Abstract
Background
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.
Methods
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.
Results
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].
Conclusion
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.
Keywords: mortality, Tp‐e interval, ventricular arrhythmias
1. INTRODUCTION
Arrhythmogenic right ventricular cardiomyopathy (ARVC), formerly called "arrhythmogenic right ventricular dysplasia" (ARVD), is an inherited cardiomyopathy characterized by a progressive fibrofatty replacement of the myocardium that predisposes to ventricular tachycardia and sudden cardiac death in young individuals and athletes (Marcus et al., 2010; McKenna et al., 1994).
Repolarization abnormalities, the significant contributor to ventricular arrhythmias and mortality, are the frequently observed ECG changes in patients with ARVC. Myocardial repolarization has been assessed with QT interval (QT), corrected QT interval (QTc), QT dispersion (QTd), and transmural dispersion of repolarization. Previous studies have indicated that the time interval between the peak and the end of the T wave (Tp‐e interval) has been proposed as markers of transmural dispersion of repolarization to identify the patients at higher risk of malignant arrhythmic events (Hevia et al., 2006; Morin et al., 2012; Mugnai et al., 2017). Corrected Tp‐e interval and Tp‐e/QT ratio have been introduced to be more convincing measures for the dispersion of ventricular repolarization compared to QTd, cQTd, and Tp‐Te intervals which are independent of alterations in heart rate (Chua et al., 2016; Gupta et al., 2008).
The present study was designed to investigate the Tp‐e interval, corrected Tp‐e interval, Tp‐e/QT ratio, Tp‐e/QTc ratio, and new repolarization indices, in predicting the risk of mortality in ARVC patients.
2. METHODS
2.1. Study population
We conducted an extensive search from 2010 to 2018 for patients diagnosed with ARVC. The following data were gathered from the patient records: age, gender clinical presentation, electrocardiographic, echocardiographic, and cardiac magnetic resonance imaging. 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).
Patients with valvular heart disease, other congenital heart diseases, documented coronary artery disease, pulmonary hypertension, chronic renal failure, chronic liver disorders, chronic lung disease, electrolyte imbalance, haematological disorders, known malignancy, thyroid dysfunction, paced rhythms, and atrioventricular conduction abnormalities on ECG and ECGs without clearly analyzable QT segment were not included. All subjects were in sinus rhythm. None were taking any antiarrhythmic drugs that could affect the electrocardiographic measurements at the time of admission. Informed consent was obtained from each patient involved in this study. The Institutional Ethics Committee approved the study.
2.2. Diagnosis of arrhythmogenic right ventricular dysplasia
The 2010 revised Task Force Criteria were selected based on analysis of receiver operator curves generated from data from 108 probands with newly diagnosed ARVC and data from normal subjects. In this study, both the original and revised criteria were used to select the patients (Marcus et al., 2010; McKenna et al., 1994). They are as follows:
Global and regional dysfunction and structural alterations
Tissue characterization of wall
Repolarization abnormalities on the ECG
Depolarization/conduction abnormalities on the ECG
Arrhythmias
Family history
Two major criteria or one major and two minor criteria or four minor criteria from different categories were accepted for the definite diagnosis of ARVC.
Echocardiography was performed with an echocardiography platform (GE Vivid 3, GE Healthcare, Piscataway, New Jersey, USA) equipped with a 1.5–3.6 MHz phased‐array probe. Right ventricular (RV) function was measured by tricuspid annular plane systolic excursion (TAPSE) and RV fractional area change (FAC) (Rudski et al., 2010). Left ventricular systolic function was measured by using the Simpson biplane method (Lang et al., 2015).
All ARVC patients underwent CMR imaging as part of their clinical workup on a 1.5‐T magnetic resonance imaging scanner (Achieva; Philips Healthcare, Best, The Netherlands) according to standard ARVC protocols (Dalal et al., 2009; Te Riele et al., 2013).
