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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.jecgonline.com/?rss=yes"><title>Journal of Electrocardiology</title><description>Journal of Electrocardiology RSS feed: Current Issue.    
 
 
 
The  Journal of Electrocardiology  is devoted exclusively to clinical and experimental studies 
of the electrical activities of the heart. It seeks to contribute significantly to the accuracy of diagnosis and prognosis and the effective 
treatment, prevention, or delay of heart disease. Editorial contents include electrocardiography, vectorcardiography, arrhythmias, membrane 
action potential, cardiac pacing, monitoring defibrillation, instrumentation, drug effects, and computer applications.   </description><link>http://www.jecgonline.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:issn>0022-0736</prism:issn><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2012</prism:publicationDate><prism:copyright> © 2012 Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002329/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002500/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611003001/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073610007831/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611001622/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002317/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002858/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002524/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611001427/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611001555/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611001531/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611001567/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002536/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002202/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611003086/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611002378/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611003293/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611004493/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207361100135X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207361100478X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073611004791/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002329/abstract?rss=yes"><title>Inadvertent interchange of electrocardiogram limb lead connections: analysis of predicted consequences: Part II: double interconnection errors</title><link>http://www.jecgonline.com/article/PIIS0022073611002329/abstract?rss=yes</link><description>Abstract: Limb lead connection errors are known to be very common in clinical practice.The consequences of all possible single limb lead interconnection errors were analyzed in an earlier publication (J Electrocardiology 2008;41:84-90). With a single limb lead interconnection error, 6 combinations of limb lead connections are possible. Two of these combinations give rise to records in which the limb lead morphology is uninterpretable. Such records show a “flat line” in lead II or III. Three of the errors give rise to records that are fully interpretable once the specific interconnection error has been identified (although one of the errors cannot reliably be recognized in the absence of a previous record for comparison). One of the errors produces no change in the electrocardiogram recording. In all cases, the precordial leads are interpretable, although there are very minor changes in the voltages.This communication predicts the changes in limb lead appearances consequent upon all possible double limb lead interchanges and illustrates these with records electively taken with such double interconnection errors. There are only 3 possible double limb lead interconnection errors. In 2 of the possible combinations, interpretation of the limb leads is impossible, and each of these errors gives rise to a flat line in lead I. In the third combination, the record is fully interpretable once the abnormality has been identified. In all 3 types, the precordial leads are interpretable, although there are very minor changes in the voltages.</description><dc:title>Inadvertent interchange of electrocardiogram limb lead connections: analysis of predicted consequences: Part II: double interconnection errors</dc:title><dc:creator>Derek J. Rowlands</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.005</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-08-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-08-25</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>ECG Acquisition and Analysis</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>6</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002500/abstract?rss=yes"><title>Influence of individual torso geometry on inverse solution to 2 dipoles</title><link>http://www.jecgonline.com/article/PIIS0022073611002500/abstract?rss=yes</link><description>Abstract: Background: The purpose of this study was to observe the influence of variety in individual torso geometries on the results of inverse solution to 2 dipoles.Methods: The inverse solution to 2 dipoles was computed from the measured data on 8 patients using either standard torso with various shapes and sizes of the heart and lungs in it or using various outer torso geometries with the same inhomogeneities. The vertical position of the heart relative to the fourth intercostal level was kept constant in all models. The results were compared with the reference solution computed in standard torso.Results: The inverse solution was influenced in 4 of 8 cases by changes of torso geometry and only in 1 of 8 cases by changes of internal inhomogeneities.Conclusions: The use of individual torso geometry with the knowledge of the true heart position is very important for correct inverse results.