Effect of Cigarette Smoking on TP-E Interval, TP-E/QT Ratio and TP-E/QTC Ratio

Introduction: Cigarette smoking increases the risk of sudden cardiac death. Smoking may predispose to ventricular fibrillation and sudden cardiac death by altering ventricular repolarization and enhancing sympathetic nervous system activity. We aimed to study the effects of smoking on ventricular repolarization. Methods: We studied 47 healthy subjects. 24 long-term heavy smokers (10 women, mean age: 40±5 years) constituted the study group. 23 non-smokers (10 women, mean age: 42±10 years) constituted the control group. ECG was obtained from all subjects. Tp-e interval, Tp-e/ QT ratio, Tp-e/QTc ratio were measured. These parameters were compared between the groups. Results: There was no significant difference at the basic clinical and echocardiographic variables (p> .05). QT interval and QTc interval were similar between smokers and nonsmokers. Tp-e interval (p=.001) and Tpe/QT (p=.003) ratio were higher in heavy smokers compared to non-smokers whereas Tpe/QTc ratio (p=.13) was marginally higher in smokers. Other ECG parameters were similar between smokers and nonsmokers groups. Conclusion: Tp-e interval and Tpe/QT ratio are prolonged in heavy smokers. www.jafib.com October, 2013 | Special Issue Effect of Cigarette Smoking on TP-E Interval, TP-E/QT Ratio and TP-E/QTC Ratio A. Tokatli, F. Kilicaslan, M. Uzun, B.S. Cebeci Department of Cardiology, Golcuk Military Hospital, Kocaeli, Turkey; GATA Haydarpasa hospital, Istanbul, Turkey Surface ECG & 24-Hour Holter Monitoring in the Evolution of Cardiac Arrhythmias Group I Non-smokers Group II Smokers p PR 157.8 ± 21.1 148.8 ± 19.9 0.025 QT 381.6 ± 24.1 341.3 ± 22.5 0.554 QTc 389.8 ± 22.3 379.8 ± 35.2 0.535 TPe 78.9 ± 7.3 85.3 ± 10.7 0.001* TPe/QT 0.21 ± 0.02 0.25 ± 0.03 0.003* TPe/QTc 0.20 ± 0.02 0.23 ± 0.03 0.136 Abstract Introduction: Is known that the QT interval duration depends on the heart rate (HR) and is related with the autonomic nervous system regulation. Patients with Long QT Syndrome (LQTS) due to mutation of the potassium channels have an abnormal response to abrupt changes in HR and to the sympathetic stimulation that occurs with the brisk standing. Electrocardiograms (ECGs) performed immediately after standing could be a diagnostic tool for this syndrome. Objectives:To describe the presence of QT interval changes provoked by standing in patients with genetic confirmation of LQTS, and compare the results with a group of family members of patients with LQTS not carrying the familial mutation. Methods: We performed an ECG in the supine position and another immediately after getting up in 27 patients with LQTS and 22 unaffected relatives. We measured the corrected QT interval (QTc) (Bazett ́s Formula) in supine position and immediately after standing in DII and V5. The increase in the QTc interval (QTc in standing-QTc in supine) was also evaluated. Results: LQTS patients had a mean age of 39 ± 18 years (mean±SD), and 40% were male. Among these, 8 (30%) had LQTS1, 16 (59%) LQTS2, and 3 (11%) LQTS7.In the control group the mean age was 42 ± 19 years, 50% males. QTc values in supine and in standing positions for both groups are shown in Table 1. Patients with LQTS mutations showed statistically significant differences between the mean QTc interval in supine and after brisk standing (p = 0.003 DII, P <0.001 V5). In contrast, the control group showed no differences (p = 0.928 DII, p = 0.432 V5). We also noted significant differences when compared the mean increase in the QTc interval between both groups (p = 0.001 DII, P = 0.015 V5). In the subgroup analysis, the increase in the mean QTc interval was 53 ± 51ms in DII and 31 ± 35ms in V5 for LQTS1; and 34 ± 34ms in DII and 29 ± 26ms in V5 for LQTS2, evidencing no significant differences between both subtypes of LQTS (p = 0,65). Conclusions: Our population of patients with congenital LQTS had an abnormal QTc interval adaptation with the standing, showing a significant increase of this measure. Since our controls did not show this behavior, the performance of this test could be a useful tool in the diagnosis of individuals with baseline QTc interval at the upper limit of normal.Introduction: Is known that the QT interval duration depends on the heart rate (HR) and is related with the autonomic nervous system regulation. Patients with Long QT Syndrome (LQTS) due to mutation of the potassium channels have an abnormal response to abrupt changes in HR and to the sympathetic stimulation that occurs with the brisk standing. Electrocardiograms (ECGs) performed immediately after standing could be a diagnostic tool for this syndrome. Objectives:To describe the presence of QT interval changes provoked by standing in patients with genetic confirmation of LQTS, and compare the results with a group of family members of patients with LQTS not carrying the familial mutation. Methods: We performed an ECG in the supine position and another immediately after getting up in 27 patients with LQTS and 22 unaffected relatives. We measured the corrected QT interval (QTc) (Bazett ́s Formula) in supine position and immediately after standing in DII and V5. The