Dispersion Of Ventricular Repolarization Research Articles

Prolonged Tpeak-Tend interval is associated with ventricular fibrillation during reperfusion in ST-elevation myocardial infarction

AimVentricular fibrillation (VF) during reperfusion in ST-elevation myocardial infarction (STEMI) is associated with increased in-hospital mortality. Dispersion of ventricular repolarization contributes to ventricular vulnerability during ischemia. Tpeak-Tend interval was proposed as a ventricular repolarization dispersion marker, however its value for prediction of reperfusion VF remains uncertain. We aimed to assess whether Tpeak-Tend before PCI in STEMI is associated with reperfusion VF. MethodsSTEMI patients admitted for primary PCI were retrospectively assessed for VF during reperfusion. Pre-PCI ECGs recorded in 40 patients with reperfusion VF (rVF group; age 65 ± 13 years, 80% male) were compared with 374 consecutive patients without reperfusion arrhythmias (No-rVF group; age 67 ± 12 years; 68% male). Digital ECGs were automatically processed and Tpeak-Tend interval computed on a per-lead basis. The global Tpeak-Tend was calculated between the earliest Tpeak and the latest Tend in any lead, and tested for association with reperfusion VF using logistic regression analysis. ResultsThe leftward shift of Tpeak toward QRS complex in ischemic leads resulted in Tpeak-Tend prolongation. Global Tpeak-Tend in rVF group was higher than in No-rVF group (142 ± 24 vs 130 ± 27 ms; p = 0.007). Global Tpeak-Tend ≥ 131 ms predicted reperfusion VF (OR = 3.41; 95% CI 1.66–7.04; p = 0.001) and remained a significant predictor of reperfusion VF in multivariable analysis. ConclusionTpeak-Tend interval before PCI in STEMI was an independent predictor of reperfusion VF. Our findings warrants further research aimed at prospective validation of Tpeak-Tend as a marker of periprocedural arrhythmic risk.

Research Progress in Formation and Application of Tp-Te Interval

Tp-Te interval refers to the duration from the peak to the end time points of T wave in electrocardiogram. Tp-Te interval is an electrocardiogram index reflecting mail-gnant ventricular arrhythmia, while Tp-Te interval mainly reflects ventricular transmural repolarization dispersion. The increase of ventricular transmural repolarization dispersion makes it easy to appear depolarization after repolarization, and forms functional conduction block between different regions, which leads to malignant arrhythmias. In this review we discuss how these markers have demonstrated to be effective to predict malignant arr- hythmias in medical conditions such as long and short QT syndromes, Brugada syndrome and so on. However, the same results have not been found in all conditions. Further studies are needed to reach a global consensus in order to incorporate these VR parameters in risk stratification of these patients.

Abnormal Cardiac Electrical Remodelling in POTS: Mechanistic Insights on Potential Autonomic Dysregulation

Background: Postural Orthostatic Tachycardia Syndrome (POTS) is a syndrome characterised by dysautonomia. It remains unknown if POTS individuals have abnormal cardiac electrical changes. Here we assessed electrocardiographic markers of interatrial and ventricular conduction delay in POTS compared to patients with vasovagal syncope (VVS). Methods: Patients who met diagnostic criteria for POTS by tilt table test and free of other autonomic or structural heart disease were compared to VVS patients. 12 lead ECGs taken pre-treatment were digitised (minimum 8 good-quality signals) and analysed by a cardiologist blinded to treatment. P wave and RT dispersion (PWD, RTD) were calculated (maximum – minimum P wave/RT interval duration). Peak of T to end of T wave (TpTe), a marker of transmural dispersion of ventricular repolarisation, also sensitive to sympathetic stimulation, was measured in lead II. Results: 11 POTS patients were compared to 9 age and sex - matched VVS patients. Mean age was similar. Atrial volumes and left ventricular ejection fraction (LVEF) were normal in all patients. There was no difference in LVEF. POTS was associated with abnormal PWD (48 ± 5, normal <38 ms) and higher RTD (66 ± 7 ms); compared to VVS (31 ± 4; P = 0.02 and 46 ± 6 ms; P = 0.04), despite lower left atrial volume. Baseline TpTe did not differ. Conclusion: Compared to VVS, POTS is associated with both longer PWD (above normal limits) and increased RTD, whilst TpTe did not differ, despite systemic sympathetic predominance. Further clinical studies are warranted to assess the relative role of subclinical cardiac structural remodeling and impaired cardiac autonomic nervous system function.