</description><dc:title>Influence of individual torso geometry on inverse solution to 2 dipoles</dc:title><dc:creator>Jana Svehlikova, Jana Lenkova, Marie Turzova, Milan Tysler, Michal Kania, Roman Maniewski</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.012</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-09-12</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-09-12</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>ECG Acquisition and Analysis</prism:section><prism:startingPage>7</prism:startingPage><prism:endingPage>12</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611003001/abstract?rss=yes"><title>Tombstone-like electrocardiographic changes during exercise stress test</title><link>http://www.jecgonline.com/article/PIIS0022073611003001/abstract?rss=yes</link><description>Abstract: A 45-year-old man showed tombstone-like electrocardiographic change during stage 1 of stress testing, using Bruce protocol. The raw rhythm strip did not show any ST-T changes. These pseudochanges were probably the result of computer-synthesized averaging algorithm errors.</description><dc:title>Tombstone-like electrocardiographic changes during exercise stress test</dc:title><dc:creator>Arunkumar Panneerselvam, Ravindranath K. Shankarappa, Manjunath C. Nanjappa</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.029</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>ECG Acquisition and Analysis</prism:section><prism:startingPage>13</prism:startingPage><prism:endingPage>14</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610007831/abstract?rss=yes"><title>Electromechanical association: a subtle electrocardiogram artifact</title><link>http://www.jecgonline.com/article/PIIS0022073610007831/abstract?rss=yes</link><description>Abstract: Artifacts on electrocardiogram (ECG) can simulate serious cardiac disorders. Although most common ECG artifacts can be easily recognized, in some exceptional situations, some patterns may hide pretty well even from experienced eyes. We recently reported an unusual ECG artifact caused by radial arterial impulse that closely imitates abnormal T wave. We now report 3 more examples and caught-in-the-act evidence of this subtle and dangerous artifact source.</description><dc:title>Electromechanical association: a subtle electrocardiogram artifact</dc:title><dc:creator>Emre Aslanger, Kivanc Yalin</dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.12.162</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-02-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-02-25</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>ECG Acquisition and Analysis</prism:section><prism:startingPage>15</prism:startingPage><prism:endingPage>17</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611001622/abstract?rss=yes"><title>Computer-based rhythm diagnosis and its possible influence on nonexpert electrocardiogram readers</title><link>http://www.jecgonline.com/article/PIIS0022073611001622/abstract?rss=yes</link><description>Abstract: Background: Systems providing computer-based analysis of the resting electrocardiogram (ECG) seek to improve the quality of health care by providing accurate and timely automatic diagnosis of, for example, cardiac rhythm to clinicians. The accuracy of these diagnoses, however, remains questionable.Objectives: We tested the hypothesis that (a) 2 independent automated ECG systems have better accuracy in rhythm diagnosis than nonexpert clinicians and (b) both systems provide correct diagnostic suggestions in a large percentage of cases where the diagnosis of nonexpert clinicians is incorrect.Methods: Five hundred ECGs were manually analyzed by 2 senior experts, 3 nonexpert clinicians, and automatically by 2 automated systems. The accuracy of the nonexpert rhythm statements was compared with the accuracy of each system statement. The proportion of rhythm statements when the clinician's diagnoses were incorrect and the systems instead provided correct diagnosis was assessed.Results: A total of 420 sinus rhythms and 156 rhythm disturbances were recognized by expert reading. Significance of the difference in accuracy between nonexperts and systems was P = .45 for system A and P = .11 for system B. The percentage of correct automated diagnoses in cases when the clinician was incorrect was 28% ± 10% for system A and 25% ± 11% for system B (P = .09).Conclusion: The rhythm diagnoses of automated systems did not reach better average accuracy than those of nonexpert readings. The computer diagnosis of rhythm can be incorrect in cases where the clinicians fail in reaching the correct ECG diagnosis.