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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//inpress?rss=yes"><title>Journal of Electrocardiology - Articles in Press</title><description>Journal of Electrocardiology RSS feed: Articles in Press. 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//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:issn>0022-0736</prism:issn><prism:publicationDate>2010-02-01</prism:publicationDate><prism:copyright> © 2010 Published by 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/PIIS0022073610000038/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207361000004X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006372/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006256/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006414/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207360900627X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006281/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006384/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006396/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006402/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006268/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006244/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006049/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006220/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006232/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006001/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006013/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006116/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005998/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006025/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005391/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609002581/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005123/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207360900538X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207360900541X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005512/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005408/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005524/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005378/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609002829/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005147/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207360900421X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609004233/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609003276/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609004221/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609003720/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609003264/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS002207360800215X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000038/abstract?rss=yes"><title>Artifacts posing as premature ventricular beats in an “event recorder” tracing - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073610000038/abstract?rss=yes</link><description></description><dc:title>Artifacts posing as premature ventricular beats in an “event recorder” tracing - Corrected Proof</dc:title><dc:creator>John E. Madias</dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.01.002</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207361000004X/abstract?rss=yes"><title>Comparison of serial measurements of infarct size and left ventricular ejection fraction by contrast-enhanced cardiac magnetic resonance imaging and electrocardiographic QRS scoring in reperfused anterior ST-elevation myocardial infarction - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207361000004X/abstract?rss=yes</link><description>Abstract: Background: Left ventricular ejection fraction (LVEF) is a powerful prognostic marker after acute myocardial infarction and is dependent on infarct magnitude. Contrast-enhanced cardiac magnetic resonance (ceCMR) represents the current criterion standard means of LVEF and infarct size measurement. Infarct size and LVEF can be estimated from the 12-lead electrocardiogram (ECG) using the Selvester QRS score. We examined for the first time the relationship between serial measures of LVEF and infarct size by ceCMR and ECG in patients with reperfused anterior ST-elevation myocardial infarction (STEMI) and depressed LVEF.Methods: Thirty-four patients (mean ± SD age, 59 ± 11.8 years; 70.6% male) underwent ceCMR and simultaneous ECG at mean 93 hours after admission and at 12 and 24 weeks. The QRS score was calculated on each ECG, from which infarct size and LVEF were estimated and compared with the equivalent ceCMR measurements.Results: Infarct size on ceCMR was higher than that by QRS score at each time-point (P &lt; .001) with modest correlation (r = 0.56-0.78, P &lt; .001). Left ventricular ejection fraction was consistently significantly higher on CMR than on ECG, with weak correlation (r = 0.37-0.51, P &lt; .05). We derived a novel equation relating QRS score to CMR-measured LVEF in the subacute phase of infarction: LVEF = 61 − (1.7 × QRS score) (%).Conclusions: In patients with reperfused anterior ST-elevation myocardial infarction and depressed LVEF, ceCMR is moderately correlated with the QRS in the serial measurement of infarct size and LVEF. Infarct size (measured by ceCMR) and LVEF are consistently higher than those calculated on the QRS score in the acute and subacute phases of infarction.</description><dc:title>Comparison of serial measurements of infarct size and left ventricular ejection fraction by contrast-enhanced cardiac magnetic resonance imaging and electrocardiographic QRS scoring in reperfused anterior ST-elevation myocardial infarction - Corrected Proof</dc:title><dc:creator>Robin A.P. Weir, Thomas N. Martin, Charles Aengus Murphy, Colin J. Petrie, Suzanne Clements, Tracey Steedman, Henry J. Dargie, Galen S. Wagner</dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.01.003</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006372/abstract?rss=yes"><title>Ischemic ST-segment episodes during the initial 24 hours of ST elevation myocardial infarction predict prognosis at 1 and 5 years - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006372/abstract?rss=yes</link><description>Abstract: Objectives: The aims of the study were to assess the prognostic value of recurrent ischemic episodes during the first 24 hours in ST elevation myocardial infarction (STEMI) treated with thrombolysis and to explore those episodes as a part of a low-risk prognostic feature.Design: Two hundred twenty patients with STEMI treated with thrombolysis were monitored for 24 hours with continuous online vectorcardiography assessing ST vector changes to record recurrent ischemic events.Results: Ischemic events measured as an increase in ST-change vector magnitude (STC-VM) more than 50 μV for at least 2 minutes during 4- to 24-hour predicted mortality in a 5-year follow-up based on a multivariable analysis (hazard ratio, 1.18/episode; confidence interval, 1.01-1.37). The more episodes there were, the worse the prognosis. A low-risk group with a 1-year mortality of 1.9% could be identified.Conclusion: Continuous ST-segment monitoring during the first 24 hours of a myocardial infarction is a valuable tool for identifying high- and low-risk patients. The STC-VM events during 4 to 24 hours of the first day of a myocardial infarction predict mortality within 5 years.</description><dc:title>Ischemic ST-segment episodes during the initial 24 hours of ST elevation myocardial infarction predict prognosis at 1 and 5 years - Corrected Proof</dc:title><dc:creator>Per Ottander, Johan B. Nilsson, Steen M. Jensen, Ulf Näslund</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.010</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-28</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-28</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006256/abstract?rss=yes"><title>QRS integral: an electrocardiographic indicator of mechanical interventricular asynchrony - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006256/abstract?rss=yes</link><description>Abstract: Aim: The aim of this study was to investigate whether interventricular asynchrony (IVA) can be measured by electrocardiography.Methods: Sixty-two patients (New York Heart Association heart failure functional class III: age, mean ± SD: 64 ± 9 years; ejection fraction, mean ± SD: 24% ± 8%; dilative cardiomyopathy/ischemic cardiomyopathy, n = 39/23) with left bundle branch block (QRS duration, mean ± SD: 165 ± 21 milliseconds) underwent a 120-channel body surface mapping. QRS integral was analyzed and compared with IVA (echo).Results: Interventricular asynchrony was associated with significantly decreased QRS integrals 15 cm cranial and 6 cm lateral from V1 in patients with normal axis (n = 36): At a cutoff value of −26 milliseconds ⁎ mV, receiver operating characteristic analysis to predict IVA revealed a sensitivity of 89% and a specificity of 83% (area under curve, mean ± SEM: 0.9 ± 0.07; P &lt; .001). In patients with left axis deviation (n = 26), IVA showed significantly decreased QRS integrals 10 cm caudal from V1: at a cutoff value of −89 milliseconds ⁎ mV, receiver operating characteristic analysis to predict IVA revealed a sensitivity of 83% and a specificity of 100% (area under curve, mean ± SEM: 0.9 ± 0.07; P &lt; .002).Conclusions: Interventricular asynchrony strongly correlates with QRS integral. Key lead positions, however, are axis dependent and outside standard leads.