Ventricular Repolarization Instability Research Articles

Prognostic significance of the Holter-derived T-wave variability in patients with ventricular tachyarrhythmias complicating acute coronary syndrome-TWIST study.

We aimed to investigate the association between ventricular repolarization instability and sustained ventricular tachycardia and ventricular fibrillation (VT/VF) occurring within 48 h (acute-phase VT/VF) after the onset of acute coronary syndrome (ACS) and the prognostic role of repolarization instability and heart rate variability (HRV) after discharge from the hospital. We studied 572 ACS patients with a left ventricular ejection fraction >35%. The ventricular repolarization instability was assessed by the beat-to-beat T-wave amplitude variability (TAV) using high-resolution 24-h Holter ECGs recorded at a median of 11 days from the date of admission. We calculated the HRV parameters including the deceleration capacity (DC) and non-Gaussian index calculated on a 25 s timescale (λ25s). The DC and λ25s were dichotomized based on previous studies' thresholds. Acute-phase VT/VF developed in 43 (7.5%) patients. In-hospital mortality was significantly higher among VT/VF patients (4.7% vs. 0.9%, p = .03). An adjusted logistic model showed that the maximum TAV (odds ratio 1.02, 95% confidence interval [CI] 1.00-1.29, p = .04) was associated with acute-phase VT/VF. During a median follow-up period of 2.1 years, 19 (3.3%) patients had cardiac deaths or resuscitated cardiac arrest. Acute-phase VT/VF (p = .12) and TAV (p = .72) were not significant predictors of survival. An age and sex-adjusted Cox model showed that the DC (p < .01), λ25s (p < .01), and emergency coronary intervention (p < .01) were independent predictors. T-wave amplitude variability was associated with acute-phase VT/VF, but the TAV was not predictive of survival post-discharge. The DC, λ25s, and emergency coronary intervention were independent predictors of survival.

Abstract 13376: Sleep-Disordered Breathing is Associated With Larger Ventricular Repolarization Instability

Introduction: Sleep-disordered breathing (SDB) is a common disorder in the general population that is associated with adverse cardiovascular events, such as sudden cardiac death, but the underlying mechanisms are unclear. Hypothesis: Ventricular repolarization instability is greater in those with severe SDB than those without SDB, independent of other risk factors. Methods: Among the participants of the Sleep Heart Health Study (SHHS), we identified those with SDB who had no diagnosed cardiovascular disease or other factors that could affect cardiac repolarization. Severe SDB was defined as having a respiratory disturbance index (RDI) &gt; 33 events/hour (top 95%ile of the SHHS cohort). We also identified a group of participants matched to the severe SDB group on age, sex, BMI, and race and had RDI &lt; 1.33 events/hour (bottom 25%ile; without SDB). Each group consisted of 61 (45 M and 16 F) participants. Oxygen saturation levels (SpO 2 ) were used to measure hypoxemia burden as the percentage of sleep time with SpO 2 &lt; 90% (T90). Heart rate (HR), heart rate variability (SDNN), and QT variability index (QTVI, a measure of ventricular repolarization instability) were calculated from one-lead ECG recordings. Student’s t- test was used to assess statistical associations. Results: The SDB group had a larger T90 than those without SDB (11.39 ± 1.42% vs 1.32 ± 0.61%, P &lt; 0.001). Participants with SDB also had greater mean HR (P = 0.028), SDNN (P = 0.017), and QTVI (P = 0.027) than those without SDB. Based on a multivariable linear model that included hypoxemia burden, age, BMI, and smoking status, T90 was the only independent predictor of QTVI (P = 0.022). Conclusion: SDB is associated with higher HR, HRV, and QTVI, an indicator of increased instability in ventricular repolarization leading to increased risk for cardiac arrhythmias and sudden cardiac death. The severity of the destabilizing effect of SDB on ventricular repolarization appears to be modified by hypoxemia burden.