</description><dc:title>Computer-based rhythm diagnosis and its possible influence on nonexpert electrocardiogram readers</dc:title><dc:creator>Nina Hakacova, Elin Trägårdh-Johansson, Galen S. Wagner, Charles Maynard, Olle Pahlm</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.05.007</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-08-04</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-08-04</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>ECG Acquisition and Analysis</prism:section><prism:startingPage>18</prism:startingPage><prism:endingPage>22</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002317/abstract?rss=yes"><title>Widening spectrum of the J-wave syndromes</title><link>http://www.jecgonline.com/article/PIIS0022073611002317/abstract?rss=yes</link><description>For decades, early repolarization characterized by elevation of the junction between the end of the QRS complex and the beginning of the ST segment (the J point) has been considered to be a normal electrocardiographic (ECG) variant. The presence of a prominent J wave, however, especially in the inferior leads, is increasingly recognized as a marker of risk for malignant cardiac arrhythmias and cardiac death. The electrophysiologic mechanism and clinical significance of J-point elevation are hotly debated. The prevailing and almost uncontested theory is that J-point elevation is a genetic and purely electrophysiologic abnormality characterized by early repolarization of certain segments of the myocardium, giving rise to prominent voltage gradients between the endocardium and the epicardium and to increased susceptibility for arrhythmias. Patients with structural heart disease, however, may have another acquired form of terminal notching of the QRS complex formerly called peri-infarction block. Peri-infarction block is caused not by early repolarization but by delayed depolarization of those segments of the myocardium that exhibit inhomogeneous scar tissue. Peri-infarction block is frequently associated with ventricular late potentials in signal-averaged ECGs and with increased risk of malignant ventricular arrhythmias and sudden death. A recent publication in this journal and an old observation from decades ago now raise the possibility of a third form of the J-wave syndrome that is associated with the presence of an accessory pathway.</description><dc:title>Widening spectrum of the J-wave syndromes</dc:title><dc:creator>Laszlo Littmann, József Tenczer</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.004</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-08-22</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-08-22</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>23</prism:startingPage><prism:endingPage>25</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002858/abstract?rss=yes"><title>Transient Super-Himalayan P-waves in severe pulmonary emphysema</title><link>http://www.jecgonline.com/article/PIIS0022073611002858/abstract?rss=yes</link><description>Abstract: Himalayan P-waves are classically associated with congenital heart diseases with right to left shunt where they indicate a dilated right atrium and tend to be persistent. We report a case of transient Himalayan P-waves of 9-mm amplitude associated with a severe emphysema exacerbation. Patient had a normal right atrial size. The giant P-waves were likely the result of severe pulmonary hyperinflation, right atrial hypoxia, and transient mechanical load on the right atrium directly resulting from the bronchospasm. Transient Himalayan P-waves of quite such amplitude have not been reported previously, which makes our case the first such report in literature.</description><dc:title>Transient Super-Himalayan P-waves in severe pulmonary emphysema</dc:title><dc:creator>Lovely Chhabra, David H. Spodick</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.016</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-09-12</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-09-12</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>26</prism:startingPage><prism:endingPage>27</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002524/abstract?rss=yes"><title>The antihypertensive treatment effect on left ventricular diastolic function is reflected in exercise electrocardiogram</title><link>http://www.jecgonline.com/article/PIIS0022073611002524/abstract?rss=yes</link><description>Abstract: Background/Purpose: Exercise electrocardiographic hump sign is associated with uncontrolled arterial hypertension (AH), left ventricular (LV) diastolic dysfunction, and false-positive exercise testing (ET). The aim of this prospective study was to evaluate the antihypertensive treatment effect on hump and on pseudoischemic ST-segment depression and potential correlations to LV diastolic function and mass changes.Methods: The study comprised 59 non–coronary artery disease patients (45.9 years; 67.8% men) with never-treated arterial hypertension (143.2/95.1 mm Hg). Treadmill ET and echocardiography were performed at baseline and 6 months after pharmaceutical blood pressure normalization. Prevalence of hump and ST depression, transmitral (E/A) and tissue Doppler imaging (E′/A′) early/late velocities ratios, E/E′ ratio, and LV mass index (LVMI) were all defined.Results: Prevalence of hump was reduced from 69.5% to 23.7% and false-positive ETs from 35.6% to 18.6% (P &lt; .05). Significant improvement (P &lt; .05) was found in E′/A′ ratio (0.68 vs 0.84), E/E′ ratio (9.3 vs 7.9), and LVMI (109.2 vs 99.8 g/m2). Changes in hump were related to ST-depression changes (r = 0.632, P &lt; .001) and to LV diastolic indices changes; patients with hump only at first ET (54.2%) improved E/A and E′/A′ ratios, whereas patients with hump only at second ET (8.5%) worsened diastolic indices with similar changes in blood pressure and LVMI.Conclusions: Antihypertensive treatment reduces the prevalence of hump and exercise ischemic-appearing ST depression probably through LV diastolic function improvement.