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        <title>Cardiovascular Pathology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Cardiovascular Pathology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cardiovascular+Pathology&t=Cardiovascular+Pathology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 09:32:32 +0100</lastBuildDate>
        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=5486661&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711001426%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Sat, 10 Dec 2011 02:43:35 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5486660&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711001414%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Sat, 10 Dec 2011 02:43:35 +0100</pubDate>
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        <item>
            <title>Looking forward for Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=5486652&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711001384%2Fabstract%3Frss%3Dyes</link>
            <description>I am honored to have been selected by the leadership of the Society for Cardiovascular Pathology to be the new Editor-in-Chief of Cardiovascular Pathology for a 5-year term beginning with this issue of the journal. I am enthusiastic about the opportunity to build on the pioneering effort of the founding editor, Dr. Stephen Factor, and the excellent work of Dr. Jagdish Butany and Dr. Avrum Gotlieb, who have served as Editors-in-Chief for the last 10 years. I am being joined in the stewardship of the journal by a reconstituted Editorial Board composed of a multidisciplinary group of experts and scholars in the areas of cardiovascular pathology, vascular and myocardial biology, and cardiovascular medicine and surgery. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Sat, 10 Dec 2011 02:43:35 +0100</pubDate>
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        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=5347184&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071100113X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Wed, 26 Oct 2011 08:34:15 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5347183&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711001128%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Wed, 26 Oct 2011 08:34:15 +0100</pubDate>
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            <title>In memoriam: Jack L. Titus, M.D., Ph.D., 1926–2011</title>
            <link>http://www.medworm.com/index.php?rid=5486659&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711001049%2Fabstract%3Frss%3Dyes</link>
            <description>Jack L. Titus, M.D., Ph.D., passed away in North Oaks, MN, after a long illness on June 15, 2011, at the age of 84 (). I will miss Jack as a friend and as a highly respected colleague and collaborator, who had a long and distinguished career. He was for me the ideal mentor at an extremely pivotal stage of my career, and we continued to be close, sharing many professional and other interests as my career continued to develop. He trained and collaborated with numerous other cardiovascular pathologists, many of whom themselves have made important contributions to the field. I and the many others he touched have lost an important leader in academic medicine and pathology, nationally and internationally, and a giant in the world of cardiovascular pathology. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=5196228&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000913%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5196227&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000901%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
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            <title>Autopsy demonstration of intramyocardial polymer gel emboli associated with a giant-cell reaction following cardiac catheterization: a case report</title>
            <link>http://www.medworm.com/index.php?rid=5486658&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000536%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Our case is the first to our knowledge to document intramyocardial vessel gel emboli following a cardiac catheterization with stenting. Although the microscopic finding of emboli within vessels does not seem to be the immediate cause of death in our case, it is highly possible that it contributed to the patient's demise. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Fri, 08 Jul 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=5020464&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000639%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5020463&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000627%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
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            <title>Regeneration, Remodeling and Repair: Mechanisms, Models and Therapies for Heart and Vascular Disease. Abstracts from the 12th Biennial Meeting of the International Society for Applied Cardiovascular Biology</title>
            <link>http://www.medworm.com/index.php?rid=5020461&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000317%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=4782365&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071100038X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Sat, 30 Apr 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4782364&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000378%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Sat, 30 Apr 2011 23:00:00 +0100</pubDate>
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            <title>New Editor-in-Chief: Dr. Maximilian Buja</title>
            <link>http://www.medworm.com/index.php?rid=4782351&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000275%2Fabstract%3Frss%3Dyes</link>
            <description>Dr. Buja is a highly accomplished and well-recognized clinician, investigator, educator and leader in the discipline of Cardiovascular Pathology, and Pathology more broadly. In his career spanning over 30 years, Dr. Buja has been engaged in academic medicine as a pathologist with subspecialty interest in cardiovascular diseases and has served in several academic leadership positions, including Dean of the University of Texas, Houston, Medical School and, subsequently, Executive Vice President for Academic Affairs at The University of Texas Health Science Center at Houston. In his current position as the Executive Director of the Houston Academy of Medicine-Texas Medical Center Library, Dr. Buja continues to serve as a Professor of Pathology and Laboratory Medicine and be active and engaged...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=4594256&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000056%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4594256</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4594255&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000044%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4594255</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
