JTc Intervals Research Articles

Effects of Gender on Electrocardiography in Subjects with Shortened Ventricular Depolarization (QRS).

Distinctions between electrocardiograms of female and male subjects have been recognized for many years. Due to these differences, arrhythmias in each gender have a tendency to differ. In our study, we aimed to compare electrocardiography intervals between men and women with short QRS durations. Subjects with a QRS interval of ≤80 ms were included in the study. Patients were grouped by gender and the parameters were compared. Patients with diseases that might affect QRS interval and/or who were on medications were excluded. The electrocardiogram intervals of the subjects were measured, Holter monitors were placed, and parameters of time-based heart rate variation were analyzed. A total of 100 patients (55% female) were included in the study. According to statistical analysis, no significant difference between the genders was observed in the heart rate or in the parameters, such as QT, JT, JTp, and TpTe intervals or heart rate-corrected QTc, JTc, JTpc, and TpTec intervals, which affect repolarization and are known to be arrhythmia precursors by shortening or elongation. No statistically significant difference was found between the two groups for the parameters of heart rate variability time measures (SDNN, SDANN, rMSSD, and pNN50). We observed that when the QRS interval gets shorter, repolarization differences between the genders disappear. New studies are required on this subject.

Abstract 15766: Repolarization Parameters are Significantly Prolonged in Many Patients With Left Bundle Branch Block and Acute Myocardial Infarction

Introduction: In patients with normal conduction, prolongation of repolarization parameters such as the QTc interval, JTc interval, and T-wave peak to end (Tpe) interval are associated with cardiac ischemia, ventricular tachydysrhythmias, and sudden cardiac death. These intervals are often considered “prolonged” at QTc >450 ms, JTc > 360 ms, and Tpe > 120 ms. We are unable to find published manuscripts that report these parameters in LBBB. Furthermore, it has been proposed that the Bazett correction formula for QTc and JTc overestimates repolarization duration in patients with conduction disturbances. Aim: To report the QTc, JTc, and Tpe intervals in ED patients with LBBB with and without MI and to compare common correction formulas. Methods: Retrospectively, we identified ED patients with LBBB and ischemic symptoms: with no MI, with NSTEMI, and with angiographically-proven acute coronary occlusion (STEMI). The QT, JT, and Tpe intervals were measured manually in leads II, V3, and V5; the longest of each was used. QTc and JTc intervals were calculated by Bazett’s, Hodges’ and Framingham formulas. Statistics were by two-tailed Student’s t-test and Mann-Whitney U test. Results: The no-MI, NSTEMI, and STEMI groups consisted of 105, 24 and 33 patients. In the STEMI group, 24.3% of patients had Tpe >= 120 ms compared to 4.8% of no-MI patients (p < 0.001). By Hodges’ formula, 53.1% of patients with LBBB had QTc >= 450 ms and 12.3% had JTc >= 360 ms. Conclusion: Repolarizaton parameters are prolonged in many patients with LBBB. The Tpe interval, which has been proposed as a marker of transmural repolarization heterogeneity due to ischemia, is significantly prolonged in patients with STEMI and LBBB when compared to LBBB patients without MI. Between the STEMI, NSTEMI, and no-MI groups there was no significant difference in QTc or JTc by any formula (see Table 1). However, the overall mean QTc by Bazett’s was significantly longer than Hodge’s or Framingham (see Table 2).

Effects of Different Ventricular Pacing Modes on Ventricular Repolarisation in Patients Undergoing Cardiac Resynchronisation Therapy: A Single-centre Study

The aims of this study were to compare ventricular repolarisation parameters in patients who underwent cardiac resynchronisation therapy (CRT) at Sun Yat-sen University Memorial Hospital under different ventricular pacing modes and to understand effects of epicardial pacing on ventricular repolarisation. The study included 55 patients who underwent CRT. During follow-up outpatient visits three months after CRT implantation, the CRT devices were programmed to deliver no pacing (with the exception of patients with third-degree atrioventricular block), biventricular pacing (BivP), right ventricular endocardial pacing (RV-EndoP), and left ventricular epicardial pacing (LV-EpiP). Signals from the standard 12-lead ECG were recorded simultaneously to measure the QT interval, JT interval, and Tp-e interval, from which the heart rate-corrected QTc interval, JTc interval, and Tp-ec interval were determined. The JTc interval and Tp-ec interval were prolonged during LV-EpiP and BivP compared with those during spontaneous cardiac rhythm and RV-EndoP. The JTc dispersion and Tp-ec dispersion were not significantly different among the four pacing modes. Epicardial pacing prolongs myocardial repolarisation time and increases transmural dispersion of repolarisation. Epicardial pacing has no significant effect on the dispersion of regional ventricular repolarisation.

