QT Peak Interval Research Articles

Repolarization and ventricular arrhythmia during targeted temperature management post cardiac arrest

BackgroundTargeted temperature management (TTM) following out-of-hospital cardiac arrest (OHCA) prolongs the QT-interval but our knowledge of different temperatures and risk of arrhythmia is incomplete. ObjectiveTo assess whether the QTc, QT-peak (QTp) and T-peak to T-end interval (TpTe) may be useful markers of ventricular arrhythmia in contemporary post cardiac arrest treatment. MethodsAn ECG-substudy of the TTM-trial (TTM at 33 °C vs. 36 °C) with serial ECGs from 680 (94%) patients. Bazett’s (B) and Fridericia’s (F) formula were used for heart rate correction of the QT, QTp and TpTe. Ventricular arrhythmia (VT/VF) were registered during the first three days of post cardiac arrest care. ResultsThe QT, QTc and QTp intervals were prolonged more at 33 °C compared to 36 °C and restored to similar and lower levels after rewarming. The TpTe-interval remained between 92–100 ms throughout TTM in both groups.The QTc intervals were associated with ventricular arrhythmia, but not after adjustment for cardiac arrest characteristics. The QTp-interval was not associated with risk of ventricular arrhythmia. Heart rate corrected TpTe-intervals were associated with higher risk of arrhythmia (Odds ratio (OR): TpTe(B): 1.12 (1.02–1.23, p = 0.01 TpTe(F): 1.12 (1.02–1.23, p = 0.02) per 20 ms). Further a prolonged TpTe-interval ≥ 90 ms was consistently associated with higher risk (ORadjusted: TpTe(B): 2.05 (1.25–3.37), p < 0.01, TpTe(F): 2.14 (1.32–3.49), p < 0.01). ConclusionsTTM prolongs the QT-interval by prolongation of the QTp-interval without association to increased risk. The TpTe-interval is not significantly affected by core temperature, but heart rate corrected TpTe intervals are robustly associated with risk of ventricular arrhythmia. Trial registrationThe TTM-trial is registered and accessible at ClinicalTrials.gov (Identifier: NCT01020916).

Mutual Information Reveals Non-linear Relationships between Electrocardiographic Conduction or Repolarization Indices and Mechanical Dispersion by Speckle-Tracking Echocardiography in the General Population

Electrical inhomogeneities can lead to regional heterogeneity in left ventricular contraction. We investigated the correlation between electrocardiographic parameters of conduction and/or repolarization and myocardial longitudinal strain-derived parameters in a general population. Mean and dispersion (maximum–minimum) values were calculated for the electrocardiographic indices: QT interval, Tpeak–Tend interval (Tpe), JTpeak interval (JTp), JTend interval (JTe), QTpeak interval (QTp). Mechanical dispersion was assessed using the standard deviation (SD) of time-to-peak longitudinal strains (MDSD) and the difference between the longest time and shortest time to peak strain (MDdelta) by speckle-tracking echocardiography. A total of 59 patients, 60 ± 12 y, were included. Tpe, Tpe/QT, Tpe/JTp and Tpe/JTe correlated well with MDSD and MDdelta (r ≥ 0.43, p < 0.001). Mutual information revealed significant non-linear relationships between most of the electrocardiographic indices measured and mechanical dispersion. In conclusion, there is a moderate linear correlation between electrocardiographic indices reflecting repolarization heterogeneities and speckle tracking-assessed mechanical dispersion.

P506Brugada Syndrome: is the addition of the electrocardiographic risk markers the clue?