Abstract 14306: Development of Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

Introduction: Sleep-disordered breathing (SDB) is a prevalent condition associated with adverse cardiovascular events, including nocturnal arrhythmias and sudden cardiac death, but the underlying mechanism is unclear. Hypothesis: Ventricular repolarization instability increases in those who develop SDB. Methods: For the participants of the Sleep Heart Health Study (SHHS), the percentage of sleep time with oxygen saturation levels &lt; 90% (T90) was measured. We identified participants who did not have SDB (T90 &lt; 0.22% = median of the SHHS cohort) during the initial study but developed SDB (T90 &gt; 10%) by the time of the 5-year follow-up. A comparator group was identified as those who matched the first group on age, sex, BMI, and race but had T90 &lt; 0.22% during both the initial and the follow-up sleep studies. Each group consisted of 25 (8 M and 17 F) participants, none of whom had any diagnosed comorbidities or prescriptions that could affect cardiac repolarization. Heart rate (HR), heart rate variability (SDNN), and QT variability index (QTVI, a measure of ventricular repolarization instability) were calculated from one-lead ECG recordings. Paired sample t- test was used to assess statistical associations. Results: The respiratory disturbance index (RDI) for the study group increased from 2.57 ± 0.74 events/hr at baseline to 14.8 ± 3.72 events/hr at follow-up (P = 0.001), while the RDI was not different for the comparators (3.08 ± 0.71 events/hr at baseline, 3.65 ± 0.68 events/hr at follow-up, P = 0.599). In those who developed SDB, HR and SDNN did not change between baseline and follow-up, but QTVI increased from -1.25 ± 0.15 to -0.85 ± 0.15 (P = 0.013). None of the measured electrocardiographic parameters differed between baseline and follow-up in comparators. Conclusion: Over a five-year follow-up, the development of SDB was associated with an increase in QT variability comparable to symptomatic heart failure. Hypoxemia appears to be the main underlying mechanism.

Abstract 12538: Intermittent Hypoxemia Progressively Destabilizes Ventricular Repolarization in Healthy Awake Subjects

Introduction : Obstructive sleep apnea (OSA) is highly prevalent in the general population. OSA is associated with adverse cardiovascular events, including sudden cardiac death, but the mechanism is unclear. Intermittent hypoxemia, a pathognomonic feature of OSA, could increase the propensity for abnormal ventricular repolarization. We previously found that short-term exposure of awake healthy subjects to recurrent hypoxic episodes increased their heart rate (HR) and HR variability. Hypothesis: Exposure to intermittent hypoxia increases ventricular repolarization instability in awake healthy subjects. Methods: Healthy adults (N = 19) were exposed to either intermittent hypoxia or air for 4 hours on two different days in a randomized order. Intermittent hypoxia was induced with exposure to hypoxic gas (95% N 2 and 5% O 2 ) or ambient air in an alternative fashion at a frequency of ⁓ 25 times/hour, mimicking moderate to severe OSA. Repolarization stability was assessed using the QT variability index (QTVI), a validated predictor of cardiac arrhythmias and mortality. HR and QTVI were measured from one-lead ECG over consecutive 5-min epochs. Paired sample t - test was used to assess statistical associations. Results: Mean oxygen saturation levels were lower during exposure to intermittent hypoxia (90.86 ± 0.19%) versus normoxia (97.37 ± 0.20%, P &lt; 10 -13 ). Electrocardiographic measures at baseline were similar between the two conditions. No changes in these measures were noted during the conditions of normoxia. However, with intermittent hypoxia, mean HR and QTVI steadily increased (HR: 63.31 ± 1.51 initial, 69.21 ± 2.14 final, P &lt; 0.001; QTVI: -1.85 ± 0.04 initial, -1.64 ± 0.07 final, P = 0.016). By the end of the 4-hour experiment, QTVI was greater in hypoxia vs. normoxia (final QTVI in hypoxia: -1.64 ± 0.07, in normoxia: -1.86 ± 0.06, P = 0.021). Conclusion: Four hours of intermittent hypoxia in awake normal healthy subjects progressively destabilized ventricular repolarization. Chronic exposure to recurrent periods of intermittent hypoxemia in OSA can increase ventricular repolarization and contribute to the OSA-associated adverse cardiovascular events, including sudden cardiac death.

