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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.jecgonline.com/?rss=yes"><title>Journal of Electrocardiology</title><description>Journal of Electrocardiology RSS feed: Current Issue. The  Journal of Electrocardiology  is devoted exclusively to clinical and experimental studies of the electrical activities 
of the heart. It seeks to contribute significantly to the accuracy of diagnosis and prognosis and the effective treatment, prevention, 
or delay of heart disease. Editorial contents include electrocardiography, vectorcardiography, arrhythmias, membrane action potential, 
cardiac pacing, monitoring defibrillation, instrumentation, drug effects, and computer applications.</description><link>http://www.jecgonline.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:issn>0022-0736</prism:issn><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:publicationDate>March 2010</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/PIIS0022073609002829/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/PIIS0022073609006049/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609005548/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073609006104/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/PIIS0022073609003720/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/PIIS0022073609004221/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/PIIS0022073610000713/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/PIIS0022073610000749/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/PIIS002207360900421X/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/PIIS0022073610000051/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073610000087/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecgonline.com/article/PIIS0022073610000099/abstract?rss=yes"/></rdf:Seq></items></channel><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</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</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 43, 2 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>91</prism:startingPage><prism:endingPage>103</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>104</prism:startingPage><prism:endingPage>112</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>113</prism:startingPage><prism:endingPage>120</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005548/abstract?rss=yes"><title>Rhythm quizlet</title><link>http://www.jecgonline.com/article/PIIS0022073609005548/abstract?rss=yes</link><description></description><dc:title>Rhythm quizlet</dc:title><dc:creator>Jonni Cooper</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.11.002</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>120</prism:startingPage><prism:endingPage>120</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609006104/abstract?rss=yes"><title>The ST injury vector: electrocardiogram-based estimation of location and extent of myocardial ischemia</title><link>http://www.jecgonline.com/article/PIIS0022073609006104/abstract?rss=yes</link><description>Abstract: Background: Analysis of ST deviations from the 12-lead electrocardiogram allows for estimation of a spatial ST injury vector. The goal of the present study was to compare the location and extent of transmural myocardial ischemia evaluated by myocardial perfusion imaging with the direction and magnitude of the ST injury vector.Methods: Twelve-lead electrocardiograms were recorded from 75 acute myocardial infarction patients with single-vessel disease and thrombolysis in myocardial infarction (TIMI) flow 0/1 (30 left anterior descending [LAD], 28 right coronary artery [RCA], 17 left circumflex artery [LCX]). ST deviations were measured in the J point in all leads and used to estimate ST injury vectors for each patient. Myocardial perfusion imaging was performed to evaluate the extent and location of myocardial ischemia at the time of coronary intervention.Results: Ninety-two percent of the patients showed ST injury vectors within the expected directional range for the identified anatomic segment of ischemia by myocardial perfusion imaging. ST injury vector direction separated LAD, RCA, and LCX occlusion patients; 90% of the LAD patients showed anterior vectors, 82% of the RCA patients showed posteroinferoseptal vectors, and 59% of the LCX patients showed posteroinferolateral vectors. Eight patients did not fulfill the ST elevation criteria for ST elevation myocardial infarction but showed anterior ST depression and prominent ST injury vectors in the posterior torso direction. There was a moderate correlation between the extent of ischemia and ST injury vector magnitude for the ischemic patients, r = 0.29.Conclusion: We found strong agreement between the direction of the ST injury vector and the location of myocardial ischemia. The ST injury vector may be the key to higher diagnostic accuracy for inferobasal transmural ischemia and may help distinguishing between RCA and LCX occlusions in the acute phase.