Evaluation of ventricular arrhythmogenesis in children with acute rheumatic carditis.

Recent studies have shown that the Tp-e interval, which on an electrocardiogram (ECG) is the interval between the peak and the end of the T wave, can be used as an index of transmural dispersion of ventricular repolarisation (TDR). Both Tp-e/QT and Tp-e/QTc ratios have also been used in that capacity. However, these novel repolarisation indices have not previously been studied in children with acute rheumaticcarditis (ARC). A hundred and thirty-nine children who were diagnosed with ARC and 153 age- and gender-matched healthy controls were retrospectively reviewed. Twelve-lead ECGs were used to evaluate P-wave, QT and QTc dispersions, Tp-e interval, and Tp-e/QT and Tp-e/QT ratios. The mean age of the patients was 10.9 ± 2.4 years. The P-wave, QT and QTc dispersions were significantly higher in patients compared to the healthy control subjects. The Tp-e interval, and Tp-e/QT and Tp-e/QTc ratios were also significantly increased in patients compared to the controls. When the patients were compared in terms of either one- or two-valve involvement, we found no difference between the groups regarding P-wave, QTd and QTc dispersions, Tp-e interval, and Tp-e/QT and Tp-e/QT c ratios. There was no correlation between acute-phase reactants, white blood cell count and these repolarisation parameters. This study showed that the new transmural dispersion of ventricular repolarisation parameters, Tp-e interval, Tp-e/QT ratios and QTd were increased in children with ARC. Prolongation of the Tp-e interval and an increased Tp-e/QT ratio might be useful markers for predicting myocardial involvement in children with ARC.

Can abnormal dispersion of ventricular repolarization be a predictor of mortality in arrhythmogenic right ventricular cardiomyopathy: The importance of Tp-e interval.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy characterized by ventricular arrhythmias and specific ventricular pathology. Repolarization abnormalities, the significant contributor to life-threatening arrhythmias and mortality, are frequently observed ECG changes in patients with ARVC. This study aimed to evaluate the changes in Tp-e interval, Tp-e/QT, Tp-e/QTc ratio, and traditional electrocardiographic features of electrical dispersion in patients with ARVC. A total of 105 participants were enrolled in the current study. The ARVC group consisted of 40 subjects (30 men, with a median of 35 (26-41) years), and the control group included of 65 age and sex-matched individuals (42 men, with a median of 37 (24-45) years). The Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were measured by the 12-lead electrocardiogram. Tp-e interval, cTp-e interval, Tp-e/QT, and Tp-e/QTc ratio were significantly higher in ARVC patients compared to the control group (all p<0.001). Tp-e interval, cTp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were significantly increased in deceased ARVC patients compared to the survival group (p=0.038, p<0.001, p=0.006, p=0.032, respectively). In the multivariate analysis, RV-FAC and cTp-e interval level (p<0.05 for each parameter) were associated with all-cause mortality [odds ratio 1.747 95% CI (1.012-3.018); p=0.045 and odds ratio 1.166, 95% CI (1.017-1.336); p=0.027, respectively]. Tp-e interval, cTp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were prolonged in patients with NC. We revealed that abnormal dispersion of ventricular repolarization suggests the increased risk of mortality in ARVC.