Estimation of the second ventilatory threshold through ventricular repolarization profile analysis.

Under the hypothesis that sympathetic control of ventricular repolarization may change once the second ventilatory threshold (VT2) has been reached, a novel methodology for non-invasive VT2 estimation based on the analysis of the T wave from the electrocardiogram (ECG) is proposed, and potential underlying physiological mechanisms are suggested. 25 volunteers (33.4 ± 5.2 years) underwent an incremental power cycle ergometer test (25 W/minute). During the test, respiratory gas exchange and multi-lead ECG were acquired. The former was employed to determine VT2, used here as a reference, whereas the latter was used to compute the temporal profiles of an index of ventricular repolarization instability (dT) and its low-frequency (LF) oscillations (LFdT). The sudden increases observed in dT and LFdT profiles above an established heart rate threshold were employed to derive VT2 estimates, referred to as VT2d T and VT2LF d T , respectively. Estimation errors of -4.7 ± 25.2 W were obtained when considering VT2d T . Errors were lower than the one-minute power increment of 25 W in 68% of the subjects and lower than 50 W in 89.5% of them. When using VT2LF d T , estimation error was of 15.3 ± 32.4 W. Most of the subjects shared common characteristic dT and LFdT profiles, which could be reflecting changes in the autonomic control of ventricular repolarization before and after reaching VT2. The analysis of ventricular repolarization dynamics during exercise allows non-invasive ECG-based estimation of VT2, possibly in relation to changes in the autonomic control of ventricular electrical activity when VT2 is reached.

Low-Frequency Oscillations in Cardiac Sympathetic Neuronal Activity.

Sudden cardiac death caused by ventricular arrhythmias is among the leading causes of mortality, with approximately half of all deaths attributed to heart disease worldwide. Periodic repolarization dynamics (PRD) is a novel marker of repolarization instability and strong predictor of death in patients post-myocardial infarction that is believed to occur in association with low-frequency oscillations in sympathetic nerve activity. However, this hypothesis is based on associations of PRD with indices of sympathetic activity that are not directly linked to cardiac function, such as muscle vasoconstrictor activity and the variability of cardiovascular autospectra. In this review article, we critically evaluate existing scientific evidence obtained primarily in experimental animal models, with the aim of identifying the neuronal networks responsible for the generation of low-frequency sympathetic rhythms along the neurocardiac axis. We discuss the functional significance of rhythmic sympathetic activity on neurotransmission efficacy and explore its role in the pathogenesis of ventricular repolarization instability. Most importantly, we discuss important gaps in our knowledge that require further investigation in order to confirm the hypothesis that low frequency cardiac sympathetic oscillations play a causative role in the generation of PRD.

Ventricular repolarization instability quantified by instantaneous frequency of ECG ST intervals.

BACKGROUND: Ventricular repolarization instabilities have been documented to be closely linked to arrhythmia development. The electrocardiogram (ECG) ST interval can be used to measure ventricular repolarization. Analyzing the duration variation of the ST intervals can provide new information about the arrhythmogenic vulnerability.OBJECTIVE: In this work, we propose a new method based on mean instantaneous frequency (IF) of the ST intervals to quantitatively evaluate the risk of sudden cardiac deaths (SCDs).METHODS: Two spectral bands, i.e. the low-frequency band (LF, 0–0.15 Hz) and the high-frequency band (HF, 0.15–0.5 Hz), are considered in this paper. Based on IF estimates, the ECG recordings from three MIT-BIH databases that represent different risk levels of SCD occurrence are used, and their mean IFs in the LF and HF bands are calculated.RESULTS: The statistical results show that healthy subjects have a higher mean IF in the HF band and a lower mean IF in the LF band. The experimental results are the opposite for patients with malignant ventricular arrhythmia.CONCLUSION: The proposed mean IF can represent an indirect measure of intrinsic ventricular repolarization instability and can mark cardiac instability associated with SCDs.