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            <title>Parasympathetic and substance P-immunoreactive nerve denervation in atrial fibrillation models</title>
            <link>http://www.medworm.com/index.php?rid=5486656&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000081%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Recent studies demonstrated that atrial fibrillation (AF) induced heterogeneous sympathetic hyperinnervation and baroreflex impartation, but the changes of vagal and afferent nerve are not clear.Methods: Six dogs underwent atrial pacing at 600 beats/min (AF group). All paced dogs developed sustained AF by 5 weeks of pacing. Tissues from six healthy dogs were used as controls. Immunohistochemistry staining of cardiac nerves was performed using anti-growth-associated protein 43 (anti-GAP43), anti-tyrosine hydroxylase, antiacetylcholine (anti-ACh), and anti-substance P (anti-SP) antibodies.Results: In AF group, the density of GAP43-positive in the right atrium (RA), atrial septum (AS), and left atrium (LA) was 5590.24±1417.51, 8083.22±1271.39, and 10854.56±1877.56 μm...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486656</comments>
            <pubDate>Fri, 25 Feb 2011 05:00:00 +0100</pubDate>
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            <title>Recommendations for processing cardiovascular surgical pathology specimens: a consensus statement from the Standards and Definitions Committee of the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=5486653&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000068%2Fabstract%3Frss%3Dyes</link>
            <description>This report is presented to aid pathologists, pathology assistants, and clinicians in maximizing the diagnostic utility of cardiovascular surgical pathology specimens for enhanced patient care. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486653</comments>
            <pubDate>Fri, 25 Feb 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Insight into pathologic abnormalities in congenital semilunar valve disease based on advances in understanding normal valve microstructure and extracellular matrix</title>
            <link>http://www.medworm.com/index.php?rid=5486657&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071100007X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Congenitally diseased valves are relatively frequent causes of significant morbidity and mortality. Pathology descriptions of such valves have primarily focused on gross structural features including the number of leaflets or commissures (bicuspid/bicommissural valve) and alterations in the contour, thickness, and consistency of the leaflets (dysplastic valve). Functional correlates of these pathologic alterations are valvar stenosis, insufficiency, or both. Further characterization of the microstructural abnormalities seen in these malformed valves may not only provide insight into the correlation of distinct pathologies with their respective pathogenesis and clinical sequelae but also prove pivotal in uncovering new avenues for therapeutic interventions and prevention regimens....</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486657</comments>
            <pubDate>Thu, 24 Feb 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>80001178</title>
            <link>http://www.medworm.com/index.php?rid=4465427&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000056%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465427</comments>
            <pubDate>Sat, 12 Feb 2011 15:47:36 +0100</pubDate>
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        <item>
            <title>80001177</title>
            <link>http://www.medworm.com/index.php?rid=4465426&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880711000044%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465426</comments>
            <pubDate>Sat, 12 Feb 2011 15:47:36 +0100</pubDate>
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        <item>
            <title>Reduced serum content and increased matrix stiffness promote the cardiac myofibroblast transition in 3D collagen matrices</title>
            <link>http://www.medworm.com/index.php?rid=5347171&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001602%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The results suggest that reduced serum and increased matrix stiffness promote the myofibroblast phenotype in the myocardium. This transition both enhances and is promoted by matrix stiffness, indicating the presence of positive feedback that may contribute to the pathogenesis of cardiac fibrosis. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347171</comments>
            <pubDate>Wed, 09 Feb 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Proteinase inhibitor 9 is reduced in human atherosclerotic lesion development</title>
            <link>http://www.medworm.com/index.php?rid=5486655&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001985%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Reduced proteinase inhibitor 9 expression in human vascular smooth muscle cells is associated with atherosclerotic disease progression and is inversely related to the extent of apoptosis within the intima. Reduced proteinase inhibitor 9 expression may contribute to increased smooth muscle cell susceptibility to granzyme-B-induced apoptosis within the plaque. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486655</comments>
            <pubDate>Tue, 08 Feb 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Mechanical function, glycolysis, and ultrastructure of perfused working mouse hearts following thoracic aortic constriction</title>
            <link>http://www.medworm.com/index.php?rid=5347173&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001997%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: The results are consistent with the view that myocyte damage, fibrosis, and suppressed glycolytic flux represent maladaptive structural and metabolic remodeling that contribute to the development of failure in high pressure load-induced LVH in the mouse. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347173</comments>
            <pubDate>Tue, 08 Feb 2011 05:00:00 +0100</pubDate>