</description><dc:title>QRS integral: an electrocardiographic indicator of mechanical interventricular asynchrony - Corrected Proof</dc:title><dc:creator>Alexander Samol, Stefan Klotz, Jörg Stypmann, Hans-Jürgen Bruns, Richard Houben, Matthias Paul, Christian Vahlhaus</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.006</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-27</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-27</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006414/abstract?rss=yes"><title>Atrioventricular block with 4:2 conduction pattern: concealed electrotonic conduction as an alternative mechanism - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006414/abstract?rss=yes</link><description>We have read with much interest a recent report by Jastrzebski and Kukla on atrioventricular (AV) block with 4:2 conduction pattern. They presented electrocardiograms showing AV block with 4:2 conduction pattern in a patient with myocardial infarction. They proposed 3 alternative explanations: (1) supernormal conduction; (2) 2-level block with 4:1 conduction ratio in the upper level and 3:2 conduction ratio in the lower level; and (3) presence of 2 populations of Purkinje cells in the remaining, critically injured, fascicle: one with the phase-3 block and the other with slow diastolic depolarization leading, during a pause after the first nonconducted P, to phase-4 block.</description><dc:title>Atrioventricular block with 4:2 conduction pattern: concealed electrotonic conduction as an alternative mechanism - Corrected Proof</dc:title><dc:creator>Shinji Kinoshita, Takakazu Katoh</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.014</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-27</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-27</prism:publicationDate><prism:section>LETTER TO THE EDITOR</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207360900627X/abstract?rss=yes"><title>New York Heart Association Functional class influences the impact of diabetes on cardiac autonomic function - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207360900627X/abstract?rss=yes</link><description>Abstract: Background: Diabetes (D) and heart failure (HF) are associated with abnormal heart rate variability (HRV). It is unclear whether the HRV effect of having both is cumulative.Methods: Pretreatment HRV (traditional, nonlinear, and heart rate [HR] turbulence) in 80 D versus 74 non-D (ND) systolic HF patients was compared by New York Heart Association II versus III among patients entered into an HF drug evaluation study.Results: Age-adjusted HR was lower in class II D versus class III and most HRV including HR turbulence was better in class II ND versus all others, with few differences between class II D and class III ND and D patients.Conclusion: The effect of D and HF on autonomic function may be cumulative in class II, but D may have little additional effect on most HRV in class III patients. The prognostic value of different HRV measures in D versus ND HF patients should be further investigated.</description><dc:title>New York Heart Association Functional class influences the impact of diabetes on cardiac autonomic function - Corrected Proof</dc:title><dc:creator>Phyllis K. Stein, Prakash Deedwania</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.008</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006281/abstract?rss=yes"><title>Association of Holter-based measures including T-wave alternans with risk of sudden cardiac death in the community-dwelling elderly: the Cardiovascular Health Study - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006281/abstract?rss=yes</link><description>Abstract: Background: Sudden cardiac death (SCD) can be the first manifestation of cardiovascular disease. Development of screening methods for higher/lower risk is critical.Methods: The Cardiovascular Health Study is a population-based study of risk factors for coronary heart disease and stroke those 65 years or older. Forty-nine (of 1649) with usable Holters and in normal sinus rhythm had SCD during follow-up and were matched with 2 controls, alive at the time of death of the case and not experiencing SCD on follow-up. Univariate and multivariate conditional logistic regression determined the association of Holter-based information and SCD.Results: In univariate models, the upper half of ventricular premature contraction (VPC) counts, abnormal heart rate turbulence, decreased normalized low-frequency power, increased T-wave alternans (TWA), and decreased the short-term fractal scaling exponent (DFA1) were associated with SCD, but time domain heart rate variability was not. In multivariate models, the upper half of VPC counts (odds ratio [OR], 6.6) and having TWA of 37 μV or greater on channel 2 (OR, 4.8) were independently associated with SCD. Also, the upper half of VPC counts (OR, 6.9) and having a DFA1 of less than 1.05 (OR, 5.0) were independently associated with SCD. When additive effects were explored, having both higher VPCs and higher TWA was associated with an OR of 8.2 for SCD compared with 2.6 for having either. Also, having both higher VPCs and lower DFA1 was associated with an OR of 9.6 for SCD compared with 3.1 for having either.Conclusions: Results support a potential role for 24-hour Holter recordings to identify older adults at increased or lower risk of SCD.</description><dc:title>Association of Holter-based measures including T-wave alternans with risk of sudden cardiac death in the community-dwelling elderly: the Cardiovascular Health Study - Corrected Proof</dc:title><dc:creator>Phyllis K. Stein, Devang Sanghavi, Nona Sotoodehnia, David S. Siscovick, John Gottdiener</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.009</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006384/abstract?rss=yes"><title>Repetitive polymorphic ventricular tachycardia initiated by phase 4 block in the His-Purkinje system - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006384/abstract?rss=yes</link><description>Abstract: We report a case of a patient who developed repetitive episodes of polymorphic ventricular tachycardia with a stereotypical pattern of initiation. A premature atrial complex would result in a brief pause followed by left bundle branch block aberrancy. Ventricular bigeminy would ensue followed by episodes of polymorphic ventricular tachycardia, some requiring cardioversion. We postulate that delay within the His-Purkinje system initiated by phase 4 block was proarrhythmic in this patient.</description><dc:title>Repetitive polymorphic ventricular tachycardia initiated by phase 4 block in the His-Purkinje system - Corrected Proof</dc:title><dc:creator>Jose' Dizon, Daniel Wang, Alan Vainrib</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.011</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006396/abstract?rss=yes"><title>Negative current of injury due to inadvertent polarity reversal during active atrial lead implantation - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006396/abstract?rss=yes</link><description>Abstract: We report an example of the negative current of injury (COI) during permanent pacemaker implantation. Cardiac perforation was our first priority. However, patient had stable hemodynamics, and the fluoroscopic location of the atrial lead was acceptable. Therefore, the connections were checked revealing the cause of the negative COI; the red (+) clips was attached to the tip of the atrial lead rather than anodal ring. Correcting the connections resolved the problem. This report shows that a negative COI might not only be due to cardiac perforation or right ventricular ischemia but that checking the lead connectivity should be carried out first.