to arrhythmogenicity. In the current study, we validate several proposed electrocardiogram (ECG) indices for RH: T-wave amplitude, -area, -complexity, and -symmetry ratio, QT dispersion, and the Tapex-end interval (the latter being an index of transmural dispersion of the repolarization (TDR)). Methods and Results: We used ECGSIM, a mathematical simulation model of ECG genesis in a human thorax, and varied global RH by increasing the standard deviation (SD) of the repolarization instants from 20 (default) to 70 msec in steps of 10 msec. T-wave amplitude, -area, -symmetry, and Tapex-end depended linearly on SD. T-wave amplitude increased from 275 ± 173 to 881 ± 456 ,V, T-wave area from 34 × 103± 21 × 103 to 141 × 103± 58 × 103,V msec, T-wave symmetry decreased from 1.55 ± 0.11 to 1.06 ± 0.23, and Tapex-end increased from 84 ± 17 to 171 ± 52 msec. T-wave complexity increased initially but saturated at SD = 50 msec. QT dispersion increased modestly until SD = 40 msec and more rapidly for higher values of SD. TDR increased linearly with SD. Tapex-end increased linearly with TDR, but overestimated it. Conclusion: T-wave complexity did not discriminate between differences in larger RH values. QT dispersion had low sensitivity in the transitional zone between normal and abnormal RH. In conclusion, T-wave amplitude, -area, -symmetry, and, with some limitations, Tapex-end and T-wave complexity reliably reflect changes in RH. [source]

QT Dispersion Does Not Represent Electrocardiographic Interlead Heterogeneity of Ventricular Repolarization

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000
MAREK MALIK Ph.D.
QT Dispersion and Repolarization Heterogeneity. Introduction: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals. Methods and Results: Seventy-eight normal subjects (47 ± 16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38 ± 15 years. 21 women), 72 dilated cardiomyopathy patients (DCM; 48 ± 15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63 ± 12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). OTd was 33.6 ± 18.3, 47.0 ± 19.3, 34.8 ± 21.2, and 57.5 ± 25.3 msec in normals, HCM, CM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%± 0.031%, 0.067%± 0.067%, 0.112%± 0.154%, and 0.186%± 0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS. other P < 0.006), The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. Conclusion: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it. [source]

Left Ventricular Mass Is Associated With Ventricular Repolarization Heterogeneity One Year After Renal Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2008
M. Arnol
Ventricular repolarization heterogeneity (VRH) is associated with the risk of arrhythmia and cardiac death. This study investigated the association between VRH and left ventricular mass (LVM) in renal transplant recipients 1 year after transplantation. Echocardiography and 5-min 12-lead electrocardiogram were recorded and GFR was estimated (eGFR) in 68 nondiabetic patients. Beat-to-beat QT interval variability algorithm was used to calculate SDNN-QT and rMSSD-QT indices of VRH. To quantify QT interval variability relative to heart rate fluctuations, QTRR index was calculated. Left ventricular hypertrophy (LVH) was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m2 compared with 40 patients with eGFR ,60 mL/min/1.73 m2 (248 ± 61 g and 86% vs. 210 ± 46 g and 50%, respectively; p < 0.01). A direct correlation was found between LVM and SDNN-QT (R = 0.47, R2= 0.23; p < 0.001), rMSSD-QT (R = 0.27; R2= 0.10; p = 0.034), and QTRR (R = 0.55; R2= 0.31; p < 0.001) indices. In conclusion, greater LVM is associated with increased VRH in renal transplant recipients, providing a link with the high risk of arrhythmia and cardiac death, specifically in patients with decreased graft function. [source]

Validation of ECG Indices of Ventricular Repolarization Heterogeneity: A Computer Simulation Study

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2005
BART HOOFT VAN HUYSDUYNEN M.D.
Introduction: Repolarization heterogeneity (RH) is functionally linked to dispersion in refractoriness and to arrhythmogenicity. In the current study, we validate several proposed electrocardiogram (ECG) indices for RH: T-wave amplitude, -area, -complexity, and -symmetry ratio, QT dispersion, and the Tapex-end interval (the latter being an index of transmural dispersion of the repolarization (TDR)). Methods and Results: We used ECGSIM, a mathematical simulation model of ECG genesis in a human thorax, and varied global RH by increasing the standard deviation (SD) of the repolarization instants from 20 (default) to 70 msec in steps of 10 msec. T-wave amplitude, -area, -symmetry, and Tapex-end depended linearly on SD. T-wave amplitude increased from 275 ± 173 to 881 ± 456 ,V, T-wave area from 34 × 103± 21 × 103 to 141 × 103± 58 × 103,V msec, T-wave symmetry decreased from 1.55 ± 0.11 to 1.06 ± 0.23, and Tapex-end increased from 84 ± 17 to 171 ± 52 msec. T-wave complexity increased initially but saturated at SD = 50 msec. QT dispersion increased modestly until SD = 40 msec and more rapidly for higher values of SD. TDR increased linearly with SD. Tapex-end increased linearly with TDR, but overestimated it. Conclusion: T-wave complexity did not discriminate between differences in larger RH values. QT dispersion had low sensitivity in the transitional zone between normal and abnormal RH. In conclusion, T-wave amplitude, -area, -symmetry, and, with some limitations, Tapex-end and T-wave complexity reliably reflect changes in RH. [source]