Abstract Background Risk stratification in Brugada Syndrome (BS) remains a clinical challenge. Several electrocardiografic (ECG) risk markers had been described, as a spontaneous type 1 Brugada pattern (ST1B), maximal time interval between the peak and the end of the t wave in precordial leads (Tpe Max), the presence of an S Wave on DI, a PR interval (PRi) ≥ 200ms and fragmented QRS (f-QRS). Purpose Evaluate the association of ECG risk markers with sudden cardiac death (SCD) or appropriate shocks (A-Sh) by implantable cardioverter defibrillator (ICD) in patients (p) with BS. Methods From a registry of 97 p with BS with a median follow up of 2.3 years (Q1 0.7-Q3 7.8), 12 lead ECG were recorded in every p. QT peak interval (QTp) was measured between the QRS onset and the peak of the T wave. Tpe was calculated between the difference of QT and QTp in precordial leads (V1 to V6). TpeMax was defined as the most prolonged Tpe. If an S-DI was present, duration and amplitude was measured. PRi was measured on DII. Baseline characteristics: Age 44 ± 13 years, male 74 (76%), secondary prevention 2 (3%), malignant syncope 10 (10%), inducible electrophysiology study 22/43 (51%), SCD on first grade family &amp;lt; 35 years 12 (12%) and ICD 34 (35%). A-Sh and SCD were compared among p with ST1B vs no ST1B, TpeMax≥100 vs &amp;lt;100ms, S-DI ≥0.4 vs &amp;lt;0.4ms, S-D ≥0.1 vs &amp;lt;0.1mV, PRi≥200 vs &amp;lt;200ms and presence of f-QRS ≥ 2 spike ≥ 2 leads. Variables that were associated with A-Sh or SCD were combined. For variables with significant difference sensibility (Sen) and specificity (Spe) was calculated. Results During follow up 6 p presented A-Sh and no p SCD. Results are described in the Table. Conclusion In our study population, there was a significant higher incidence of A-Sh in p with ST1B, Tpe Max ≥ 100ms and S-DI ≥ 0.1mV. We found that the presence of one ECG risk marker had a high sensibility to predict A-Sh. The presence of the 3 ECG risk markers highly increased specificity to predict A-Sh. Further trials should be carried out to asses if ECG risk markers would allow us to differentiate which asymptomatic patients could benefit from electrophysiological study for risk stratification (high sensibility - One ECG Risk marker) or would benefit from ICD implantation (high specificity - 3 ECG Risk markers). Abstract Figure.

Electrocardiogram Characteristics and Arrhythmic Events during Fever in Patients with Fever-Induced Brugada Syndrome

Introduction: Changes in electrocardiogram (ECG) parameters and the incidence of arrhythmic events in patients with fever-induced Brugada syndrome (BrS) remain unknown. Objective: We aimed to investigate the effect of hyperthermia on the ECG pattern and the occurrence of fever-triggered arrhythmic events (FTAEs) in patients with fever-induced BrS. Methods: We retrospectively analyzed a series of fever-induced BrS cases from January 1966 to November 2018. Clinical characteristics and ECG parameters were evaluated in the presence or absence of fever. Results: Syncope and implantable cardioverter defibrillator implantation occurred more frequently in BrS patients with FTAEs than in patients without FTAEs. In BrS patients <16 years old, more arrhythmia events occurred in patients with FTAEs than in patients without FTAEs (p = 0.04). During follow-up, 2 patients in the FTAEs group suffered new malignant arrhythmic events. Compared to the afebrile state, the J point increased significantly in precordial leads V1, V2, and V3 during the febrile state (all p < 0.01). The corrected QTpeak intervals in V1 and V2 were significantly longer in the FTAEs group than in the non-FTAEs group (354.5 ± 37.0 vs. 334.3 ± 45.5 ms, p < 0.01 and 368.0 ± 43.4 vs. 330.9 ± 41.5 ms, p < 0.01, respectively). An increased corrected QT dispersion and a lengthened corrected Tpeak-Tend dispersion were also observed during fever. Conclusions: Fever may not only reveal BrS but also induce life-threatening arrhythmic events, especially in children and adolescents.

FEATURES OF STRUCTURAL AND ELECTRICAL REMODELING OF THE HEART ASSOCIATED WITH HIGH RISK OF LIFETHREATENING VENTRICULAR TACHYARRHYTHMIAS IN PATIENTS WITH ISCHEMIC AND NON-ISCHEMIC CARDIOMYOPATHIES