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            <title>Giant cell aortitis: a difficult diagnosis assessing risk for the development of aneurysms and dissections</title>
            <link>http://www.medworm.com/index.php?rid=5020458&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001626%2Fabstract%3Frss%3Dyes</link>
            <description>We describe the main clinical features of the patients in conjunction with a review of the literature to identify any common clinical presentations that manifest in these patients. Giant cell aortitis in the absence of previously established GC arteritis is difficult to identify, and a careful analysis of the history and presentation along with appropriate investigations (e.g., erythrocyte sedimentation rate) may prompt the clinician to consider GC aortitis and suggest immunosuppressant therapy. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
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            <pubDate>Wed, 02 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Insulin-like growth factor-1 overexpression in cardiomyocytes diminishes ex vivo heart functional recovery after acute ischemia</title>
            <link>http://www.medworm.com/index.php?rid=5486654&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001936%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Chronic insulin-like growth factor-1 overexpression is associated with reduced functional recovery after acute ischemic insult. Collagen deposition is elevated in transgenic αMHC-IGF-1 Ea hearts, but there is no change in expression of the myocardial structural proteins desmin and laminin. These findings suggest that sustained cardiac elevation of insulin-like growth factor-1 may not be beneficial in the setting of an acute ischemic insult. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5486654</comments>
            <pubDate>Thu, 27 Jan 2011 05:00:00 +0100</pubDate>
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            <title>Incidental finding of cor triatriatum sinister in an adult post-myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=5196219&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001675%2Fabstract%3Frss%3Dyes</link>
            <description>We report a case of a 51-year-old man who was transferred from a community hospital to our institution in cardiogenic shock after thrombolytic therapy for myocardial infarction. At autopsy, a cor triatriatum sinister was found. This may have contributed to his poor outcome post infarction. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196219</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
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        <item>
            <title>Bicuspid aortic valve disease: the role of oxidative stress in Lrp5 bone formation</title>
            <link>http://www.medworm.com/index.php?rid=4782357&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001730%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The bicuspid aortic valve is a common congenital cardiac anomaly, having a prevalence of 0.9% to 1.37% in the general population and a male preponderance ratio of 2:1. The recognition of a bicuspid aortic valve is clinically relevant because of its association with aortic stenosis or regurgitation, aortic aneurysm or dissection, and infective endocarditis. Although some patients with a bicuspid aortic valve may go undetected without clinical complications for a lifetime, the vast majority will require intervention, most often surgery, at some point. In fact, the natural history of bicuspid aortic valve is that of valve calcification and progressive stenosis that typically occur at a faster rate than in tricuspid aortic valves. This pattern of presentation supports the hypothesis ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782357</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782357</guid>        </item>
        <item>
            <title>The aortic valve microenvironment and its role in calcific aortic valve disease</title>
            <link>http://www.medworm.com/index.php?rid=4782358&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001948%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In calcific aortic valve disease, fibrotic and calcific lesions form focally in the fibrosa layer of the valve leaflets. Layer-specific pathosusceptibility suggests that the fibrosa microenvironment is permissive to pathological development. The cellular microenvironment in the aortic valve is defined by a variety of biomechanical-, biochemical-, and extracellular-mediated factors, some of which are unique to the fibrosa. Growing evidence supports the role of these microenvironmental cues in the local regulation of side-specific valve cell phenotypes and focal pathological alterations, revealing new insights into the cellular and molecular processes that contribute to calcific aortic valve disease. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782358</comments>
            <pubDate>Fri, 21 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782358</guid>        </item>
        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=4295569&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001778%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295569</comments>
            <pubDate>Wed, 29 Dec 2010 23:15:16 +0100</pubDate>
            <guid isPermaLink="false">4295569</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4295568&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001766%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295568</comments>
            <pubDate>Wed, 29 Dec 2010 23:15:16 +0100</pubDate>
            <guid isPermaLink="false">4295568</guid>        </item>
        <item>
            <title>Cardiovascular Pathology: a new journal for an old need</title>
            <link>http://www.medworm.com/index.php?rid=4295551&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001729%2Fabstract%3Frss%3Dyes</link>
            <description>The advent of a new journal is always an exciting event for those people involved with its genesis: the editor, the editorial board, the publisher, and the sponsoring society, if any. On the other hand, for many people, the reaction is precisely that expressed to me by a prominent cardiovascular pathologist with some exasperation: “What do we need another journal for?” At first glance, this is a reasonable question. There are certainly many journals in the fields of experimental and human pathology, cardiology, cardiovascular surgery, and atherosclerosis that publish cardiovascular pathology articles. But with the growth of cardiovascular pathology as a recognized discipline, and with the growth and acceptance of the Society for Cardiovascular Pathology as a representative of that disc...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295551</comments>
