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QT Dispersion (qt + dispersion)
Selected AbstractsQT Dispersion Does Not Represent Electrocardiographic Interlead Heterogeneity of Ventricular RepolarizationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000MAREK 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] The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2009MUSTAFA HASSAN M.D. Background: An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress-induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia. Objectives: To examine the effects of psychological stress on QT dispersion (QTd) among CAD patients and whether these effects are mediated via the development of myocardial ischemia. Methods: Psychological stress was induced using a public speaking task. Twelve-lead electrocardiograms (ECG) were recorded at rest, during mental stress, and during recovery. QTd was calculated as the difference between the longest and the shortest QT interval in the 12-lead ECG. Rest-stress myocardial perfusion imaging was also performed to detect mental stress-induced myocardial ischemia. Results: Mental stress induced a significant increase in QTd compared to the resting condition (P < 0.001). This effect persisted beyond the first 10 minutes of recovery (P < 0.001). QTd was significantly associated with the development of mental stress ischemia with ischemic patients having significantly higher QTd during mental stress than nonischemic patients (P = 0.006). This finding remained significant after controlling for possible confounding factors (P = 0.01). Conclusion: An acute psychological stress induces a significant increase in QTd, which persists for more than 10 minutes after the cessation of the stressor. This effect seems to be, at least partially, mediated by the development of mental stress-induced myocardial ischemia. [source] Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular HypertrophyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2004Laura Maria Lonati M.D. Objective:,The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. Methods:,A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 ± 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 ± 6.1 years), and 17 normotensive healthy subjects as control group (24.8 ± 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12-lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, ,QT, ,QTc). Results:,There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 ± 45.2/93.5 ± 4.9 mmHg) versus athletes (120.9 ± 10.8/77.1 ± 6.0 mmHg) and controls (123.5 ± 4.8/78.8 ± 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 ± 21.1 g/m2) and hypertensives (117.1 ± 15.2 g/m2) versus controls (81.1 ± 14.5 g/m2; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m2) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (,QT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ,QTc 88 ± 2.0, 47 ± 1.4, 54 ± 2.7; P < 0.01). Conclusions:,LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion. [source] QT Dispersion and Mortality in the ElderlyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2001Juha 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] Hormone Replacement Therapy Shortens QT Dispersion in Healthy Postmenopausal WomenANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2001Aylin Yildirir M.D. Background: The aim of the study was to investigate the effects of hormone replacement therapy (HRT) on myocardial repolarization characteristics in postmenopausal women without coronary artery disease. Methods: Fifty-one consecutive healthy postmenopausal women (age 48 ±; 5) with negative exercise stress testing were prospectively enrolled into the study. Standard 12-lead electrocardiograms were obtained to evaluate the effects of 6 months of HRT on QT intervals, corrected QT intervals (QTcmax and QTcmin), QT dispersion (QTd), and corrected QTd (QTcd). Hormone regimens were continuous 0.625 mg/day conjugated equine estrogen (CEE) plus 2.5 mg/day medroxyprogesterone acetate (MPA) or 0.625 mg/day CEE alone depending on the hysterectomy status. Results: Although not statistically significant, CEE alone or in combination with MPA increased QTmax and QTmin values. However, the increase in QTmin was greater than the increase in QTmax, which resulted in statistically significant shortening of QTd (P = 0.007 in CEE and P < 0.001 in CEE + MPA groups). There was a significant prolongation of QTcmin values after 6 months in patients assigned to the CEE group (P = 0.001). The QTcd values were significantly shortened by HRT with both regimens (for CEE group 49 ±; 13 ms vs 38 ±; 13 ms, P = 0.01; for CEE + MPA group 49 ±; 14 ms vs 36 ±; 13, P < 0.001). Conclusion: HRT significantly decreased the QTd and QTcd in postmenopausal women without coronary artery disease, independent of the addition of MPA to the regimen. This improvement in myocardial repolarization may be one of the mechanisms of the favorable effects of HRT on cardiovascular system. However, the clinical implications of the