</description><dc:title>Negative current of injury due to inadvertent polarity reversal during active atrial lead implantation - Corrected Proof</dc:title><dc:creator>Mohammad Kafi, Amir Aslani, Majid Haghjoo</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.012</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006402/abstract?rss=yes"><title>T-wave alternans in 24-hour ambulatory electrocardiogram monitoring in healthy newborn of first to fourth day of life - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006402/abstract?rss=yes</link><description>The contribution of Makarov et al published in the January-February 2010 issue of the Journal provides a unique opportunity to assess a possible association (previously proposed) of T-wave alternans (TWA) magnitudes (MTWA) and the amplitudes of the T-waves (ATW), used for the calculation of TWA, because it provides serial data, with circadian reference, in a cohort of healthy newborns, where one could assume that the TWAs measured are of the type expected in healthy subjects (unrelated to increased arrhythmogenicity), as was also noted in adults. The authors studied 20 healthy newborns serially using 24-hour ambulatory electrocardiogram (AECG) monitoring on days 1, 2, and 4 after birth. The modified moving average time-domain method was used for the assessment of TWA. Their Table 1 shows that the peak values of TWA were 28 ± 6, 34 ± 7, and 30 ± 4 μV on days 1, 2, and 4 after birth, correspondingly. Most probably, the peak TWA values were obtained from different leads in different newborns, although in adults, one expects peak TWA values to be recorded from the modified V2 lead. The authors speculate that the “peculiarities” of the TWA in their study “possibly reflect restructuring of heart activity in the developing heart.” Such “peculiarities” may also affect the ATW. In this context, one wonders: (1) What was the relation between the MTWA and the corresponding ATW in the 3 modified chest leads, V2, V5, and aVF, in each newborn throughout of the AECG monitoring? (2) What was the relation between the MTWA and the corresponding ATW on the AECG monitoring from the 3 different days, days 1, 2, and 4, in each newborn? The essence of these questions pertains to the speculation that changes in MTWA are determined by changes in the corresponding ATW and do not reflect necessarily only changes in underlying propensity to malignant ventricular arrhythmias. The cohort of the healthy newborns 1 to 4 days old is the ideal data set to explore this speculation. Could the authors oblige us with a response?</description><dc:title>T-wave alternans in 24-hour ambulatory electrocardiogram monitoring in healthy newborn of first to fourth day of life - Corrected Proof</dc:title><dc:creator>John E. Madias</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.013</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate><prism:section>LETTER TO THE EDITOR</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006268/abstract?rss=yes"><title>Pleomorphic ventricular tachycardia originating from Purkinje fiber network of left anterior fascicle - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006268/abstract?rss=yes</link><description>Abstract: A 55-year-old woman with recurrent syncope and palpitation experienced polymorphic ventricular tachycardia (VT) and more than 3 monomorphic VTs with a right bundle branch block configuration as inferior, middle, and superior axis. During the pleomorphic VT, the diastolic potential (dp) was recorded at the anterolateral left ventricle. Changes in the QRS morphology were associated with the time between dp and onset of QRS complex (dp-V interval), and prolongation of dp-V interval terminated the VT. In addition, the delayed potentials were seen during sinus rhythm around this area. Delivery of radiofrequency current targeting the delayed potentials abolished all the VTs. Different exits from relatively large area of slow conduction in the left anterior fascicle might have produced the pleomorphic VTs.</description><dc:title>Pleomorphic ventricular tachycardia originating from Purkinje fiber network of left anterior fascicle - Corrected Proof</dc:title><dc:creator>Hisashi Yokoshiki, Hirofumi Mitsuyama, Masaya Watanabe, Masayuki Sakurai, Hiroyuki Tsutsui</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.007</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-21</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-21</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006244/abstract?rss=yes"><title>Open-loop, clockwise QT-RR hysteresis immediately before the onset of torsades de pointes in type 2 long QT syndrome - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006244/abstract?rss=yes</link><description>Abstract: Delay of QT interval adaptation to sudden heart rate change causes hysteresis in dynamic QT-RR relationship. We analyzed QT-RR plotting during and after exercise in a patient with genetically identified type 2 long QT syndrome before and after starting oral propranolol. Blunted QT shortening by exercise and augmented postexercise QT prolongation resulted in an open-loop, clockwise QT-RR hysteresis immediately before the onset of torsades de pointes before propranolol. However, this hysteresis was eliminated by propranolol. QT-RR analysis provided insight into the mechanisms of the onset of torsades de pointes at least in this case of type 2 long QT syndrome.</description><dc:title>Open-loop, clockwise QT-RR hysteresis immediately before the onset of torsades de pointes in type 2 long QT syndrome - Corrected Proof</dc:title><dc:creator>Gen Nakaji, Masahiko Fujiwara, Mitsuhiro Fukata, Shioto Yasuda, Keita Odashiro, Toru Maruyama, Koichi Akashi</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.005</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-18</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-18</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006049/abstract?rss=yes"><title>Comparison of high-frequency QRS components and ST-segment elevation to detect and quantify acute myocardial ischemia - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006049/abstract?rss=yes</link><description>Abstract: Objective: This study tests the ability of high-frequency components of the depolarization phase (HF-QRS) vs conventional ST-elevation criteria to detect and quantify myocardial ischemia.Methods: Twenty-one patients admitted for elective percutaneous coronary intervention were included. Quantification of the ischemia was made by myocardial scintigraphy. High-resolution electrocardiogram before and during percutaneous coronary intervention was recorded and signal averaged. The HF-QRS were determined within the frequency band 150 to 250 Hz. ST-segment deviation was measured in the standard frequency range (&lt;100 Hz).Results: HF-QRS criteria were met by 76% of the patients, whereas 38% met the ST-elevation criteria (P = .008). Both HF-QRS reduction and ST elevation correlated significantly with the amount of ischemia (HF-QRS: r = 0.59, P = .005 for extent and r = 0.69, P = .001 for severity; ST elevation: r = 0.49, P = .023 for extent and r = 0.57, P = .007 for severity).Conclusions: This study suggests that HF-QRS analysis could provide valuable information both to detect acute ischemia and to quantify myocardial area at risk.</description><dc:title>Comparison of high-frequency QRS components and ST-segment elevation to detect and quantify acute myocardial ischemia - Corrected Proof</dc:title><dc:creator>Michael Ringborn, Jonas Pettersson, Eva Persson, Stafford G. Warren, Pyotr Platonov, Olle Pahlm, Galen S. Wagner</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.009</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006220/abstract?rss=yes"><title>The diagnostic utility of heart rate–corrected ST-segment depression during adenosine nuclear stress testing - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006220/abstract?rss=yes</link><description>Abstract: Background: Vasodilator stress testing relies heavily on the imaging portion so that clinically useful information from the electrocardiogram may be overlooked. Stress-induced ST-segment depression, although uncommon, is highly predictive of severe disease. We investigated whether minor ST depressions during adenosine nuclear stress testing corrected for the modest heart rate increases (ST/HR slope and ST/HR index) might be clinically relevant.Methods: The study included 74 consecutive patients with electrocardiograms interpretable for ischemia who underwent coronary angiography within the following 6 months.Results: Abnormal responses using conventional thresholds for ischemic ST depression, the ST/HR slope, and ST/HR index were present in 8%, 20%, and 27%, respectively. The sensitivity for conventional ST depression was 11% and, when corrected for heart rate, increased to 27% and 36%, (P = .012), without adversely affecting the high positive predictive accuracy (83%, 80%, and 80%). Even with a normal perfusion scan, heart rate correction was highly predictive of multivessel coronary artery disease (4/5 patients).Summary: Heart rate correction of ST depression during adenosine nuclear stress improves on conventional ST depression and may compliment perfusion imaging in detecting multivessel disease.