</description><dc:title>The antihypertensive treatment effect on left ventricular diastolic function is reflected in exercise electrocardiogram</dc:title><dc:creator>Charalampos I. Liakos, Andreas P. Michaelides, Gregory P. Vyssoulis, Evaggelos I. Chatzistamatiou, Polychronis E. Dilaveris, Maria I. Markou, Christodoulos I. Stefanadis</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.014</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-09-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-09-16</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>28</prism:startingPage><prism:endingPage>35</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611001427/abstract?rss=yes"><title>The prevalence of early repolarization in Wolff-Parkinson-White syndrome with a special reference to J waves and the effects of catheter ablation</title><link>http://www.jecgonline.com/article/PIIS0022073611001427/abstract?rss=yes</link><description>Abstract: We determined the prevalence of J waves in the electrocardiograms (ECG) of 120 patients with Wolff-Parkinson-White syndrome in comparison with J-wave prevalence in a control group of 1936 men and women with comparable demographic and ECG characteristics and with normal atrioventricular conduction. J waves were present only during manifest preexcitation in 22 of 120 patients (18.3%), disappearing after catheter ablation and suggesting that J waves were associated with the presence of preexcitation. J waves were present in 19 (15.8%) of 120 patients only after ablation, apparently having been masked by early depolarization of the preexcited myocardial region, and in 22 patients (18.3%), J waves were not altered significantly by preexcitation. Thus, the overall J-wave prevalence was 52.5% (63/120) and, excluding those apparently due to preexcitation, 34.8% (41/120), both substantially higher than the prevalence (11.5%) in the control group (P &lt; .001 for both). The patients with J waves appearing only during preexcitation were younger, predominantly females. The presence of J waves after ablation was associated with a history of atrial fibrillation and shorter ventricular effective refractory period. It is concluded that the prevalence of J waves is high in patients with Wolff-Parkinson-White syndrome and is influenced by manifest preexcitation.</description><dc:title>The prevalence of early repolarization in Wolff-Parkinson-White syndrome with a special reference to J waves and the effects of catheter ablation</dc:title><dc:creator>Nobue Yagihara, Akinori Sato, Kenichi Iijima, Daisuke Izumi, Hiroshi Furushima, Hiroshi Watanabe, Tadanobu Irie, Yoshiaki Kaneko, Masahiko Kurabayashi, Masaomi Chinushi, Masahito Satou, Yoshifusa Aizawa</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.04.006</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-06-27</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-06-27</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>36</prism:startingPage><prism:endingPage>42</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611001555/abstract?rss=yes"><title>The prognostic significance of electrocardiographic changes in Chagas disease</title><link>http://www.jecgonline.com/article/PIIS0022073611001555/abstract?rss=yes</link><description>Abstract: Introduction: The meaning of electrocardiographic changes appearing during the clinical follow-up of Chagas disease (ChD) is unknown. In this study, a patient cohort with ChD was followed to describe the electrocardiographic changes that may make it possible to identify patients whose left ventricular function has deteriorated.Methods: The study sample consisted of a prospective cohort followed since 1998 to 1999, involving 220 patients aged 15 to 55 years, 30 controls, and 190 with ChD, without other comorbidities. The group was reexamined between 2004 and 2006, and new electrocardiograms were obtained for 153 patients, 25 (83%) of 30 in the control group and 128 (72%) of 177 in the ChD group. Electrocardiographic variables associated with a significant decrease in ejection fraction (5% or more) were identified.Results: A significant decrease in ejection fraction was observed in 21 patients in the ChD group (18.7%) but in none of the non-ChD group (P = .024). Only the presence of a new electrocardiographic abnormality and an increase in QRS duration correlated with a decrease in an ejection fraction of 5% or more. QRS duration was correlated with both an increase in left ventricle diastolic diameter and a deterioration in the ejection fraction (rs = 0.225, P = .017, and rs = −0.300, P &lt; .001). A QRS increase of 5 milliseconds had 77.8% sensitivity and 62.2% specificity for identifying patients with significant decrease in ejection fraction.Conclusion: The increase in the duration of the QRS complex and the appearance of new electrocardiographic alterations may help in identifying patients with a significant decrease (of 5% or more) in left ventricle ejection fraction.</description><dc:title>The prognostic significance of electrocardiographic changes in Chagas disease</dc:title><dc:creator>Bruno Ramos Nascimento, Christiano Gonçalves Araújo, Manoel Otávio Costa Rocha, José Darlan Pinheiro Domingues, Aline Braga Rodrigues, Márcio Vinicius Lins Barros, Antonio Luiz Pinho Ribeiro</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.04.011</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-06-27</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-06-27</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>43</prism:startingPage><prism:endingPage>48</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611001531/abstract?rss=yes"><title>Ventricular repolarization sequences on the epicardium and endocardium. Monophasic action potential mapping in healthy pigs</title><link>http://www.jecgonline.com/article/PIIS0022073611001531/abstract?rss=yes</link><description>Abstract: To investigate repolarization sequence, monophasic action potentials were recorded from a mean of 153 ± 54 left and right ventricular epicardial and endocardial sites in 10 pigs using the CARTO mapping system (Biosense Webster, Waterloo, Belgium). The activation time and end-of-repolarization (EOR) time were measured and 3-dimensional maps of activation and repolarization sequences constructed.Results: In 8 of 9 pigs, both the activation and EOR times appeared first in the septum and last in the latero-basal areas on the endocardium, not on the epicardium. The EOR followed the activation sequence, both on the epicardium (in 8/9 pigs) and endocardium (in 8/8 pigs). The maximal EOR differences were 84 ± 20 ms, whereas the local EOR differences between paired sites against each other on the left ventricular epicardium and endocardium were 11 ± 9 ms in the apex and 12 ± 12 ms in the anterior wall.Conclusion: The EOR follows the activation sequence both on the epicardium and endocardium. The apico-basal gradients are predominant repolarization gradients, as compared with the epicardial–endocardial gradients.</description><dc:title>Ventricular repolarization sequences on the epicardium and endocardium. Monophasic action potential mapping in healthy pigs</dc:title><dc:creator>Ole Kongstad, Yunlong Xia, Ying Liu, Yanchun Liang, Bertil Olsson, Shiwen Yuan</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.04.009</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-06-22</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-06-22</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>49</prism:startingPage><prism:endingPage>56</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611001567/abstract?rss=yes"><title>Pacemaker electrocardiogram with new large negative T waves: what is the cause?</title><link>http://www.jecgonline.com/article/PIIS0022073611001567/abstract?rss=yes</link><description>A 59-year-old woman with a history of severe nonischemic dilated cardiomyopathy with left bundle-branch block, status post implantation of a biventricular pacemaker-cardioverter-defibrillator (BiV/ICD) 3 years before, presented with atypical chest pain. She denied any recent physical or emotional stress. The patient had 2 cardiac catheterizations in the past without demonstrable coronary artery disease. After implantation of the BiV/ICD, her heart failure symptoms have essentially resolved, and her left ventricular ejection fraction has increased from 30% to 50%. On presentation, the patient's vital signs were normal, and her cardiovascular examination result was negative. Chest x-ray revealed trivial cardiomegaly and clear lung fields; the pacemaker and ICD leads were in the appropriate positions. Routine laboratory test results were normal. The admission electrocardiogram (ECG) demonstrated sinus P waves and a ventricular paced rhythm (A). Repeat ECG 8 hours later still showed a ventricular paced rhythm but now with large, almost giant negative T waves in the chest leads with more shallow negative T waves in the inferior leads (B). The patient did not experience any cardiac symptoms during the time interval between the 2 recorded ECGs. What could have been the cause of this dramatic change in the T-wave morphology over 8 hours?</description><dc:title>Pacemaker electrocardiogram with new large negative T waves: what is the cause?</dc:title><dc:creator>Laszlo Littmann</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.05.001</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-06-22</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-06-22</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>57</prism:startingPage><prism:endingPage>59</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002536/abstract?rss=yes"><title>Prediction of sudden cardiac death in patients after acute myocardial infarction using T-wave alternans: a prospective study</title><link>http://www.jecgonline.com/article/PIIS0022073611002536/abstract?rss=yes</link><description>Abstract: Background and Purpose: We assessed the value of T-wave alternans (TWA) in prediction of sudden cardiac death (SCD) in patients with acute myocardial infarction (AMI).Methods: Consecutive patients (N = 227) were enrolled and were monitored with 24-hour ambulatory electrocardiogram within 1 to 15 days after AMI. T-wave alternans was identified by a modified moving average (MMA) algorithm computer software. The primary end point was SCD or lethal ventricular arrhythmia. We analyzed the hazard ratios (HRs) using the previously determined 47 μV TWA cutpoint.Results: During the 16 ± 7-month follow-up, 10 (4.4%) patients died suddenly. T-wave alternans (≥47 μV) predicted SCD (HR, 17.78 [95% confidence interval, 3.75-84.31]; P &lt; .0001). Moreover, patients with 5 or more TWA episodes (≥47 μV) were at higher risk for SCD (HR, 20.75 [95% confidence interval, 5.77-74.57]; P &lt; .0001).Conclusions: T-wave alternans (≥47 μV) monitored at 1 to 15 days after AMI-predicted heightened risk of SCD. Prediction is improved when the frequency of TWA episodes (≥47 μV) is analyzed.