shortening of QTd in postmenopausal women with HRT must be clarified. A.N.E. 2001; 6(3):193,197 [source] The Effect of Sleep Apnea on QT Interval, QT Dispersion, and ArrhythmiasCLINICAL CARDIOLOGY, Issue 6 2010Kitti Barta MD Background QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. Hypothesis The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. Methods A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. Results Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 ± 34.6 ms, daytime QT interval: 381.6 ± 33.8 ms, 24-hour QT interval: 394.7 ± 31.1 ms). However, during the nighttime QT interval (422.8 ± 14.9 ms), QTd (31.2 ± 11.0 ms) and QT dispersion (30.5 ± 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 ± 14.2 ms, QTd: 28.8 ± 9.4 ms, QTcd: 30.5 ± 9.43 ms) and daytime levels (QTc interval: 423.9 ± 14.3 ms, QTd: 27.3 ± 10.7 ms, QTcd: 29.9 ± 11.1 ms). None of the patients had ventricular arrhythmias. Conclusions QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period. Copyright © 2010 Wiley Periodicals, Inc. [source] The 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] The Relationship Between Left Ventricular Shape and QT Interval DispersionECHOCARDIOGRAPHY, Issue 8 2002F.A.C.C., Kishore J. Harjai M.D. Left ventricular geometry is suspected to affect heterogeneity of myocardial repolarization; therefore, it is plausible but unproven that increased sphericity of the left ventricle is associated with greater QT interval dispersion. In 60 patients with dilated cardiomyopathy with left ventricular ejection fraction , 30%, we found that spherical distortion of the left ventricle was associated with increased QT dispersion, implying increased heterogeneity of myocardial repolarization. [source] Effects of adrenaline and potassium on QTc interval and QT dispersion in manEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2003S. 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] Evidences of the gender-related differences in cardiac repolarization and the underlying mechanisms in different animal species and humanFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2006Jianhua 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] 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] Validation of ECG Indices of Ventricular Repolarization Heterogeneity: A Computer Simulation StudyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2005BART 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 RepolarizationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2000MAREK 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] Acute Effects of Low Doses of Red Wine on Cardiac Conduction and Repolarization in Young Healthy SubjectsALCOHOLISM, Issue 12 2009Matteo Cameli Background:, Moderate to high blood concentrations of ethanol have been shown to yield acute changes in cardiac electrophysiological properties, but the effect of low concentrations have never been assessed. The role of concomitant changes in clinical variables or cardiac dimensions is also still unknown. This study aimed at exploring the acute effects of low doses of ethanol, administered as Italian red wine, on conduction, depolarization, and repolarization electrocardiographic (ECG) intervals in a population of healthy subjects. Methods:, Forty healthy young volunteers drank a low quantity of red wine (5 ml/kg), and an equal volume of fruit juice in separate experiments. Heart rate, P-wave duration, PR interval, QRS duration, QT interval, corrected QT interval, QT dispersion, and corrected QT dispersion were assessed at baseline and after 60 minutes from challenge. Results:, Mean blood ethanol concentration after drinking was 0.48 ± 0.06 g/l. Compared to the control challenge, significant changes after red wine intake were observed in P-wave duration (from 101 ± 11 to 108 ± 14 milliseconds, p = 0.0006), PR interval (from 153 ± 15 to 167 ± 17 milliseconds, p < 0.0001), QT interval (from 346 ± 28 to 361 ± 24 milliseconds, p < 0.0001), and corrected QT interval (from 388 ± 24 to 402 ± 30 milliseconds, p = 0.0006). None of these changes showed correlations with modifications in clinical or echocardiographic variables. In multivariate analyses aimed at exploring predictors of ECG changes, none of the variables entered the final models. Conclusions:, Low doses of red wine acutely slow cardiac conduction and prolong repolarization in normal individuals. These changes are poorly predictable. The potential arrhythmogenic impact of these effects is worthy of exploration. [source] Anterior Mitral Valve Length is Associated with Ventricular Tachycardia in Patients with Classical Mitral Valve ProlapsePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2010MURAT AKCAY M.D. Background: The aim of this study was to investigate the electrocardiographic and echocardiographic predictors of ventricular tachycardia (VT) in patients with classical mitral valve prolapse (MVP). Methods: Thirty patients (nine men and 21 women; mean age, 41.5 ± 15 years) in sinus rhythm with