</description><dc:title>The diagnostic utility of heart rate–corrected ST-segment depression during adenosine nuclear stress testing - Corrected Proof</dc:title><dc:creator>Attila S. Nemeth, Robert C. Bahler, Robert S. Finkelhor</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.003</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-08</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006232/abstract?rss=yes"><title>Significance of a prominent Q wave in lead negative aVR (−aVR) in acute anterior myocardial infarction - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006232/abstract?rss=yes</link><description>Abstract: Purpose: The aim of this study was to clarify the significance of a Q wave in lead negative aVR (−aVR) in anterior wall acute myocardial infarction (AMI).Methods: Eighty-seven patients with a first anterior wall AMI were classified into 2 groups according to the presence (n = 17, group A) or absence (n = 70, group B) of a prominent Q wave (duration ≥20 milliseconds) in lead −aVR at predischarge. Group A had a higher prevalence of a long left anterior descending coronary artery (LAD), a lower left ventricular ejection fraction, and more reduced regional wall motion in the apical and inferior regions than group B. None of group A patients had an LAD that did not reach the apex.Conclusion: A prominent Q wave in lead −aVR in anterior wall AMI is related to severe regional wall motion abnormality in the apical and inferior regions, with an LAD wrapping around the apex.</description><dc:title>Significance of a prominent Q wave in lead negative aVR (−aVR) in acute anterior myocardial infarction - Corrected Proof</dc:title><dc:creator>Munenori Kotoku, Akira Tamura, Yusei Abe, Junichi Kadota</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.004</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-01-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-08</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006001/abstract?rss=yes"><title>How to increase the accuracy of electrocardiogram's interpretation and stimulate the interest of the interpreters? - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006001/abstract?rss=yes</link><description>The questions posed in the title imply that there is room for improving the accuracy of the computer-generated electrocardiographic diagnosis and the vigilance of the overreaders. To back up the above 2 “accusations,” I will rely on personal observations that do not include electrocardiogram (ECG) in pediatric practice. Before discussing the accuracy of the ECG report and its verification, I will address the present role of the ECG in clinical practice and in postgraduate education.</description><dc:title>How to increase the accuracy of electrocardiogram's interpretation and stimulate the interest of the interpreters? - Corrected Proof</dc:title><dc:creator>Borys Surawicz</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.005</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006013/abstract?rss=yes"><title>Fact or artifact? The electrocardiographic diagnosis of orthostatic tremor - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006013/abstract?rss=yes</link><description>Abstract: Orthostatic tremor is a rare but disabling neurologic condition characterized by unsteadiness when standing accompanied by rapid leg tremor and frequent falls. We present the case of a 57-year-old man who presented with a several-month history of falls and was found to have orthostatic tremor. Telemetry strips while standing revealed continuous gross 13 to 18 Hz of oscillatory artifact, identical to the frequency range of oscillations recorded with electromyographic recordings of the thigh muscles in patients with orthostatic tremor. If confirmed in other cases, electrocardiogram recorded in the standing position could become a simple noninvasive tool to screen for or to support the clinical diagnosis of orthostatic tremor.</description><dc:title>Fact or artifact? The electrocardiographic diagnosis of orthostatic tremor - Corrected Proof</dc:title><dc:creator>Laszlo Littmann</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.006</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006116/abstract?rss=yes"><title>Effect of Periodontitis on Susceptibility to Atrial Fibrillation in an Animal Model - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006116/abstract?rss=yes</link><description>Abstract: Background: Inflammation is implicated in the pathophysiology of atrial fibrillation (AF). Periodontitis causes a general inflammatory response. Whether periodontitis is related to AF is unknown.Objective: The aim of the study was to test the hypothesis that inflammation facilitates AF.Methods: Twenty-two adult mongrel canines of either sex were used for this study. Periodontitis was induced in 12 dogs (periodontitis group) by tying 2-0 silk ligatures at the second premolar of mandibula. Ten healthy dogs were used as controls. Before the ligation procedure and on the day 30, 60, and 90 after ligation, an electrophysiologic evaluation was performed to measure atrial refractoriness and AF inducibility by delivering a single atrial extrastimuli in the high right atrium, atrial septum (AS), and coronary sinus (CS), respectively. Before each electrophysiologic study, blood samples were taken for determining the levels of C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α). Animals were killed after 90 days. The hearts and mandibulae were harvested for morphological study, and the periodontal disease severity was quantiﬁed.Results: Atrial effective refractory period (AERP) shortened, and AF inducibility increased progressively in the periodontitis group. At a drive length of 300 milliseconds, AERP in the CS was 126.7 ± 13.0 milliseconds and 107.5 ± 9.7 milliseconds after 60 and 90 days of ligation, respectively (vs 165.8 ± 10.8 milliseconds at baseline; P &lt; .001). By CS pacing, AF was induced in 5 and 10 of 12 dogs on day 60 and 90 after ligation, respectively (vs 1/12 at baseline; P &lt; .05 and P &lt; .01, respectively). Elevation of CRP and TNF-α occurred after 60 days of ligation (CRP, 13.42 ± 2.21 mg/L vs control, 1.92 ± 0.38 mg/L; P &lt; .001; TNF-α, 9.85 ± 1.72 mg/L vs control, 3.36 ± 0.75 mg/L; P &lt; .001) and reached the peak at the end of the study (CRP, 31.38 ± 2.69 mg/L vs control, 1.99 ± 0.40 mg/L; P &lt; .001; TNF-α, 12.32 ± 1.07 mg/L vs control, 3.24 ± 0.53 mg/L; P &lt; .001). There was a negative correlation between the levels of serum inflammatory factors and AERP values (P &lt; .05). Alveolar bone level decreased in the periodontitis group (P &lt; .001). The long axis (P &lt; .001) of atrial cardiomyocytes including the right atrial appendage (25.50 ± 3.58 μm vs 18.14 ± 3.32 μm), AS (24.78 ± 3.45 μm vs 17.47 ± 2.57 μm), and left atrial appendage (31.90 ± 4.80 μm vs 18.78 ± 2.42 μm) from the periodontitis group was larger than the control group. The short axis of atrial cardiomyocytes was larger than the control group, too (P &lt; .001). Inflammatory cells were more generally found in the atria of the periodontitis group (P &lt; .001). Myolysis affected some atrial cardiomyocytes of the dogs with periodontitis.Conclusion: Periodontitis led to inflammatory responses in the atrial myocardium, which disturbed the structural and electrophysiologic properties of the atrium and facilitated AF.