</description><dc:title>The ST injury vector: electrocardiogram-based estimation of location and extent of myocardial ischemia</dc:title><dc:creator>Mads P. Andersen, Christian J. Terkelsen, Jacob T. Sørensen, Anne K. Kaltoft, Søren S. Nielsen, Johannes J. Struijk, Hans E. Bøtker</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.12.001</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>121</prism:startingPage><prism:endingPage>131</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-10-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-08</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Acute Coronary Syndromes</prism:section><prism:startingPage>132</prism:startingPage><prism:endingPage>135</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-09-16</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-09-16</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Pacing</prism:section><prism:startingPage>136</prism:startingPage><prism:endingPage>141</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005408/abstract?rss=yes"><title>A case of late-term lead endocarditis causing pacemaker dysfunction</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</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 43, 2 (2010)</dc:source><dc:date>2009-11-25</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-25</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Letter to the Editor</prism:section><prism:startingPage>142</prism:startingPage><prism:endingPage>143</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609004221/abstract?rss=yes"><title>Wolf-Parkinson-White alternans diagnosis unveiled by adenosine stress test</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</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 43, 2 (2010)</dc:source><dc:date>2009-09-30</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-09-30</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>WPW</prism:section><prism:startingPage>144</prism:startingPage><prism:endingPage>145</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>WPW</prism:section><prism:startingPage>146</prism:startingPage><prism:endingPage>154</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000713/abstract?rss=yes"><title>Answers to Quiz</title><link>http://www.jecgonline.com/article/PIIS0022073610000713/abstract?rss=yes</link><description></description><dc:title>Answers to Quiz</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(10)00071-3</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>WPW</prism:section><prism:startingPage>154</prism:startingPage><prism:endingPage>154</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073609005123/abstract?rss=yes"><title>Electrophysiologic and anatomical relationships studied in primum atrioventricular septal defect</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</dc:title><dc:creator>Nina Hakacova</dc:creator><dc:identifier>10.1016/j.jelectrocard.2009.09.005</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Septal Defects</prism:section><prism:startingPage>155</prism:startingPage><prism:endingPage>160</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000749/abstract?rss=yes"><title>Articles Appearing in the Next Issue</title><link>http://www.jecgonline.com/article/PIIS0022073610000749/abstract?rss=yes</link><description></description><dc:title>Articles Appearing in the Next Issue</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(10)00074-9</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Septal Defects</prism:section><prism:startingPage>160</prism:startingPage><prism:endingPage>160</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Septal Defects</prism:section><prism:startingPage>161</prism:startingPage><prism:endingPage>166</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-10-08</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-08</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Cardiomyopathies</prism:section><prism:startingPage>167</prism:startingPage><prism:endingPage>172</prism:endingPage></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</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</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 43, 2 (2010)</dc:source><dc:date>2009-10-05</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2009-10-05</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Cardiomyopathies</prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>176</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000051/abstract?rss=yes"><title>Poster Session 1</title><link>http://www.jecgonline.com/article/PIIS0022073610000051/abstract?rss=yes</link><description>An abstract entitled “A novel low-tilt waveform for the internal defibrillation of ventricular fibrillation” by J.R. Bennett, K.M. Daragh, S.J. Walsh, J.D. Allen, J. Anderson, A.A.J. Adgey, and G. Manoharan was inadvertently not printed in the November/December 2008 issue (41/6) of Journal of Electrocardiology. We have included the missing material below.</description><dc:title>Poster Session 1</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jelectrocard.2010.01.004</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Erratum</prism:section><prism:startingPage>177</prism:startingPage><prism:endingPage>177</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000087/abstract?rss=yes"><title>Editorial Board</title><link>http://www.jecgonline.com/article/PIIS0022073610000087/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(10)00008-7</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.jecgonline.com/article/PIIS0022073610000099/abstract?rss=yes"><title>Contents</title><link>http://www.jecgonline.com/article/PIIS0022073610000099/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0022-0736(10)00009-9</dc:identifier><dc:source>Journal of Electrocardiology 43, 2 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of Electrocardiology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>43</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0022-0736(10)X0002-4</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A4</prism:endingPage></item></rdf:RDF>