Objective: to identify the features of myocardial fibrosis and ventricular repolarization disorders associated with malignant ventricular tachyarrhythmias (VT) in patients with ischemic (ICM) and non-ischemic cardiomyopathy (NICM).Material and Methods. Fifty consecutive patients (41 men and 9 women aged 60±13 years; 30 patients with ICM and 20 patients with NICM) underwent contrast magnetic resonance imaging (MRI) of the heart, QT dispersion analysis of 12-lead Holter ECG followed by implantation of cardioverter-defibrillator (ICD) or resynchronizing device with defibrillator (CRTD) to prevent sudden cardiac death.Results. According to data of 32 (28–43)-month follow up, VT paroxysms were registered in 20 of 30 patients (67%) with ICM and in 5 of 20 patients (25%) with NICM on follow-up. Data of successive univariate and ROC analyses of MRI indices differed between patients with and without recurrence of VTs in ICM and NICM patient groups. In ICM patients, VTs were associated with the values of QT (peak) interval dispersion over 80 mc according to data of Holter ECG monitoring and higher gray zone in the left ventricle (≥27%) according to contrast-enhanced MRI. Similar analyses in NICM patients showed that the most valuable diagnostic signs associated with the right ventricular tachycardias were the values of QT (peak) interval dispersion over 90 mc according to data of Holter ECG monitoring and the presence of non-transmural fibrosis of the left ventricle (≥27%) according to contrast-enhanced MRI.Conclusion. The features of structural remodeling of the left ventricle predisposing to VTs significantly differ in patients with ICM and NICM. Nevertheless, the presence of ventricular repolarization disorders, associated with onset of VTs, is universal in patients with ischemic and non-ischemic cardiomyopathies.

FEATURES OF STRUCTURAL AND ELECTRICAL REMODELING OF THE HEART ASSOCIATED WITH HIGH RISK OF LIFETHREATENING VENTRICULAR TACHYARRHYTHMIAS IN PATIENTS WITH ISCHEMIC AND NON-ISCHEMIC CARDIOMYOPATHIES

Objective: to identify the features of myocardial fibrosis and ventricular repolarization disorders associated with malignant ventricular tachyarrhythmias (VT) in patients with ischemic (ICM) and non-ischemic cardiomyopathy (NICM).Material and Methods. Fifty consecutive patients (41 men and 9 women aged 60±13 years; 30 patients with ICM and 20 patients with NICM) underwent contrast magnetic resonance imaging (MRI) of the heart, QT dispersion analysis of 12-lead Holter ECG followed by implantation of cardioverter-defibrillator (ICD) or resynchronizing device with defibrillator (CRTD) to prevent sudden cardiac death.Results. According to data of 32 (28–43)-month follow up, VT paroxysms were registered in 20 of 30 patients (67%) with ICM and in 5 of 20 patients (25%) with NICM on follow-up. Data of successive univariate and ROC analyses of MRI indices differed between patients with and without recurrence of VTs in ICM and NICM patient groups. In ICM patients, VTs were associated with the values of QT (peak) interval dispersion over 80 mc according to data of Holter ECG monitoring and higher gray zone in the left ventricle (≥27%) according to contrast-enhanced MRI. Similar analyses in NICM patients showed that the most valuable diagnostic signs associated with the right ventricular tachycardias were the values of QT (peak) interval dispersion over 90 mc according to data of Holter ECG monitoring and the presence of non-transmural fibrosis of the left ventricle (≥27%) according to contrast-enhanced MRI.Conclusion. The features of structural remodeling of the left ventricle predisposing to VTs significantly differ in patients with ICM and NICM. Nevertheless, the presence of ventricular repolarization disorders, associated with onset of VTs, is universal in patients with ischemic and non-ischemic cardiomyopathies.

Electrocardiographic T-wave parameters in families with long QT syndrome.

T-wave parameters, especially the Tpeak-Tend interval (TpTe), reflect the total dispersion of repolarization, whose amplification may lead to the development of life-threatening ventricular arrhythmias observed in the long QT syndrome (LQTS). The study attempted to evaluate QT, QTp (Q-Tpeak) and TpTe (Tpeak-Tend) intervals in unaffected and affected blood relatives of children with clinically confirmed LQTS as well as to determine whether the values of these repolarization parameters may be used in clinical practice. The study group included 47 affected blood relatives (27 LQTS1 and 20 LQTS2) and 68 unaffected family members without clinically confirmed LQTS symptoms. The TpTe, QT and QTp intervals were measured manually in the lead V5 of standard ECGs and corrected using Bazett's and Fridericia's formulas. The RR, QT, QTp and TpTe intervals with their corrected values were significantly longer (p < 0.0001) in the affected subjects than in the unaffected subjects and, similarly, in LQTS1 and LQTS2 patients compared with the unaffected family members. The TpTe interval in LQTS2 showed only a tendency to be longer compared to LQTS1, but did not reach statistical significance (p = 0.0933). For affected blood relatives, only the TpTe interval (p < 0.0409) and QT interval, corrected with Bazett's (p < 0.0393) and Fridericia's (p < 0.0495) formulas, enabled differentiation between LQTS1 (mean TpTe = 103 ±15) and LQTS2 women (mean TpTe = 106 ±17). Moreover, there were statistically significant differences (p < 0.05) in the TpTe interval between the 6 sex subgroups: unaffected women and men as well as women and men with LQTS1 and LQTS2. The electrocardiographic Tpeak-Tend parameter, in addition to the QT interval, is helpful in identifying affected blood relatives of children with LQTS, particularly for the group of LQTS1 and LQTS2 women. Further studies are required to assess the clinical importance of the TpTe interval in families with long QT syndrome.