increase in the QTc interval (QTc in standing-QTc in supine) was also evaluated. Results: LQTS patients had a mean age of 39 ± 18 years (mean±SD), and 40% were male. Among these, 8 (30%) had LQTS1, 16 (59%) LQTS2, and 3 (11%) LQTS7.In the control group the mean age was 42 ± 19 years, 50% males. QTc values in supine and in standing positions for both groups are shown in Table 1. Patients with LQTS mutations showed statistically significant differences between the mean QTc interval in supine and after brisk standing (p = 0.003 DII, P <0.001 V5). In contrast, the control group showed no differences (p = 0.928 DII, p = 0.432 V5). We also noted significant differences when compared the mean increase in the QTc interval between both groups (p = 0.001 DII, P = 0.015 V5). In the subgroup analysis, the increase in the mean QTc interval was 53 ± 51ms in DII and 31 ± 35ms in V5 for LQTS1; and 34 ± 34ms in DII and 29 ± 26ms in V5 for LQTS2, evidencing no significant differences between both subtypes of LQTS (p = 0,65). Conclusions: Our population of patients with congenital LQTS had an abnormal QTc interval adaptation with the standing, showing a significant increase of this measure. Since our controls did not show this behavior, the performance of this test could be a useful tool in the diagnosis of individuals with baseline QTc interval at the upper limit of normal. www.jafib.com October, 2013 | Special Issue The Response of the QT Interval to Standing as a New Diagnostic Tool for Long QT Syndrome C. Muñoz-Esparza1, M. Salar Alcaraz1, E. Zorio Grima2, P. Peñafiel Verdú1, J. José Sánchez Muñoz1, A. García Alberola1, M. Valdés-Chávarri1, J. R. Gimeno Blanes1 1Hospital Clínico Universitario Virgen de la Arrixaca, El Palmar, Murcia, Spain 2Hospital Politécnico y Universitario La Fe, Valencia, Spain QTc DII in supine QTc DII in standing QTc DII increment QTc V5 in supine QTc V5 in standing QTc V5 increment LQTS 477±66 516±50 45±47 472±33 510±45 36±39 Controls 423±33 417±42 0±31 423±34 425±40 6±33 Abstract Introduction: Increased P-wave dispersion is well known to be the predictor of recurrences after cardioversion in patients with atrial fibrillation. However, there is little data about relation between recurrence of atrial fibrillation and increased P-wave dispersion in normal LA sized patients after electrical cardioversion. Methods: We reviewed the electrocardiograms taken within a day in atrial fibrillation patients with successful cardioversion. All patients received antiarrhythmic drug after cardioversion. We compared P wave dispersion and maximum P-wave duration between recurrent group and non-recurrent group. Results: In 27 patients with persistent atrial fibrillation with normal LA size, 14 patients (51.8%) recurred atrial fibrillation after cardioversion. There were no difference in baseline characteristics including sex, age, hypertension and diabetes between two groups. P wave dispersions were significantly higher in the recurrent group than the nonrecurrent group (44.5±20 vs 30±12 ms, P<0.038). Furthermore, recurrent group showed significantly prolonged maximum P wave compared with that of nonrecurrent group (134±16 vs. 118±19, p=0.035). Conclusions: Increased P wave dispersion and prolonged maximum P-wave duration were associated with the recurrence of atrial fibrillation in patients with normal LA size after electrical cardioversion.Introduction: Increased P-wave dispersion is well known to be the predictor of recurrences after cardioversion in patients with atrial fibrillation. However, there is little data about relation between recurrence of atrial fibrillation and increased P-wave dispersion in normal LA sized patients after electrical cardioversion. Methods: We reviewed the electrocardiograms taken within a day in atrial fibrillation patients with successful cardioversion. All patients received antiarrhythmic drug after cardioversion. We compared P wave dispersion and maximum P-wave duration between recurrent group and non-recurrent group. Results: In 27 patients with persistent atrial fibrillation with normal LA size, 14 patients (51.8%) recurred atrial fibrillation after cardioversion. There were no difference in baseline characteristics including sex, age, hypertension and diabetes between two groups. P wave dispersions were significantly higher in the recurrent group than the nonrecurrent group (44.5±20 vs 30±12 ms, P<0.038). Furthermore, recurrent group showed significantly prolonged maximum P wave compared with that of nonrecurrent group (134±16 vs. 118±19, p=0.035). Conclusions: Increased P wave dispersion and prolonged maximum P-wave duration were associated with the recurrence of atrial fibrillation in patients with normal LA size after electrical cardioversion. www.jafib.com October, 2013 | Special Issue P Wave Dispersion and Recurrences After Cardioversion in Atrial Fibrillation Patients with Normal Left Atrium Size Y.J. Song1, D.K. Kim1, D.S. Kim1, T.H. Yang1, J.S. Jang1, J.S. Seo1, H.Y. Jin1, Y.A. Park1, J.I. Yang1, H.Y. Lee1, K.H. Kim2 1 Department of Cardiology, Busan paik Hospital, Busan, Republic of Korea 2 Department of Cardiology, Haeundae paik Hospital, Busan, Republic of Korea