2.3. Demographic and Clinical data, Follow‐up
Demographic and clinical data including age, sex, and the presence of hypertension, diabetes mellitus, and smoking status were recorded. The blood pressure of the patients was measured, while the patient was seated, after a 5‐min rest. HT was diagnosed if the systolic blood pressure was 140 mm Hg or the diastolic blood pressure 90 mm Hg in at least two separate measurements, or if the patient was taking any antihypertensive medication. DM was defined as a fasting blood glucose level of 126 mg/dl on two separate occasions or if the patient was being treated with oral antihyperglycemic agents or insulin. Smoking status was defined as currently smoking. Clinical follow‐up was performed by review of hospital medical records. All subsequent hospital admissions during follow‐ups were recorded.
2.4. Electrocardiogram analysis
The 12‐lead ECG was recorded at a paper speed of 50 mm/s at rest in the supine position with amplification of 20 mm/mV. Epsilon(e) waves, defined according to McKenna et al. (1994). as distinct waves of small amplitude that occupy the QT segment in the right precordial leads, complete right bundle branch block (RBBB), defined as a prolonged QRS complex ≥120 ms. The heart rate was measured from the ECG data. QT interval (from the onset of the QRS complex to the end of the T wave) and corrected QT interval (according to the Bazett's formula (QTc = QT/RR)) were measured manually after twofold magnification. QT dispersion (the difference between the maximum and minimum QT intervals) and QTc dispersion (the difference between the maximum and minimum QTc intervals) were also analyzed (Day, McComb, & Campbell, 1990).
Tp‐e (Tp‐e tangent) interval was defined as the time from the peak of the T wave to the intersection between the tangent line and the isoelectric line in the tangent method (Erikssen, Liestøl, Gullestad, Haugaa, & Bendz, 2012). Tp‐e (Tp‐e tail) was defined as the time from the peak of the T wave to the end of the T wave in the tail method (Figure 1; Salles, Cardoso, Leocadio, & Muxfeldt, 2008). The primary difference between the two methods is that the tail method also includes the terminal phase of the T wave. Measurements of Tp‐e interval were performed from precordial leads (II, V2, and V5), and the mean value of the measurements was used in the analysis and corrected for the heart rate (cTp‐e) (Hevia et al., 2006). If U wave interrupts the descending limb of the preceding T wave, the T‐wave offset was considered to be at nadir between the T and U waves. If T wave was low voltage, biphasic or negative, the QT interval was measured from the time of the final return of the deflection to the baseline (Goldenberg, Moss, & Zareba, 2006). If the T‐wave amplitude was <1.5 mm in the lead, that lead was excluded from the analysis. All findings appeared on Tp‐e in this article are based on the tail method choosing the lead with the longest Tp‐e. The Tp‐e/QT and Tp‐e/QTc ratios were also measured from these values. Neither intraobserver nor interobserver variability was assessed in random samples of 20 ECGs measured by two other cardiologists. Intraobserver and interobserver coefficients of variation (standard deviation [SD] of differences between two observations divided by the mean value and expressed as the percent) were found to be 2.3% and 2.2%, respectively.
Figure 1.
Measurement of the Tp‐e interval by both the tail and the tangent methods. Tp‐e, interval between the peak and the end of the T wave
2.5. Statistical analysis
All statistical analyses were carried out using SPSS, version 22.0 (SPSS for Mac; SPSS Inc., Chicago, Illinois, USA). Subjects were grouped into ARVC and control group. The variables were investigated using visual (histograms, probability plots) and analytical methods (Kolmogorov–Smirnov/Shapiro–Wilk test) to determine whether or not they are normally distributed. Continuous measurements were summarized as a mean and standard deviation or median [interquartile range], whereas categorical variables were summarized as the number of cases with the percentage (%). Overall comparisons of categorical variables were performed using Pearson's chi‐square test and Fisher's exact test. Student's t test was used for normally distributed parameters, whereas Mann–Whitney U test was used for the parameters not distributed normally. The capacity of cTp‐e interval and FAC (%) in predicting mortality was analyzed using the receiver operating characteristics (ROC) curve analysis. When a significant cutoff value was observed, the sensitivity, specificity, and positive and negative predictive values were presented. For clinical outcomes, Kaplan–Meier estimates and curves were generated. Two separate log‐rank tests were used to identify the independent effect of prolonged cTp‐e interval and reduced FAC (r FAC) on survival. Forward stepwise multivariate logistic regression models were created to determine the independent predictors of mortality. A P value <0.05 was considered statistically significant.