Assessment of ventricular repolarization instability in terms of T-wave alternans induced by head-down bed-rest immobilization

Objective: To assess the effects of different durations of simulated microgravity exposure on ventricular repolarization (VR) in terms of T-wave alternans (TWA) as well as to test whether an increase in VR heterogeneity could be detected once normal gravity was restored. Approach: A total of 63 healthy volunteers were recruited in several head-down bed-rest (HDBR) experiments in the context of the European Space Agency bed-rest strategy. TWA is evaluated during the night period using ambulatory ECG recordings, before, during and after long- (60 d), mid- (21 d) and short- (5 d) duration HDBR by the long-term averaging technique. Main results: 5–21 d of exposure to simulated microgravity by means of the HDBR model do not lead to a significant increase of cardiac electrical instability in healthy myocardial substrates up to the point of eliciting TWA on the surface ECG. However, TWA indices increased after long-term HDBR exposure, once normal gravity was re-established, indicative of incipient electrical instability on VR at the conclusion of 60 d of HDBR. Significance: The results of this work underline the importance of focusing future research on immediate effects after long-term microgravity exposure, both simulated by HDBR or from space mission scenarios, once partial gravity conditions are re-established. A deeper insight in the understanding of human body reactions in these scenarios results crucial in the design of future long-duration spaceflight missions, to mitigate any potential risk that can limit astronaut’s performance.

Sudden cardiac death and pump failure death prediction in chronic heart failure by combining ECG and clinical markers in an integrated risk model.

BackgroundSudden cardiac death (SCD) and pump failure death (PFD) are common endpoints in chronic heart failure (CHF) patients, but prevention strategies are different. Currently used tools to specifically predict these endpoints are limited. We developed risk models to specifically assess SCD and PFD risk in CHF by combining ECG markers and clinical variables.MethodsThe relation of clinical and ECG markers with SCD and PFD risk was assessed in 597 patients enrolled in the MUSIC (MUerte Súbita en Insuficiencia Cardiaca) study. ECG indices included: turbulence slope (TS), reflecting autonomic dysfunction; T-wave alternans (TWA), reflecting ventricular repolarization instability; and T-peak-to-end restitution (ΔαTpe) and T-wave morphology restitution (TMR), both reflecting changes in dispersion of repolarization due to heart rate changes. Standard clinical indices were also included.ResultsThe indices with the greatest SCD prognostic impact were gender, New York Heart Association (NYHA) class, left ventricular ejection fraction, TWA, ΔαTpe and TMR. For PFD, the indices were diabetes, NYHA class, ΔαTpe and TS. Using a model with only clinical variables, the hazard ratios (HRs) for SCD and PFD for patients in the high-risk group (fifth quintile of risk score) with respect to patients in the low-risk group (first and second quintiles of risk score) were both greater than 4. HRs for SCD and PFD increased to 9 and 11 when using a model including only ECG markers, and to 14 and 13, when combining clinical and ECG markers.ConclusionThe inclusion of ECG markers capturing complementary pro-arrhythmic and pump failure mechanisms into risk models based only on standard clinical variables substantially improves prediction of SCD and PFD in CHF patients.

Epilepsy is associated with ventricular alterations following convulsive status epilepticus in children.

