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<p>
<b>Atrial fibrillation and congestive heart failure: should we aim to control the heart's rate or its rhythm?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1377">doi:10.1038/ncpcardio1377</a>
</p>
<p>Author: Alessandro Capucci</p>
]]></content:encoded>
<dc:title>Atrial fibrillation and congestive heart failure: should we aim to control the heart's rate or its rhythm?</dc:title>
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<description/>
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<p>
<b>Are pediatricians responsible for prevention of adult cardiovascular disease?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1389">doi:10.1038/ncpcardio1389</a>
</p>
<p>Authors: Henry C McGill, C Alex McMahan
&amp; Samuel S Gidding</p>
]]></content:encoded>
<dc:title>Are pediatricians responsible for prevention of adult cardiovascular disease?</dc:title>
<dc:creator>Henry C McGill</dc:creator>
<dc:creator>C Alex McMahan</dc:creator>
<dc:creator>Samuel S Gidding</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1389</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-28</dc:date>
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<description/>
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<p>
<b>Translation of evidence-based guidelines in preventive cardiology: the EUROACTION program</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1386">doi:10.1038/ncpcardio1386</a>
</p>
<p>Author: Thomas A Pearson</p>
]]></content:encoded>
<dc:title>Translation of evidence-based guidelines in preventive cardiology: the EUROACTION program</dc:title>
<dc:creator>Thomas A Pearson</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1386</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-21</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-21</prism:publicationDate>
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<title>Assessment of microvascular injury after acute myocardial infarction: importance of the area at risk</title>
<link>http://dx.doi.org/10.1038/ncpcardio1373</link>
<description/>
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<p>
<b>Assessment of microvascular injury after acute myocardial infarction: importance of the area at risk</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1373">doi:10.1038/ncpcardio1373</a>
</p>
<p>Authors: Igor Klem
&amp; Raymond J Kim</p>
]]></content:encoded>
<dc:title>Assessment of microvascular injury after acute myocardial infarction: importance of the area at risk</dc:title>
<dc:creator>Igor Klem</dc:creator>
<dc:creator>Raymond J Kim</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1373</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-14</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
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<prism:startingPage/>
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<title>Home blood pressure monitoring: a new standard method for monitoring hypertension control in treated patients</title>
<link>http://dx.doi.org/10.1038/ncpcardio1374</link>
<description/>
<content:encoded><![CDATA[

<p>
<b>Home blood pressure monitoring: a new standard method for monitoring hypertension control in treated patients</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1374">doi:10.1038/ncpcardio1374</a>
</p>
<p>Author: Thomas G Pickering</p>
]]></content:encoded>
<dc:title>Home blood pressure monitoring: a new standard method for monitoring hypertension control in treated patients</dc:title>
<dc:creator>Thomas G Pickering</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1374</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-14</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
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<title>Implantable cardioverter-defibrillator lead failure: how weak is the link?</title>
<link>http://dx.doi.org/10.1038/ncpcardio1367</link>
<description/>
<content:encoded><![CDATA[

<p>
<b>Implantable cardioverter-defibrillator lead failure: how weak is the link?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1367">doi:10.1038/ncpcardio1367</a>
</p>
<p>Author: Jeffrey A Brinker</p>
]]></content:encoded>
<dc:title>Implantable cardioverter-defibrillator lead failure: how weak is the link?</dc:title>
<dc:creator>Jeffrey A Brinker</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1367</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-07</dc:date>
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<description/>
<content:encoded><![CDATA[

<p>
<b>Early repolarization and sudden cardiac arrest: theme or variation on a theme?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1354">doi:10.1038/ncpcardio1354</a>
</p>
<p>Authors: Robert J Myerburg
&amp; Agustin Castellanos</p>
]]></content:encoded>
<dc:title>Early repolarization and sudden cardiac arrest: theme or variation on a theme?</dc:title>
<dc:creator>Robert J Myerburg</dc:creator>
<dc:creator>Agustin Castellanos</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1354</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-07</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-07</prism:publicationDate>
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<prism:startingPage/>
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<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1368">
<title>Is an invasive interventional strategy of value in non-ST-elevation acute coronary syndromes?</title>
<link>http://dx.doi.org/10.1038/ncpcardio1368</link>
<description/>
<content:encoded><![CDATA[