3. RESULTS
The baseline demographic and clinical data are presented in Table 1. The study population was divided into two groups which were similar regarding sex distribution, age, body mass index, risk factors including hypertension, diabetes mellitus, and smoking status. When compared to the control group, the patients with ARVC had significantly lower right ventricular FAC (31.2 ± 2.6, 35.2 ± 2.6; p < 0.001, respectively) and TAPSE (1.75 ± 0.2, 2.53 ± 0.3; p < 0.001, respectively). When ARVC patients compared according to their LV EF, no significant difference was found (LVEF ranged from 57% to 64%, with a median of 60%, LVEF ranged from 60% to 65%, with a median of 61%; p = 0.804, respectively).
Table 1.
Clinical characteristics and echocardiographic findings of the study population
| Variables | ARVC (n = 40) | Control group (n = 65) | p Value |
|---|---|---|---|
| Clinical characteristics | |||
| Age (years) | 35 (26–41) | 37 (24–45) | 0.151 |
| Men, n (%) | 30 (75 ) | 42 (64.6) | 0.288 |
| Body mass index (kg/m2) | 23.8 ± 1.5 | 24.1 ± 2.2 | 0.532 |
| Hypertension, n (%) | 2 (5) | 4 (6.2) | 0.585 |
| Diabetes, n (%) | 2 (5) | 3 (4.7) | 0.641 |
| Smoking, n (%) | 11 (27.5) | 16 (24.6) | 0.457 |
| Mortalite, n(%) | 10 (25) | – | |
| 2D Echocardiographic parameters | |||
| LV Ejection fraction, % | 60 (57,64) | 61 (60, 65) | 0.804 |
| RV‐FAC,% | 31.2 ± 2.6 | 35.2 ± 2.6 | <0.001 |
| TAPSE(mm) | 1.75 ± 0.2 | 2.53 ± 0.3 | <0.001 |
ARVC: arrhythmogenic right ventricular cardiomyopathy; cTp‐e: corrected Tp‐e; LV: left ventricle; QTc: corrected QT; RV‐FAC: right ventricular fractional area change.
Values are median (IQR), mean ± SD, or n (%)
Electrocardiographic parameters of the groups are shown in Table 2. No significant differences were found in the heart rate, and QRS interval between the groups. QT interval, QTc interval, QTd, and QTc dispersion were significantly increased in ARVC patients compared to the controls (all p < 0.001). Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratio were also significantly higher in ARVC patients compared to the control group (all p < 0.001). Of 40 patients in ARVC group, nine (22.5%) had epsilon wave, 11 (27.5%) had isolated RBBB, and 12 (30%) had precordial T‐wave inversion (Table 2).
Table 2.