SummaryObjectiveConvulsive status epilepticus can exert profound cardiovascular effects in adults, including ventricular depolarization–repolarization abnormalities. Whether status epilepticus adversely affects ventricular electrical properties in children is less understood. Therefore, we sought to characterize ventricular alterations and the associated clinical factors in children following convulsive status epilepticus.MethodsWe conducted a 2‐year retrospective case–control study. Children between 1 month and 21 years of age were included if they were admitted to the pediatric intensive care unit with primary diagnosis of convulsive status epilepticus and had 12‐lead electrocardiogram (ECG) within 24 h of admission. Children with heart disease or ion channelopathy, or who were on vasoactive medications were excluded. Age‐matched control subjects had no history of seizures or epilepsy. The primary outcome was ventricular abnormalities represented by ST segment changes, abnormal T wave, QRS axis deviation, and corrected QT (QTc) interval prolongation. The secondary outcomes included QT/RR relationship, beat‐to‐beat QTc interval variability, ECG interval measurement between groups, and clinical factors associated with ECG abnormalities.ResultsOf 317 eligible children, 59 met the inclusion criteria. History of epilepsy was present in 31 children (epileptic) and absent in 28 children (nonepileptic). Compared with the control subjects (n = 31), the status epilepticus groups were more likely to have an abnormal ECG, with overall odds ratios of 3.8 and 7.0 for the nonepileptic and the epileptic groups, respectively. Simple linear regression analysis demonstrated that children with epilepsy exhibited impaired dependence and adaptation of the QT interval on heart rate. Beat‐to‐beat QTc interval variability, a marker of ventricular repolarization instability, was increased in children with epilepsy.SignificanceConvulsive status epilepticus can adversely affect ventricular electrical properties and stability in children, especially those with epilepsy. These findings suggest that children with epilepsy may be particularly vulnerable to seizure‐induced arrhythmias. Therefore, postictal cardiac surveillance may be warranted in this population.

Recording duration and short-term reproducibility of heart rate and QT interval variability in patients with myocardial infarction

Beat-to-beat variability of the QT interval (QTV) measured on surface ECG has emerged as a potential marker for ventricular repolarization instability and has been used along with heart rate variability (HRV) to predict arrhythmic risk. Since measurement modalities of QTV have not been standardized, the objective of this study was to investigate the effect of ECG recording duration on QTV as well as HRV. Using a database of 30 min ECG recorded from 500 patients with acute myocardial infraction during rest, we extracted RR and QT interval time series and estimated different HRV and QTV metrics over windows of varying length. Analysis of variance (ANOVA) and intra-class correlation analyses were computed to investigate the effect of recording length on consistency and short-term reproducibility of HRV and QTV variables. Good consistency (non-significant ANOVA results) and short-term reproducibility (intra-class correlation coefficients >0.8) were demonstrated for all but standard deviation based metrics when at least 200 beats were included in the estimation. In conclusion, QTV can be quantified from resting ECG with good short-term consistency and reproducibility that is comparable to that of HRV.

Usefulness of microvolt T-wave alternans for predicting outcome in patients with Chagas disease with implantable cardioverter defibrillators

BackgroundChagas disease (ChD) may lead to life-threatening heart disease, including malignant ventricular arrhythmias. The use of implantable cardioverter defibrillators (ICDs) has become the main therapeutic strategy for secondary prevention of SCD in Chagas disease (ChD). Microvolt T-wave alternans (MTWA) is a direct measure of ventricular repolarization instability and has emerged as a potentially useful way of determining arrhythmia vulnerability. However, this methodology has not been evaluated in patients with ChD. ObjectiveTo evaluate the predictive value of MTWA testing for appropriate therapy or death in ChD patients with ICDs. MethodsThis prospective study included consecutive patients who received ICD implantations in a Brazilian tertiary referral center. ResultsSeventy-two patients were followed for a median time of 422 (range 294–642) days. Thirty-three patients had ChD. The MTWA was non-negative (positive or indeterminate) in 27 (81.8%) of ChD patients. The combined primary outcome (appropriate ICD therapy or death) occurred in 29 patients (40.3%); 17 out 33 ChD patients presented the primary outcome. There was a statistically significant difference in event-free survival between ChD patients with negative and non-negative MTWA results (p=0.02). Non-negative MTWA tests nearly triple the risk of appropriate ICD therapy or death (HR=2.7, 95% CI: 1.7–4.4, p=0.01) in patients with ChD and was the only variable associated with outcomes. The sensitivity and the negative predictive value was 100% in ChD patients. ConclusionsMTWA may be useful in recognizing high-risk ICD patients who may require adjunctive therapies with antiarrhythmic drugs or catheter ablation.