</description><dc:title>Prediction of sudden cardiac death in patients after acute myocardial infarction using T-wave alternans: a prospective study</dc:title><dc:creator>Hou Yu, Fang Pi-hua, Wu Yuan, Li Xiao-feng, Liu Jun, Li Zhi, Lei Sen, Shu Zhang</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.015</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-09-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-09-16</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>60</prism:startingPage><prism:endingPage>65</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002202/abstract?rss=yes"><title>Heart rate adjustment of PR interval in middle-aged and older adults</title><link>http://www.jecgonline.com/article/PIIS0022073611002202/abstract?rss=yes</link><description>Abstract: Prolonged PR interval has been associated with adverse cardiac events. Consequently, the scientific community and regulatory agencies have become concerned about PR interval prolongation induced by cardioactive agents. We evaluated PR dependence on heart rate (HR) in 5757 men and women aged 40 years and older from the US third National Health and Nutrition Survey with the objective to determine if rate adjustment for the PR interval is warranted as is the case with QT interval. Electrocardiograms were computer-processed in a central electrocardiogram laboratory. There was a statistically significant negative correlation between PR and HR (r = −0.15; P &lt; .001); notably weaker than that between QT and HR (r = −0.76; P &lt; .001). Evaluation of subgroups stratified by sex, race, and age revealed a significant interaction between PR and HR with age (P = .006). A subsequent search for optimal rate-adjusted PR (PRa) formula that eliminates PR dependence on HR within each age group produced the formula: PRa = PR + 0.26 (HR − 70) for age group younger than 60 years and PRa = PR + 0.42 (HR − 70) for age group 60 years or older. The application of this formula in the study population effectively made the PR interval rate-invariant (residual slope of regression, −0.0054; 95% confidence interval, −0.064 to 0.053; P = .86). Based on the distribution of PRa, the 98th percentile limit of 220 milliseconds would be a reasonable overall threshold for defining first-degree AV block, with the 95th percentile limit of 205 as a threshold for borderline PR prolongation. In conclusion, the association between PR and HR is age- and rate-dependent and a separate rate-adjustment formula is needed for adults in younger and older age groups. The prognostic significance of the rate-adjusted PR needs to be investigated.</description><dc:title>Heart rate adjustment of PR interval in middle-aged and older adults</dc:title><dc:creator>Elsayed Z. Soliman, Pentti M. Rautaharju</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.06.003</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-07-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-07-25</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>66</prism:startingPage><prism:endingPage>69</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611003086/abstract?rss=yes"><title>Heart rate deceleration runs for postinfarction risk prediction</title><link>http://www.jecgonline.com/article/PIIS0022073611003086/abstract?rss=yes</link><description>Abstract: A method for counting episodes of uninterrupted beat-to-beat heart rate decelerations was developed.Methods: The method was set up and evaluated using 24-hour electrocardiogram Holter recordings of 1455 (training sample) and 946 (validation sample) postinfarction patients. During a median follow-up of 24 months, 70, 46, and 19 patients of the training sample suffered from total, cardiac, and sudden cardiac mortality, respectively. In the validation sample, these numbers were 39, 25, and 15. Episodes of consecutive beat-to-beat heart rate decelerations (deceleration runs [DRs]) were characterized by their length.Results: Deceleration runs of 2 to 10 cycles were significantly less frequent in nonsurvivors. Multivariate model of DRs of 2, 4, and 8 cycles identified low-, intermediate-, and high-risk groups. In these groups of the training sample, the total mortalities were 1.8%, 6.1%, and 24%, respectively. In the validation sample, these numbers were 1.8%, 4.1%, and 21.9%.Conclusion: Infrequent DRs during 24-hour Holter indicate high risk of postinfarction mortality.</description><dc:title>Heart rate deceleration runs for postinfarction risk prediction</dc:title><dc:creator>Przemyslaw Guzik, Jaroslaw Piskorski, Petra Barthel, Axel Bauer, Alexander Müller, Nadine Junk, Kurt Ulm, Marek Malik, Georg Schmidt</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.08.006</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-09-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-09-16</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>70</prism:startingPage><prism:endingPage>76</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611002378/abstract?rss=yes"><title>Bivariate phase-rectified signal averaging for assessment of spontaneous baroreflex sensitivity: normalization of the results</title><link>http://www.jecgonline.com/article/PIIS0022073611002378/abstract?rss=yes</link><description>Abstract: Background: Previously proposed technique for assessment of spontaneous baroreflex sensitivity (BRS) based on bivariate phase-rectified signal averaging measures averaged R-R interval (RRI) changes triggered by beat-to-beat increases in systolic blood pressure (SBP). In this study, we investigate a normalized version of the method that relates the averaged RRI changes to the triggering blood pressure changes, thus providing the results in measurement units comparable with existing literature.Methods: Data of previously reported prospective observational study were used. In each of 146 heart failure patients presenting with sinus rhythm, 10-minute recordings of electrocardiogram and arterial and blood pressures were obtained in the supine resting position. The averaged RRI increases initiated by beat-to-beat SBP increases were measured (original BRS result in milliseconds) and normalized for the averaged beat-to-beat SBP increases (normalized BRS result in milliseconds per millimeters of mercury). Both results were compared in terms of predicting all-cause mortality during a mean follow-up of 2.7 ± 1.1 years when 42 patients (28.8%) died.Results: Both types of results were highly correlated (r = 0.938, P &lt; .001) and led to similarly strong separation of high- and low-risk groups. The receiver operator characteristics of both indices were well within the 95% confidence intervals of each other, and the areas under the characteristics were practically identical: 71.1% (95% confidence interval, 60.7%-80.9%) for original BRS and 69.7% (58.9%-79.2%) for normalized BRS.Conclusion: The results might question the concept of a linear relationship between the SBP changes and RRI changes. The phase-rectified signal averaging–based assessment of BRS may be used with equal legitimacy in the nonnormalized and normalized forms; the normalized form provides results in conventional measurement units.