The utilization of twelve-lead electrocardiography for predicting sudden cardiac death after heart transplantation

Sudden cardiac death (SCD) occurs commonly after heart transplantation (HTX). The utilization of surface electrocardiography (ECG) to assess post-HTX SCD has not been investigated thoroughly. This study aimed to investigate the specific changes in surface ECG in HTX patients with SCD. A total of 227 HTX patients (age 48 ± 14 y/o, mean donor age 34 ± 14 y/o, 173 males) were followed up regularly at the outpatient clinic. Twelve-lead ECG's were recorded during 1-2 monthly visits. Serial ECG parameters and relevant clinical data were collected and analyzed. During the follow-up period of 96 ± 51 months, SCD occurred in 28 (12.3%) patients. The baseline ECG parameters were comparable between patients with and without SCD. Important ECG trends of rising rest heart rates and prolongation of corrected QT (QTc) and JT (JTc) intervals were observed prior to development of SCD. After adjustment for other clinical variables, the independent predictors for SCD were older donor age (p = 0.014, OR 1.05, 95% CI 1.01-1.09), faster heart rate (p = 0.006, OR 1.06, 95% CI 1.02-1.1) and longer JTc interval (p = 0.015, OR 1.03, 95% CI 1.01-1.06). SCD occurred in 71.4% patients presenting with all three risk predictors. Besides older donor age, important ECG signs, including prolongation of the JTc interval and increased heart rate during post HTX follow up, could predict SCD.

Effect of Artesunate on Electrocardiographic QT Interval in Patients with Plasmodium Falciparum Malaria

Background: Several anti-malarial drugs are associated with adverse cardiovascular effects. There are a few reports available on the potential cardiac effects ( QTc interval) of artesunate, which includes an increased risk of potentially ventricular arrhythmia. This study aimed to evaluate the electrocardiographic (ECG) Changes (QTc interval ) in malaria patients treated with artesunate. Method: Total 32 (16 malea16 female ) patients with severe Falciparum malaria enrolled in medical ward, CIMS hospital Bilaspur (C.G) were selected. Electrocardiogram was recorded, and QTc interval was calculated before and after administration of three doses of artesunate given by intravenous injection in all patients who were positive for Falciparum malaria. Results: The mean QTc interval was not affected by intravenous artesunate (2.4 mg/kg) given at different time intervals(p>0.05). There was no significant effect observed on the JTc or PR interval, QRS width, blood pressure and heart rate. Intravenous artesunate does not have significant other cardiovascular effects in patients with severe Falciparum malaria. Conclusion: Intravenous artesunate does not have significant cardiovascular effects in patients with falciparum malaria.

Facilitating assessment of QT interval duration during ventricular pacing

We aimed to facilitate the assessment of the QT interval duration during conventional right ventricular pacing (VP) by uncovering relationships with the underlying QT interval during intrinsic atrioventricular conduction (IC). The study patients (n = 122, age 68 ± 11 years) were dual-chamber device recipients with preserved IC and narrow QRS complexes. Patients were classified into either 'normal-QT' (n = 70) or 'prolonged-QT' (n = 52) group. Incremental atrial pacing rates were exercised to record serial QT/JT intervals over 5 min periods in IC mode and then in VP mode. Six different QT correction methods for heart rate were applied to assess the effect (i) of pacing mode (IC vs. VP) and (ii) of heart rate on the derived QT(c)/JT(c) intervals by mixed-effects linear models. Following VP, the uncorrected QT/JT intervals as well as the JTc intervals shortened (P < 0.001), whereas the QTc intervals prolonged (P < 0.001). In both patient groups, the Framingham and Nomogram methods demonstrated the optimal balance to assess QTc, with low heart rate dependence during VP and minimal interaction between pacing mode and heart rate. The Rautaharju formula provided excellent correction for the QT changes induced by VP, but the QTc interval responded differently to rate changes in IC vs. VP mode. Bazett's formula exaggerated QTc/JTc rate dependency during VP. The Framingham and Nomogram correction methods perform most reliably in assessing the underlying QT interval during IC from the ventricular paced QT interval.