Ventricular repolarization wave variations during the amiodarone treatment course

The aim of this study was to assess ventricular repolarization wave variations during the amiodarone treatment course for patients with ventricular arrhythmias and atrial fibrillation.Sixty-nine patients with ventricular arrhythmias and 9 patients with persistent atrial fibrillation were treated with intravenous injection of a 150 mg loading dose of amiodarone, followed by 1 mg/minute for 6 hours and 0.5 mg/minute for 48 hours. After the initial 24 hours of intravenous injection, amiodarone was also administered orally at a dose of 0.2 g tid for 1 week; followed by 0.2 g bid for 1 week and 0.2 g qd for maintenance. During the procedure, the heart rate, QT, QTc, QTd, QTcd TpTe, TpTe-c, TpTe-d, TpTe/QT, and QTp were measured on days 1, 3, 7, 10, 14, 17, and 20 of amiodarone treatment.The control rate of arrhythmias was 91.0% (71/78). The heart rate dropped significantly on the 7th day after treatment initiation and reached the minimal value on day 14. The QT interval was prolonged from day 3; TpTe was prolonged from day 7 to day 14; QTp was prolonged from day 1 to day 20. The longest QT interval (441.2 ± 33.9 ms) and TpTe (95.0 ± 18.0 ms) occurred on day 14. QTc, QTd, QTcd, TpTe-c, TpTe-d, and TpTe/QT showed no significant changes throughout the treatment.Amiodarone lowers the heart rate, prolongs QT and QTp intervals, and transiently prolongs TpTe. However, it has no effects on QTc, QTd, QTcd, TpTe-c, TpTe-d or TpTe/QT. Amiodarone prolongs QT interval evenly, showing no effects on repolarization dispersion. TpTe/QT is a better indicator of ventricular transmural repolarization dispersion compared with TpTe.

Meta-analysis of Tpeak–Tend and Tpeak–Tend/QT ratio for risk stratification in congenital long QT syndrome

Background and objectivesCongenital long QT syndrome (LQTS) predisposes affected individuals to ventricular tachycardia/fibrillation (VF/VF), potentially resulting in sudden cardiac death. The Tpeak–Tend interval and the Tpeak–Tend/QT ratio, electrocardiographic markers of dispersion of ventricular repolarization, were proposed for risk stratification but their predictive values in LQTS have been controversial. A systematic review and meta-analysis was conducted to examine the value of Tpeak–Tend intervals and Tpeak–Tend/QT ratios in predicting arrhythmic and mortality outcomes in congenital LQTS. MethodPubMed and Embase databases were searched until 9th May 2017, identifying 199 studies. ResultsFive studies on long QT syndrome were included in the final meta-analysis. Tpeak–Tend intervals were longer (mean difference [MD]: 13ms, standard error [SE]: 4ms, P=0.002; I2=34%) in congenital LQTS patients with adverse events [syncope, ventricular arrhythmias or sudden cardiac death] compared to LQTS patients without such events. By contrast, Tpeak–Tend/QT ratios were not significantly different between the two groups (MD: 0.02, SE: 0.02, P=0.26; I2=0%). ConclusionThis meta-analysis showed that Tpeak–Tend interval is significant higher in individuals who are at elevated risk of adverse events in congenital LQTS, offering incremental value for risk stratification.

Myocardial repolarization is affected in patients with ascending aortic aneurysm

ObjectiveAscending aortic aneurysm (AAA) is one of the major causes of ventricular diastolic dysfunction. Diastolic dysfunction can induce ventricular repolarization dispersion. Nevertheless, myocardial repolarization dispersion is not yet to be fully evaluated in patients with AAA. We aimed to evaluate ventricular repolarization using QT and Tp-Te interval and corrected (c) Tp-Te/QT ratio in patients with AAA. MethodsOne hundred-four patients with AAA without coronary artery disease (CAD) served as the aneurysm group and 82 patients having a normal aortic diameter as the control group. All patients underwent transthoracic echocardiography (TTE) for measurements of LV diastolic function and underwent electrocardiography (ECG) to calculate RR, QT, Tp-Te intervals and QT dispersion. Bazett's formula was used to calculate QTc and cTp-Te intervals. cTp-Te/QT ratio was also calculated. ResultsThe groups were similar according to basal characteristics. We found left ventricular diastolic properties were impaired and QT dispersion, QTc interval, and both of Tp-Te and cTp-Te intervals were significantly prolonged in the aneurysm group than the control group. There were also significant correlations between TTE and ECG parameters. On multivariate linear regression analysis, indexed ascending aortic dimension (AAoD), LA diameter and E/e′ ratio were independent predictors of ventricular repolarization dispersion in AAA patients. ConclusionsOur study results showed that patients with AAA may have an increased risk for ventricular arrhythmogenesis because of deteriorated the left ventricular diastolic function.

