Heterogeneity Of Ventricular Repolarization Research Articles

Impact of coronary collateral circulation on QT dispersion in patients with coronary artery disease

The aim of this study was to assess the effect of coronary collateral circulation (CCC) on QT dispersion (QTD) in coronary artery disease. A prolonged QTD has been linked to increased heterogeneity of ventricular repolarization implicated in the genesis of ventricular arrhythmias and has been associated with an adverse prognosis in patients with coronary artery disease. CCC and corrected QTD (QTcD) were established in patients who had at least 85% stenosis in the left anterior descending coronary artery or in proximal part or in the body of the right coronary artery. Furthermore, left ventricular function score was determined for all the patients. While CCC was not present (CCC grade 0) in 32 patients, 68 patients were observed with CCC (CCC grade > or =1). Mean QTcD was higher in patients who had CCC grade > or =1 than in patients with grade 0 (64.3+/-3.5 and 46.8+/-2.7, respectively, P=0.002). We detected a significant correlation between the collateral score and QTcD (r=0.354, P=0.001). CCC grade > or =1 patients had higher mean left ventricular function scores than grade 0 patients (P=0.048). Left ventricular function score and QTcD were observed to be correlated (r=0.200, P=0.046). CCC in chronic coronary artery disease was not established to have a positive decreasing effect on QTcD. On the contrary, QTcD values were observed to be even higher in patients with well developed CCC. Further research including larger series and long-term follow-up is required to investigate this issue.

Human antibodies with muscarinic activity modulate ventricular repolarization: Basis for electrical disturbance

Introduction In chronic chagasic patients sudden death has been reported when QT interval dispersion is increased and antibodies with muscarinic-like activity have been demonstrated to trigger arrhythmias. The aims were to investigate, in vivo and in vitro, relation between these antibodies and heterogeneity of ventricular repolarization and to identify predictors of cardiac death in chronic chagasic patients. Methods and results Clinical, electrocardiograph and echocardiograph variables from 32 chronic chagasic patients with moderate to severe left ventricular dysfunction, followed-up for 10 years were analyzed. Sera from chronic chagasic patients with or without muscarinic activity were tested in isolated rabbit hearts to study ventricular repolarization. Stepwise multivariate logistic analysis was applied to identify independent predictors of cardiac death. QT interval dispersion of patients with muscarinic activity (75.9 ± 5.5 ms) was larger than that of patients without muscarinic activity (51.3 ± 4.0 ms, p < 0.001). Maximum uncorrected and corrected QT intervals were not significantly different between groups of patients. Sera from patients with muscarinic activity significantly and reversibly increased QT interval in isolated rabbit hearts ( p = 0.002). This effect was abolished in the presence of the muscarinic antagonist atropine. Multivariate analysis identified maximum corrected QT intervals and left ventricular end diastolic index as independent predictors of cardiac death ( p = 0.03 and p = 0.02, respectively). Conclusions Sera with muscarinic activity from chagasic patients have a strong contribution to evoke ventricular repolarization rhythm disorder. In these patients, ventricular repolarization heterogeneity is increased significantly. In vitro, muscarinic sera reversibly increased repolarization duration. Maximum corrected QT intervals and left ventricular end diastolic index are independent predictors of cardiac death.

Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients

The aim of our study was to evaluate the effect of cardiac resyncronization therapy on QT dispersion (QTd), JT dispersion (JTd), and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. Fifty patients (43 male, 7 female, age 60.2+/-3.1 years) suffering from congestive heart failure (n=39 NYHA class III; n=11 NYHA class IV) as a result of coronary artery disease (n=19) or of dilated cardiomyopathy (n=31), with sinus rhythm (SR), QRS duration >120 ms (mean QRS duration=156+/-21 ms), an ejection fraction <35%, left ventricular end-diastolic diameter >55 mm, presence of atrioventricular asynchrony, intra- and inter-ventricular asynchrony, underwent permanent biventricular pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing (BiVP) and QTd, JTd, and TDR were assessed. BiVP significantly reduced QTd (73.93+/-19.4 ms during BiVP vs. 91+/-6.7 ms in SR, P=0.004), JTd (73.18+/-17.16 ms during BiVP vs. 100.72+/-39.04 at baseline, P=0.003), TDR (93.16+/-15.60 vs. 101.55+/-19.08 at baseline, P<0.004), compared with SR. Right ventricular endocardial pacing and left ventricular epicardial pacing both increased QTd (RVendoP 94+/-51 ms, P<0.03; LVepiP 116+/-71 ms, P<0.02), and TDR (RVendoP 108.13+/-19.94 ms, P<0.002; LVepiP 114.71+/-26.1, P<0.05). There was no effect on JTd during right and left ventricular stimulation. BiVP causes a statistically significant reduction of ventricular heterogeneity of repolarization and has an electrophysiological anti-arrhythmic influence on the arrhythmogenic substrate of dilated cardiomyopathy.