Electrocardiographic findings of the study population
| Variables | ARVC (n = 40) | Control group (n = 65) | p Value |
|---|---|---|---|
| Heart rate (beat/min) | 69.8 ± 6.3 | 73.4 ± 12.3 | 0.133 |
| QRS interval (ms) | 104.3 ± 16.1 | 101.2 ± 15.5 | 0.378 |
| QT interval (ms) | 448.1 ± 55.0 | 395.1 ± 30.4 | <0.001 |
| QT dispersion of the 12 leads (ms) | 29.7 ± 5.1 | 21.3 ± 6.6 | <0.001 |
| QTc interval (ms) | 481.8 ± 58.6 | 427.6 ± 31.8 | <0.001 |
| QTc dispersion of the 12 leads (ms) | 31.8 ± 5.3 | 23.3 ± 6.5 | <0.001 |
| Tp‐e interval (ms) | 99.1 ± 10.6 | 87.1 ± 14.4 | <0.001 |
| cTp‐e interval (ms) | 102.1 ± 12.0 | 86.2 ± 11.0 | <0.001 |
| Tp‐e/QT ratio | 0.22 ± 0.02 | 0.19 ± 0.02 | <0.001 |
| Tp‐e/QTc ratio | 0.21 ± 0.05 | 0.18 ± 0.02 | <0.001 |
| Epsilon wave n, (%) | 9 (22.5) | – | – |
| RBBB n, (%) | 11 (27.5) | – | – |
| Precordial T‐wave inversion, n, (%) | 12 (30) | – | – |
cTp‐e: corrected Tp‐e.; QTc: corrected QT; RBBB: right bundle branch block; Tp‐e: the interval between the peak and the end of the T wave.
Values are mean ± SD.
From the medical records began with the patient's first admission as an inpatient or attendance as an outpatient to the last medical reports (94.5 ± 30.5 months), 10 (25%) patients died in ARVC group. Patients were divided into two groups: the deceased group (group A) (n = 10), who died during the follow‐up period, and the survival group (group B) (n = 30).
QRS interval, QT dispersion, QTc interval, QTc dispersion, Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratio were significantly increased in group A patients compared to the group B (p = 0.002, p = 0.006, p = 0.001, p = 0.020, p = 0.001, p = 0.020, p = 0.038, p < 0.001, p = 0.006, p = 0.032, respectively) (Table 3). There was no significant difference in epsilon waves as well as RBBB between group A and group B. Group A significantly showed the higher number of precordial T‐wave inversion (p = 0.026). The patients in group A had significantly lower right ventricular FAC (28.8 ± 2.2, 32.1 ± 2.2; p < 0.001, respectively) and TAPSE (1.51 ± 0.2, 1.83 ± 0.2; p < 0.001, respectively).
Table 3.
Comparison of electrocardiographic and echocardiographic findings between patients in group A and group B
| Variables | Group A (n = 10) | Group B (n = 30) | p Value |
|---|---|---|---|
| Heart rate (beat/min) | 72.0 ± 1.0 | 69.1 ± 7.1 | 0.225 |
| QRS interval (ms) | 113.0 ± 3.1 | 101.5 ± 17.6 | 0.002 |
| QT interval (ms) | 467.0 ± 47.4 | 441.6 ± 56.7 | 0.212 |
| QT dispersion of the 12 leads (ms) | 31.0 ± 4.8 | 26.0 ± 4.2 | 0.006 |
| QTc interval (ms) | 531.5 ± 26.8 | 465.3 ± 57.1 | 0.001 |
| QTc dispersion of the 12 leads (ms) | 33.0 ± 5.1 | 28.5 ± 4.7 | 0.020 |
| Tp‐e interval (ms) | 105.1 ± 12.1 | 97.1 ± 9.5 | 0.038 |
| cTp‐e interval (ms) | 113.3 ± 10.0 | 99.1 ± 10.5 | <0.001 |
| Tp‐e/QT ratio | 0.23 ± 0.01 | 0.21 ± 0.02 | 0.006 |
| Tp‐e/QTc ratio | 0.22 ± 0.02 | 0.20 ± 0.02 | 0.032 |
| Epsilon wave n, (%) | 3 (30) | 6 (20) | 0.517 |
| RBBB n, (%) | 4 (40) | 7 (21.8) | 0.301 |
| Precordial T‐wave inversion, n, (%) | 6 (60) | 6 (20) | 0.026 |
| RV‐FAC,% | 28.8 ± 2.2 | 32.1 ± 2.2 | <0.001 |
| TAPSE(mm) | 1.51 ± 0.2 | 1.83 ± 0.2 | <0.001 |
cTp‐e: corrected Tp‐e; QTc: corrected QT; Tp‐e interval between the peak and the end of the T wave.
