scholarly journals Relationship between transmural dispersion of repolarization, Tpeak-Tend interval, and ventricular arrhythmias: reply

EP Europace ◽  
2007 ◽  
Vol 9 (1) ◽  
pp. 61-61
Author(s):  
L. Santangelo ◽  
E. Ammendola ◽  
V. Russo ◽  
C. Cavallaro ◽  
F. Vecchione ◽  
...  
Author(s):  
Yazdan Ghandi ◽  
Bita Ghahremani ◽  
Danial Habibi ◽  
Afsane Pouya ◽  
Saiid Sadrnia

Background: Children with mitral valve prolapse (MVP) may be prone to ventricular arrhythmias due to transmural dispersion of repolarization (TDR). This study aimed to assess alterations in ventricular repolarization in children with MVP and to investigate their relationships with the degree of mitral regurgitation. Methods: Fifty children with MVP and 50 age- and sex-matched healthy children as controls were studied. Twelve-lead electrocardiography and echocardiography were performed in all the subjects. TDR parameters were QT and QTc intervals, QTc dispersion, Tp-e interval, Tp-e interval dispersion, Tp-e/QT, Tp-e/QTc, JTc, JTc dispersion, Tp-e/JT, and Tp-e/JTc. Results: The mean age of the 50 patients with MVP was 12.45±2.50 years (F/M: 15/35). There were no significant differences in QT and QTc intervals between the 2 groups. QTc dispersion (P=0.001), Tp-e dispersion interval (P=0.002), Tp-e/QTc (P=0.001), JTc dispersion (P=0.023), Tp-e/JT (P=0.004), and Tp-e/JTc (P=0.002) were significantly higher in the patients with MVP than in the healthy controls. Positive correlations were found between Tp-e dispersion interval and Tp-e/QTc and an increase in the degree of mitral regurgitation (P=0.012, r=0.42 and P=0.004, r=0.31, respectively). Additionally, positive correlations were detected between JTc dispersion and Tp-e/JTc and an increase in the degree of mitral regurgitation (P=0.032, r=0.20 and P=0.024, r=0.42, correspondingly). Conclusion: In this study, TDR was damaged in children with MVP and was positively correlated with an increase in the degree of mitral regurgitation. It appears that children with MVP are prone to life-threatening ventricular arrhythmias.


Author(s):  
CENGİZ BURAK ◽  
ERKAN BAYSAL ◽  
MUHAMMED SÜLEYMANOĞLU ◽  
ÇAĞRI YAYLA ◽  
SERKAN ÇAY ◽  
...  

Background/aim: The number of patients with heart transplantation has dramatically increased in the last decade. Considerable studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (Tp-e) may correspond to the transmural dispersion of repolarization and increased Tp-e interval and Tp-e/QT ratio are associated with malignant ventricular arrhythmias. We analyzed the dispersion of myocardial repolarization using electrocardiographic Tp-e interval and Tp-e/QTc ratio in patients with heart transplantation.
 Materials and methods: This observational study included 38 patients (12 female and 26 male) with heart transplantation and 38 well-matched controls. From electrocardiograms, Tp-e interval and Tp-e/QTc ratio were calculated and compared between the 2 groups. Results: Noninvasive arrhythmia indicators including Tp-e interval (84.63 ± 14.17 ms vs 71.82 ± 7.47 ms, p < 0.001), Tp-e/QTc ratio (0.19 ± 0.04 vs 0.16 ± 0.02 p < 0.001) and QTc interval except QT interval were significantly higher in transplanted hearts compared to normal hearts. Conclusion: Patients with heart transplantation have increased myocardial dispersion of repolarization. Keywords: Tp-e/QTc ratio, heart transplantation, myocardial dispersion of repolarization


2009 ◽  
Vol 297 (3) ◽  
pp. H1048-H1057 ◽  
Author(s):  
Lin Wu ◽  
Sridharan Rajamani ◽  
Hong Li ◽  
Craig T. January ◽  
John C. Shryock ◽  
...  

Reduction of repolarization reserve increases the risk of arrhythmia. We hypothesized that inhibition of K+ current ( IK) to decrease repolarization reserve would unmask the proarrhythmic role of endogenous, physiological late Na+ current (late INa). Monophasic action potentials (MAP) and 12-lead electrocardiogram were recorded from female rabbit isolated hearts. To block IK and reduce repolarization reserve, E-4031, 4-aminopyridine, and BaCl2 were used; to block endogenous late INa, tetrodotoxin (TTX) and ranolazine were used. E-4031 (1–60 nM) concentration-dependently prolonged MAP duration (MAPD90) and increased duration of the T wave from Tpeak to Tend (Tpeak-Tend), transmural dispersion of repolarization (TDR), and beat-to-beat variability (BVR) of MAPD90. E-4031 caused spontaneous and pause-triggered polymorphic ventricular tachycardia [ torsade de pointes (TdP)]. In the presence of 60 nM E-4031, TTX (0.6–3 μM) and ranolazine (5–10 μM) shortened MAPD90, decreased TDR, BVR, and Tpeak-Tend ( n = 9–20, P < 0.01), and abolished episodes of TdP. In hearts treated with BaCl2 or 4-aminopyridine plus E-4031, TTX (0.6–3 μM) shortened MAPD90 and decreased Tpeak-Tend. Ranolazine could not reverse the effect of E-4031 to inhibit human ether-a-go-go-related gene (HERG) K+ current; thus, the reversal by ranolazine of effects of E-4031 was likely due to inhibition of late INa and not to antagonism of the HERG-blocking action of E-4031. We conclude that endogenous, physiological late INa contributes to arrhythmogenesis in hearts with reduced repolarization reserve. Inhibition of this current partially reverses MAPD prolongation and abolishes arrhythmic activity caused by IK inhibitors.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Alexey V Glukhov ◽  
Vadim V Fedorov ◽  
Kelley V Foyil ◽  
Nader Moazami ◽  
Igor R Efimov

Transmural dispersion of repolartization (DR) has been studied in numerous animal models. Some studies presented evidence of midmyocardial population of M-cells that possess distinctly long action potential duration (APD). We aimed to investigate APD and DR in explanted failing human left ventricles (LV). We optically mapped APD in coronary-perfused human LV wedge preparations (n=4) using CMOS camera in presence of blebbistatin (BB, 10 μ M). Microelectrode recordings were used to validate BB in human LV. RESULTS: During slow pacing (S1S1=2,000ms), APD at the endo-, mid-, and epicardium was 586±27ms, 578±19ms, and 496±14ms, respectively. Maximum APD gradient was 24±5 ms/mm, DR was 35±6 ms. Progressive decrease in S1S1 up to functional refractory period (460±26 ms) induced an inhomogeneous shortening of APD (up to 350±26 ms, 352±36 ms and 346±30 ms, respectively), decrease in APD gradient and DR (4±3 ms/mm and 20±4 ms, respectively, p<0.01) We present for the first time evidence of transmural APD gradient in failing human LV. However, we could not confirm presence of distinct population of M-cells that were found in several animal models.


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