T-wave Morphology Descriptors Research Articles

T-wave morphology descriptors in patients with bulimia nervosa

Bulimia nervosa (BN) is associated with increased risk of cardiovascular disease and arrhythmias. Some reports found abnormal electrocardiographic markers of arrhythmias in BN, while others did not. This study investigated novel parameters of T-wave morphology that were reported to be associated with adverse cardiovascular outcomes in other patient groups, among patients with BN under medical care. Thirty-five BN patients and 76 healthy controls were included. Total cosine R to T (TCRT) and T-wave Morphology Dispersion (TMD) parameters were computed according to accepted standards for an average beat and a random beat. Patients were followed for 11.1 ± 0.1years for the emergence of arrhythmias or events of sudden death. Twenty-five (71.4%) BN patients were hospitalized when enrolled, for a mean duration of 1.1 ± 0.2months. The rest were ambulatory patients. The BN group had lower blood pressure, more smokers, and used antidepressants, neuroleptic drugs and benzodiazepines more than controls did. Other demographic parameters were comparable between groups. TCRT and TMD parameters were statistically similar and within the normal ranges reported by other research groups. None of the BN patients had prolonged QTc interval or electrolyte abnormalities on inclusion. During the follow-up period, no clinical symptoms suggestive of arrhythmias were reported, and no cardiovascular-related hospitalizations or deaths occurred in either group. Medically treated BN patients have normal T-wave morphology parameters and hence, low risk for repolarization-associated malignant ventricular arrhythmias. The prognostic importance of these novel repolarization parameters remains to be explored among untreated patients, those who ingest emetic substances and patients with electrolyte imbalance. Level III.

Effect of Loss of Heart Rate Variability on T-Wave Heterogeneity and QT Variability in Heart Failure Patients: Implications in Ventricular Arrhythmogenesis.

Heart rate variability (HRV) modulates dynamics of ventricular repolarization. A diminishing value of HRV is associated with increased vulnerability to life-threatening ventricular arrhythmias, however the causal relationship is not well-defined. We evaluated if fixed-rate atrial pacing that abolishes the effect of physiological HRV, will alter ventricular repolarization wavefronts and is relevant to ventricular arrhythmogenesis. The study was performed in 16 subjects: 8 heart failure patients with spontaneous ventricular tachycardia [HFVT], and 8 subjects with structurally normal hearts (H Norm). The T-wave heterogeneity descriptors [total cosine angle between QRS and T-wave loop vectors (TCRT, negative value corresponds to large difference in the 2 loops), T-wave morphology dispersion, T-wave loop dispersion] and QT intervals were analyzed in a beat-to-beat manner on 3-min records of 12-lead surface ECG at baseline and during atrial pacing at 80 and 100bpm. The global T-wave heterogeneity was expressed as mean values of each of the T-wave morphology descriptors and variability in QT intervals (QTV) as standard deviation of QT intervals. Baseline T-wave morphology dispersion and QTV were higher in HFVT compared to H Norm subjects (p≤0.02). While group differences in T-wave morphology dispersion and T-wave loop dispersion remained unaltered with atrial pacing, TCRT tended to fall more in HFVT patients compared to H Norm subjects (interaction p value=0.086). Atrial pacing failed to reduce QTV in both groups, however group differences were augmented (p<0.0001). Atrial pacing and consequent loss of HRV appears to introduce unfavorable changes in ventricular repolarization in HFVT subjects. It widens the spatial relationship between wavefronts of ventricular depolarization and repolarization. This may partly explain the concerning relation between poorer HRV and the risk of ventricular arrhythmias.

136-02: Effect of Loss of Heart Rate Variability on T-wave Heterogeneity and QT Variability in Heart Failure Patients: Implications in Ventricular Arrhythmogenesis