mitral valve prolapse who had VT in 24-hour Holter analysis and 30 patients with MVP without VT (eight men and 22 women; mean age, 43 ± 16 years) were included in this study. Transthoracic echocardiography, QT analyses from 12-lead electrocardiography, and 24-hour Holter electrocardiogram recordings were performed. Results: Mitral posterior leaflet thickness (0.48 ± 0.03 cm vs 0.43 ± 0,08 cm, P = 0.025), mitral anterior leaflet length (3.2 ± 0.24 cm vs 2.9 ± 0.36, P < 0.001), mitral posterior leaflet length (2.2 ± 0.3 cm vs 1.9 ± 0.35 cm, P = 0.01), left atrium anteroposterior diameter (4.2 ± 0.8 cm vs 3.5 ± 0.5 cm, P = 0.001), and mitral annulus circumference (15.7 ± 1.3 cm vs 14.6 ± 1.6 cm, P = 0.004) were increased significantly in MVP cases with VT. No significant difference was found between the cases with and without VT in terms of frequency- and time-domain analysis. QT dispersion (72 ± 18 ms vs 55 ± 15 ms, P = 0.0002) and corrected QT dispersion (QTcD) (76 ± 18 ms vs 55 ± 15 ms, P = 0.0002) were significantly increased in cases with VT compared with those without VT. Based on logistic regression analysis for MVP cases, in the case of VT, an enhancement in QTcD (P = 0.01) and the mitral anterior leaflet length (P = 0.003) were the independent predictors of VT. Conclusion: Mitral anterior leaflet length and enhanced QTcD are closely related with VT in patients with classical MVP. (PACE 2010; 33:1224,1230) [source] The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2009MUSTAFA HASSAN M.D. Background: An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress-induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia. Objectives: To examine the effects of psychological stress on QT dispersion (QTd) among CAD patients and whether these effects are mediated via the development of myocardial ischemia. Methods: Psychological stress was induced using a public speaking task. Twelve-lead electrocardiograms (ECG) were recorded at rest, during mental stress, and during recovery. QTd was calculated as the difference between the longest and the shortest QT interval in the 12-lead ECG. Rest-stress myocardial perfusion imaging was also performed to detect mental stress-induced myocardial ischemia. Results: Mental stress induced a significant increase in QTd compared to the resting condition (P < 0.001). This effect persisted beyond the first 10 minutes of recovery (P < 0.001). QTd was significantly associated with the development of mental stress ischemia with ischemic patients having significantly higher QTd during mental stress than nonischemic patients (P = 0.006). This finding remained significant after controlling for possible confounding factors (P = 0.01). Conclusion: An acute psychological stress induces a significant increase in QTd, which persists for more than 10 minutes after the cessation of the stressor. This effect seems to be, at least partially, mediated by the development of mental stress-induced myocardial ischemia. [source] Spatial Distribution of Repolarization Times in Patients with Coronary Artery DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2003PETER VAN LEEUWEN The potential clinical value of QT dispersion (QTd), a measure of the interlead range of QT interval duration in the surface 12-lead ECG, remains ambiguous. The aim of the study was the temporal and spatial analysis of the QT interval in healthy subjects and in patients with coronary artery disease (CAD) using magnetocardiography (MCG) and surface ECG. Standard 12-lead ECG and 37-channel MCG were performed in 20 healthy subjects, 23 patients with CAD without prior myocardial infarction (MI), 31 MI patients and 11 MI patients with ventricular tachycardia (VT). QTd was increased in CAD without MI compared to normals (ECG46.1 ± 6.0vs42.8 ± 5.0, P < 0.05; MCG66.8 ± 20.3vs49.7 ± 10.8, P < 0.01) and in VT compared to MI (ECG66.8 ± 16.5vs51.9 ± 16.6, P < 0.05; MCG93.6 ± 29.6vs66.8 ± 20.8, P < 0.005). In MCG, spatial distribution of QT intervals in patient groups differed from those in healthy subjects in three ways: (1) greater dispersion, (2) greater local variability, and (3) a change in overall pattern. This was quantified on the basis of smoothness indexes (SI). Normalized SI was higher in CAD without MI compared to normals (3.8 ± 1.1vs2.7 ± 0.6, P < 0.001) and in VT compared to MI (6.4 ± 1.6vs4.2 ± 1.4, P < 0.0005). For the normal-CAD comparison a sensitivity of 74% and a specificity of 80% was obtained, for MI-VT, 100% and 77%, respectively. The results suggest that examining the spatial interlead variability in multichannel MCG may aid in the initial identification of CAD patients with unimpaired left ventricular function and the identification of post-MI patients with augmented risk for VT. (PACE 2003; 26:1706,1714) [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] Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003DALIA GIEDRIMIENE GIEDRIMIENE, D., et al.: Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary Disease. To evaluate if QT dispersion (QTd) may be affected by the number of obstructed coronary arteries (CAs) in patients with acute myocardial infarction (MI) and undergoing angioplasty, and to evaluate if QTd may be affected by ejection function of the heart. The infarct related CA was identified by coronary angiography in 141 patients (97 men, mean age61.6 ± 12.9years) with acute MI undergoing percutaneous angioplasty. Successful reperfusion was defined as TIMI III flow with <20% residual stenosis. QTd, calculated by subtracting the shortest from the longest QT interval on 12-lead electrocardiograms, was examined immediately before and after angioplasty, at 24 hours, and 3 days after angioplasty. Successful reperfusion was achieved in 98 (69.5%) patients. Prolonged QTd at baseline was found in all patients with ischemia. A trend toward a decrease in QTd was observed immediately after angioplasty and at 24 hours, and a significant decrease at 3 days in patients with successful reperfusion regardless of the number of occluded CAs. There was no change in QTd found in patients with no reperfusion. An increase in QTd was observed in patients with acute ischemia due to single or multivessel disease. (PACE 2003; 26[Pt. II]:390,393) [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] Clinical Value of Electrocardiographic Parameters in Genotyped Individuals with Familial Long QT SyndromePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2001GEROLD MOENNIG MOENNIG, G., et al.: Clinical Value of Electrocardiographic Parameters in Genotyped Individuals with Familial Long QT Syndrome. Rate corrected QT interval (QTc) and QT dispersion (QTd) have been suggested as markers of an increased propensity to arrhythmic events and efficacy of therapy in patients with long QT syndrome (LQTS). To evaluate whether QTc and QTd correlate to genetic status and clinical symptoms in LQTS patients and their relatives, ECGs of 116 genotyped individuals were analyzed. JTc and QTc were longest in symptomatic patients (n = 28). Both QTd and JTd were significantly higher in symptomatic patients than in asymptomatic (n = 29) or unaffected family members (n = 59). The product of QTd/JTd and QTc/JTc was significantly different among all three groups. Both dispersion and product put additional and independent power on identification of mutation carriers when adjusted for sex and age in a logistic regression analysis. Thus, symptomatic patients with LQTS show marked inhomogenity of repolarization in the surface ECG. QT dispersion and QT product might be helpful in finding LQTS mutation carriers and might serve as additional ECG tools to identify asymptomatic LQTS patients. [source] Dispersion of QT Intervals: A Measure of Dispersion of Repolarization or Simply a Projection Effect?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2000DIEGO DI BERNARDO QT interval dispersion may provide little information about repolarization dispersion. Some clinical measurements demonstrate an association between high QT interval dispersion and high morbidity and mortality, but what is being measured is not clear. This study was designed to help resolve this dilemma. We compared the association between different clinical measures of QT interval dispersion and the ECG lead amplitudes derived from a heart vector model of repolarization with no repolarization dispersion whatsoever. We compared our clinical QT interval dispersion data obtained from 25 subjects without cardiac disease with similar data from published studies, and correlated these QT dispersion results with the distribution of lead amplitudes derived from the projection of the heart vector onto the body surface during repolarization. Published results were available for mean relative QT intervals and mean differences from the maximum QT interval. The leads were derived from Uijen and Dower lead vector data. Using the Uijen lead vector data, the correlation between measurements of dispersion and derived lead amplitudes ranged from 0.78 to 0.99 for limb leads, and using the Dower values ranged from 0.81 to 0.94 for the precordial leads. These results show a clear association between the measured QT interval dispersion and the variation in ECG lead amplitudes derived from a simple heart vector model of repolarization with no regional information. Therefore, measured QT dispersion is related mostly to a projection effect and is not a true measure of repolarization dispersion. Our existing interpretation of QT dispersion must be reexamined, and other measurements that provide true repolarization dispersion data investigated. [source] Impact of QT Variables on Clinical Outcome of Genotyped Hypertrophic CardiomyopathyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009Katsuharu 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] Circadian Variation in QT Dispersion Determined from a 12-Lead Holter Recording: A Methodological Study of an Age- and Sex-Stratified Group of Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007Stig Hansen M.D. Background: QT dispersion is