A novel algorithm to predict the QT interval during intrinsic atrioventricular conduction from an electrocardiogram obtained during ventricular pacing

QT interval prolongation is a major arrhythmia risk factor. Standard QT interval limits are defined for preserved intrinsic atrioventricular and interventricular conduction. However, ventricular pacing (VP) prolongs the QRS duration, induces electrical remodeling, and therefore obscures the intrinsic QT interval. No consensus exists on QT interval monitoring during VP. The aim of this study was to develop an algorithm to predict the QT interval during intrinsic conduction (IC) from the VP electrocardiogram. We measured electrocardiographic intervals QRS, QT, QTpeak, JTpeak, and TpeakTend in 38 participants with cardiac devices and preserved atrioventricular and interventricular conduction. We performed paired measurements in AAI (IC) and DDD (VP) pacing modes at equal heart rates at baseline and after 1 week of VP. We fit linear mixed models to predict IC QT intervals from VP intervals and compared their fit with other proposed methods of IC QT interval estimation. After 1 week of VP, the IC QT interval prolonged while the VP QT interval shortened from their respective baseline values. VP QT interval shortening was due to TpeakTend interval shortening. JTpeak and QTpeak intervals prolonged in both pacing modes at 1 week. A formula using VP QTpeak interval and heart rate closely predicted the IC QT interval (r = 0.94), outperforming other methods, including subtraction of "excess" QRS duration from the actual QT interval (r = 0.64) and subtraction of fixed values from heart rate-corrected QT interval (r = 0.58 and r = 0.69). Validation in 2000 bootstrapped data sets confirmed the model's performance (r = 0.93) compared to others (r = 0.43-0.58). In patients with VP, a formula using the QTpeak interval accurately predicts the intrinsic QT interval.

Increased Tpeak-Tend interval is highly and independently related to arrhythmic events in Brugada syndrome

Risk stratification in Brugada syndrome (BS) remains controversial. The time interval between the peak and the end of the T wave (Tpe interval), a marker of transmural dispersion of repolarization, has been linked to malignant ventricular arrhythmias in various settings but leads to discordant results in BS. We study the correlation of the Tpe interval with arrhythmic events in a large cohort of patients with BS. A total of 325 consecutive patients with BS (mean age 47±13 years, 259 men-80%) with spontaneous (n=143, 44%) or drug-induced (n=182, 56%) type 1 electrocardiogram were retrospectively included. 235 were asymptomatic (70%), 80 presented with unexplained syncope (22%), and 10 presented with sudden death (SD) or appropriate implantable cardioverter-defibrillator therapy (AT) (8%) at diagnosis or over a mean follow-up of 48 ± 34 months. The Tpe interval was calculated as the difference between the QT interval and the QT peak interval as measured in each of the precordial leads. The Tpe interval from lead V1 to lead V4, maximum value of the Tpe interval (max Tpe), and Tpe dispersion in all precordial leads were significantly higher in patients with SD/AT or in patients with syncope than in asymptomatic patients (P < .001). A max Tpe of ≥100 ms was present in 47 of 226 asymptomatic patients (21%), in 48 of 73 patients with syncope (66%), and in 22 of 26 patients with SD/AT (85%) (P < .0001). In multivariate analysis, a max Tpe of ≥100 ms was independently related to arrhythmic events (odds ratio 9.61; 95% confidence interval 3.13-29.41; P < .0001). The Tpe interval in the precordial leads is highly related to malignant ventricular arrhythmias in this large cohort of patients with BS. This simple electrocardiographic parameter could be used to refine risk stratification.