Background: A diminishing value of heart rate variability (HRV) robustly increases vulnerability to life-threatening ventricular arrhythmias, yet the electrophysiological mechanism of this dynamic relationship is still not well understood. We evaluated if fixed-rate atrial pacing, that abolishes the effect of physiological HRV, will modulate ventricular repolarization wavefronts and is relevant to ventricular arrhythmogenesis. Methods: The study was performed in 16 subjects: 8 heart failure patients with history of spontaneous ventricular tachycardia [HFVT], and 8 subjects with structurally normal hearts (HNorm). The T-wave heterogeneity descriptors [total cosine angle between QRS and T-wave loop vectors (TCRT, negative value corresponds to large difference in the 2 loops), T-wave morphology dispersion, T-wave loop dispersion] and QT intervals were analyzed in a beat-to-beat manner on 3-minutes records of 12-lead surface ECG at baseline and during atrial pacing at physically inert rates of 80 and 100 bpm. The global T-wave heterogeneity was expressed as mean values of each of the T-wave morphology descriptors and variability in QT intervals (QTV) as standard deviation of QT intervals. Results: Baseline T-wave morphology dispersion and QTV were higher in HFVT compared to HNorm subjects (p ≤ 0.02). While group differences in T-wave morphology dispersion and T-wave loop dispersion remained unaltered with atrial pacing, TCRT tended to fall more in HFVT patients compared to HNorm subjects (interaction p value = 0.086). Atrial pacing failed to reduce QTV in both groups, however group differences were augmented (p < 0.0001). Conclusions: Atrial pacing and consequent loss of HRV appears to introduce unfavorable changes in ventricular repolarization in HFVT subjects. It widens the spatial relationship between wavefronts of ventricular depolarization and repolarization (Figure). This may partly explain the concerning relation between poorer HRV and the risk of ventricular arrhythmias.

Repolarisation descriptors and heart rate variability in hemodialysed patients.

T wave morphology (TWM) descriptors derived from Holter electrocardiograms during hemodialysis (HD) are of potential value for cardiac risk assessment in HD patients. Our knowledge on autonomic regulation of TWM descriptors is limited. The purpose of this study was to investigate the association between TWM parameters and heart rate variability (HRV) during intradialytic monitoring. In each of 81 patients on maintenance HD, continuous electrocardiograms were recorded 5 times during HD on alternate weeks. TWM descriptors were calculated every 5 s in overlapping 10-s ECG segments and Low Frequency (LF) (0.04 Hz to 0.15 Hz), High Frequency (HF) (0.15 Hz to 0.40 Hz) powers of the spectrum of HRV were calculated every five min. The calculated values of TWM and HRV were averaged during the first hour of the recordings and subsequently over all recordings in each subject. Analyzable data for HRV and TWM were available in 71 HD patients (aged 61+/-15, 36 % diabetics, 32 % females). LF in normalized units correlated positively with Total Cosine R to T (r=0.374, p=0.001) and negatively with T wave morphology dispersion (r=-0.253, p=0.033) after adjusting for heart rate. A heart rate independent association between repolarisation descriptors and HRV exists in HD patients. Autonomic modulation needs to be considered when using TWM characteristics for risk profiling of HD patients.

T-wave morphology descriptors during hemodialysis

T-wave morphology descriptors during hemodialysis

Defibrillation threshold testing does not cause acute electrocardiographic changes in cardiomyopathy patients undergoing insertion of an implantable cardioverter defibrillator

and repeated five times at 2-week intervals. T-wave morphology descriptors [TCRT, T-wave morphology dispersion (TMD) and CRA parameter] were calculated every 5 seconds in overlapping 10-second ECG segments. Recordings with fewer than total 1000 analyzable segments or fewer than 100 segments during the first or the last hour of the recording were excluded. Results: A total of 187 intradialytic recordings were included in the final analysis containing on average 2699 ± 592 ECG segments. Mean intradialytic values were as follows: CRA 0.204 ± 0.101, TMD 32.14 ± 21, and TCRT 0.282 ± 0.583.There was a positive correlation between CRA and TMD (p = 0.000, CE .528) and CRA and TCRT (0.312, p = 0.000). Comparison between averaged values during the first and after the third hours of recordings showed statistically significant differences in CRA, TCRT and TMD [independent-sample t test p b 0.05 for 182 (97.3%), 179 (95.7%) and 180 (96.3%) of comparisons respectively]. Intradialytic changes were expressed as (last hour value − first hour value)/first hour value and denoted as CRAD, TMDD and TCRTD. More than 10% intradialytic increase was noted in 55.5%, 41.8 %, and 55.5% while more than 10% decrease in 8.2%, 35% and 12.3% of the overall recordings for CRA, TCRT and TMD, respectively. There was a positive relationship between intradialytic change of CRA and TMD (correlation coefficient of 0.211, p = 0.05). Repeated-measures ANOVA of average CRA, TMD, TCRT and their intradialytic changes (CRAD, TMDD and TCRTD) in subjects with five consecutive analyzable recordings showed intrasubject stability (CRA F = 0.558, p = 0.694; TMD F = 0.770, p = 0.483; TCRT F = 1.966, p = 0.135; CRAD F = 0.356, p = 0.839; TMDD F = 0.533, p = 0.630; TCRTD F = 1.498, p = 0.239). Pre-dialysis hyponatremia was associated with higher intradialytic changes in CRA (independent-sample t test p = 0.019). Conclusion: T-wave morphology descriptors exhibit differential subject specific dynamic profiles in response to fluid and electrolyte changes on dialysis. Predialysis hyponatremia may have a role in intradialytic CRA changes.