Optimal QT/JT Interval Assessment in Patients with Complete Bundle Branch Block

Prolonged ventricular repolarization duration confers increased risk for malignant ventricular arrhythmias. We sought to clarify the optimal method of QT/JT interval assessment in patients with complete bundle branch block (BBB). Study patients (n = 71) were dual-chamber device recipients with baseline left or right BBB who preserved intrinsic ventricular activation during incremental atrial pacing. Patients were classified according to the presence or not of structural heart disease. The former group received chronic amiodarone therapy. QT and JT intervals were recorded at baseline heart rate of 51 ± 4 beats/min and during atrial pacing at 60, 80, and 100 beats/min. We used linear mixed-effects models to assess the effect of heart rate on the derived QTc and JTc values with the use of six different heart rate correction formulae. Heart rate had a significant effect on the QTc and the JTc intervals regardless of the correction formula used (P < 0.001 for all formulae). The formula of Hodges demonstrated the least variability in QTc and JTc measurements across the different heart rates in both patients groups without (F = 15.05 and F = 13.53, respectively) and with structural heart disease (F = 5.71 and F = 7.69, respectively), followed by the Nomogram and Framingham methods, whereas the uncorrected QT and JT intervals showed comparable heart rate-dependency. The application of Bazett's JTc and QTc led to the most pronounced interval variations in any case with BBB. The Hodges, Nomogram and Framingham correction methods provide best assessment of QT/JT intervals in BBB, whereas Bazett's formula exaggerates heart rate-dependency of ventricular repolarization intervals.

Analysis and Dispersion of QT, JT and Tpeak-Tend Intervals in Elite Female Water Polo Players

Background The physiology of water polo has been difficult to study d ue to the characteristics of the game in the field of play. Little is known about cardiac electrophysiology in these athletes, particularly in women. The electrocardiographic findings in elite water polo athletes have been rarely studied. Objectives To analyze the ventricular repolarization in female water polo players from the Cuba’s National Preliminary Squad. M aterial and Methods W e conducted a cross-sectional study in a sample of two groups of women, one with 20 athletes and another with 20 healthy non-athletes. The electrocardiographic parameters of ventricular repolarization were compared in both groups. Results Mean age was 22.45±5.30 years vs. 22.45±5.30 years; p >0.05. Weight was greater in athletes compared to non-athletes (69.63±7.73 kg vs. 51.20±6.63 kg; p <0.001 ). Mean duration of sporting practice was 13.5 years. There were no significant differences in QTc and JTc intervals in lead DII between both groups, yet the intervals measured in lead V5 were longer in athletes (QTc: 405 ms vs. 424 ms; p <0.05 - JTc: 307 ms vs. 329 ms; p <0.05 ). QT interval dispersion was greater in athletes compared to non-athletes (74 ms vs. 43 ms; p <0.001). Tpeak-Tend interval was greater in athletes in leads V1 (64 ms vs. 81 ms; p <0.05), V3 (78 ms vs. 92 ms; p< 0.05), V4 (72 ms vs. 83 ms; p <0.05) and V5 (63 ms vs. 80 ms; p <0.05). Conclusions QTc and JTc intervals and QT interval dispersion were significantly greater in athletes. Tpeak-Tend interval was significantly greater in athletes in leads V1, V3, V4 and V5; Tpeak-Tend interval dispersion was greater, though not statistically significant in athletes.