AB40-2: Why is it difficult to detect transmural heterogeneity of ventricular repolarization In vivo?

Transmural heterogeneity in ventricular repolarization demonstrated in vitro has been difficult to confirm in vivo. Whether this discrepancy reflects a physiological phenomenon or a methodological problem is still a matter of debate. Thus, transmural refractory measurements obtained in vivo were repeated in the same heart and at identical sites in vitro with uni- and bipolar recordings to determine the role of the type of preparation and methodology applied.

Why does not QT dispersion reflect the heterogeneity in ventricular repolarization?

Why does not QT dispersion reflect the heterogeneity in ventricular repolarization?

Increased ventricular repolarization heterogeneity in patients with ventricular arrhythmia vulnerability and cardiomyopathy: a human in vivo study

Increased repolarization heterogeneity can provide the substrate for reentrant ventricular arrhythmias in animal models of cardiomyopathy. We hypothesized that ventricular repolarization heterogeneity is also greater in patients with cardiomyopathy and ventricular arrhythmia vulnerability (inducible ventricular tachycardia or positive microvolt T wave alternans, VT/TWA) compared with a similar patient population without ventricular arrhythmia vulnerability (no VT/TWA). Endocardial and epicardial repolarization heterogeneity was measured in patients with (n = 12) and without (n = 10) VT/TWA by using transvenous 26-electrode catheters placed along the anteroseptal right ventricular endocardium and left ventricular epicardium. Local activation times (AT), activation-recovery intervals (ARI), and repolarization times (RT) were measured from unipolar electrograms. Endocardial RT dispersion along the apicobasal ventricle was greater (P < 0.005) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.005). AT dispersion was similar between the two groups. Epicardial RT dispersion along the apicobasal ventricle was greater (P < 0.05) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.05). AT dispersion was similar between the two groups. A plot of AT as a function of ARI revealed an inverse linear relationship for no VT/TWA such that progressively later activation was associated with progressively shorter ARI. The AT-ARI relationship was nonlinear in VT/TWA. In conclusion, patients with cardiomyopathy and VT/TWA have greater endocardial and epicardial repolarization heterogeneity than those without VT/TWA without associated conduction slowing. The steep repolarization gradients in VT/TWA may provide the substrate for functional conduction block and reentrant ventricular arrhythmias.

Effect of lidocaine and amiodarone on transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia

To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, mid-myocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5 +/- 3.9 ms to 31.2 +/- 4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P < 0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P < 0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.

Relationship between prolongation of QTc and prolongation of the peak of T (Tp) to the end of T (Te)

Introduction Lengthening of ventricular repolarization is known to be a risk factor for development of torsade de pointes, a form of ventricular tachycardia thought to be initiated by an early after depolarization and to be sustained by a novel reentrant mechanism precipitated, putatively, by heterogeneity of repolarization among ventricular myocytes. While prolongation of QT and QTc are good predictors of torsdogenic potential, the duration from the peak to the end of the T wave (Tp–Te) is thought to be a more accurate reflection of heterogeneity of ventricular repolarization. This study, conducted on Langendorff guinea pig hearts, was designed to compare lengthening of QTc with lengthening of Tp–Te for 16 test articles known to be and 7 known not to be torsadogenic. Methods Bipolar, transventricular electrograms, recorded from 83 guinea pig hearts perfused according to methods of Langendorff, were exposed to escalating concentrations of test articles. RR, QT, QTc and Tp–Te were measured. QTc was calculated by the method of Fridericia. Data was analyzed using a mixed model ANOVA where least squared means ( t-test) was used for comparing males vs. females and for concentration levels for each parameter studied. Results QTc lengthened in 16 of 16 test articles known to be torsadogenic and did not lengthen in 7 of 7 test articles known not to be torsadogenic—sensitivity and specificity of 1.0. In 9 out of 16 torsadogenic test compounds, the Tp–Te interval increased parallel with QTc. In 7 test compounds known not to be torsadogenic, two test compounds increased Tp–Te. Discussion It is clear that QTc prolongation is a more robust predictor of torsadogenicity than Tp–Te in the male guinea pig heart.