Evidences of the gender-related differences in cardiac repolarization and the underlying mechanisms in different animal species and human

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2006
Jianhua Cheng
Abstract Clinical and experimental studies have shown that gender differences exist in cardiac repolarization in various animal species and human, as is evidenced by significantly longer QT, JT intervals and action potential duration in females than in males due to a reduced repolarization reserve in females. The latter is shown by the relatively greater increase in ventricular repolarization and higher incidence of torsades de pointes (TdP) in preparations from females by drugs blocking repolarizing K+ currents. These results can be modulated by gonadectomy, suggesting that gonadal steroids are important determinants of gender difference in repolarization. In human subjects, QT and JT intervals are longer in women, whereas QT dispersion and Tp-e interval (the interval from the peak to the end of T wave) are longer in men. At slow heart rates greater prolongation in QT and increase in transmural repolarization heterogeneity (i.e. increase in Tp-e) may predispose to TdP tachycardias in women. In healthy postmenopausal women, hormone replacement therapy with estrogen alone usually produced a prolongation of QT interval, while estrogen plus progesterone had no significant effects on QT interval but reduced QT dispersion. Along with these, there are still conflicting data reported. Further work is needed before the elucidation of the basis of gender differences in ventricular repolarization. [source]

Transmural Action Potential Repolarization Heterogeneity Develops Postnatally in the Rabbit

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2004
Ph.D., SALIM F. IDRISS M.D.
Introduction: In the hereditary long QT syndrome, arrhythmia risk changes with age despite the presence of an ion channel mutation throughout development. Age-dependent changes in the transmural dispersion of repolarization may modulate this vulnerability. We recorded cardiac action potentials in infant, periadolescent, and adult rabbit myocardium to determine if transmural heterogeneities in repolarization are developmentally determined. Methods and Results: Arterially perfused ventricular preparations were studied from 2-week (n = 7), 7-week (n = 7), and adult (n = 6) NZW rabbits. Action potentials were recorded with microelectrodes in five regions: epicardium (epi), subepicardium (subepi), midwall (mid), subendocardium (subendo), and endocardium (endo) during endocardial S1 pacing at cycle lengths of 2,000, 1,000, and 500 ms. At 2 weeks, the transmural APD90 profile was flat. With age, APD prolongation from subepi to endo created a transmural repolarization gradient. At 7 weeks, APD90 was significantly longer at subendo [204 ± 2 ms (mean ± SE) 2,000-ms cycle length, P < 0.05] vs both endo (193 ± 2 ms) and epi (172 ± 2 ms), causing a heterogeneous transmural APD90 gradient. In adults, the transmural gradient was a smooth continuum such that APD was shortest in epicardium and longest in endocardium. Conclusion: The transmural distribution of APD is developmentally determined. Tissue-specific age-dependent changes in APD can result in transmural repolarization heterogeneity. These age-related effects may modulate arrhythmia vulnerability during development. (J Cardiovasc Electrophysiol, Vol. 15, pp. 795-801, July 2004) [source]

QT Dispersion Does Not Represent Electrocardiographic Interlead Heterogeneity of Ventricular Repolarization

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000
MAREK MALIK Ph.D.
QT Dispersion and Repolarization Heterogeneity. Introduction: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals. Methods and Results: Seventy-eight normal subjects (47 ± 16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38 ± 15 years. 21 women), 72 dilated cardiomyopathy patients (DCM; 48 ± 15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63 ± 12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). OTd was 33.6 ± 18.3, 47.0 ± 19.3, 34.8 ± 21.2, and 57.5 ± 25.3 msec in normals, HCM, CM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%± 0.031%, 0.067%± 0.067%, 0.112%± 0.154%, and 0.186%± 0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS. other P < 0.006), The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. Conclusion: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it. [source]

Left Ventricular Mass Is Associated With Ventricular Repolarization Heterogeneity One Year After Renal Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2008
M. Arnol
Ventricular repolarization heterogeneity (VRH) is associated with the risk of arrhythmia and cardiac death. This study investigated the association between VRH and left ventricular mass (LVM) in renal transplant recipients 1 year after transplantation. Echocardiography and 5-min 12-lead electrocardiogram were recorded and GFR was estimated (eGFR) in 68 nondiabetic patients. Beat-to-beat QT interval variability algorithm was used to calculate SDNN-QT and rMSSD-QT indices of VRH. To quantify QT interval variability relative to heart rate fluctuations, QTRR index was calculated. Left ventricular hypertrophy (LVH) was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m2 compared with 40 patients with eGFR ,60 mL/min/1.73 m2 (248 ± 61 g and 86% vs. 210 ± 46 g and 50%, respectively; p < 0.01). A direct correlation was found between LVM and SDNN-QT (R = 0.47, R2= 0.23; p < 0.001), rMSSD-QT (R = 0.27; R2= 0.10; p = 0.034), and QTRR (R = 0.55; R2= 0.31; p < 0.001) indices. In conclusion, greater LVM is associated with increased VRH in renal transplant recipients, providing a link with the high risk of arrhythmia and cardiac death, specifically in patients with decreased graft function. [source]