<p>
<b>Is an invasive interventional strategy of value in non-ST-elevation acute coronary syndromes?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1368">doi:10.1038/ncpcardio1368</a>
</p>
<p>Author: William S Weintraub</p>
]]></content:encoded>
<dc:title>Is an invasive interventional strategy of value in non-ST-elevation acute coronary syndromes?</dc:title>
<dc:creator>William S Weintraub</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1368</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-07</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-07</prism:publicationDate>
<prism:section>Clinical Advance</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1401">
<title>Hypertrophic obstructive cardiomyopathy and sleep-disordered breathing: an unfavorable combination</title>
<link>http://dx.doi.org/10.1038/ncpcardio1401</link>
<description>In this thought-provoking Viewpoint and accompanying clinical vignettes, Sengupta and colleagues posit that clinicians should be aware of obstructive sleep apnea in patients with hypertrophic obstructive cardiomyopathy. They hypothesize that this sleep disorder could be the reason cardiomyopathy symptoms remain despite therapy and could also contribute to a raised gradient seen in some patients.</description>
<content:encoded><![CDATA[

<p>
<b>Hypertrophic obstructive cardiomyopathy and sleep-disordered breathing: an unfavorable combination</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1401">doi:10.1038/ncpcardio1401</a>
</p>
<p>Authors: Partho P Sengupta, Dan Sorajja, Mackram F Eleid, Virend K Somers, Steve R Ommen, James M Parish, Bijoy Khandheria
&amp; A Jamil Tajik</p>
]]></content:encoded>
<dc:title>Hypertrophic obstructive cardiomyopathy and sleep-disordered breathing: an unfavorable combination</dc:title>
<dc:creator>Partho P Sengupta</dc:creator>
<dc:creator>Dan Sorajja</dc:creator>
<dc:creator>Mackram F Eleid</dc:creator>
<dc:creator>Virend K Somers</dc:creator>
<dc:creator>Steve R Ommen</dc:creator>
<dc:creator>James M Parish</dc:creator>
<dc:creator>Bijoy Khandheria</dc:creator>
<dc:creator>A Jamil Tajik</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1401</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-11-18</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-11-18</prism:publicationDate>
<prism:section>Viewpoint</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1371">
<title>Myocardial protection: is primary PCI enough?</title>
<link>http://dx.doi.org/10.1038/ncpcardio1371</link>
<description/>
<content:encoded><![CDATA[

<p>
<b>Myocardial protection: is primary PCI enough?</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1371">doi:10.1038/ncpcardio1371</a>
</p>
<p>Authors: Derek J Hausenloy
&amp; Derek M Yellon</p>
]]></content:encoded>
<dc:title>Myocardial protection: is primary PCI enough?</dc:title>
<dc:creator>Derek J Hausenloy</dc:creator>
<dc:creator>Derek M Yellon</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1371</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-14</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-14</prism:publicationDate>
<prism:section>Viewpoint</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1366">
<title>The relevance of prosthesis&#8211;patient mismatch after aortic valve replacement</title>
<link>http://dx.doi.org/10.1038/ncpcardio1366</link>
<description>Patient-prosthesis mismatch (PPM) is common after aortic valve replacement and has been shown to be associated with poor hemodynamic and symptomatic status, a high rate of cardiac events, and increased mortality. In this article, Philippe Pibarot and Jean G. Dumesnil highlight the importance of defining and recognizing PPM and its clinical impact. They also assert that, because PPM is a predictable and modifiable risk factor, it is vital to identify susceptible patients and to apply preventive strategies to avoid PPM or reduce its severity.</description>
<content:encoded><![CDATA[

<p>
<b>The relevance of prosthesis&#8211;patient mismatch after aortic valve replacement</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1366">doi:10.1038/ncpcardio1366</a>
</p>
<p>Authors: Philippe Pibarot
&amp; Jean G Dumesnil</p>
]]></content:encoded>
<dc:title>The relevance of prosthesis&#8211;patient mismatch after aortic valve replacement</dc:title>
<dc:creator>Philippe Pibarot</dc:creator>
<dc:creator>Jean G Dumesnil</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1366</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-07</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-07</prism:publicationDate>
<prism:section>Viewpoint</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1372">
<title>Platelet ADP-receptor antagonists for cardiovascular disease: past, present and future</title>
<link>http://dx.doi.org/10.1038/ncpcardio1372</link>
<description>Aspirin can effectively prevent arterial thrombosis; however, its efficacy is limited as it inhibits the synthesis of only one platelet agonist (thromboxane A2). Here Raju and colleagues review agents that target ADP-mediated platelet activation. They examine controversies and unresolved issues associated with clopidogrel&#8212;the optimum loading dose, duration of treatment and incomplete platelet inhibition&#8212;and the new ADP-receptor antagonists prasugrel, AZD6140 and cangrelor, and explore their potential relative to each other and to clopidogrel.</description>
<content:encoded><![CDATA[