Acute cardiovascular effects of tacrolimus in the isolated guinea pig heart

Tacrolimus is an immunosuppressive, macrolide antibioticfrequently used to minimize transplant rejections. It has alsobeen used as a topical ointment to treat atopic dermatitis (Kappet al., 2003), and as an immunosuppressant in kidney trans-plants in dogs (Griffin et al., 1992). Macrolide antibiotics areknown to prolong ventricular repolarization, and to produce thepotentially fatal arrhythmia torsade de pointes (TdP).Reports by Johnson et al. (1992) and Hodak et al. (1998)describe TdP in patients receiving tacrolimus. TdP is a rapid,polymorphic, ventricular tachycardia produced most often bydrugs that lengthen the duration of depolarization and repolar-ization measured as the QT duration in the electrocardiogram(ECG). Tacrolimus has been shown to increase QTc (QT correctedfor heart rate) dispersion in patients with kidney transplants,implying a risk for TdP (Gerhart et al., 2001). A second study byGonza´lez et al. (1999) reported shortening of QTc in patientswith liver transplants treated with tacrolimus. The QTc disper-sion refers to the difference in durations of QTcs from numerousleads, and is thought to reflect heterogeneity of ventricularrepolarization, an electrophysiological substrate for early afterdepolarizations and re-entrant ventricular arrhythmias. Minem-atsu et al. (1999) demonstrated lengthening of QTc in a use-dependent manner showing counterclockwise hysteresis inanesthetized guinea pigs. Thus, the QTc lengthened more athigher heart rates than at lower heart rates – a pattern oppositeto that of most torsadogenic agents, which lengthen QTc in areverse-use dependent manner.There are two mechanisms by which tacrolimus may retardventricular repolarization. Tacrolimus blocks intermediate-con-ductance K

396 Validation of ECG indices of ventricular repolarization heterogeneity: a computer simulation study

396 Validation of ECG indices of ventricular repolarization heterogeneity: a computer simulation study

396 Validation of ECG indices of ventricular repolarization heterogeneity: a computer simulation study

396 Validation of ECG indices of ventricular repolarization heterogeneity: a computer simulation study

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

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)). 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 muV, T-wave area from 34 x 10(3)+/- 21 x 10(3) to 141 x 10(3)+/- 58 x 10(3)muV 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. 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.

Relation of QT c duration heterogeneity to mortality following orthotopic heart transplantation

Studies of heart failure patients have demonstrated that serial QT prolongation and abnormally prolonged QT intervals are associated with greater mortality. Serial QT interval measurements in patients who undergo orthotopic heart transplantation (OHT) may quantify the degree of myocardial repolarization heterogeneity and serve as a marker of arrhythmogenic substrate. In this study, the mean survival for those with "stable" QT(c) intervals (a change of -10 to 10 ms/year) was 124 +/- 8 months versus 63 +/- 25 months in those with annual QT(c) changes of >10 ms (p = 0.009). Ventricular repolarization heterogeneity may serve as a marker of identifying high-risk patients after OHT.

The Acute Effects of Cigarette Smoking on the Heterogeneity of Ventricular Repolarization in Healthy Subjects: The Relationship between QT Dispersion and Coronary Flow Reserve