Effects of propofol on ventricular repolarization and incidence of malignant arrhythmias in adults

BackgroundPropofol is commonly used for procedural sedation in interventional electrophysiology. However, ventricular arrhythmias under Propofol have been reported. Our aim was to investigate ventricular repolarization and incidence of ventricular arrhythmias under Propofol infusion in adults with cardiac arrhythmias. MethodsQRS, QTcB (Bazett), QTcFri (Fridericia), JTc, measurement of T peak to Tend time (Tp-e) at baseline and under Propofol infusion was performed in 235 patients. Screening for unexpected ventricular arrhythmias was performed in 1165 patients undergoing EP procedures under Propofol. ResultsA significant prolongation of Tp-e under Propofol infusion (79.7±17.3 vs. 86.4±22.5ms, p<0.001) and of QTcFri (429.3±35.8 vs. 435.5±36.5, p=0.033) was detected. No significant change of the QTcB interval, JTc interval or QRS duration was observed. One case (0.09%) of ventricular fibrillation during rapid ventricular pacing under Propofol occurred. ConclusionAlthough transmural dispersion of ventricular repolarisation is increased under Propofol, incidence of malignant ventricular arrhythmias is low. For evaluation of QT interval under Propofol, Fridericia's correction formula should be used rather than Bazett's formula.

Echocardiography and Electrocardiography Variables Correlate With the New York Heart Association classification: An Observational Study of Ischemic Cardiomyopathy Patients.

The aim of our study was to determine whether combinations of ultrasound echocardiography (UCG) and electrocardiography (EKG) parameters correlated with the functional status of ischemic cardiomyopathy (ICM) patients according to the New York Heart Association (NYHA) classification system.We assessed 536 elderly Chinese ICM patients according to the NYHA criteria, which included 196 patients with type 2 diabetes mellitus (T2DM). All of the patients underwent UCG. Transmural dispersion of ventricular repolarization was examined using EKG. Cumulative odds logistic regression was performed to evaluate associations between NYHA class and the demographic, clinical, UCG, and EKG variables based on the odds ratio (OR) and 95% confidence interval (CI). A Pearson analysis was also performed to examine correlations between the NYHA classification and the UCG and EKG variables.Based on the NYHA assessment, 140, 147, 138, and 111 patients were identified as class I, II, III and IV, respectively. A comparison of UCG and EKG variables based on T2DM status showed that CO and Tp-e differed significantly between all NYHA classes (P < .05 for all), with values of each increasing with increasing NYHA class regardless of T2DM status. Multivariate logistic regression analysis showed that the disease course (OR: 1.30; 95% CI: 1.20-1.40), heart rate (OR: 1.16; 95% CI: 1.12-1.21), T wave peak to endpoint (Tp-e; OR: 1.22; 95% CI: 1.18-1.27), dispersion of the QT interval (OR: 0.98; 95% CI: 0.95-1.22), left ventricular fractional shortening (OR: 0.82; 95% CI: 0.78-0.87), cardiac output (CO; OR: 5.58; 95% CI: 3.08-10.13) were significantly associated with the NYHA class (P < .0001 for all). A Pearson correlation analysis showed that Tp-e (r = 0.75982, P < .0001), CO (r = 0.56072, P < .0001), and stroke volume (r = -0.14839, P = .0006) significantly correlated with the NYHA class.An index consisting of Tp-e and CO will be useful for corroborating the results of the NYHA assessment of ICM patients.