Electrocardiographic P-Wave Duration, QT Interval, T Peak to End Interval and Tp-e/QT Ratio in Pregnancy with Respect to Trimesters.

P-wave duration helps to determine the risk of atrial arrhythmia, especially atrial fibrillation. QT interval, T peak to end interval (Tp-e), and Tp-e/QT ratio are electrocardiographic indices related to ventricular repolarization which are used to determine the risk of ventricular arrhythmias. We search for any alterations in electrocardiographic indices of arrhythmia in the pregnancy period with respect to trimesters. We enrolled 154 pregnant and 62 nonpregnant, healthy women into this cross-sectional study. Maximum and minimum P-wave durations (Pmax, Pmin), and QT intervals (QTmax, QTmin) were measured from 12 leads. QT measurements were corrected using Fridericia (QTc-Fr) and Bazett's (QTc-Bz) correction. Tp-e interval was obtained from the difference between QT interval, and QT peak interval (QTp) measured from the beginning of the QRS until the peak of the T wave. Tp-e/QT ratio was calculated using these measurements. Pmax were 93.0 ± 9.1, 93.9 ± 8.9, 97.9 ± 5.6, 99.0 ± 6.1 in nonpregnant women, first, second, third trimesters of pregnancy, respectively (P = 0.001); whereas Pmin values were not significantly different. QTc-Fr max were 407.4 ± 14.2, 408.5 ± 16.1, 410.1 ± 13.1, 415.1 ± 10.1 (P = 0.007); Tp-e were 72.7 ± 6.2, 73.2 ± 6.5, 77.2 ± 8.9, 87.2 ± 9.6 (P < 0.001); and Tp-e/QT were 0.17 (0.14-0.20), 0.17 (0.14-0.20), 0.18 (0.15-0.23), 0.20 (0.16-0.25) in nonpregnant women, first, second, and third trimesters of pregnancy respectively (P < 0.001). None of the participants experienced any arrhythmic event. P-wave duration is prolonged in the second trimester, and resumes a plateau thereafter. Maximum QTc interval, Tp-e interval and Tp-e/QT ratio are increased in the late pregnancy. Although these indices are altered during the course of pregnancy, they all remain in the normal ranges.

The phenotype characteristics of type 13 long QT syndrome with mutation in KCNJ5 (Kir3.4-G387R)

Long QT syndrome type 13 (LQT13) is caused by loss-of-function mutation in the KCNJ5-encoded cardiac G-protein-coupled inward rectifier potassium channel subtype 4 protein. The electrocardiographic (ECG) features of LQT13 are not described yet. To describe for the first time in detail the phenotype-genotype relationship of the ECG and clinical features in patients with LQT13. The 12-lead ECGs, 24-hour Holter recordings, and clinical information from KCNJ5-G387R mutation carriers of a fourth-generation Han Chinese family with LQT13 and a group of healthy Chinese individuals were analyzed. Compared with the analysis of the healthy group (n = 8), age- and sex-matched pair analysis revealed that the mutation carriers (n = 8) had ventricular repolarization abnormality results in the prolongation of corrected QT and QTpeak intervals (P < .01); greater combined measure of repolarization morphology (T-wave morphology combination score) based on asymmetry, flatness, and notch (P < .01); and reduced low frequency/high frequency ratio of heart rate variability (P < .01) as a reflection of cardiac autonomic imbalance. Mean heart rate, time domain parameters of heart rate variability, time interval from T-wave peak to T-wave end, and T-wave amplitude were similar. This study demonstrates for the first time the ECG features of patients with LQT13. Our data suggest that QTpeak intervals and T-wave morphology combination score may be the better parameters than the corrected QT interval to predict the phenotype-genotype relationship in patients with LQT13.