Background and Objectives：Although cigarette smoking is a known risk factor for sudden cardiac death, little is known about the effects of smoking on the heart. The QT interval and QT dispersion prolongation have been associated with a lower ventricular fibrillation threshold and the occurrence of sudden cardiac death. Smoking has an unfavorable influence on the autonomic balance and myocardial blood flow. The objective of the current study was to evaluate the relationship between the QT dispersion and coronary flow reserve (CFR) in healthy young male subjects. Subjects and Methods：The study included a sample of 30 healthy young male cigarette smokers. The catecholamines level, QTc dispersion, heart rate variability and myocardial blood flow were measured, immediately before and 5 minutes after and during the smoking of 3 cigarettes. Results：Short-term smoking caused significant increases in the serum cortisol (10.9±4.9 vs. 15.0±7.0 μg/dL, p<0.01), serum epinephrine (0.038±0.026 vs. 0.046±0.026 ng/mL, p=0.044), heart rate (78±9 vs. 85±8 beats/min, p< 0.01), maximal QTc interval (412±22 vs. 435±20 ms, p<0.01), QTc dispersion (43±14 vs. 62±17 ms, p<0.01), LFnu (68±9 vs. 78±6%, p<0.01), LF/HF (3.25±2.15 vs. 5.22±1.89, p<0.01) and peak diastolic velocity (21.7±3.9 vs. 23.9±5.5 cm/sec, p=0.005), and a decrease in the CFR (3.71±0.56 vs. 3.42±0.76, p=0.024). The change in the QTc dispersion was closely related to the change in the CFR (r=-0.357, p=0.043). Conclusion：The present study is the first to demonstrate that the impaired coronary flow reserve after smoking may contribute to the increased inhomogeneity of ventricular repolarization in healthy young male smokers. (Korean Circulation J 2005;35:448-453)

Dispersion of the corrected QT interval in acute carbon monoxide poisoning

Carbon monoxide (CO) poisoning is known to cause myocardial toxicity and life-threatening arrhythmias. Corrected QT dispersion (QTdc) of the ECG is an indirect measure of heterogeneity of ventricular repolarisation, which may contribute to ventricular arrhythmias. The aim of the study was to evaluate the relationship between the carboxyhemoglobin (COHb) level and QTdc during carbon monoxide poisoning. This study was prospectively performed in 104 patients who diagnosed CO intoxication. Patients were assigned to two groups according to COHb levels 25% (Group II, n = 72). In each ECG lead, the QT interval and QRS duration were measured in the two groups and corrected for heart rate (QTc) using Bazett's formula (QT/RR1/2). QTdc is then the difference between the leads with the shortest and longest QTc intervals. Measurement of QT intervals were calculated at admission and in 24-hour and 48-hour ECGs after admission. Cardiac enzymes were measured at each stage. The myocardial perfusion after exercise and at rest 4 hours after exercise were determined in all patients 1 week after admission. QT, QTc and QTd intervals were not significantly different in both of groups each stage whereas the values of the QTdc after 24 hours were significantly greater than QTdc at admission in Group II but not in Group I. Comparison of QTdc for the two groups demonstrated significant differences after 24 hours (P < 0.05) (Table ​(Table1).1). Plasma creatinine phosphokinase (CPK) and CPK-MB levels at admission, and 24 and 48 hours later in Group II were significantly higher than the other group (P < 0.05). Seven patients in Group I and 23 patients in Group II had an extent of myocardial ischemia on scintigraphy. Table 1 The reduced threshold for arrhythmias in CO poisoning may be due to inhomogeneous repolarization of ventricles, assessed by QTdc. Measuring QTdc for monitoring after CO poisoning may be suggestive of the potential danger of high levels of COHb to cardiac-disabled individuals.

The Relation of Circadian Blood Pressure Variation to Left Ventricular Mass, Diastolic Function, and Dynamic QT Dispersion