Ventricular repolarization duration and dispersion adaptation after atropine induced rapid heart rate increase in healthy adults

BackgroundProper adaptation of ventricular repolarization (VR) to rapid heart rate (HR) increase is crucial for cardiac electro-mechanical function. The pattern and temporal aspects of this adaptation and its components (duration and dispersion) during normal conduction are, however, incompletely known in humans and were the topic of this study. Methods & resultsThe VR duration (QT & QTpeak) and dispersion (Tamplitude, Tarea & ventricular gradient; VG) responses were studied by continuous vectorcardiogram after a bolus injection of atropine 0.04mg/kg b.w. in 31 healthy young adults (16 men). The primary measure (T90 End) was the time to reach 90% change from baseline to end value 300s later.Mean (SD) of T90 End was 23 (9) s for a 41% RR decrease, 130 (35) s for a 16% QTend decrease and 110 (36) s for a 19% QTpeak decrease; the response was single-exponential for these measures. For 35–43% decreases of Tamplitude, Tarea & VG, mean (SD) of T90 End were 21 (10), 38 (20) and 40 (23) s and the response pattern was double-exponential with varying overshoot. ConclusionsVR duration and dispersion responses to a very rapid HR increase during normal conduction differed substantially. In contrast to the well-known single-exponential delay in VR duration adaptation the responses of VR dispersion measures were double-exponential and much more rapid. We describe a new and completely non-invasive phenotypic characterization of different components of VR adaptation.

Early remodeling of repolarizing K+ currents in the αMHC403/+ mouse model of familial hypertrophic cardiomyopathy

Familial hypertrophic cardiomyopathy (HCM), linked to mutations in myosin, myosin-binding proteins and other sarcolemmal proteins, is associated with increased risk of life threatening ventricular arrhythmias, and a number of animal models have been developed to facilitate analysis of disease progression and mechanisms. In the experiments here, we use the αMHC403/+ mouse line in which one αMHC allele harbors a common HCM mutation (in βMHC, Arg403 Gln). Here, we demonstrate marked prolongation of QT intervals in young adult (10–12week) male αMHC403/+ mice, well in advance of the onset of measurable left ventricular hypertrophy. Electrophysiological recordings from myocytes isolated from the interventricular septum of these animals revealed significantly (P<0.001) lower peak repolarizing voltage-gated K+ (Kv) current (IK,peak) amplitudes, compared with cells isolated from wild type (WT) littermate controls. Analysis of Kv current waveforms revealed that the amplitudes of the inactivating components of the total outward Kv current, Ito,f, Ito,s and IK,slow, were significantly lower in αMHC403/+, compared with WT, septum cells, whereas Iss amplitudes were similar. The amplitudes/densities of IK,peak and IK,slow were also lower in αMHC403/+, compared with WT, LV wall and LV apex myocytes, whereas Ito,f was attenuated in αMHC403/+ LV wall, but not LV apex, cells. These regional differences in the remodeling of repolarizing Kv currents in the αMHC403/+ mice would be expected to increase the dispersion of ventricular repolarization and be proarrhythmic. Quantitative RT-PCR analysis revealed reductions in the expression of transcripts encoding several K+ channel subunits in the interventricular septum, LV free wall and LV apex of (10–12week) αMHC403/+ mice, although this transcriptional remodeling was not correlated with the observed decreases in K+ current amplitudes.

Evaluation of the Tp-e Interval and Tp-e/QT Ratio in Patients with Mitral Annular Calcification