</description><dc:title>Bivariate phase-rectified signal averaging for assessment of spontaneous baroreflex sensitivity: normalization of the results</dc:title><dc:creator>Alexander Müller, Adrian Morley-Davies, Petra Barthel, Katerina Hnatkova, Axel Bauer, Kurt Ulm, Marek Malik, Georg Schmidt</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.07.010</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-08-22</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-08-22</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>77</prism:startingPage><prism:endingPage>81</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611003293/abstract?rss=yes"><title>Assessment of autonomic control of the heart during transient myocardial ischemia</title><link>http://www.jecgonline.com/article/PIIS0022073611003293/abstract?rss=yes</link><description>Abstract: Introduction: In the presence of coronary artery obstruction, complex cardiovascular reflexes may lead to changes in heart rate and even to the precipitation of malignant arrhythmias. The autonomic nervous system (ANS) has traditionally been considered to be “balanced” between continuously interacting sympathetic and parasympathetic outflows. The purpose of this study was to assess ANS control of the heart during prolonged coronary balloon occlusion procedures of one of the major coronary arteries.Methods: R-R intervals were obtained from continuous electrocardiographic data of 90 patients undergoing selective percutaneous coronary interventions (PCI) with balloon inflation periods ranging from 3 to 10 minutes (4.7 ± 1.1 minutes). Three 3-minute stages were chosen: (1) preinflation (baseline), (2) from the start of occlusion (PCI), and (3) immediately post deflation. The dynamics of the ANS was evaluated by heart rate variability analysis using standard time and frequency domain indices and the short-term fractal-like index (α1).Results: During PCI, time and frequency domain measures related to vagal control decreased significantly with respect to baseline (significantly in left anterior descending [LAD] artery occlusions). During the postdeflation stage, heart rate variability and high-frequency power increased (P &lt; .01) in the group with right coronary artery occlusions, whereas a marked sympathetic increase, as assessed by an increase (P &lt; .01) of normalized low-frequency power and the low/high-frequency ratio was observed in the LAD group after balloon deflation. Fractal index α1 decreased during the PCI period but increased significantly after balloon deflation.Conclusions: Significant changes in autonomic control of heart rate that were a function of the affected artery occurred during and after coronary artery occlusions. Occlusion of the LAD resulted in a significant reduction of vagal activity and a decrease of the short-term fractal index during PCI and a marked sympathetic response after postdeflation. However, a marked increment of vagal activity between the occlusion stage and postdeflation period was found in the right coronary artery group. These results may relate the site of the occlusion and lack of blood supply to different parts of the left ventricle.</description><dc:title>Assessment of autonomic control of the heart during transient myocardial ischemia</dc:title><dc:creator>Pedro Gomis, Pere Caminal, Montserrat Vallverdú, Stafford G. Warren, Phyllis K. Stein, Galen S. Wagner</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.08.013</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Mini Symposium: Myocardial Depolarization and Repolarization and its Neurological Regulation</prism:section><prism:startingPage>82</prism:startingPage><prism:endingPage>89</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611004493/abstract?rss=yes"><title>T-wave alternans immediately after an acute myocardial infarction</title><link>http://www.jecgonline.com/article/PIIS0022073611004493/abstract?rss=yes</link><description>The article by Yu et al published ahead of print in the Journal on September 13, 2011, assessed the value of T-wave alternans (TWA) in predicting sudden cardiac death (SCD) in 227 consecutive patients 1 to 15 days after an acute myocardial infarction (AMI) using the modified moving average in 24-hour ambulatory electrocardiograms. The authors showed that TWA 47 μV or more predicted SCD or malignant ventricular arrhythmia, and its predictive value improved further when the frequency of TWA to 5 episodes or more, with this threshold, increased. What is unique about the study is that it focuses on the immediate period after an AMI in contrast to the bulk of relevant studies that have evaluated patients with chronic myocardial infarction leading to ischemic cardiomyopathy and the introduction of the frequency of 5 or more episodes of TWA above the threshold of 47 μV or more chosen a priori as a predictive variable of SCD, which was evaluated in a multivariate analysis. I would