Values are mean ± SD.
In the ROC curve analysis, Tp‐e interval cutoff value of ≥107 ms with the sensitivity of 90% and the specificity of 88% (AUC = 0.886, p < 0.001) and, RV‐FAC cutoff value of ≤30% with the sensitivity of 80% and the specificity of 88% (AUC = 910, p < 0.001) for the prediction of mortality in patients with ARVC. Figure 2 shows that patients in group B had superior survival compared with those in group A.
Figure 2.
Kaplan–Meier survival curves for patients with cTp‐e tail < 107 ms and cTp‐e tail ≥ 107 ms and RV‐FAC < 30% and RV‐FAC ≥ 30%. Dots indicate censored individuals. RV‐FAC = right ventricular fractional area change; Tp‐e; the interval between the peak and the end of the T wave
Univariate and multivariate logistic regression analysis for the predictors of all‐cause mortality in the study group are presented in Table 4. In the univariate analysis, right ventricular FAC, QTc interval, Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc were associated with all‐cause mortality. Variables with a P value less than 0.05 in univariate analysis were included in the multivariate model. 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].
Table 4.
Univariate and multivariate analysis for the predictors of all‐cause mortality in the study population
| Univariate analysis | Multivariate analysisa | |||
|---|---|---|---|---|
| OR (95% CI) | p | OR (95% CI) | p | |
| RV‐FAC, % | 2.236 (1.336–3.743) | 0.002 | 1.747 (1.012–3.018) | 0.045 |
| TAPSE (mm) | 2.132 (1.263–3.598) | 0.005 | ||
| Tp‐e interval (ms)b | 1.081 (1.016–1.150) | 0.013 | – | – |
| cTp‐e interval (ms)b | 1.163 (1.064–1.271) | 0.001 | 1.166 (1.017–1.336) | 0.027 |
| Tp‐e/QT ratiob | 1.562 (1.125–2.168) | 0.008 | – | – |
| Tp‐e/QTc ratiob | 1.584 (1.128–2.225) | 0.008 | – | – |
CI: confidence interval; EF: ejection fraction; OR: odds ratio; Tp‐e: interval between the peak and the end of the T wave.
Variables with a p < 0.05 in univariate analysis were included in the multivariate model.
Each parameter was studied separately using multiple regression analysis.
4. DISCUSSION
The main findings of this study are the following:
Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratios were prolonged in patients with ARVC as compared to healthy subjects.
The detailed analysis showed that the risk of mortality was significantly higher in the setting of reduced FAC, TAPSE and prolonged QTc, QTc dispersion, Tp‐e intervals, Tp‐e/QT, and Tp‐e/QTc ratios in ARVC.
Corrected QT interval and QT dispersion, known as traditional ventricular repolarization markers, have been used in many diseases characterized by malignant ventricular arrhythmias, such as myocardial infarction, coronary artery disease, long‐QT syndrome, hypertrophic cardiomyopathy, and chronic heart failure (Buja, Miorelli, Turrini, Melacini, & Nava, 1993; Day et al., 1990; De Bruyne et al., 1998; Perkiömaki, Koistinen, Yli‐Mayry, & Huikuri, 1995; Zareba, Moss, & Cessie, 1994).