</description><dc:title>Effect of Periodontitis on Susceptibility to Atrial Fibrillation in an Animal Model - Corrected Proof</dc:title><dc:creator>Guang Yu, Yang Yu, Yi Ning Li, Rong Shu</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.002</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005998/abstract?rss=yes"><title>Assessment of atrial electromechanical delay by tissue Doppler echocardiography in patients with nonischemic dilated cardiomyopathy - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005998/abstract?rss=yes</link><description>Abstract: Background: Atrial electromechanical delay (AEMD) calculated from tissue Doppler imaging (TDI) echocardiography can be an alternative to invasive electrophysiologic studies. We investigated whether the AEMD obtained from TDI is prolonged in patients with nonischemic dilated cardiomyopathy (DCM).Methods: Fifty-five patients with nonischemic DCM (23 men/32 women; age, 43.9 ± 14.8 years) and 55 controls (20 men/35 women; age, 41.3 ± 13.4 years) were included in this study. Atrial electromechanical delay (the time interval from the onset of P wave on electrocardiogram to the beginning of late diastolic wave [Am wave] on TDI) was calculated from the lateral and septal mitral annulus, and lateral tricuspid annulus (PA lateral, PA septum, and PA tricuspid, respectively). P-wave dispersion was calculated from the 12-lead electrocardiogram.Results: PA lateral and PA septum duration were significantly longer in patients with nonischemic DCM than the controls (78.4 ± 19.7 versus 53.8 ± 6.6 and 55.2 ± 16.3 versus 40.5 ± 6.2, P &lt; .0001 for both; respectively). However, PA tricuspid duration was statistically similar between the 2 groups (36.4 ± 10.9 versus 37.2 ± 5.7, P ≥ .05). P-wave dispersion was significantly higher in nonischemic DCM patients than the controls (53.0 ± 14.4 versus 37.5 ± 5.5, P &lt; .0001). PA lateral was correlated with the left atrial maximal volume (r = 0.64, P &lt; .0001), P-wave dispersion (r = 0.65, P &lt; .0001), and log B-type natriuretic peptide (NT proBNP) (r = 0.63, P &lt; .0001). There was a statistically significant and negative correlation between the PA lateral and left ventricular ejection fraction (r = −0.63, P &lt; .0001) and E-wave deceleration time (r = −0.34, P &lt; .0001). Multivariate analysis revealed that left atrial maximal volume and log NT proBNP were the independent predictors of PA lateral (P &lt; .0001 and P = .003, respectively).Conclusion: The AEMD was significantly prolonged in patients with nonischemic DCM. Left atrial enlargement and log NT proBNP were the independent predictors of this prolongation.</description><dc:title>Assessment of atrial electromechanical delay by tissue Doppler echocardiography in patients with nonischemic dilated cardiomyopathy - Corrected Proof</dc:title><dc:creator>Selcuk Pala, Kursat Tigen, Tansu Karaahmet, Cihan Dundar, Alev Kilicgedik, Ahmet Güler, Cihan Cevik, Cevat Kirma, Yelda Basaran</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.004</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006025/abstract?rss=yes"><title>Nine times measure, 10th cut away - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006025/abstract?rss=yes</link><description>There is a Lithuanian proverb saying: “nine times measure, 10th time cut away.”   With great delight, I have read the “AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: acute ischemia/infarction,” prepared by Wagner et al and published in the Journal of the American College of Cardiology in 2009. They are in line with the latest data about the electrocardiographic identification of the obstructed coronary artery and the proximal or distal location of the obstruction within that artery. This new information is a great addition to the “Universal definition of myocardial infarction—ESC/ACCF/AHA/WHF expert consensus document.” Much information about the identification of the obstructed coronary artery and the proximal or distal location of the obstruction within that artery was published in the issues of the Journal of Electrocardiology of year 2009 (eg, reference ). Thus, the Journal of Electrocardiology in 2009 was of great importance and interest.</description><dc:title>Nine times measure, 10th cut away - Corrected Proof</dc:title><dc:creator>Egle Kalinauskiene</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.007</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:section>LETTER TO THE EDITOR</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005391/abstract?rss=yes"><title>Calculating Cornell voltage from nonstandard chest electrode recording site in the Reasons for Geographic And Racial Differences in Stroke study - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005391/abstract?rss=yes</link><description>Abstract: Background: To minimize participants' burden and the need for disrobing, a 7-lead electrocardiogram (ECG) recording using a single mid-sternal chest lead was recorded at the initial stages of The REasons for Geographic And Racial Differences in Stroke (REGARDS) study. Electrocardiogram-detected left ventricular hypertrophy (ECG-LVH) by Cornell voltage (RaVL + S-wave amplitude in V3 [SV3]) cannot be assessed from this method because of the absence of V3. We examined the possibility that the S-wave amplitude in the mid-sternal lead (SV) could be used as a surrogate for SV3.Methods: The REGARDS study is a US national study where 7-lead ECGs were performed in 8,330 (29%) participants and standard 12-lead EGCs were performed in 20 811 (71%). Cornell voltage was calculated as the sum of aVL amplitude + SV (in the 7-lead group) or SV3 (in the 12-lead group). Logistic regression analysis was used to examine and compare the magnitude of the association between the LVH risk factors with ECG-LVH in both groups, and Cox proportional hazards analysis was used to examine and compare the hazard ratios of overall mortality and cardiovascular mortality associated with ECG-LVH in both groups.Results: Regardless of the Cornell voltage calculation method, ECG-LVH was significantly associated with LVH risk factors; and with the exception of sex, there was no evidence of a difference in the magnitude of the association. ECG-LVH from both approaches were significantly and similarly associated with both all-cause and cardiovascular mortality.Conclusion: ECG-LVH by Cornell voltage calculated from a 7-lead ECG (using SV in the formula) has demographic and clinical associations that are similar to that calculated from a standard 12-lead ECG (using SV3). In epidemiologic studies recording 7-lead ECG, SV could be used as an alternative to SV3 in the Cornell voltage formula.</description><dc:title>Calculating Cornell voltage from nonstandard chest electrode recording site in the Reasons for Geographic And Racial Differences in Stroke study - Corrected Proof</dc:title><dc:creator>Elsayed Z. Soliman, George Howard, Ronald J. Prineas, Leslie A. McClure, Virginia J. Howard</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.002</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-10</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-10</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609002581/abstract?rss=yes"><title>Ventricular fibrillation during the use of an electric shaver? - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609002581/abstract?rss=yes</link><description></description><dc:title>Ventricular fibrillation during the use of an electric shaver? - Corrected Proof</dc:title><dc:creator>Kurt S. Hoffmayer, Nora Goldschlager</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.06.013</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-04</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-04</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005123/abstract?rss=yes"><title>Electrophysiologic and anatomical relationships studied in primum atrioventricular septal defect - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005123/abstract?rss=yes</link><description>Abstract: Anatomy and pattern of electrical activation predict the function and contraction pattern of the heart. Patients with primum atrioventricular septal defect (primum AVSD) present with abnormality of both anatomical arrangements and electric activation and serve therefore as an interesting population for studying electro-anatomic relationships in the heart.Understanding the relationships between anatomic and electrophysiologic abnormality is appropriate not only for diagnosis, therapy, and prognosis in patients with primum AVSD but also for understanding the developmental relationship between the conduction system and heart structures, in general.This article presents a review of the anatomical and electrophysiologic characteristics of patients with primum AVSD and provides recent knowledge of electroanatomical relationships of the heart.