Abnormalities of Cardiac Repolarization in Williams Syndrome

Williams syndrome (WS) affects 1 in 8,000 live births and has a high risk of sudden death. No previous studies have evaluated corrected QT (QTc) prolongation in WS. Retrospective review of all patients with WS evaluated at our institution from January 1, 1980 to December 31, 2007 was performed. WS was diagnosed by a medical geneticist and/or by fluorescence in situ hybridization. Patients with ≥1 electrocardiogram (ECG) with sinus rhythm and measurable intervals were included. Normal control ECGs were identified from a large clinical database. Corrected JT (JTc) interval was calculated when QRS and QTc intervals were prolonged. QTc interval ≥460 ms and JTc interval >340 ms were defined as prolonged. Prevalence comparisons were made using Fisher's exact test. Statistical probability of <0.05 was considered significant. Of 270 patients identified, 188 had ECGs for review. Complete data were present in 499 of 517 ECGs (patients' mean age 10.3 ± 9.9 years); 1,522 normal ECGs of age-similar patients composed the control group. QTc prolongation prevalences were 2.0% in controls and 13.6% in WS (p <0.0001); in those, JTc prolongation prevalences were 1.8% in controls and 11.7% in WS (p <0.0001). Four patients died during follow-up; 2 had QTc prolongation and 1 died during noncardiac surgery. Another patient with QTc prolongation sustained cardiac arrest during a procedure. In conclusion, cardiac repolarization is prolonged in WS. Presence of prolonged cardiac repolarization may contribute to the high incidence of periprocedural mortality in these patients. All patients with WS should be screened for cardiac repolarization abnormalities, especially before surgery.

Changes in the QTc interval after administration of flecainide acetate, with and without coadministered Paroxetine, in Relation to Cytochrome P450 2D6 Genotype: Data from an open-label, two-period, single-sequence crossover study in healthy Korean male subjects

Background: Flecainide acetate is a class Ic antiarrythmic agent that is metabolized by the cytochrome P450 (CYP) 2D6 isozyme. A previous open-label, 2-period, single-sequence crossover study in healthy Korean male volunteers found differences in the pharmacokinetics of flecainide between subjects with the CYP2D6 wild-type allele and those with the CYP2D6*10 allele, as well as differences in the pharmacokinetic interaction between flecainide and the CYP2D6 inhibitor paroxetine between genotype groups. Objective: This study evaluated QTc-interval changes after administration of a single oral dose of flecainide, with and without paroxetine, in relation to CYP2D6 genetic polymorphism. Methods: This was a follow-on to the previous pharmacokinetic study and used data from the same group of healthy Korean male volunteers. Subjects were grouped by CYP2D6 genotype as follows: CYP2D6*1/*1 or CYP2D6*1/*2 (group 1, extensive metabolizers); CYP2D6*1/*10 (group 2, intermediate metabolizers); and CYP2D6*10/*010 or CYP2D6*10/*36 (group 3, poor metabolizers). Flecainide 200 mg was administered on day 1 (period 1); after a 7-day washout period, subjects received paroxetine 20 mg once daily from day 8 to day 14, and flecainide 200 mg on day 15 (period 2). On days 1 and 15, serial 12-lead ECGs were obtained before flecainide dosing and at 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, and 24 hours after dosing. Baseline ECGs were obtained at the same time points on days -1 and 14. Machine-read changes in the QT interval corrected using the Fridericia formula (QTcF) and manually read changes in the QT interval individually corrected using mixed-effects modeling (QTcI) from time-matched baseline were analyzed by genotype and by period (baseline and paroxetine-inhibited state). The QRS duration and JTc interval (QTcF - QRS) were also determined. Results: Twenty-one healthy volunteers (mean [SD] age, 24.5 [3.0] years; mean height, 173.5 [4.6] cm; mean weight, 69.1 [4.5] kg), 7 in each group, were enrolled in and completed the study. In period 1, all genotype groups had significant increases from time-matched baseline in both the QTcF interval (group 1:17.4 milliseconds [90% CI, 9.9-24.9], P < 0.001; group 2: 11.1 milliseconds [90% CI, 7.9-14.3], P = 0.013; and group 3: 20.5 milliseconds [90% CI, 12.8-28.2], P < 0.001) and the QTcI interval (group 1:15.4 milliseconds [90 % CI, 8.0-22.9], P = 0.001; group 2: 9.1 milliseconds [90% CI, 6.5-11.8], P = 0.030; and group 3:16.4 milliseconds [90% CI, 9.3-23.5], P = 0.001); the extent of increase did not differ significantly between groups. In groups 1 and 2, the least squares mean difference between period 1 and period 2 was statistically significant for the change in QTcF interval (6.5 milliseconds [90 CI, 3.2-9.8], P = 0.002; and 6.7 milliseconds [90% CI, 3.6-9.7], P = 0.001, respectively) and QTcI interval (6.9 milliseconds [90% CI, 4.1-9.8], P < 0.001; and 5.8 milliseconds [90% CI, 3.4-8.3], P < 0.001). In group 3, the least squares mean difference between period 1 and period 2 was statistically significant for the change in QTcI interval (3.9 milliseconds [90% CI, 1.3-6.5], P = 0.015) but not for the change in QT cF interval. The changes in QRS duration did not differ significantly by genotype or period. Consistent with the findings for the QTc interval, the least squares mean difference between period 1 and period 2 was statistically significant for the change in JTc interval in groups 1 and 2 (6.9 milliseconds [90% CI, 3.7-10.2], P = 0.001; and 5.4 milliseconds [90% CI, 2.7-8.2], P = 0.001, respectively) but not in group 3. Conclusion: The extent of drug interaction between flecainide and paroxetine, as reflected in the change in QTc interval (used as a pharmacodynamic biomarker), was influenced by the CYP2D6*10 allele in these healthy Korean male volunteers.