considered to reflect inhomogeneity of myocardial repolarization. Method: The circadian variation of QT interval dispersion was examined in 95 healthy subjects using 24-hour Holter monitoring. Three different methods of lead selection were applied: all 12 leads (QTdisp 12), only precordial leads (QTdisp 6), and the pair of leads selected at 3 a.m. in which the longest and shortest QT intervals were found in each individual subject (QTdisp 2). Results: A preliminary methodological study including measurements from every minute in 10 subjects revealed no significant circadian variation using mean values of QTdisp 12, QTdisp 6, or QTdisp 2 obtained every hour, every 2, or every 4 hours, except in QTdisp 6, which demonstrated a significant circadian variation (P < 0.01) in 1-hour measurements. Analysis of all 95 subjects using measurements obtained every 4 hours revealed a significant circadian variation in QTdisp 12 and QTdisp 6 (P < 0.0001), whereas no circadian variation was seen in QTdisp 2. A subdivision into 10-year age groups revealed that subjects at age >50 years had a significant circadian variation in QTdisp 12 and QTdisp 6, but not in QTdisp 2. Only in males a significant circadian variation was seen in QTdisp 12 (P < 0.0001), whereas QTdisp 6 demonstrated a circadian variation both in females (P < 0.001) and in males (P < 0.0001). Conclusions: Selection of leads is of crucial importance for repetitive measurements of QT dispersion. Circadian variation was detected in subjects over 50 years of age, when all 12 or only the 6 precordial leads were taken into account. [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. [source] Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular HypertrophyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2004Laura Maria Lonati M.D. Objective:,The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. Methods:,A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 ± 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 ± 6.1 years), and 17 normotensive healthy subjects as control group (24.8 ± 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12-lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, ,QT, ,QTc). Results:,There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 ± 45.2/93.5 ± 4.9 mmHg) versus athletes (120.9 ± 10.8/77.1 ± 6.0 mmHg) and controls (123.5 ± 4.8/78.8 ± 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 ± 21.1 g/m2) and hypertensives (117.1 ± 15.2 g/m2) versus controls (81.1 ± 14.5 g/m2; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m2) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (,QT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ,QTc 88 ± 2.0, 47 ± 1.4, 54 ± 2.7; P < 0.01). Conclusions:,LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion. [source] Hormone Replacement Therapy Shortens QT Dispersion in Healthy Postmenopausal WomenANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2001Aylin Yildirir M.D. Background: The aim of the study was to investigate the effects of hormone replacement therapy (HRT) on myocardial repolarization characteristics in postmenopausal women without coronary artery disease. Methods: Fifty-one consecutive healthy postmenopausal women (age 48 ±; 5) with negative exercise stress testing were prospectively enrolled into the study. Standard 12-lead electrocardiograms were obtained to evaluate the effects of 6 months of HRT on QT intervals, corrected QT intervals (QTcmax and QTcmin), QT dispersion (QTd), and corrected QTd (QTcd). Hormone regimens were continuous 0.625 mg/day conjugated equine estrogen (CEE) plus 2.5 mg/day medroxyprogesterone acetate (MPA) or 0.625 mg/day CEE alone depending on the hysterectomy status. Results: Although not statistically significant, CEE alone or in combination with MPA increased QTmax and QTmin values. However, the increase in QTmin was greater than the increase in QTmax, which resulted in statistically significant shortening of QTd (P = 0.007 in CEE and P < 0.001 in CEE + MPA groups). There was a significant prolongation of QTcmin values after 6 months in patients assigned to the CEE group (P = 0.001). The QTcd values were significantly shortened by HRT with both regimens (for CEE group 49 ±; 13 ms vs 38 ±; 13 ms, P = 0.01; for CEE + MPA group 49 ±; 14 ms vs 36 ±; 13, P < 0.001). Conclusion: HRT significantly decreased the QTd and QTcd in postmenopausal women without coronary artery disease, independent of the addition of MPA to the regimen. This improvement in myocardial repolarization may be one of the mechanisms of the favorable effects of HRT on cardiovascular system. However, the clinical implications of the shortening of QTd in postmenopausal women with HRT must be clarified. A.N.E. 2001; 6(3):193,197 [source] The Effect of Sleep Apnea on QT Interval, QT Dispersion, and ArrhythmiasCLINICAL CARDIOLOGY, Issue 6 2010Kitti Barta MD Background QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. Hypothesis The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. Methods