It is known that ARVC's characteristic pathologic finding, fibrofatty replacement of the right ventricular myocardium, predisposes to ventricular arrhythmias and sudden cardiac death. The process is divided into three progressive phases: In the early “concealed phase,” patients are mostly asymptomatic; in the overt “electrical phase,” patients present with symptomatic arrhythmias; finally, in the diffuse disease, patients may present with the right, left, or biventricular heart failure with associated ventricular arrhythmias. However, lethal ventricular arrhythmias can be the first clinical presentation in a concealed phase even typical echocardiographic findings are still absent (Dalal et al., 2005). ECG abnormalities are found in up to 90% of ARVC patients. T‐wave inversion (TWI), showing abnormal ventricular repolarization, in leads V1–V3 is a well‐established ECG feature of ARVD/C, and in the absence of a RBBB is considered as a minor diagnostic criterion. Besides, Turrini et al. (2001) provided information about QT dispersion, which was significantly correlated with the dispersion of ventricular recovery time, was significantly greater in the patients who died suddenly compared with living patients with different arrhythmic profiles. Consistent with their study, we found that QTc, QT dispersion, and corrected QT dispersion were significantly higher in ARVC patients when compared to controls.
Recently, a new marker, the Tp‐e interval, which is an index of the transmural dispersion of ventricular repolarization, shows the action potential duration differences in the epicardium, endocardium, and M cells from the heart. Previous studies have presented that prolonged Tp‐e interval and Tp‐e/QTc ratio are strongly associated with sudden cardiac death probably due to an increased sensitivity to arrhythmias caused by ventricular reentry (Erikssen et al., 2012; Wang et al., 2007). The present study demonstrated that Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratios were prolonged in patients with ARVC as compared to healthy subjects. Inconsistent with our study, Alizade et al. (2017) reported for the first time that Tp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratio were significantly prolonged in the early stage of ARVD patients compared to controls. In addition to their results, the most apparent findings to emerge from our analysis were that the increased cTp‐e interval, Tp‐e interval, Tp‐e/QT ratio, reduced FAC, and TAPSE were along with the mortality. A cutoff value ≥107 ms for cTp‐e interval and a cutoff value of ≤30% for FAC had good sensitivity and specificity in predicting the occurrence of death (Figure 2). The reason behind could be the loss of myocardial cells with fibrofatty replacement, and the scar formation was a substrate for potentially lethal ventricular arrhythmias and sudden death in ARVD patients Zorzi et al. (2013) findings confirmed that the extent of RV fibrofatty tissue is correlated with the amount of repolarization abnormality. RV fibrofatty tissue which is much more abundant in the epicardium may provoke electrical inhomogeneity and micro‐reentry resulting in ventricular arrhythmias and sudden cardiac death. This present study supports the fact that abnormal repolarization is a significant contributor to the arrhythmic substrate. In our study, 10 (25%) ARVC patients died, five (50%) of whom had documented ventricular tachycardia/ventricular fibrillation.
The findings of our study should be interpreted with caution because of the limited sample size and retrospective origin. We investigated the electrocardiographic features of ARVC patients, either deceased or survived, before starting antiarrhythmic drug therapy. The subsequent follow‐up of these patients on antiarrhythmic drug treatment or after implantation of cardioverter defibrillator was not addressed; therefore, prospective randomized studies in a larger population are required to confirm our results.
5. CONCLUSION
In conclusion, the fundamental strength of the present study is to show prolongation of Tp‐e interval, cTp‐e interval, Tp‐e/QT ratio, and Tp‐e/QTc ratio in ARVC patients. Furthermore, this appears to be the first study to reveal the strong relationship between the new repolarization abnormality markers and the mortality in ARVC patients. Hence, our findings may highlight the potential usefulness of ECG markers to define better which patients having ARVC benefit from placement of an ICD to prevent lethal cardiac arrhythmias and cardiac death.
CONFLICT OF INTEREST
There is no conflict of interest.
Cekirdekci EI, Bugan B. Can abnormal dispersion of ventricular repolarization be a predictor of mortality in arrhythmogenic right ventricular cardiomyopathy: The importance of Tp‐e interval. Ann Noninvasive Electrocardiol. 2019;24:e12619 10.1111/anec.12619
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