Effect of atorvastatin on dynamic parameters of myocardial repolarization in healthy subjects

BackgroundAntiarrhythmic properties of statins were suggested as a part of their pleiotropic effects. The aim of the present study was to evaluate the effects of atorvastatin on myocardial repolarization as manifested on surface electrocardiograms (ECGs) in healthy subjects. Methods and ResultsForty young healthy volunteers (20 men, 20 women) underwent a single-dose double-blind 3-way crossover study of 20 and 80 mg of atorvastatin and placebo. Long-term 13-hour 12-lead ECGs were obtained in each subject and each study period starting 15 minutes before drug administration. Each study period contained 18 time-points of 5-minute durations when the subjects were in resting supine positions. Digital ECG recordings were analyzed automatically, and the results were completed blindly before statistical analyses. Dynamic parameters of myocardial repolarization and T-wave morphology descriptors were evaluated. Although some trends were observed, no significant drug-related changes in any of investigated ECG repolarization descriptors were found. ConclusionIn comparison with placebo, single doses of atorvastatin had no effect on repolarization heterogeneity in healthy subjects. The observation confirms safe profile of the drug with limited proarrhythmic potential.

Risk stratification by T-wave morphology for cardiovascular mortality in patients with systolic heart failure

The objective was to investigate the prognostic value of T-wave morphology in systolic heart failure patients. T-wave morphology descriptors on standard 12-lead electrocardiograms (ECG) have been shown to have prognostic importance concerning the arrhythmic susceptibility of patients with previous myocardial infarction. However, these descriptors have not been considered with regard to further risk stratification in patients with systolic heart failure. Patients with systolic heart failure [defined by a left ventricular ejection fraction (LVEF) <50%] were enrolled. Standard digitized 12-lead ECGs were used for analysis of T-wave morphology descriptors [lead dispersion, T-wave morphology dispersion, percentage of the loop area, percentage of the outer area, and the total cosine between QRS and T-wave (TCRT)]. A total of 650 patients with a mean age of 63 +/- 14 years were enrolled and followed-up for 2.7 +/- 1.8 years. The mean LVEF was 36 +/- 9%. During this study, the total mortality rate was 32.7% and cardiovascular mortality rate was 22.3%. A stepwise backward Cox regression analysis showed that cardiovascular mortality was significantly associated with age (P < 0.001), diabetes mellitus (P = 0.022), haemoglobin (P = 0.001), LVEF (P = 0.001), and TCRT (P = 0.003). On the basis of a median TCRT of -0.473 as a cut-off point, a significant difference in cardiovascular mortality was observed from a Kaplan-Meier survival curve (P = 0.01). Total cosine between QRS and T-wave further stratified the risk of LVEF (P = 0.007), age (P = 0.001), haemoglobin (P < 0.001), and diabetes mellitus (P < 0.001) in cardiovascular mortality for these patients. Total cosine between QRS and T-wave may provide further risk stratification for and therefore impact on the prognosis of patients with systolic heart failure.

The Association between T‐Wave Morphology and Life‐Threatening Ventricular Tachyarrhythmias in Patients with Congestive Heart Failure

Whether T-wave morphology descriptors on the 12-lead electrocardiogram (ECG) can predict the occurrence of life-threatening ventricular arrhythmia in patients with advanced congestive heart failure is unclear. Standard 12-lead ECGs were photoscanned and digitized for analysis in 27 heart failure patients with ventricular tachycardia/ventricular fibrillation (VT/VF; study group), as well as in 54 age- and sex-matched heart failure patients without life-threatening ventricular arrhythmia as a control group. Novel T-wave morphology descriptors were compared. The results showed that the temporal descriptor, the lead dispersion (LD; 426.5 +/- 279.8 vs 189.0 +/- 125.7, P < 0.001), was significantly higher in the study than in the control group. The other T-wave morphology parameters, such as the T-wave morphology dispersion (45.7 +/- 20.1 vs 44.9 +/- 18.6), the total cosine between QRS and T wave (TCRT; -0.4 +/- 0.4 vs -0.5 +/- 0.3), and the normalized T-loop area (NTLA; 0.5 +/- 0.1 vs 0.4 +/- 0.1), were not significantly different between the two groups (all P value > 0.05). After an adjustment for other clinical variables, increased LD (odds ratio: 9.9, 95% confidence interval [CI]: 2.9-33.4, P < 0.001) or decreased NTLA (odds ratio: 0.4, 95% CI: 0.1-1.0, P =0.05) was associated with VT/VF. The novel T-wave morphology analysis may help in identifying heart failure patients at high risk for VT/VF.