The Relationship of Bipolar Left Ventricular Pacing Stimulus Intensity to Cardiac Depolarization and Repolarization in Humans with Cardiac Resynchronization Devices

Myocardial depolarization can be altered by varying pacing stimulus output. This may have implications on response rates for cardiac resynchronization therapy (CRT). The purpose of our study was to determine the relationship of left ventricular (LV) pacing stimulus intensity to measures of depolarization and repolarization in humans with CRT devices. In 37 patients with a CRT device and bipolar LV leads, bipolar LV-only pacing from maximum output to threshold was performed. The presence of changes in depolarization was defined by predetermined changes in ECG morphology that accompanied a change in bipolar stimulus amplitude. ECG parameters and the EGMs were analyzed at various LV pacing stimulus intensities. Changes in ECG morphology were apparent in 70% of patients. These occurred at a mean LV stimulus amplitude of greater than 2.7 +/- 0.8 V at 1 ms. Of the patients with changes in surface ECG, the transventricular conduction time decreased from 155 +/- 41 ms at low output to 141 +/- 39 ms at high output (P < 0.01). Despite a significant reduction in QRS duration with high output, mean QTc and JTc interval increased with increasing LV stimulus strength (539 +/- 45 vs 559 +/- 46 ms (P < 0.01) and 353 +/- 31 ms vs 377 +/- 32 (P < 0.01)). Increased LV stimulus intensity, independent of RV anodal capture, is associated with faster transventricular conduction time, changes in myocardial depolarization, and longer QT intervals. These findings have important implications on the relationship of programmed LV pacing output to pacing-induced proarrhythmia and clinical CRT response rates.

Catheter Ablation of a Posteroseptal Accessory Pathway in a Case With Congenital Long QT Syndrome

A 23-year-old woman with pre-excitation who was resuscitated from ventricular fibrillation underwent electrophysiologic testing. Successful catheter ablation of a left posteroseptal accessory pathway was achieved. Though the JT and JTc intervals as well as QT and QTc intervals were prolonged before and one day after the ablation, they normalized within about 5 hours after the ablation. This case demonstrated that in a patient with pre-excitation and long QT syndrome (LQTs), the JTc interval was useful for diagnosing LQTs and a longer follow-up of the JTc interval after the ablation was necessary in order not to miss the diagnosis of LQTs.

Does Artesunate Prolong the Electrocardiograph QT Interval in Patients with Severe Malaria?

Several antimalarials can cause significant prolongation of the electrocardiograph QT interval, which can be associated with an increased risk of potentially lethal ventricular arrhythmias. High doses of artemether and artemotil have been associated with QT prolongation in dogs, raising the possibility of a class effect with the artemisinin derivatives. Serial electrocardiograms were recorded, and QTc interval was calculated before and after administration of artesunate by intravenous injection in patients with severe falciparum malaria in Bangladesh. Of 21 adult patients with severe malaria enrolled, 8 (38%) died. The mean QTc interval was unaffected by bolus intravenous artesunate (2.4 mg/kg). In two patients, the QTc interval exceeded 0.5 seconds, but in both cases, an alternative explanation was plausible. No effect was observed on the JTc or PR interval, QRS width, blood pressure, or heart rate. Intravenous artesunate does not have significant cardiovascular effects in patients with severe falciparum malaria.