Objective: Mitral annular calcification (MAC) is regarded as a manifestation of cardiovascular disease. Recent studies have shown that prolongation of the interval between the peak and end of the T wave on electrocardiogram (Tp-e), which is accepted as an index of transmural dispersion of ventricular repolarization, and the Tp-e/QT ratio are associated with ventricular arrhythmias. In the present study, we aimed to evaluate ventricular repolarization using the Tp-e interval and Tpe/ QT ratio in patients with MAC. Methods: Fifty patients with MAC (27 females and 23 males; mean age 71.6 ± 8.0 years) and 50 patients without MAC (26 females and 24 males; mean age 69.3 ± 6.2 years) were included in this study. Maximum and minimum QT and Tp-e intervals as well as corrected values according to heart rate were calculated using a 12- lead electrocardiogram. QT dispersion and Tp-e/QT ratios were calculated. All parameters were compared between the two groups. Results: Patients with MAC had significantly higher Tp-e (75.8 ± 11.6 vs. 62.1 ± 8.7; p<0.001) and cTp-e intervals (84.9 ± 14.3 vs. 67.5 ± 9.7; p<0.001), Tp-e/QT (0.19 ± 0.02 vs. 0.15 ± 0.02; p<0.001) and cTp-e/QT ratios (0.19 ± 0.03 vs. 0.15 ± 0.02; p<0.001), and cQT values (390.1 ± 31.5 vs. 373.8 ± 26.1; p=0.006) compared with the control subjects. There were positive correlations between E/Em ratio and cTp-e interval (r=0.396; p=0.004) and between the E/Em ratio and cTp-e/QT ratio (r=0.535; p<0.001) in the MAC group. Conclusion: Our findings indicate that the patients with MAC had higher Tp-e and cTp-e intervals and Tp-e/QT and cTp-e/QT ratios compared with the subjects without MAC.

Diffuse interstitial fibrosis assessed by cardiac magnetic resonance is associated with dispersion of ventricular repolarization in patients with hypertrophic cardiomyopathy

BackgroundHypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias. MethodsECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look–Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1–V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG. ResultsAll patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1–V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1–V4 (odds ratio, 1.011 [1.004–1.0178, p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion. ConclusionDiffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1–V4.

Transcranial direct current stimulation improves the QT variability index and autonomic cardiac control in healthy subjects older than 60 years.

BackgroundNoninvasive brain stimulation technique is an interesting tool to investigate the causal relation between cortical functioning and autonomic nervous system (ANS) responses.ObjectiveThe objective of this report is to evaluate whether anodal transcranial direct current stimulation (tDCS) over the temporal cortex influences short-period temporal ventricular repolarization dispersion and cardiovascular ANS control in elderly subjects.Subjects and methodsIn 50 healthy subjects (29 subjects younger than 60 years and 21 subjects older than 60 years) matched for gender, short-period RR and systolic blood pressure spectral variability, QT variability index (QTVI), and noninvasive hemodynamic data were obtained during anodal tDCS or sham stimulation.ResultsIn the older group, the QTVI, low-frequency (LF) power expressed in normalized units, the ratio between LF and high-frequency (HF) power, and systemic peripheral resistances decreased, whereas HF power expressed in normalized units and α HF power increased during the active compared to the sham condition (P<0.05).ConclusionIn healthy subjects older than 60 years, tDCS elicits cardiovascular and autonomic changes. Particularly, it improves temporal ventricular repolarization dispersion, reduces sinus sympathetic activity and systemic peripheral resistance, and increases vagal sinus activity and baroreflex sensitivity.

Variability of Ventricular Repolarization Dispersion Quantified by Time-Warping the Morphology of the T-Waves.

We propose two electrocardiogram (ECG)-derived markers of T-wave morphological variability in the temporal, dw, and amplitude, da, domains. Two additional markers, dwNL and daNL, restricted to measure the nonlinear information present within dw and da are also proposed. We evaluated the accuracy of the proposed markers in capturing T-wave time and amplitude variations in 3 situations: 1) In a simulated set up with presence of additive Laplacian noise, 2) when modifying the spatio-temporal distribution of electrical repolarization with an electro-physiological cardiac model, and 3) in ECG records from healthy subjects undergoing a tilt table test. The metrics dw, da , dwNL , and daNL followed T-wave time- and amplitude-induced variations under different levels of noise, were strongly associated with changes in the spatio-temporal dispersion of repolarization, and showed to provide additional information to differences in the heart rate, QT and Tpe intervals, and in the T-wave width and amplitude. The proposed ECG-derived markers robustly quantify T-wave morphological variability, being strongly associated with changes in the dispersion of repolarization. The proposed ECG-derived markers can help to quantify the variability in the dispersion of ventricular repolarization, showing a great potential to be used as arrhythmic risk predictors in clinical situations.