<p>
<b>Platelet ADP-receptor antagonists for cardiovascular disease: past, present and future</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1372">doi:10.1038/ncpcardio1372</a>
</p>
<p>Authors: Nina C Raju, John W Eikelboom
&amp; Jack Hirsh</p>
]]></content:encoded>
<dc:title>Platelet ADP-receptor antagonists for cardiovascular disease: past, present and future</dc:title>
<dc:creator>Nina C Raju</dc:creator>
<dc:creator>John W Eikelboom</dc:creator>
<dc:creator>Jack Hirsh</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1372</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-28</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-28</prism:publicationDate>
<prism:section>Review</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1370">
<title>Structural remodeling in atrial fibrillation</title>
<link>http://dx.doi.org/10.1038/ncpcardio1370</link>
<description>Atrial fibrillation is characterized by structural remodeling of the atrial myocardium&#8212;a slow process that comprises morphological changes that affect atrial myocardial architecture and atrial ultrastructure. Here Corradi  et al. examine the morphological changes that characterize the fibrillating atrial myocardium at histological and ultrastructural levels, and explore how the pathogenetic mechanisms involved in AF could lead to new treatments.</description>
<content:encoded><![CDATA[

<p>
<b>Structural remodeling in atrial fibrillation</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1370">doi:10.1038/ncpcardio1370</a>
</p>
<p>Authors: Domenico Corradi, Sergio Callegari, Roberta Maestri, Stefano Benussi
&amp; Ottavio Alfieri</p>
]]></content:encoded>
<dc:title>Structural remodeling in atrial fibrillation</dc:title>
<dc:creator>Domenico Corradi</dc:creator>
<dc:creator>Sergio Callegari</dc:creator>
<dc:creator>Roberta Maestri</dc:creator>
<dc:creator>Stefano Benussi</dc:creator>
<dc:creator>Ottavio Alfieri</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1370</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-14</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-14</prism:publicationDate>
<prism:section>Review</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1375">
<title>Vascular complications of selected cancer therapies</title>
<link>http://dx.doi.org/10.1038/ncpcardio1375</link>
<description>Vascular complications following cancer treatment are relatively common, particularly in patients with advanced stages of cancer. In this Review, Dr Daher and Dr Yeh describe the vascular complications of treatment with 5-fluorouracil, bevacizumab, and several new tyrosine kinase inhibitors, with special emphasis on thrombotic complications and hypertension.</description>
<content:encoded><![CDATA[

<p>
<b>Vascular complications of selected cancer therapies</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1375">doi:10.1038/ncpcardio1375</a>
</p>
<p>Authors: Iyad N Daher
&amp; Edward TH Yeh</p>
]]></content:encoded>
<dc:title>Vascular complications of selected cancer therapies</dc:title>
<dc:creator>Iyad N Daher</dc:creator>
<dc:creator>Edward TH Yeh</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1375</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-14</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-14</prism:publicationDate>
<prism:section>Review</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1355">
<title>Acute hemodynamic changes in percutaneous transluminal septal coil embolization for hypertrophic obstructive cardiomyopathy</title>
<link>http://dx.doi.org/10.1038/ncpcardio1355</link>
<description>Ramcharitar and colleagues present an interesting case of a patient with drug-refractory hypertrophic obstructive cardiomyopathy and NYHA class II&#8211;III heart failure who was treated with septal coil embolization. This article demonstrates, for the first time, the acute changes in hemodynamics that occur following septal coil embolization, and shows that this treatment is a viable alternative to percutaneous coronary intervention.</description>
<content:encoded><![CDATA[

