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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 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:issn>0022-0736</prism:issn><prism:publicationDate>2010-03-08</prism:publicationDate><prism:copyright> © 2010 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/PIIS0022073610000853/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006037/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073610000026/abstract?rss=yes"/><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/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/PIIS0022073609005512/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/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/PIIS0022073610000853/abstract?rss=yes"><title>Intravenous electrocardiographic guidance for placement of peripherally inserted central catheters - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073610000853/abstract?rss=yes</link><description>Abstract: Background: Correct positioning of peripherally inserted central catheters (PICCs) is essential to avoid complications. We evaluated intravenous electrocardiogram (ECG) recordings during PICC placement to assess the effectiveness of this guidance technique to reduce complications resulting from incorrect catheter placement.Methods: Six patients undergoing PowerPICC catheter insertion were included in this pilot study. Venography through the PICC was performed to identify the superior vena cava–right atrial (SVC-RA) junction. Unipolar ECG recordings from the catheter stylet measured P-wave changes during PICC insertion.Results: The peak P-wave amplitude was highest at the SVC-RA junction. With catheter insertion into the RA, P-wave amplitude decreased and eventually became negative. With catheter withdrawal into the SVC, P-wave amplitude decreased.Conclusions: P-wave amplitude was highest when the PICC catheter was in the optimal location at the SVC-RA junction. Intravenous ECG monitoring during PICC insertion seems to be a promising technique to guide catheter positioning.</description><dc:title>Intravenous electrocardiographic guidance for placement of peripherally inserted central catheters - Corrected Proof</dc:title><dc:creator>Brigham Smith, Renée M. Neuharth, Mary Ann Hendrix, Daniel McDonnall, Andrew D. Michaels</dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.02.003</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006037/abstract?rss=yes"><title>Posterior or lateral involvement in nonanterior wall infarction. What's in a name? - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073609006037/abstract?rss=yes</link><description>The surface electrocardiogram (ECG) was one of the first clinical tools to register structural aspects of the normal and diseased heart. The electrocardiogram could be used for that purpose because structural heart disease leads to changes in electrical activation of the heart chambers. To assess the accuracy of the ECG in this regard, information from the electrical wave forms was compared with other imaging techniques. Early electrical-structural correlations were based on the study of postmortem pathologic findings or other electrical techniques such as vectorcardiography.</description><dc:title>Posterior or lateral involvement in nonanterior wall infarction. What's in a name? - Corrected Proof</dc:title><dc:creator>Anton P.M. Gorgels, Kirian van der Weg</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.008</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-02-15</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-02-15</prism:publicationDate><prism:section>LETTER TO THE EDITOR</prism:section></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000026/abstract?rss=yes"><title>How many leads through persistent left superior vein cava and coronary sinus? - Corrected Proof</title><link>http://www.jecgonline.com/article/PIIS0022073610000026/abstract?rss=yes</link><description>Abstract: In the modern implanting era with progressive expanding indications to resynchronization therapy, upgrading procedure is a relatively common event. Persistent left superior vena cava (PLSVC), the most common venous abnormality, may exacerbate technical difficulties. We describe the procedure of upgrading from a dual chamber pacemaker to resynchronization/defibrillation system with a total of 4 leads through a PLSVC entering a dilated coronary sinus (CS) never described before. The case report, in addition to the description of a unique technical approach, raises a lot of clinical questions about how many leads we can introduce in such a venous structure and inside CS without hemodynamic impact on venous drainage potentially leading to life-threatening situations.</description><dc:title>How many leads through persistent left superior vein cava and coronary sinus? - Corrected Proof</dc:title><dc:creator>Giovanni Morani, Corinna Bergamini, Mauro Toniolo, Corrado Vassanelli</dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.01.001</dc:identifier><dc:source>Journal of Electrocardiology (2010)</dc:source><dc:date>2010-02-15</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-02-15</prism:publicationDate></item><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/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/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/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/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>