Tpeak-to-Tend/QT is an independent predictor of early ventricular arrhythmias and arrhythmic death in anterior ST elevation myocardial infarction patients.

The aim of our study was to analyse the markers of transmural dispersion of ventricular repolarization, especially Tpeak-to-Tend and Tpeak-to-Tend /QT ratio, in patients with anterior ST elevation myocardial infarction on admission and to evaluate their association with in-hospital life-threatening arrhythmias and mortality. A total of 223 consecutive patients with anterior wall ST elevation myocardial infarction admitted to our Division of Cardiology between January 2010 and December 2012 were prospectively evaluated. A standard electrocardiogram was obtained on admission and then analysed. The primary end point was constituted by in-hospital ventricular arrhythmias and arrhythmic death. At univariate analysis heart rate (odds ratio = 1.03; 95% confidence intervals 1.006-1.05; p=0.001), maximal ST elevation (odds ratio =1.25; 95% confidence intervals 1.10-1.43; p=0.0001), QTc Bazett (odds ratio = 1.01; 95% confidence intervals 1.006-1.02; p=0.002), QT dispersion (odds ratio = 1.02; 95% confidence intervals 1.002-1.04; p=0.02) and both Tpeak-to-Tend and Tpeak-to-Tend/QT (odds ratio = 1.02; 95% confidence intervals 1.01-1.03; p<0.0001 and OR = 1.07; 95% confidence intervals 1.03-1.11; p<0.0001 respectively) were significantly associated with ventricular arrhythmias and arrhythmic mortality. Of note, Tpeak-to-Tend /QT remained a predictor of early ventricular arrhythmias and arrhythmic death (odds ratio = 1.04; 95% confidence intervals 1.003 - 1.10; p=0.03) independently from heart rate and maximal ST elevation. Receiver operating characteristic curve analysis showed that Tpeak-to-Tend /QT values <0.31 had a predictive negative value of 92% for the prediction of the composite outcome. Tpeak-to-Tend /QT was an independent predictor of early ventricular arrhythmias and arrhythmic mortality in patients with anterior ST elevation myocardial infarction. Especially, Tpeak-to-Tend /QT <0.31 may identify a subgroup of ST elevation myocardial infarction patients with low risk of early arrhythmias and arrhythmic death.

Prolonged Tp-e interval and Tp-e/QT correlates well with modified Rodnan skin severity score in patients with systemic sclerosis.

Ventricular arrhythmias can be seen in systemic sclerosis (SSc) patients and are thought to be a result of fibrosis or ischemia of the ventricular myocardium. Tp-e interval and Tp-e/QT ratio are electrocardiographic (ECG) indices to predict ventricular tachyarrhythmia and cardiovascular mortality. We aimed to evaluate Tp-e interval and Tp-e/QT ratio in patients with SSc. A total of 107 patients with SSc (mean age, 48.6 ± 14.0 years; 96 females) and 100 healthy controls (mean age, 49.4 ± 8.6 years; 90 females) were enrolled. The standard 12-lead ECG was recorded; QTc, Tp-e interval and Tp-e/QT ratio were measured. Modified Rodnan skin severity score (MR-SSS) calculated for all SSc patients. Tp-e interval (90.7 ± 23.8 ms vs. 84.0 ± 20.6 ms, p = 0.032) and Tp-e/QT ratio (0.20 ± 0.05 vs. 0.18 ± 0.04, p = 0.007, respectively) were significantly prolonged in SSc patients than in the control group. Pearson's correlation analyses revealed positive correlations of MR-SSS with QTc (r = 0.427, p = 0.001), Tp-e interval (r = 0.620, p = 0.001) and Tp-e/ /QT ratio (r = 0.615, p = 0.001). MR-SSS (b = 2.108, p = 0.001) and CRP (b = 2.273, p = 0.027) were found to be significant independent predictors of Tp-e interval. Similarly, MR-SSS (b = 0.004, p = 0.001) was only a significant independent predictor of Tp-e/QT ratio among patients with SSc. The patients with SSc had a prolonged Tp-e interval and Tp-e/QT ratio compared with normal subjects. Furthermore, this prolongation was well correlated with clinical severity score among patients with SSc. Ventricular repolarization dispersion as a predictor of ventricular arrhythmias was found to be diminished in patients with SSc. Patients with SSc, particularly with higher MR-SSS, should be followed closely for adverse cardiovascular outcomes.