Does artesunate prolong the electrocardiograph QT interval in patients with severe malaria?

Several antimalarials can cause significant prolongation of the electrocardiograph QT interval, which can be associated with an increased risk of potentially lethal ventricular arrhythmias. High doses of artemether and artemotil have been associated with QT prolongation in dogs, raising the possibility of a class effect with the artemisinin derivatives. Serial electrocardiograms were recorded, and QTc interval was calculated before and after administration of artesunate by intravenous injection in patients with severe falciparum malaria in Bangladesh. Of 21 adult patients with severe malaria enrolled, 8 (38%) died. The mean QTc interval was unaffected by bolus intravenous artesunate (2.4 mg/kg). In two patients, the QTc interval exceeded 0.5 seconds, but in both cases, an alternative explanation was plausible. No effect was observed on the JTc or PR interval, QRS width, blood pressure, or heart rate. Intravenous artesunate does not have significant cardiovascular effects in patients with severe falciparum malaria.

Advanced electrocardiographic predictors of mortality in familial dysautonomia

Objective To identify electrocardiographic predictors of mortality in patients with familial dysautonomia (FD). Methods Ten-minute resting high-fidelity 12-lead electrocardiograms (ECGs) were obtained from 14 FD patients and 14 age/gender-matched healthy subjects. Multiple conventional and advanced ECG parameters were studied for their ability to predict mortality over a subsequent 4.5-year period, including representative parameters of heart rate variability (HRV), QT variability (QTV), T-wave complexity, signal averaged ECG, and 3-dimensional ECG. Results Four of the 14 FD patients died during the follow-up period, three with concomitant pulmonary disorder. Of the ECG parameters studied, increased non-HRV-correlated QTV and decreased HRV were the most predictive of death. Compared to controls as a group, FD patients also had significantly increased ECG voltages, JTc intervals and waveform complexity, suggestive of structural heart disease. Conclusion Increased QTV and decreased HRV are markers for increased risk of death in FD patients. When present, both markers may reflect concurrent pathological processes, especially hypoxia due to pulmonary disorders and sleep apnea.

Biventricular Pacing and QT Interval Prolongation

The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB). One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 +/- 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 +/- 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 +/- 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 +/- 9 ms during BiV pacing vs 178 +/- 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 +/- 34 ms with BiV pacing versus 445 +/- 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 +/- 9 ms vs 320 +/- 20 ms, P < 0.0001). During a mean follow-up of 24 +/- 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued. Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.

Repolarization Duration in Patients With Conduction Disturbances After Myocardial Infarction

This study compared different measurements of repolarization duration in patients after infarction with and without conduction disturbances and evaluated the prognostic significance of repolarization parameters for predicting mortality in patients with conduction abnormalities. The study population consisted of 3,282 patients after recent myocardial infarction. Repolarization duration was measured using Bazett QTc and JTc (QTc minus QRS) and Rautaharju QT and JT(RR) formulas. All-cause mortality was the end point of the predictive models. In 259 patients with conduction disturbances, 76 (2.3%) had indeterminate ventricular conduction disturbances, 126 (3.8%) had right bundle branch block, and 47 (1.4%) had left bundle branch block. Patients with left bundle branch block demonstrated excessive prolongation of the QTc interval, which was not observed when using the JT(RR) interval. There were no significant differences in repolarization duration by gender in patients with conduction abnormalities. Repolarization parameters were uniformly dichotomized at the 75th percentile (QTc interval >490 ms, JTc interval >360 ms, QT(RR,QRS) interval >433 ms, JT(RR) interval >359 ms) to determine their prognostic significance for predicting mortality. After adjustment for significant clinical predictors of mortality, the hazard ratios were 1.65 for QTc interval (p = 0.062), 1.46 for JTc interval (p = 0.168), 1.71 for QT(RR,QRS) interval (p = 0.043), and 1.70 for JT(RR) interval (p = 0.044)(.) In conclusion, patients with left bundle branch block, right bundle branch block, or indeterminate ventricular conduction disturbances show longer repolarization duration than patients without these conduction disturbances, and QT(RR,QRS) and JT(RR) intervals reflect better than QTc repolarization duration in patients with conduction disturbances. QT(RR) and JT(RR) intervals significantly and independently predict mortality in patients after infarction with conduction disturbances.