Normal standards for computer-ECG programs for prognostically and diagnostically important ECG variables derived from a large ethnically diverse female cohort: The Women's Health Initiative (WHI)

BackgroundSubstantial new information has emerged recently about the prognostic value for a variety of new ECG variables. The objective of the present study was to establish reference standards for these novel risk predictors in a large, ethnically diverse cohort of healthy women from the Women's Health Initiative (WHI) study. Methods and ResultsThe study population consisted of 36,299 healthy women. Racial differences in rate-adjusted QT end (QTea) and QT peak (QTpa) intervals as linear functions of RR were small, leading to the conclusion that 450 and 390ms are applicable as thresholds for prolonged and shortened QTea and similarly, 365 and 295ms for prolonged and shortened QTpa, respectively. As a threshold for increased dispersion of global repolarization (TpeakTend interval), 110ms was established for white and Hispanic women and 120ms for African-American and Asian women. ST elevation and depression values for the monitoring leads of each person with limb electrodes at Mason-Likar positions and chest leads at level of V1 and V2 were first computed from standard leads using lead transformation coefficients derived from 892 body surface maps, and subsequently normal standards were determined for the monitoring leads, including vessel-specific bipolar left anterior descending, left circumflex artery and right coronary artery leads. The results support the choice 150μV as a tentative threshold for abnormal ST-onset elevation for all monitoring leads. Body mass index (BMI) had a profound effect on Cornell voltage and Sokolow–Lyon voltage in all racial groups and their utility for left ventricular hypertrophy classification remains open. ConclusionsCommon thresholds for all racial groups are applicable for QTea, and QTpa intervals and ST elevation. Race-specific normal standards are required for many other ECG parameters.

Electrocardiographic estimates of regional action potential durations and repolarization time subintervals reveal ischemia-induced abnormalities in acute coronary syndrome not evident from global QT

We evaluated electrocardiogram estimates of repolarization times (RTs) and action potential durations (APD) separately for initial and terminal repolarization periods in a reference group of 5376 healthy men and women and in 125 acute coronary syndrome patients with and 657 without diagnostic ST elevation (ST-elevation myocardial infarction [STEMI] and non-STEMI [NSTEMI], respectively). Two key covariates in the model are the rate-adjusted QT peak interval (QTpa), assigned to earliest epicardial RT (RTepi), and (Tp-Txd), the rate-invariant interval from Tp to the inflection point (Txd) at T wave downstroke. (Tp-Txd) defines the crossmural RT gradient (XMRTgrad). Transmural RTgrad (TMRTgrad) is obtained as CosΘ(Rmax|Tmax)*XMRTgrad, where Θ is the spatial angle between the maximal QRS and T vectors. Derived endocardial variables are the XMRTendo, equal to QTpa + XMRTgrad and TMRTendo, equal to QTpa + TMRTgrad. Noting that excitation time (ET) and RT define APD, APDepi = RTepi - QRp in V6 and TMAPDendo = TMRTendo - 10 milliseconds. Compared to the reference group, the estimates for APDepi and TMAPDendo were shortened in STEMI by 20 and 31 milliseconds, respectively, (p <0.001 for both) signifying transmural ischemia. In contrast, in NSTEMI, TMAPDendo was shortened by 28 milliseconds (P <0.001) with a lesser, 5 millisecond shortening of APDepi, signifying subendocardial ischemia. QT was prolonged by 6 milliseconds in STEMI (P <0.05) and by 8 milliseconds in NSTEMI (P <0.001). Prolonged QT with shortened APDepi suggests that prolonged repolarization in terminal possibly non-ischemic regions accounts for QT prolongation in both myocardial infarction groups. These substantial differences in ischemia-induced regional manifestations of repolarization abnormalities revealed by the repolarization model were not evident from evaluation of the global QT.

Electrocardiographic estimates of action potential durations and transmural repolarization time gradients in healthy subjects and in acute coronary syndrome patients—profound differences by sex and by presence vs absence of diagnostic ST elevation