Effect of intravenous zoledronic acid infusion on electrocardiographic parameters in patients with osteoporosis.

The aim of the present study was to evaluate the early and late effects of ZA therapy on ECG parameters which might be associated with the tendency for atrial and ventricular arrhythmias. Consecutive patients with osteoporosis who were admitted to our clinic between December 2013 and December 2014 and who were scheduled to receive ZA infusion constituted our study population. Twelve-lead surface ECGs were obtained from all patients before and after ZA infusion on the same day as well as 1month after the infusion. All ECG parameters were measured and compared with each other for each patient. Data of 100 patients were used in the analysis (9 male; 70.5±11.6years of age). There were no significant differences between repeated measurements regarding pmax, pmin, and p dispersion values. QT max and QT min values were significantly increased after infusion; however, there were no significant changes in QT dispersion, Tp-e interval, and Tp-e dispersion values. ZA infusion did not affect P wave dispersion both at the immediate post-infusion period and 1month after infusion. QT values were significantly increased early after ZA infusion; however, there were no significant differences in parameters reflecting disparity of ventricular recovery times and transmural dispersion of ventricular repolarization. Based on these observations, it may be suggested that ZA infusion did not have any short- or long-term effect on any parameter that might be associated with the tendency for atrial fibrillation or ventricular arrhythmias.

Inhibition of the cardiac late sodium current with eleclazine protects against ischemia-induced vulnerability to atrial fibrillation and reduces atrial and ventricular repolarization abnormalities in the absence and presence of concurrent adrenergic stimulation

Myocardial ischemia carries dual risk for initiating atrial and ventricular arrhythmias that can be exacerbated by adrenergic stimulation. The purpose of this study was to investigate whether selective inhibition of the cardiac late sodium current (INa) with eleclazine decreases susceptibility to ischemia-induced atrial fibrillation (AF) and atrial and ventricular repolarization abnormalities before and after epinephrine infusion. In chloralose-anesthetized, open-chest, male Yorkshire pigs (n = 12), atrial and ventricular ischemia was induced by partial occlusion of the left circumflex coronary artery proximal segment to reduce flow by 75%. Epinephrine (0.5 µg/kg IV bolus over 1 minute; n = 6) was infused before and at 2 hours after eleclazine (0.9 mg/kg IV bolus over 15 minutes). Left circumflex coronary artery occlusion significantly increased ventricular dispersion of repolarization (T-wave alternans [TWA] by 861%, T-wave heterogeneity by 286%, Tpeak-Tend interval by 74%) and atrial repolarization alternans (TWAa) by 2850% and lowered AF threshold by 65%. Eleclazine reduced the ischemia-induced surge in TWA by 81% (P = .007), T-wave heterogeneity by 23% (P = .035), and Tpeak-Tend by 28% (P = .014), suppressed the ischemia-induced surge in atrial TWAa by 64% (P = .002), and reduced the ischemia-induced fall in AF threshold to 20%. It shortened baseline QT interval by 6% (P <.001), JT interval by 8% (P <.001), and atrial action potential duration (PTa) by 8% (P = .002). Similar beneficial effects of eleclazine were observed after epinephrine infusion without reducing contractility (P = .054). Selective inhibition of cardiac late INa with eleclazine confers dual protection against vulnerability to ischemia-induced AF and reduces atrial and ventricular repolarization abnormalities before and during adrenergic stimulation without negative inotropic effects.