</description><dc:title>Electrophysiologic and anatomical relationships studied in primum atrioventricular septal defect - Corrected Proof</dc:title><dc:creator>Nina Hakacova</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.005</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207360900538X/abstract?rss=yes"><title>The utility of modified Butler-Leggett criteria for right ventricular hypertrophy in detection of clinically significant shunt ratio in ostium secundum–type atrial septal defect in adults - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207360900538X/abstract?rss=yes</link><description>Abstract: Background: This study was performed to test the hypothesis that there exists a correlation between the Butler-Leggett (BL) criterion for right ventricular hypertrophy on the electrocardiogram and the Qp/Qs shunt ratio in adults with ostium secundum atrial septal defects (ASDs).Methods: Demographic, cardiac catheterization, ASD closure, and electrocardiographic data were acquired on 70 patients with secundum ASDs closed percutaneously. Simple linear regression and logistic regression models were created to test the hypothesis.Results: The mean Qp/Qs ratio and BL criterion value were 1.61 ± 0.46 and 0.11 ± 0.41, respectively. The BL criterion values correlated with shunt ratios (r2 = 0.11 and P = .004). A BL criterion value greater than 0 mV predicted a significant shunt ratio (Qp/Qs ≥1.5) (odds ratio, 4.8; 95% confidence interval, 1.3, 18.1; P = &lt;.0001) with a sensitivity of 0.68 and specificity of 0.65.Conclusion: Our results indicate that there is limited utility of the BL criterion at detecting right ventricular volume overload, although a BL criterion value greater than 0 mV being used to identify patients with significant intracardiac shunts yielded a sensitivity of 0.68 and specificity of 0.65.</description><dc:title>The utility of modified Butler-Leggett criteria for right ventricular hypertrophy in detection of clinically significant shunt ratio in ostium secundum–type atrial septal defect in adults - Corrected Proof</dc:title><dc:creator>Adeel M. Siddiqui, Zainab Samad, Nina Hakacova, James Kinsella, Cary Ward, Michael White, Anna Lisa C. Crowley, Galen S. Wagner, J. Kevin Harrison</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.001</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207360900541X/abstract?rss=yes"><title>Ischemia-induced repolarization response in relation to the size and location of the ischemic myocardium during short-lasting coronary occlusion in humans - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207360900541X/abstract?rss=yes</link><description>Abstract: Background: The ventricular repolarization (VR) response to short-lasting coronary occlusion has been characterized by 3-dimensional vectorcardiography (VCG) in humans; the T vector loop becomes distorted and more circular. The purpose of this study was to relate these changes to the size of the myocardium at risk (MAR) and its location.Methods: Continuous VCG was applied during transient coronary occlusion in 35 elective angioplasty patients, and the size of the MAR was estimated by single-photon emission computed tomography. Three VR aspects were assessed at baseline vs maximum ischemia: the ST segment, the T vector angles, and the T vector loop morphology.Results: The T loop morphology changes were significantly associated with MAR size, but also dependent of its location. In contrast, the early phase of VR reflected by the ST segment responded to acute ischemia in relation to the MAR size independent of location.Conclusion: The VR changes were related both to the size and the location of the MAR and most pronounced during occlusion of the left anterior descending artery.</description><dc:title>Ischemia-induced repolarization response in relation to the size and location of the ischemic myocardium during short-lasting coronary occlusion in humans - Corrected Proof</dc:title><dc:creator>Aigars Rubulis, Steen M. Jensen, Ulf Näslund, Gunilla Lundahl, Jens Jensen, Lennart Bergfeldt</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.004</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005512/abstract?rss=yes"><title>The diagnostic use of respiratory artifact - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005512/abstract?rss=yes</link><description></description><dc:title>The diagnostic use of respiratory artifact - Corrected Proof</dc:title><dc:creator>Laszlo Littmann</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.005</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005408/abstract?rss=yes"><title>A case of late-term lead endocarditis causing pacemaker dysfunction - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005408/abstract?rss=yes</link><description>With regard to pacemakers, lead endocarditis is a rare condition noted for causing difficulties in patient management. It has been reported in the literature that lead endocarditis may occur even after 10 years. In general, the incidence of pacemaker infections has not been carefully documented. The prevalence and incidence of pacemaker lead dysfunctions due to lead endocarditis have not been researched previously. We present a case of pacemaker dysfunction related to infective endocarditis.</description><dc:title>A case of late-term lead endocarditis causing pacemaker dysfunction - Corrected Proof</dc:title><dc:creator>Mehmet Kayrak, Osman Sonmez, Enes Elvin Gul, Mehmet Gunduz</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.003</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-11-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-25</prism:publicationDate><prism:section>LETTER TO THE EDITOR</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005524/abstract?rss=yes"><title>Variable presentation of ventricular tachycardia-like electrocardiographic artifacts - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005524/abstract?rss=yes</link><description>Abstract: Diagnosis of clinically significant ventricular tachycardia (VT) relies on accurate electrocardiogram (ECG) interpretation, in the context of a convincing clinical picture. ECG artifacts resembling VT are common and can be misleading. We present two instances of VT-like ECG artifacts, which demonstrate the variable presentation of such artifacts and highlight ways in which these ECG tracings can be distinguished from true VT.</description><dc:title>Variable presentation of ventricular tachycardia-like electrocardiographic artifacts - Corrected Proof</dc:title><dc:creator>Jason M. Tarkin, Nearchos Hadjiloizou, Sam Kaddoura, Julian Collinson</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.10.006</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-11-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-25</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005378/abstract?rss=yes"><title>Angiotensinogen polymorphisms and acquired atrial fibrillation in Chinese - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005378/abstract?rss=yes</link><description>Abstract: Genetic predisposition may be underlying the prevalence of acquired atrial fibrillation (AF). We investigated the association between polymorphism in angiotensinogen (AGT) and angiotensin-converting enzyme gene and risk of acquired AF in a pair-matched case-control study conducted in Chinese Hans. We selected 9 single nucleotide polymorphisms (SNPs) in the AGT gene and 3 SNPs in the angiotensin-converting enzyme gene using a tagging-SNP strategy. We observed significant association between tagging-SNP rs699 (M235T), located in exon 2 of the AGT gene, and AF. The AA genotype of rs699 increased the risk of AF by 70% (95% confidence interval, 1.01-2.85; P = .044) under a recessive model (AA vs AG + GG). The significance remained after controlling for covariates age, smoking, body mass index, hypertension, diabetes, and left atrial dimension, with an increased risk of AF by 90% (95% confidence interval, 1.04-3.46; P = .036). We provide evidence that polymorphism in AGT gene may confer predisposition to acquired atrial fibrillation in Chinese Hans.