like to engage the authors on the following issues, hoping that I will receive a response. (1) The authors “selected 2 precordial leads V2 and V5 because TWA is a regionally specific phenomenon, and unipolar leads are capable of detecting TWA in ischemic and scar area of cardiac muscle,” to use their words verbatim, yet they did not use an inferior lead or consider the different culprit coronary artery in AMI, or AMI location, as variables; is it not possible that an inferior and/or posterior AMI would not yield a TWA of 47 μV or more by the V2 and V5 precordial leads? (2) The authors used “one maximum TWA value, for each 15 seconds of the ECG recording, calculated as the maximum difference between successive T waves of the respective moving averages for each 15-second beat stream” in “the section between the end points of QRS wave (J point) and T wave” and “the resulting maximum value was recorded.” Cardiologists routinely interpreting Holter recordings of ambulatory electrocardiograms witness a massive change of the amplitude of the T waves and the J-T intervals, with variation in the different leads used, and occurring without an explanation over the course of 24 hours. Is it not possible that the TWA magnitude is affected by the T-wave amplitude? Is it not possible that 1 threshold value (as herein, ≥47 μV) does not fit all patients, irrespective of the sometimes massive differences in the amplitude of the T waves in their electrocardiograms? The above concerns apply to the same lead at different time points and to 2 or more leads recorded simultaneously. Is it not reasonable that we should rethink this issue and consider an adjustment of the TWA magnitude by the corresponding T-wave amplitude?</description><dc:title>T-wave alternans immediately after an acute myocardial infarction</dc:title><dc:creator>John E. Madias</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.10.003</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-11-10</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-11-10</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>90</prism:startingPage><prism:endingPage>90</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207361100135X/abstract?rss=yes"><title>“Reperfusion ST-elevation peak”: an interesting phenomenon that needs to be studied and implemented further</title><link>http://www.jecgonline.com/article/PIIS002207361100135X/abstract?rss=yes</link><description>The report by Demidova et al and the accompanying editorial by Terkelsen, in the January/February issue of the Journal of Electrocardiology, focuses on the “reperfusion peak” (RP), that is, the transient additional ST-elevation (STE) detected in both the porcine model after restoration of coronary flow, and patients with an STE myocardial infarction, undergoing primary percutaneous coronary intervention. The realization of the phenomenon of paradoxical increase in STE after reperfusion is not new. It has been described in several articles as occurring during intravenous thrombolytic therapy. At first, it was thought to represent a good sign of reperfusion. Later, the concept has been changed suggesting that the RP represents some form of “reperfusion injury.” Although it is far from certain that we know the exact mechanism of the phenomenon, as Terkelsen explains, the RP predicts a large final infarct size and an unfavorable outcome, a lower left ventricular ejection fraction, higher levels of troponin T and N-terminal pro-brain natriuretic peptide release, and delay in STE resolution, it does not reflect the initial extent of the myocardium at risk, and it may be a sign of impaired myocardial reperfusion, despite the achievement of Thrombolysis in Myocardial Infarction-3 flow. However, the elegant analysis of Terkelsen notwithstanding, I do not understand the exclusion of the embolization of thrombus as a cause of the RP in the porcine model. Is it because of the initial intravenous heparin injection, or because one should not expect the column of blood in the coronary artery, distal to the inflated balloon, to thrombose in the course of 40 minutes? Certainly, it would be easy to examine whether thrombus is the cause of RP, especially in the porcine model, although in the clinical setting, it may be more difficult. The RP phenomenon is observed also in patients without angiographically visible thrombus, although in such a case, one cannot exclude microembolization.</description><dc:title>“Reperfusion ST-elevation peak”: an interesting phenomenon that needs to be studied and implemented further</dc:title><dc:creator>John E. Madias</dc:creator><dc:identifier>10.1016/j.jelectrocard.2011.04.003</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2011-06-10</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2011-06-10</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>90</prism:startingPage><prism:endingPage>91</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207361100478X/abstract?rss=yes"><title>Editorial Board</title><link>http://www.jecgonline.com/article/PIIS002207361100478X/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(11)00478-X</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073611004791/abstract?rss=yes"><title>Table of Contents</title><link>http://www.jecgonline.com/article/PIIS0022073611004791/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(11)00479-1</dc:identifier><dc:source>Journal of Electrocardiology 45, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>45</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S0022-0736(11)X0007-9</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A4</prism:endingPage></item></rdf:RDF>