Female Mice Lacking Estrogen Receptor β Display Prolonged Ventricular Repolarization and Reduced Ventricular Automaticity After Myocardial Infarction

Major gender-based differences in the incidence of ventricular tachyarrhythmia after myocardial infarction have been shown in humans. Although the underlying mechanisms are unclear, earlier studies suggest that estrogen receptor-mediated effects play a major role in this process. We examined the effect of estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) on the electrophysiological phenotype in female mice with and without chronic anterior myocardial infarction. There was no significant difference in overall mortality, infarct size, and parameters of left ventricular remodeling when we compared infarcted ERalpha-deficient and ERbeta-deficient mice with infarcted wild-type animals. In the 12-hour telemetric ECG recording 6 weeks after myocardial infarction, surface ECG parameters did not show significant differences in comparisons of ERalpha-deficient mice versus wild-type controls, infarcted versus noninfarcted ERalpha-deficient mice, and infarcted ERalpha-deficient versus infarcted wild-type mice. However, infarcted ERbeta-deficient versus noninfarcted ERbeta-deficient mice showed a significant prolongation of the QT (61+/-6 versus 48+/-8 ms; P<0.05) and QTc intervals (61+/-7 versus 51+/-9 ms; P<0.05) and the JT (42+/-6 versus 31+/-4 ms; P<0.05) and JTc intervals (42+/-7 versus 33+/-4 ms; P<0.05). Furthermore, infarcted ERbeta-deficient versus infarcted wild-type mice showed a significant prolongation of the QT (61+/-6 versus 53+/-8 ms; P<0.05) and QTc intervals (61+/-7 versus 53+/-7 ms; P<0.05) and the JT (42+/-6 versus 31+/-5 ms; P<0.05) and JTc intervals (42+/-7 versus 31+/-5 ms; P<0.05), accompanied by a significant decrease of ventricular premature beats (7+/-21/h versus 71+/-110/h; P<0.05). Finally, real-time polymerase chain reaction-based quantitative analysis of mRNA levels showed a significantly lower expression of Kv4.3 (coding for I(to)) in ERbeta-deficient mice (P<0.05). Estrogen receptor beta deficiency results in prolonged ventricular repolarization and decreased ventricular automaticity in female mice with chronic myocardial infarction.

JTC interval prolongation is associated with ventricular arrhythmia events post cardiac resynchronization therapy

Background: Epicardial left ventricular pacing for cardiac resynchronization therapy (CRT) has been shown to prolong the QT interval and predispose to ventricular arrhythmia events (VAE) early on after implantation. The prognostic value of cardiac repolarization changes on long-term follow-up has not been reported. We sought to determine the relationship of VAE with post-CRT cardiac repolarization changes.

The effects of sotalol on ventricular repolarization during exercise

Although after pacing animal and human studies have demonstrated a rate-dependent effect of sotalol on ventricular repolarization, there is little information on the effects of sotalol on ventricular repolarization during exercise. This study attempted to show the effects of sotalol on ventricular repolarization during physiological exercise. Thirty-one healthy volunteers (18 males, 13 females) were enrolled in the study. Each performed a maximal treadmill exercise test according to the Bruce protocol after random treatment with sotalol, propranolol and placebo. Sotalol significantly prolonged QTc (corrected QT) and JTc (corrected JT) intervals at rest compared with propranolol (QTc 324.86 ms vs 305.21 ms, P<0.001; JTc 245.04 ms vs 224.17 ms, P<0.001) and placebo (QTc 324.86 ms vs 314.06 ms, P<0.01; JTc 245.04 ms vs. 232.69 ms, P<0.001). The JTc percent reduction increased progressively with each stage of exercise and correlated positively with exercise heart rate (r=0.148, P<0.01). The JTc percent reduction correlation with exercise heart rate did not exist with either propranolol or placebo. These results imply that with sotalol ventricular repolarization is progressively shortened after exercise. Thus the specific class III antiarrhythmic activity of sotalol, present as delay of ventricular repolarization, may be attenuated during exercise. Such findings may imply the need to consider other antiarrythmic therapy during periods of stress-induced tachycardia.