Background and Objectives:A non-dipping pattern in hypertensive patients has been shown to be associated with a greater left ventricular (LV) hypertrophy, LV diastolic impairments and prolonged ventricular repolarization. The dynamic parameters of the QT dispersion (QTd) have been highlighted as markers of ventricular repolarization heterogeneity. The aim of this study was to demonstrate if the extent of nocturnal blood pressure (BP) fall was related to the LV mass, LV diastolic function and dynamic parameters of the QTd. Subjects and Methods:122 subjects, receiving electrocardiography, 24-hour ambulatory BP monitoring, 12 lead-24hr Holter monitoring and 2-dimensional Doppler echocardiography examinations, were enrolled. The subjects were classified as normotensive, dipper and non-dipper. The LV mass (LVM) and LV diastolic indices were measured. Using the QT Guard software, with 12 lead-24hr Holter monitoring, the QTd, mean QTd, QTd variation (the difference between the maximum minus the minimum QTd value observed over the recording time), QTd maximum (the maximum difference of QTd between consecutive beats) and QTd variability (QTd standard deviation) were analyzed. Results:Of the 122 patients, 39 and 40 were placed in the dipper and non-dipper groups, respectively. The non-dipper group had a greater LVM index (LVMI) than the dipper group (p<0.01). The nondipper group had greater increases in their A velocity (p<0.01), and more prolonged deceleration (p<0.01) and isovolumic relaxation (p<0.01) times than the dipper group. There were no significant differences in the QT and QTc interval between the 3 groups, but the QTd was much more increased in the non-dipper than the dipper and normotensive groups (p<0.01). For the dynamic parameters of the QTd, the QTd variation, QTd maximum and QTd variability were significantly increased in the non-dipper compared to the dipper and normotensive groups (p<0.05). Comparing the dipper and normotensive groups, there were no significant differences in the LVMI, LV diastolic indices, QTd and dynamic parameters of the QTd. Conclusion:The nondipper group of hypertensive patients had a greater LVMI, more impaired LV diastolic function and greater increases in their QTd and dynamic parameters of the QTd compared to the dipper and normotensive groups, suggesting the possibility of a much greater chance of cardiovascular events, and their complications, in the nondipper compared to the dipper group. (Korean Circulation J 2005;35:382-388)

Prognostic value of heterogeneity of ventricular repolarization in survivors of acute myocardial infarction

The expansion of indications for implantation of cardioverter-defibrillators (ICD) has enhanced the need for risk stratification of patients post myocardial infarction (MI), while the improved treatment of acute MI has decreased mortality and diminished the prognostic power of traditional risk variables. Increased heterogeneity of ventricular repolarization quantified by TCRT (total cosine R-to-T, angular difference between spatial QRS and T loops, decreased with increase in repolarization heterogeneity) is an independent predictor of mortality in patients post MI. Left ventricular ejection fraction (EF), QRS duration on signal-averaged ECG, number of ventricular ectopic beats (VE)/h, heart rate variability (HRV) triangular index, heart rate turbulence slope on 24-h Holter recording, and TCRT were analyzed in 334 survivors of acute MI followed up for 41 +/- 20 months. In multivariate analysis, EF < 35% (relative risk [RR] 2.3, 95% confidence interval [CI] 1.1-4.7, p = 0.023), VE > 10/h (RR 2.2, CI 1.0-4.6, p = 0.044), HRV < 20 U (RR 2.2, CI 1.1-4.5, p = 0.032), and TCRT < -0.896 (RR 4.3, CI 2.2-8.5, p = 0.00001) were independent predictors of cardiac mortality (11%). Independent predictors of arrhythmic mortality (5%) were VE, HRV, and TCRT (RR 5.8, CI 2.1-15.6, p = 0.0004). Cardiac and arrhythmic mortality of patients with both EF <35% and TCRT < -0.896 were >60 and >30%, respectively, compared with 17 and 7% in those with only EF <35% or TCRT < -0.896. Decreased TCRT, which reflects increased repolarization heterogeneity, is a strong and independent predictor of cardiac and arrhythmic death in patients post MI.

The indices of ventricular repolarization heterogeneity may be used as diagnostic criteria for left ventricular hypertrophy in patients with arterial hypertension. Analyzing the variability of T-wave amplitudes and repolarization integrals