A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. Results Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 ± 34.6 ms, daytime QT interval: 381.6 ± 33.8 ms, 24-hour QT interval: 394.7 ± 31.1 ms). However, during the nighttime QT interval (422.8 ± 14.9 ms), QTd (31.2 ± 11.0 ms) and QT dispersion (30.5 ± 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 ± 14.2 ms, QTd: 28.8 ± 9.4 ms, QTcd: 30.5 ± 9.43 ms) and daytime levels (QTc interval: 423.9 ± 14.3 ms, QTd: 27.3 ± 10.7 ms, QTcd: 29.9 ± 11.1 ms). None of the patients had ventricular arrhythmias. Conclusions QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period. Copyright © 2010 Wiley Periodicals, Inc. [source] New parameters in the interpretation of exercise testing in women: QTC dispersion and QT dispersion ratio differenceCLINICAL CARDIOLOGY, Issue 4 2002Kurtulu, Özdemr M.D. Abstract Background: It has been reported that the increase of QT dispersion (QTD) that occurs due to increased inhomogeneity of the ventricular repolarization because of transient ischemia obtained by standard 12-lead electrocardiogram (ECG), the changes during exercise, and the differences between exercise and rest increase the accuracy of exercise test in the diagnosis of coronary artery disease (CAD). Hypothesis: This study was designed to investigate the value of QTD parameters, which are reported to increase the diagnostic accuracy of exercise test in women. Methods: Ninety-seven women who had undergone coronary angiography and exercise test were evaluated for diagnosis of chest pain. QT dispersion was calculated using the measurements of the highest and lowest values of QT interval obtained by ECG during peak exercise. The QTc using Bazett's equation, and the QTD ratio (QTDR) using QT/RR were calculated, and QTcD and QTD ratios were obtained. The difference between QTcD and QTDR was determined by extracting the rest values from the exercise values. Results: The groups with normal coronaries (n = 48), single-vessel CAD (n= 24), and multivessel CAD (n= 25) were compared. The obtained QTD parameters at peak exercise and their differences between exercise and rest were found to be significantly increased in patients with CAD (p<0.001). Furthermore, these parameters were found to be higher in the patients with multivessel CAD than in those with single-vessel disease (p < 0.05). With the parameters QTcD > 60 ms and QTDR > 10%, greater sensitivity and specificity were obtained compared with ST-segment depression. The highest diagnostic accuracy was obtained with the QTD parameters calculated from the differences between rest and exercise values. The diagnostic accuracy of the difference of QTcD > 15 ms and the difference of QTDR > 5% was relatively higher than the other parameters (sensitivity, specificity, and negative and positive predictor values are 84,88,84, 87% and 84, 96, 85, 95%, respectively). Conclusion: The use of QTD parameters as variables of ECG, which is easily obtainable in the evaluation of exercise ECG in women, increases the diagnostic accuracy of the exercise test. In addition, the evaluation of QTD variables may provide information about the incidence of CAD. [source] Changes of QT dispersion in patients with coronary artery disease dependent on different methods of stress inductionCLINICAL CARDIOLOGY, Issue 3 2000B. Hailer M.D. Abstract Background: Episodes of stress-induced myocardial ischemia in patients with coronary artery disease (CAD) may cause increases of QT dispersion (QTd). Hypothesis: Aim of this study was to analyze the effect of increasing heart rates on QTd and to compare the effect of different methods of stress induction in patients with varying degrees of CAD when estimating QTd. Methods: We studied 58 patients, 22 with prior myocardial infarction (MI), 25 without MI or wall motion disturbances at rest, and 11 patients without evidence of CAD. Prior to coronary angiography, standard 12-lead ECGs were obtained at rest as well as during dynamic exercise and pharmacologic stress using arbutamine simultaneously with echocardiography. QTd was determined at each stress level by subtracting minimal from maximal QT interval duration. Results: QTd values at rest were not consistently higher in the patients with CAD. At maximal heart rate, QTd was statistically significantly higher in patients with CAD with a better discrimination between groups for pharmacologic stress (p < 0.005 for exercise, p < 0.0001 for arbutamine). Patients after MI had higher QTd values under all conditions than did the groups without MI. As in patients with CAD, the values of this group changed more radically as a result of pharmacologic stress. Conclusion: Patients with CAD can be identified on the basis of QTd under stress. These changes were not as marked in patients with MI as their rest values were already increased. Overall, drug-induced stress produced greater differences than dynamic exercise, suggesting that the ischemic threshold might be lower in the former. [source] | |||||||||||||||||||||||||