</description><dc:title>Angiotensinogen polymorphisms and acquired atrial fibrillation in Chinese - Corrected Proof</dc:title><dc:creator>Qun-shan Wang, Yi-gang Li, Xing-dong Chen, Jie-fei Yu, Jun Wang, Jian Sun, Shang-biao Lu, Li Jin, Xiao-feng Wang</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.009</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-11-23</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-23</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609002829/abstract?rss=yes"><title>Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609002829/abstract?rss=yes</link><description>Abstract: The electrocardiogram (ECG) remains the most immediately accessible and widely used diagnostic tool for guiding emergency treatment strategies. The ECG recorded during acute myocardial ischemia is of diagnostic, therapeutic, and prognostic significance. In patients with myocardial ischemia as a result of decreased blood supply, the initial 12-lead ECG typically shows (1) predominant ST-segment elevation (STE) as part of STE acute coronary syndrome (STE-ACS), or (2) no predominant STE, that is, non–STE ACS (NSTE-ACS). Patients with predominant STE are classified as having either aborted myocardial infarction (MI) or ST-elevation MI (STEMI) based on the absence or presence of biomarkers of myocardial necrosis. The MI may be aborted either by spontaneous or therapeutic reperfusion of the ischemic myocardium before development of myocardial cell necrosis. NSTE-ACS patients are classified as having either unstable angina or NSTE-MI, based also on the absence or presence of biomarkers of mycardial necrosis.The information obtained from the 12-lead ECG at presentation should be complemented by repeated ECGs especially during symptoms indicative of ischemia and, if applicable, by comparing the findings with reference ECGs. Also, continuous ECG recording in a coronary care setting, including the comparison of ECGs with and without pain, adds to the information gained at patient presentation.In this article, mechanisms of ischemic ECG changes and the ECG patterns recorded in both STE-ACS and NSTE-ACS are described. ECG patterns of NSTE-ACS, which include ST depression, negative T wave, and even normal ECG, need to be better defined in future studies to correlate them with the severity and extent of ischemia and to explore to what extent they are explained by acute active ischemia or represent consequences of ischemia. One of the aims of this article is to propose a classification of the ECG patterns encountered in different clinical scenarios of ACS. How these patterns will aid in guiding the diagnostic and therapeutic process is discussed.</description><dc:title>Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology - Corrected Proof</dc:title><dc:creator>Kjell Nikus, Olle Pahlm, Galen Wagner, Yochai Birnbaum, Juan Cinca, Peter Clemmensen, Markku Eskola, Miquel Fiol, Diego Goldwasser, Anton Gorgels, Samuel Sclarovsky, Shlomo Stern, Hein Wellens, Wojciech Zareba, Antoni Bayés de Luna</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.07.009</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005147/abstract?rss=yes"><title>Dilated cardiomyopathy in children with ventricular preexcitation: the location of the accessory pathway is predictive of this association - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609005147/abstract?rss=yes</link><description>Abstract: Background: Ventricular preexcitation may be associated with dilated cardiomyopathy, even in the absence of recurrent and incessant tachycardia.Methods: This report describes the clinical and electrophysiologic characteristics of 10 consecutive children (6 males), with median age of 8 years (range, 1-17 years), who presented with dilated cardiomyopathy and overt ventricular preexcitation on the 12-lead electrocardiogram. Incessant tachycardia as the cause of dilated cardiomyopathy could be excluded. Coronary angiography, right ventricular endomyocardial biopsy (4/10 patients), and metabolic and microbiologic screening were nondiagnostic.Results: The electrocardiograms suggested right-sided pathways in all patients. A right-sided accessory pathway was demonstrated in 8 patients during invasive electrophysiologic study (superoparaseptal, n = 5; septal, n = 2; fasciculoventricular, n = 1). All pathways were successfully ablated (radiofrequency ablation in 7, cryoablation in 1). Two patients had spontaneous loss of ventricular preexcitation during follow-up. Left ventricular (LV) function completely recovered after a loss of preexcitation in all patients.Conclusions: Right-sided accessory pathways with overt ventricular preexcitation and LV dyssynchrony may cause dilated cardiomyopathy. An association between such pathways and dilated cardiomyopathy is suggested by the rapid normalization of ventricular function and reverse LV remodeling after a loss of ventricular preexcitation.</description><dc:title>Dilated cardiomyopathy in children with ventricular preexcitation: the location of the accessory pathway is predictive of this association - Corrected Proof</dc:title><dc:creator>Floris E.A. Udink ten Cate, Markus A. Kruessell, Kerstin Wagner, Uwe Trieschmann, Mathias Emmel, Konrad Brockmeier, Narayanswami Sreeram</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.007</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207360900421X/abstract?rss=yes"><title>Correlation of ST-segment “hump sign” during exercise testing with impaired diastolic function of the left ventricle - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207360900421X/abstract?rss=yes</link><description>Abstract: Background: The appearance of a discrete upward deflection of the ST segment, termed the ST hump sign during exercise testing has been associated with resting hypertension and exaggerated blood pressure response to exercise.Objective: We investigated the correlation between the presence of hump sign during exercise testing with coexisting impaired diastolic function of the left ventricle (LV) at these patients.Methods: We formed a cohort of 237 nonconsecutive patients (140 males, 41 ± 5 years old) having undergone a treadmill test, according to the Bruce protocol, which divided into 2 groups: group A, including 130 patients which presented ST-segment hump sign at any of the leads of the electrocardiograms recorded during exercise, and group B, including 107 patients that didn't. All patients subsequently underwent an echocardiographic estimation of the LV diastolic function, using conventional and Tissue Doppler Imaging techniques.Results: From 237 patients included in our study, 106 had echocardiographic signs of diastolic LV dysfunction. Among them, the appearance of ST hump sign at the peak of exercise testing was observed in 93 patients (88%), particularly in the inferior and lateral leads, while no ST hump sign was observed only in 13 patients (12%) with impaired diastolic LV function.Conclusions: The appearance of ST segment hump sign during exercise testing is strongly correlated with diastolic LV dysfunction and can be used as an exercise electrocardiographic index of diastolic LV dysfunction, independently from the echocardiographic study.</description><dc:title>Correlation of ST-segment “hump sign” during exercise testing with impaired diastolic function of the left ventricle - Corrected Proof</dc:title><dc:creator>Andreas P. Michaelides, Leonidas G. Raftopoulos, Constantina Aggeli, Charalambos Liakos, Charalambos Antoniades, Christos Fourlas, Elias Stamatopoulos, Nikolaos Ioakeimides, Dimitrios Soulis, Christodoulos Stefanadis</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.001</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-10-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-08</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609004233/abstract?rss=yes"><title>ST-segment depression in aVR as a predictor of culprit artery and infarct size in acute inferior wall ST-segment elevation myocardial infarction - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609004233/abstract?rss=yes</link><description>Abstract: Background: ST-segment depression in lead aVR in acute inferior wall ST-segment elevation myocardial infarction (STEMI) has recently been suggested as a predictor of left circumflex (LCx) artery involvement. The purpose of this study is to evaluate the clinical significance of aVR depression during inferior wall STEMI.Methods: This study included 106 consecutive patients who presented with inferior wall STEMI and underwent urgent coronary angiogram. Clinical and angiographic findings were compared between patients with and without aVR depression ≥0.1 mV.Results: The sensitivity and specificity of aVR depression as a predictor of LCx infarction were 53% and 86%, respectively. In patients with right coronary artery infarction, aVR depression was associated with increased cardiac enzymes and the involvement of a large posterolateral branch, which may explain the larger infarction.Conclusions: ST-segment depression in lead aVR in inferior wall STEMI predicts LCx infarction or larger RCA infarction involving a large posterolateral branch.