New descriptors of T-wave morphology are independent of heart rate

T-wave morphology descriptors are sensitive to drug-induced changes and may be a useful addition to the QT interval in cardiac safety trials. Intrasubject heart rate dependence of T-wave morphology was investigated in a sample of 39 healthy individuals. Ten-second electrocardiograms were obtained from daytime Holter recordings. Duration parameters (QT, ToTe, TpTe, and others), a number of basic T-wave morphology parameters (amplitude, area, and others) as well as advanced morphology descriptors (asymmetry, flatness, and others) were measured automatically. Heart rate dependence was examined by means of analysis of covariance. The results showed clear heart rate dependence for the QT interval ( R 2 = 0.53-0.57) and a moderate degree of heart rate dependence for the basic morphology parameters (amplitude, area, and others) ( R 2 = 0.17-0.42). Both the advanced T-wave descriptors (asymmetry, flatness, and others), ToTe intervals and TpTe intervals, were practically independent of heart rate ( R 2 = 0-0.08), making heart rate correction unnecessary for these parameters.

Relation of twelve-lead electrocardiographic T-wave morphology descriptors to left ventricular mass

Echocardiographically detected left ventricular (LV) hypertrophy is an independent risk factor for sudden cardiac death, and the relative risk increases as LV mass increases. 1 Experimental studies strongly suggest that development of LV hypertrophy creates arrhythmia-generating repolarization abnormalities. 2‐6 The inscription of the T wave on the body surface electrocardiogram (ECG) is generated by repolarization gradients at the myocardial level. 7,8 A change in these gradients has an effect on T-wave morphology. 7‐10 Thus, repolarization gradients, arrhythmic vulnerability, and T-wave morphology are interrelated. 8,11 Recently, novel T-wave morphology descriptors on the 12-lead ECG 12 were shown to carry important prognostic information on arrhythmic susceptibility in patients with coronary artery disease. 13,14 We examined whether T-wave morphology descriptors are associated with echocardiographically determined LV hypertrophy and correlate with the degree of LV hypertrophy. ••• We studied 50 subjects who participated in an ongoing study examining the capability of body surface mapping techniques to detect LV hypertrophy. The LV hypertrophy group (n 35) consisted of 24 patients with hemodynamically significant aortic stenosis and 11 patients with essential arterial hypertension, all of whom had echocardiographic LV hypertrophy by gender-specific criteria (LV mass indexed to body surface area 116 g/m 2 in men; 104 g/m 2 in women). 15 No patient had echocardiographic wall motion abnormalities or pathologic Q waves on the ECG. In addition, no patient with aortic stenosis had 70% stenosis of the luminal diameter in epicardial arteries on routine coronary angiography, and no patient with essential hypertension had a history of effort angina. The control group consisted of 15 healthy middleaged volunteers who had no cardiovascular risk factors or a history or signs of heart disease. In these 15 subjects, a screening echocardiogram showed no evidence of anatomic or valvular abnormalities, and a symptom-limited exercise test without ST-segment

Analysis of 12-Lead T-Wave Morphology for Risk Stratification After Myocardial Infarction

The stratification of post-myocardial infarction (MI) patients at risk of sudden cardiac death remains important. The aim of the present study was to assess the prognostic value of novel T-wave morphology descriptors derived from resting 12-lead ECGs. In 280 consecutive post-MI patients, a 12-lead ECG was recorded before discharge, optically scanned, and digitized. For the present study, 5 T-wave morphology descriptors were automatically calculated after singular value decomposition of the ECG signal. The total cosine R-to-T (TCRT [describes the global angle between repolarization and depolarization wavefront]) and the T-wave loop dispersion were univariately associated (P:=0.0002 and P:<0.002, respectively, U: test) with 27 prospectively defined clinical events in 261 patients (mean follow-up 32+/-10 months). Kaplan-Meier event probability curves for strata above and below the median confirmed the strong risk discrimination by TCRT and T-wave loop dispersion (P:<0.003 and P:<0.001, respectively, log-rank test). On Cox regression analysis, with the entering of age, left ventricular ejection fraction, heart rate, QRS width, reperfusion therapy, beta-adrenergic-blocker treatment, and standard deviation of R-R intervals on 24-hour Holter monitoring, TCRT (P:<0.03) yielded independent predictive value, whereas T-wave loop dispersion was of borderline independence (P:=0.064). Heart rate (P:<0.02), left ventricular ejection fraction (P:<0.02), and reperfusion therapy (P:<0.02) also remained in the final model. Computerized T-wave morphology analysis of the 12-lead resting ECG permits independent assessment of post-MI risk and an improved risk stratification when combined with other risk markers.