Techniques for Ventricular Repolarization Instability Assessment From the ECG

Instabilities in ventricular repolarization have been documented to be tightly linked to arrhythmia vulnerability. Translation of the information contained in the repolarization phase of the electrocardiogram (ECG) into valuable clinical decision-making tools remains challenging. This work aims at providing an overview of the last advances in the proposal and quantification of ECG-derived indices that describe repolarization properties and whose alterations are related with threatening arrhythmogenic conditions. A review of the state of the art is provided, spanning from the electrophysiological basis of ventricular repolarization to its characterization on the surface ECG through a set of temporal and spatial risk markers.

Beat-to-beat T-wave amplitude variability in the risk stratification of right ventricular outflow tract-premature ventricular complex patients.

Premature ventricular complexes (PVCs) originating from the right ventricular outflow tract (RVOT) may occasionally trigger monomorphic ventricular tachycardia (MVT), polymorphic ventricular tachycardia (PVT), or ventricular fibrillation (VF). We examined whether an analysis of the ventricular repolarization instability could differentiate PVT/VF triggered by RVOT-PVCs from benign RVOT-PVCs or MVT. We evaluated the ventricular repolarization instability as assessed by the beat-to-beat T-wave amplitude variability (TAV) using Holter recordings in patients with RVOT-PVCs but with no structural heart disease. We determined the prematurity index, defined as the ratio of the coupling interval of the first ventricular tachycardia (VT) beat or isolated PVC to the preceding R-R interval just before the VT or isolated PVC in the Holter recordings. The study patients were classified into RVOT-PVCs/MVT (n = 33) and PVT/VF (n = 10). The two groups did not differ with respect to the age, sex, and left ventricular ejection fraction. There was no significant difference in the prematurity index between the two groups (RVOT-PVCs/MVT 0.66 ± 0.16 vs. PVT/VF 0.61 ± 0.13, P = 0.60). The patients with PVT/VF had a significantly larger maximum TAV than those with RVOT-PVCs/MVT (31 ± 13 vs. 68 ± 40 µV, P < 0.001). Patients with a higher than median value of the TAV (33 µV) were at increased risk of PVT/VF vs. those with a lower than median value, after adjusting for the age and sex [9.25 (95% confidence interval: 1.27-19.2); P = 0.03]. The TAV analysis is a useful measure to identify the subset of usually benign RVOT-PVC/MVT patients prone to PVT/VF.

The Presence of Electromechanical Mismatch In Nonischemic Dilated Cardiomyopathy Is Associated With Ventricular Repolarization Instability

BackgroundWe analyzed electromechanical mismatch (EMM) and its relationship to ventricular repolarization in patients with nonischemic dilated cardiomyopathy (DCM). Methods and ResultsIn 39 DCM patients with left ventricular ejection fraction (LVEF) <40% and New York Heart Association functional class ≥III, electroanatomic mapping was used to quantify areas of EMM. High-resolution electrocardiograph was used to measure heart rate variability (HRV) and QT variability index (QTVI). EMM was present in 22 patients (56%, group 1), whereas 17 patients presented no mismatched segments (44%, group 2). The groups did not differ in age (56 ± 10 years in group 1 vs 57 ± 7 years in group 2; P = .82), sex (male: 82% vs 94%; P = .40), LVEF (27 ± 8% vs 25 ± 6%; P = .18), or N-terminal pro–B-type natriuretic peptide (2,350 pg/mL vs 2,831 pg/mL; P = .32). Although heart rate and HRV were similar in both groups (rate: 80 ± 20 beats/min in group 1 vs 74 ± 19 beats/min in group 2 [P = .47]; standard deviation of normal-to normal RR intervals: 106 ± 79 vs 88 ± 115 [P = .61]), we found significantly higher QTVI values in patients from group 1 (−1.15 ± 0.46 vs −1.62 ± 0.51 in group 2; P = .005). In patients with implantable cardioverter-defibrillators, ventricular arrhythmias recorded ≤1 year before enrollment were more frequent in group 1 than in group 2 (58% vs 13%; P = .02). ConclusionsEMM is present in a majority of patients with DCM and is associated with ventricular repolarization instability.

Assessing real-time RR-QT frequency-domain measures of coupling and causality through inhomogeneous point-process bivariate models.