</description><dc:title>ST-segment depression in aVR as a predictor of culprit artery and infarct size in acute inferior wall ST-segment elevation myocardial infarction - Corrected Proof</dc:title><dc:creator>Yumiko Kanei, Jyoti Sharma, Ravi Diwan, Ron Sklash, Lori L. Vales, John T. Fox, Paul Schweitzer</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.003</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-10-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-08</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609003276/abstract?rss=yes"><title>The electrocardiographic paradox of tako-tsubo cardiomyopathy–comparison with acute ischemic syndromes and consideration of molecular biology and electrophysiology to understand the electrical-mechanical mismatching - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609003276/abstract?rss=yes</link><description>Abstract: From the electrocardiographic (ECG) point of view, the tako-tsubo cardiomyopathy (TTC) behaves like an acute subepicardial circumferential ischemic syndrome. The electrical manifestations are significantly different from those of acute transmural segmental ischemia, in which the ECG primarily expresses the electrophysiologic and metabolic changes occurring in the subepicardial layer. In comparison with transmural anterior ischemia and despite acute contraction impairment (circumferential middle and apical dyskinesis and basal hyperkinesis), in TTC there is typically only moderate ST elevation in the precordial leads.This paradox can be understood by taking into consideration the molecular biology and basic electrophysiology. In the senescent female with hypoestrogenemia, the subepicardium is almost totally unprotected against “adrenergic storm.” In the fertile female, estrogen plays the pivotal role of protecting the myocardium at many levels of the metabolic cascade, such as in the regulation of the presynaptic release of adrenergic substances and by increasing the release of adenosine. There is consequental increase of the adenosine triphosphate (ATP)–sensitive K+ channels, thus regulating the inward flow of Ca2+ toward the sarcoplasmic reticulum. The ATP-sensitive K+ channels hyperpolarize the subepicardial cells during extremely aggressive situations such as ischemia and adrenergic storm. The hyperpolarization of the subepicardium is manifested in the ECG by tall, peaked T waves, indicating an increase of the repolarization gradient between the subendocardial and subepicardial layers. In the absence of estrogen, there are severe decreases in the concentration of adenosine and in the density of the ATP-sensitive K+ channels. The subepicardial myocytes cannot be hyperpolarized, and the adrenergic storm is manifested by moderate ST-T elevation. Furthermore, the very rapid appearance and disappearance of a Q wave are “against the rules.” This is a classical example of electrical stunning, that disappears before mechanical stunning in which contraction is typically recovered only after 1 week.</description><dc:title>The electrocardiographic paradox of tako-tsubo cardiomyopathy–comparison with acute ischemic syndromes and consideration of molecular biology and electrophysiology to understand the electrical-mechanical mismatching - Corrected Proof</dc:title><dc:creator>Samuel Sclarovsky, Kjell Nikus</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.07.015</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-10-05</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-05</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609004221/abstract?rss=yes"><title>Wolf-Parkinson-White alternans diagnosis unveiled by adenosine stress test - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609004221/abstract?rss=yes</link><description>Abstract: The case of a 41-year-old woman who presented to her primary care physician with atypical chest pain was reported. An electrocardiogram (ECG) was performed in his office and the patient was told she had left bundle-branch block and an old infarct. The patient was very concerned and referred to cardiology for further evaluation/testing. An ECG at the cardiologist's office was normal. The cardiologist however suspected the ECG performed at the primary care physician office to be preexcitation (Wolf-Parkinson-White). During an adenosine nuclear stress test, intermittent preexcited beats occurred transiently to confirm the diagnosis of Wolf-Parkinson-White. Wolf-Parkinson-White can mimic multiple other ECG changes including a pseudoinfarct pattern and hence be misleading. The figure of the unique ECG, during the adenosine stress test, of intermittent preexcited (preexcitation alternans) complexes is included.</description><dc:title>Wolf-Parkinson-White alternans diagnosis unveiled by adenosine stress test - Corrected Proof</dc:title><dc:creator>Rami N. Khouzam</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.002</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-09-30</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-09-30</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609003720/abstract?rss=yes"><title>Effects of left ventricular lead positions and coronary venous microanatomy on Cardiac pacing parameters - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609003720/abstract?rss=yes</link><description>Abstract: We describe effects of pacing lead position and cardiac microanatomy on electrical pacing parameters. Passive fixation transvenous pacing leads were implanted in anterior interventricular veins in isolated swine hearts (n = 6). Electrical pacing parameters were measured in 3 implant positions (5 implant sites each): touching myocardial side of venous wall, not touching venous wall, and touching epicardial side of venous wall. After perfusion fixing hearts, veins were sectioned perpendicular to vein's length from base to apex. Slides were prepared and analyzed for measurement of vein wall thickness/circumference, and distances between vein walls and myocardium. Average pacing thresholds were greater when pacing leads were free-floating (5.45 ± 3.29 V) or oriented in epicardial positions (6.81 ± 2.96 V) compared with myocardial positions (3.79 ± 3.46 V; P = not significant). Vein circumferences were significantly larger in basal regions (8.31 ± 2.28 mm) compared with mid (6.90 ± 1.46 mm) and apical (6.40 ± 1.92 mm) regions (P &lt; .05). Variability in pacing thresholds and impedances indicates that pacing lead placement in left ventricular coronary veins significantly affects electrical pacing parameters.</description><dc:title>Effects of left ventricular lead positions and coronary venous microanatomy on Cardiac pacing parameters - Corrected Proof</dc:title><dc:creator>Sara E. Anderson, Paul A. Iaizzo</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.08.002</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-09-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-09-16</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609003264/abstract?rss=yes"><title>Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609003264/abstract?rss=yes</link><description>Abstract: The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics.Material and Methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index.Results: The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria.Conclusion: We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed.</description><dc:title>Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study - Corrected Proof</dc:title><dc:creator>Ljuba Bacharova, Vavrinec Szathmary, Matej Kovalcik, Anton Mateasik</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.07.014</dc:identifier><dc:source>Journal of Electrocardiology (2009)</dc:source><dc:date>2009-08-27</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-08-27</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS002207360800215X/abstract?rss=yes"><title>WITHDRAWN: “Pseudo-high lateral leads Brugada pattern” due to lead reversal - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS002207360800215X/abstract?rss=yes</link><description>Available online August 26, 2008This article has been withdrawn consistent with Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). The publisher apologizes for any inconvenience this may cause.</description><dc:title>WITHDRAWN: “Pseudo-high lateral leads Brugada pattern” due to lead reversal - Corrected Proof</dc:title><dc:creator>Adrian Baranchuk, Jaskaran Kang, Hoshiar Abdollah, Christopher Simpson, Damian P. Redfearn</dc:creator><dc:identifier>10.1016/j.jelectrocard.2008.07.008</dc:identifier><dc:source>Journal of Electrocardiology (2008)</dc:source><dc:date>2008-08-26</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2008-08-26</prism:publicationDate></item></rdf:RDF>