Action potential duration (APD) changes increasing repolarization time (RT) dispersion are potentially arrhythmogenic. A repolarization model developed from electrocardiographic data of 5376 healthy men and women was used to derive parameter estimates for APD and RT and their transmural gradients (RT grad and APD grad, respectively) in myocardial infarction patients, 126 with and 658 without diagnostic ST elevation (STEMI and NSTEMI, respectively). The model uses, as covariates, rate-adjusted QT and QT peak intervals (QT a and QT pa, respectively) and diagonal crossmural RT grad derived as T p-T xd, the interval from T p to the inflection point at descending limb of global T wave. An additional parameter is Θ(T|T ref), the spatial angle between a subject's T vector and the average T vector of the normal reference group. If Θ(T|T ref) >0, QT pa is assigned to RT epi and QT pa + RT grad to RT endo, with RT epi and RT endo assignments reversed if Θ(T|T ref) ≤0. Parameter estimates for APD epi and APD endo were shorter in men than in women (by 17 ms and 14 ms, respectively, P < .001 for both). Compared to the reference group, RT epi in the STEMI group was shortened by 14 ms in men and by 18 ms in women ( P < .001 for both) with a lesser decrease in RT endo suggesting predominantly subepicardial ischemia. In NSTEMI only RT endo was shortened, by 6 ms in males ( P < .01) and 10 ms in females ( P < .001), suggesting subendocardial ischemia. RT grad signifying local crossmural RT dispersion was prolonged in STEMI by 8 ms in men and by 11 ms in men ( P < .001 for both). RT grad was not changed significantly in NSTEMI. Rate-adjusted T p-T e interval signifying global RT dispersion was increased in both MI and in both sex groups ( P <.001 for all). In conclusion, QT prolongation observed in NSTEMI without prolongation of RT grad and APD epi suggests a delay during terminal repolarization, and in contrast, in STEMI, QT is not changed significantly in spite of prolonged RT grad because of shortened APD epi and RT epi. These repolarization abnormalities are not revealed by QT alone but readily by the repolarization model.

Difference of Class III Drug Effects after ICD Shock in Brugada Syndrome

Purpose: To compare drug effects on the spatial and transmural dispersion of repolarization (SDR and TDR) just after ICD shock between amiodarone (AMD) and nifekalant (NIF) in patients with Brugada syndrome (BS). Methods: We enrolled 22 consecutive patients with BS with ICD, and divided them into 2 groups: AMD group (N=12) and NIF group (N=10). We recorded 87-lead body surface ECGs before (CONTROL) and after only drug administration, and just after ICD shocks with and without drug. Corrected QT interval (QTc), QT peak interval (cQTp), and TDR (cTDR; QTc-cQTp) were measured. As an index of SDR, the dispersion of QTc (QTc-D) in 87 leads was measured. Results: Compared with CONTROL, QTc-D in both groups was significantly deteriorated by ICD shocks (AMD group; 85±12, 105±19 ms1⁄2, and NIF group; 79±10, 96±7 ms1⁄2, respectively, p<0.05). QTc-D with drug did not differ between with and without ICD shocks (AMD group; 91±19, 94±15 ms1⁄2, and NIF group; 80±13, 79±14 ms1⁄2, respectively). AMD did not increase cTDR. cTDR after drug with and without ICD shock in NIF group were larger than those in AMD group (NIF group; 148±24, 144±28 ms1⁄2, and AMD group; 123±29, 123±25 ms1⁄2, respectively, p<0.05). Conclusion: Both drugs suppressed the deterioration of SDR by ICD shocks. AMD may be more useful to suppress instability of repolarization just after ICD shocks.

Comparison of QT peak and QT end interval responses to autonomic adaptation in asymptomatic LQT1 mutation carriers

BackgroundLQT1 subtype of long QT syndrome is characterized by defective IKs, which is intrinsically stronger in the epicardium than in the midmyocardial region. Electrocardiographic QT peak and QT end intervals may reflect complete repolarization of epicardium and midmyocardial region of the ventricular wall, respectively. Repolarization abnormalities in LQT1 carriers may therefore be more easily detected in the QT peak intervals.MethodsAsymptomatic KCNQ1 mutation carriers (LQT1, n = 9) and unaffected healthy controls (n = 8) were studied during Valsalva manoeuvre, mental stress, handgrip and supine exercise. Global QT peak and QT end intervals derived from 25 simultaneous electrocardiographic leads were measured beat to beat with an automated method.ResultsIn unaffected subjects, the percentage shortening of QT peak was greater than that of QT end during mental stress and during the recovery phases of Valsalva and supine exercise. In LQT1 carriers, the percentage shortening of the intervals was similar. At the beginning of Valsalva strain under abrupt endogenous sympathetic activation, QT peak shortened in LQT1 but not in control patients yielding increased electrocardiographic transmural dispersion of repolarization in LQT1.ConclusionsIn asymptomatic KCNQ1 mutation carriers, repolarization abnormalities are more evident in the QT peak than in the QT end interval during adrenergic adaptation, possibly related to transmural differences in the degree of IKs block.

Is there a significant transmural gradient in repolarization time in the intact heart?

Is there a significant transmural gradient in repolarization time in the intact heart?