<p>
<b>Acute hemodynamic changes in percutaneous transluminal septal coil embolization for hypertrophic obstructive cardiomyopathy</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1355">doi:10.1038/ncpcardio1355</a>
</p>
<p>Authors: Steve Ramcharitar, Emanuele Meliga, Sharon W Kirschbaum, Folkert J ten Cate, Robert Jan van Geuns
&amp; Patrick W Serruys</p>
]]></content:encoded>
<dc:title>Acute hemodynamic changes in percutaneous transluminal septal coil embolization for hypertrophic obstructive cardiomyopathy</dc:title>
<dc:creator>Steve Ramcharitar</dc:creator>
<dc:creator>Emanuele Meliga</dc:creator>
<dc:creator>Sharon W Kirschbaum</dc:creator>
<dc:creator>Folkert J ten Cate</dc:creator>
<dc:creator>Robert Jan van Geuns</dc:creator>
<dc:creator>Patrick W Serruys</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1355</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-07</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-07</prism:publicationDate>
<prism:section>Case Study</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1388">
<title>Combined delivery approach of bone marrow mononuclear stem cells early and late after myocardial infarction: the MYSTAR prospective, randomized study</title>
<link>http://dx.doi.org/10.1038/ncpcardio1388</link>
<description>Combined intracoronary and intramyocardial administration might improve outcomes for bone-marrow-derived stem cell therapy for acute myocardial infarction. In this paper patients with left ventricular ejection fraction less than 45% after acute myocardial infarction were randomly assigned stem cell delivery via intramyocardial injection and intracoronary infusion 3&#8211;6 weeks or 3&#8211;4 months after AMI. Their data shows that combined cardiac stem cell delivery induces a moderate but significant improvement in myocardial infarct size and left ventricular function.</description>
<content:encoded><![CDATA[

<p>
<b>Combined delivery approach of bone marrow mononuclear stem cells early and late after myocardial infarction: the MYSTAR prospective, randomized study</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1388">doi:10.1038/ncpcardio1388</a>
</p>
<p>Authors: Mariann Gy&#246;ngy&#246;si, Irene Lang, Markus Dettke, Gilbert Beran, Senta Graf, Heinz Sochor, No&#233;mi Nyolczas, Silvia Charwat, Rayyan Hemetsberger, G&#252;nter Christ, Istv&#225;n &#201;des, L&#225;szl&#243; Balogh, Korff Thomas Krause, Kai Jaquet, Karl-Heinz Kuck, Imre Benedek, Theodora Hintea, R&#243;bert Kiss, Istv&#225;n Pr&#233;da, Vladimir Kotevski, Hristo Pejkov, Sholeh Zamini, Aliasghar Khorsand, Gottfried Sodeck, Alexandra Kaider, Gerald Maurer
&amp; Dietmar Glogar</p>
]]></content:encoded>
<dc:title>Combined delivery approach of bone marrow mononuclear stem cells early and late after myocardial infarction: the MYSTAR prospective, randomized study</dc:title>
<dc:creator>Mariann Gy&#246;ngy&#246;si</dc:creator>
<dc:creator>Irene Lang</dc:creator>
<dc:creator>Markus Dettke</dc:creator>
<dc:creator>Gilbert Beran</dc:creator>
<dc:creator>Senta Graf</dc:creator>
<dc:creator>Heinz Sochor</dc:creator>
<dc:creator>No&#233;mi Nyolczas</dc:creator>
<dc:creator>Silvia Charwat</dc:creator>
<dc:creator>Rayyan Hemetsberger</dc:creator>
<dc:creator>G&#252;nter Christ</dc:creator>
<dc:creator>Istv&#225;n &#201;des</dc:creator>
<dc:creator>L&#225;szl&#243; Balogh</dc:creator>
<dc:creator>Korff Thomas Krause</dc:creator>
<dc:creator>Kai Jaquet</dc:creator>
<dc:creator>Karl-Heinz Kuck</dc:creator>
<dc:creator>Imre Benedek</dc:creator>
<dc:creator>Theodora Hintea</dc:creator>
<dc:creator>R&#243;bert Kiss</dc:creator>
<dc:creator>Istv&#225;n Pr&#233;da</dc:creator>
<dc:creator>Vladimir Kotevski</dc:creator>
<dc:creator>Hristo Pejkov</dc:creator>
<dc:creator>Sholeh Zamini</dc:creator>
<dc:creator>Aliasghar Khorsand</dc:creator>
<dc:creator>Gottfried Sodeck</dc:creator>
<dc:creator>Alexandra Kaider</dc:creator>
<dc:creator>Gerald Maurer</dc:creator>
<dc:creator>Dietmar Glogar</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1388</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-11-11</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-11-11</prism:publicationDate>
<prism:section>Clinical research</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1364">
<title>Circulating white blood cells and platelets amplify oxidative stress in heart failure</title>
<link>http://dx.doi.org/10.1038/ncpcardio1364</link>
<description>Mitochondria of circulating white blood cells (WBC) and platelets sense oxidative stress during capillary passage and react by producing reactive oxygen species (ROS). Evidence indicates that congestive heart failure (CHF) is associated with oxidative stress; however, the role of WBC and platelets as mediators in CHF has not been investigated. In this paper the authors conducted an observational study to investigate the degree of oxidation in WBC and platelets in patients with CHF and healthy volunteers. Their data shows that in CHF, the proportion of WBC and platelets that are ROS positive is raised. The raised numbers of circulating ROS-positive WBC and platelets amplify oxidative stress in CHF.</description>
<content:encoded><![CDATA[