Ventricular repolarization instability is known to be related to arrhythmogenesis and increased risk of sudden cardiac death. These repolarization dynamics are linked to the distance between T-wave and Q-wave occurrences (QT) on the ECG, and they are coupled with R-wave to R-wave interval variability (RRV). Several efforts have been dedicated to the analysis of QT-RR interactions in order to provide both a quantification of the coupling and estimates of intrinsic repolarization dynamics. However, a methodology able to quantify dynamic changes in repolarization variability unrelated to RRV dynamics is still needed. In this study, we propose a bivariate model embedded within a multiple inhomogeneous point-process framework to obtain time-varying tracking of (causal) interactions between QT variability (QTV), a marker of repolarization variability, and RRV. Data from 15 healthy subjects undergoing a tilt table test were analyzed. Our results demonstrate that the model effectively captures the time-varying mutual QTV-RRV interactions. The analysis of time-varying coherence confirms that head-up tilt is associated with a decrease in linear QTV-RRV coupling, while time-varying directed coherence shows that intrinsic QTV becomes more prominent during head-up tilt.

Ventricular Repolarization Instability in Patients with a Malignant Form of Ventricular Extrasystoles Originating from the Right Ventricular Outflow Tract

Objective:Ventricular extrasystoles (VEs) originating from the right ventricular outflow tract (RVOT) are considered benign, but sometimes lead to sudden cardiac death due to polymorphic ventricular tachycardia or ventricular fibrillation (PVT/VF). Previous case reports suggested that patients with a malignant form of RVOT-VE exhibited a left bundle-branch block morphology and positive deflection in lead I. We assessed the hypothesis that patients with a malignant form of RVOT-VE may have ventricular repolarization instability.Methods and Results:We studied 3 patients with a malignant form of RVOT-VE (age, 34±17 years, 2 males) and compared them to 40 control subjects without structural heart disease. All patients underwent high-resolution digital Holter recording (ela medical) and we determined the maximum value of the beat-to-beat T-wave variability (TAV). The patients with a malignant form of RVOT-VE had a higher maximum value of the TAV than the controls (max TAV: 69±9 µV vs. 20±7 µV, p<0.001). During the follow-up, two males experienced shock deliveries for VF by an implantable cardioverter-defibrillator (ICD). The remaining one female had survived after a radiofrequency catheter ablation and no ICD was implanted.Conclusions:Our results suggest that patients with a malignant form of RVOT-VE may have a ventricular repolarization instability.

Relationships between Brain Natriuretic Peptide, Troponin I and QT Dispersion in Asymptomatic Dialysis Patients

Objectives. The relationships between increased wall stress, myocyte death, and ventricular repolarization instability in patients with heart failure were reported. Design and Methods. The relationships between brain natriuretic peptide (BNP), a predictor of increased wall stress of hearth; troponin I (cTnI), a predictor of myocyte death; and QT dispersion (QTd), a reflection of ventricular repolarization instability were evaluated in age- and sex-matched asymptomatic 29 hemodialysis (HD) patients and 26 peritoneal dialysis (PD) patients, and the finding were compared. Results. Serum BNP and cTnI levels in HD patients (722.9 ± 907.9 pg/mL, 0.05 ± 0.07 μg/L, respectively), just before HD, were significantly higher than those of PD patients (255.4 ± 463.7 pg/mL, 0.02 ± 0.02 μg/L, respectively; p < 0.05). There was no significant difference between groups with regard to corrected QTd and maximum and minimum QT intervals (p > 0.05). Serum cTnI levels were significantly and positively correlated with serum BNP levels in both dialysis groups (r = 0.447, p = 0.048). No relationship was found between plasma BNP and ECG parameters studied in both groups (p > 0.05). Conclusion. Increased serum cTnI levels were associated with elevated BNP levels in both dialysis groups. The increases in BNP and troponin I are more likely to reflect hypervolemia. Although CAPD patients were receiving dialysis daily and HD patients were more hypervolemic, CAPD patients have similar QTdc and accordingly a similar tendency toward arrhythmias. This suggests that factors other than electromechanical interaction may be important in determining the QT interval length in patients on dialysis.