T peakT end interval in long QT syndrome

Background The T peakT end (T pT e) interval is believed to reflect the transmural dispersion of repolarization. Accordingly, it should be a risk factor in long QT syndrome (LQTS). The aim of the study was to determine the effect of genotype on T pT e interval and test whether it was related to the occurrence of syncope. Methods Electrocardiograms were taken in 95 patients with LQTS drawn from the Danish long QT registry (44 patients with KvLQT1, 43 with HERG, and 8 with SCN5A mutations) and manually evaluated for the QT, QT peak, and RR interval. Results and conclusion (1) T pT e cannot be used to distinguish symptomatic from asymptomatic patients with LQTS; (2) HERG patients have longer T pT e than KvLQT1 patients; and (3) there is no need to heart rate–correct T pT e intervals in patients with LQTS.

Beat‐to‐Beat QT Interval Variability Is Primarily Affected by the Autonomic Nervous System

Beat-to-beat QT interval variability is associated with life-threatening arrhythmias and sudden death, however, its precious mechanism and the autonomic modulation on it remains unclear. The purpose of this study was to determine the effect of drugs that modulate the autonomic nervous system on beat-to-beat QT interval. RR and QT intervals were determined for 512 consecutive beats during fixed atrial pacing with and without propranolol and automatic blockade (propranolol plus atropine) in 11 patients without structural heart disease. Studied parameters included: RR, QTpeak (QRS onset to the peak of T wave), QTend (QRS onset to the end of T wave) interval, standard deviation (SD) of the RR, QTpeak, and QTend (RR-SD, QTpeak-SD, and QTend-SD), coefficients of variation (RR- CV, QTpeak-CV, and QTend-CV) from time domain analysis, total power (TP; RR-TP, QTpeak-TP, and QTend-TP), and power spectral density of the low-frequency band (LF; RR-LF, QTpeak-LF, and QTend-LF) and the high-frequency band (HF; RR-HF, QTpeak-HF and QTend-HF). Administration of propranolol and infusion of atropine resulted in the reduction of SD, CV, TP, and HF of the QTend interval when compared to controlled atrial pacing (3.7 +/- 0.6 and 3.5 +/- 0.5 vs 4.8 +/- 1.4 ms, 0.9 +/- 0.1 and 0.9 +/- 0.1 vs 1.2 +/- 0.3%, 7.0 +/- 2.2 and 7.0 +/- 2.2 vs 13.4 +/- 8.1 ms(2), 4.2 +/- 1.4 and 4.2 +/- 1.2 vs 8.4 +/- 4.9 ms(2), respectively). Administration of propranolol and atropine did not affect RR interval or QTpeak interval indices during controlled atrial pacing. Beat-to-beat QT interval variability is affected by drugs that modulate the autonomic nervous system.

Clinical Implications of QRS Duration and QT Peak Prolongation in Patients with Suspected Coronary Disease Referred for Elective Cardiac Catheterization

The electrocardiogram (ECG) remains a simple, universally available, and prognostically powerful investigation in heart failure, and acute coronary syndromes. We sought to assess the prognostic utility of clinical, angiographic, and simple ECG parameters in a large cohort of patients undergoing elective cardiac catheterization (CC) for known or suspected coronary artery disease. Consecutive consenting patients undergoing CC for coronary disease were enrolled at a single tertiary center. Patient data, drug therapy, catheter reports, and ECG recordings were prospectively recorded in a validated electronic archive. The primary outcome measure was death or nonfatal myocardial infarction (MI) over 1 year or until percutaneous or cardiac surgical intervention. Independent prognostic markers were identified using the Cox proportional hazard model. A total of 682 individuals were recruited of whom 17(2.5%) died or suffered a nonfatal MI in 1 year. In multivariate analysis QRS duration (ms) (HR 1.03 95% CI 1.01-1.05, P = 0.003), extent of coronary disease (HR 2.01 95% CI 1.24-3.58, P = 0.006), and prolonged corrected QT peak interval in lead I (HR 1.02 95% CI 1.00-1.03, P = 0.044) were independently associated with death or nonfatal MI. Receiver-operator characteristic (ROC) analysis for the multivariate model against the primary end point yielded an area under the curve of 0.759 (95% CI 0.660-0.858), P < 0.001. QRS duration and QT peak are independently associated with increased risk of death or nonfatal MI in stable patients attending for coronary angiography.