<p>
<b>Circulating white blood cells and platelets amplify oxidative stress in heart failure</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1364">doi:10.1038/ncpcardio1364</a>
</p>
<p>Authors: Alexander JJ IJsselmuiden, Ren&#233; JP Musters, Gijsbert de Ruiter, Loek van Heerebeek, Frans Alderse-Baas, Muriel van Schilfgaarde, Anja Leyte, Geert-Jan Tangelder, Gerrit J Laarman
&amp; Walter J Paulus</p>
]]></content:encoded>
<dc:title>Circulating white blood cells and platelets amplify oxidative stress in heart failure</dc:title>
<dc:creator>Alexander JJ IJsselmuiden</dc:creator>
<dc:creator>Ren&#233; JP Musters</dc:creator>
<dc:creator>Gijsbert de Ruiter</dc:creator>
<dc:creator>Loek van Heerebeek</dc:creator>
<dc:creator>Frans Alderse-Baas</dc:creator>
<dc:creator>Muriel van Schilfgaarde</dc:creator>
<dc:creator>Anja Leyte</dc:creator>
<dc:creator>Geert-Jan Tangelder</dc:creator>
<dc:creator>Gerrit J Laarman</dc:creator>
<dc:creator>Walter J Paulus</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1364</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-28</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-28</prism:publicationDate>
<prism:section>Clinical research</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
<item rdf:about="http://dx.doi.org/10.1038/ncpcardio1369">
<title>Retrospective study to identify predictors of the presence and rapid progression of aortic dilatation in patients with bicuspid aortic valves</title>
<link>http://dx.doi.org/10.1038/ncpcardio1369</link>
<description>Aortic dilatation is common among adults with bicuspid aortic valves (BAV). Predictors of risk and progression of aortic dilatation are not well described in this setting. In this retrospective analysis the authors study data on the presence of dilation in several aortic segments in 156 adult patients with BAV who had serial echocardiograms performed at least 1 year apart. Their data shows that patients with BAV and increased age, high body surface area, and moderate to severe aortic regurgitation are more likely to have a dilated aorta. Patients with right-to-left leaflet fusion are at increased risk of rapid aortic dilatation.</description>
<content:encoded><![CDATA[

<p>
<b>Retrospective study to identify predictors of the presence and rapid progression of aortic dilatation in patients with bicuspid aortic valves</b>
</p>
<p>Nature Clinical Practice Cardiovascular Medicine. <a href="http://dx.doi.org/10.1038/ncpcardio1369">doi:10.1038/ncpcardio1369</a>
</p>
<p>Authors: George Thanassoulis, James WL Yip, Kris Filion, Michal Jamorski, Gary Webb, Samuel C Siu
&amp; Judith Therrien</p>
]]></content:encoded>
<dc:title>Retrospective study to identify predictors of the presence and rapid progression of aortic dilatation in patients with bicuspid aortic valves</dc:title>
<dc:creator>George Thanassoulis</dc:creator>
<dc:creator>James WL Yip</dc:creator>
<dc:creator>Kris Filion</dc:creator>
<dc:creator>Michal Jamorski</dc:creator>
<dc:creator>Gary Webb</dc:creator>
<dc:creator>Samuel C Siu</dc:creator>
<dc:creator>Judith Therrien</dc:creator>
<dc:identifier>doi:10.1038/ncpcardio1369</dc:identifier>
<dc:source>Nature Clinical Practice Cardiovascular Medicine</dc:source>
<dc:date>2008-10-21</dc:date>
<prism:publicationName>Nature Clinical Practice Cardiovascular Medicine</prism:publicationName>
<prism:publicationDate>2008-10-21</prism:publicationDate>
<prism:section>Clinical research</prism:section>
<prism:startingPage/>
<prism:endingPage/>
</item>
</rdf:RDF>