Background. The values of ventricular repolarization variability are higher in patients with hypertensive left ventricular hypertrophy (LVii) and (hey correlate with the left ventricular myocardial mass index (LVMMl). Objective. To develop diagnostic criteria for LVH, which are based on the analysis of the values of ventricular repolarization heterogeneity, the indices of the variability of a T-wave amplitude. Subjects and methods. The study included 69 patients with arterial hypertension and 20 patients without cardiovascular diseases who were divided, on the basis of echocardiography determination of LVMMI into groups with or without LVH. The par of the variability of repolarization parameters were analyzed. These included dispersion (Disp), normalized dispersion (Dispnorm), root mean square deviation (RMSD) of T-wave amplitude, as well as total repolarization integrals (TRI, a product of JT end interval, and the T-wave amplitude), early repolarization integrals (ERI, a product of the JT apex interval, and the T-wave amplitude,) late repolarization integrals (LRI, a product of the T apex - T end interval, and the T-wave amplitude.) of EGG leads 12 and V 1 -V 6 . Results. An analysis of V 1 -V 6 leads has indicated that as compared to male patients with normal l.VMMI. the males with I.VII had higher values of T-wave amplitude variability and increased values of the variability of total and early repolarization integrals (of Disp, Dispnorm and RMSD), which correlated with LVMMI. A regression analysis has shown that LVMMI was an independent predictor of the dispersion of T-wave amplitudes and that of the variability of Disp, Dispnorm, of TRI, the relative thickness of the walls of the left ventricle is an independent predictor of Dispnorm and RMSD of T-wave amplitudes, as well RMSDo f TRI and ERI variability. The best diagnostic characteristics were demonstrated by RMSD of T amp of ≥ 37 ms (39 % sensitivity, 91 % specificity, 86 % positive predictive value, and 51 % negative predictive value) and Dispnorm of TRI of ≥ 300 mV x msec (45 % sensitivity, 91 % specificity, 88 % positive predictive value, and 54 % negative predictive value). These characteristics were comparable with those for the Cornell criteria, but they were less than those for the Sokolov-Lyons criteria in sensitivity. In females with LVH, the values of the variability of T-wave amplitudes and repolarization integrals did not differ from those with normal LVMMI. The correlation of LVMMI and the values of the variability of T-wave amplitudes and repolarization integrals was insignificant. Conclusion. The values of the amplitude heterogeneity of ventricular repolarization and variability of repolarization integrals may be used as independent criteria of LVH in males with arterial hypertension.

QT and JT dispersion in the drug-induced long QT syndrome in anaesthetized rabbits is accurately detected by a three-lead surface ECG measurement

Introduction: QT dispersion (QTd) can be measured from three leads of the ECG in patients with myocardial ischemia. However, whether QT and JT dispersion (QTd, JTd) can be calculated from a three-lead of the ECG in drug-induced long QT syndrome (LQTS) in animals remains elusive. Therefore, we determined to what extent a three-lead measurement of the surface ECG accurately detects dispersion of QT and JT in comparison with multi-lead assessments in anaesthetized rabbits, challenged with methoxamine and additionally infused intravenously with solvent or dofetilide. Methods: Using several ECG leads in anaesthetized rabbits challenged intravenously with an α 1-adrenoceptor agonist methoxamine, we assessed the QT and JT interval, as well as QT and JT dispersion, at baseline and in response to solvent or dofetilide (0.02 or 0.04 mg/kg/min iv for 60 min), an I Kr blocker. For that purpose, we recorded and analyzed the surface ECG and assessed QT and JT dispersion by four methods: (1) 12-lead ECG; (2) six precordial leads (V1–V6); (3) three leads most likely to contribute to the dispersion (aVF, V1, and V4); (4) three quasi-orthogonal leads (aVF, I, and V2). QT and JT dispersion were significantly lower in 6- and 3-lead measurements than in 12-lead measurement, both at baseline and during infusion of solvent or dofetilide. At 5 and 10 min of infusion, dofetilide at 0.02 or 0.04 mg/kg/min iv markedly increased QT and JT dispersion by 100% to 500% in all four ECG lead combinations. This dose regimen of dofetilide markedly prolonged QT and JT intervals in lead II, and was associated with high incidences of polymorphous ventricular tachycardia (PVT: 30% at 0.02 mg/kg/min; 100% at 0.04 mg/kg/min) and of ventricular fibrillation (VF: 17% with 0.02 mg/kg/min; 58% with 0.04 mg/kg/min). Conclusion: Our present study shows that the measurement of QT and JT dispersion in three surface ECG leads only (aVF, I, V2 or aVF, V1 V4), instead of 12 ECG leads, is an appropriate approach to assess drug-induced heterogeneity or dispersion of ventricular repolarization in anaesthetized rabbits, both at baseline and during arrhythmogenic sensitization with methoxamine and challenged with dofetilide.

P-217 Increased heterogeneity of ventricular repolarisation in first degree relatives of patients with arrhythmogenic right ventricular cardyomyopathy

P-217 Increased heterogeneity of ventricular repolarisation in first degree relatives of patients with arrhythmogenic right ventricular cardyomyopathy