            <pubDate>Wed, 29 Dec 2010 23:15:09 +0100</pubDate>
            <guid isPermaLink="false">4295551</guid>        </item>
        <item>
            <title>Cardiovascular pathology at the crossroads: the dilemma of cardiac pathologists</title>
            <link>http://www.medworm.com/index.php?rid=4295550&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001717%2Fabstract%3Frss%3Dyes</link>
            <description>What are cardiac pathologists? What role do they play? Do we need them? And if so, where do they fit in the academic structure? These are questions often asked nowadays.  In the past, a cardiac pathologist was interested in coronary artery disease, did research on atherosclerosis, or was an expert on congenital heart diseases. Today, the definition of a cardiac pathologist is much more complex. The reason for this is the changing role of the cardiac pathologist in a large medical center. On an average day, a modern cardiac pathologist might be found signing out diagnostic endomyocardial biopsies or biopsies on cardiac transplant recipients; reviewing gross and microscopic features of hearts from postoperative patients or from very complex congenital heart disease; participating in the broa...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295550</comments>
            <pubDate>Wed, 29 Dec 2010 23:15:08 +0100</pubDate>
            <guid isPermaLink="false">4295550</guid>        </item>
        <item>
            <title>The twentieth birthday of Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=4295549&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001705%2Fabstract%3Frss%3Dyes</link>
            <description>It is our pleasure to write this editorial on the occasion of the 20th birthday of the journal of the Society for Cardiovascular Pathology. As the journal reaches this milestone of 20 years we, your co-editors-in-chief, will simultaneously be approaching our own milestone of two full terms of stewardship of your journal. We thank the chair of the publications committee, Dr. Frederick Schoen, and the committee for having given us this opportunity. We also thank the founding editor, Dr. Stephen Factor, who put in a tremendous amount of work to bring the society's dream to life and to keep it going for the first, most difficult, 10 years. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295549</comments>
            <pubDate>Wed, 29 Dec 2010 23:15:08 +0100</pubDate>
            <guid isPermaLink="false">4295549</guid>        </item>
        <item>
            <title>Re: Inherited cardiomyopathies mimicking arrhythmogenic right ventricular cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=5347182&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001687%2Fabstract%3Frss%3Dyes</link>
            <description>We read with interest the case reports by Roberts et al. in the September issue of Cardiovascular Pathology . The authors describe two explant cases of cardiomyopathy that had morphologic features of arrhythmogenic right ventricular cardiomyopathy (ARVC), i.e., fibrofatty replacement of the ventricular walls. However, data from genetic testing, histologic evaluation, and family history led to diagnoses of hypertrophic cardiomyopathy (HC) and PRKAG2 cardiac syndrome, respectively, in these two patients. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347182</comments>
            <pubDate>Mon, 27 Dec 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347182</guid>        </item>
        <item>
            <title>Scopulariopsis brevicaulis infection of prosthetic valve resembling aspergilloma on histopathology</title>
            <link>http://www.medworm.com/index.php?rid=5347179&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001699%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Fungal prosthetic valve endocarditis is an infrequent but serious complication of valve replacement surgery. Approximately 75% of patients are affected with Candida species. Scopulariopsis species affecting prosthetic valve is rarely reported in the literature. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347179</comments>
            <pubDate>Mon, 27 Dec 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347179</guid>        </item>
        <item>
            <title>Differential proteoglycan and hyaluronan distribution in calcified aortic valves</title>
            <link>http://www.medworm.com/index.php?rid=5347172&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001614%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The three proteoglycans and hyaluronan demonstrated distinctive localization relative to nodules within calcified aortic valves, where they likely mediate lipid retention, cell proliferation, and extracellular matrix remodeling, and motivate further study. Comparisons between expression of these components in mature nodules and prenodules suggest distinct roles for these components in nodule progression, especially in the tissues surrounding the nodules. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347172</comments>
            <pubDate>Mon, 27 Dec 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347172</guid>        </item>
        <item>
            <title>Protective effect of grape seed proanthocyanidins against cholesterol cholic acid diet-induced hypercholesterolemia in rats</title>
            <link>http://www.medworm.com/index.php?rid=5347175&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001377%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Grape seed proanthocyanidins have cardioprotective effects against CC diet-induced hypercholesterolemia via their ability to reduce, directly or indirectly, free radicals in the myocardium. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347175</comments>
            <pubDate>Fri, 03 Dec 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347175</guid>        </item>
        <item>
            <title>Unusual autopsy finding in a case of metastatic teratocarcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5347180&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001390%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: An unusual autopsy finding was seen in a young case of metastatic teratocarcinoma of the right testis. The patient presented with features of myocardial ischemia and died of sudden cardiac arrest. At autopsy, the lungs were studded with variably sized metastatic nodules composed of glistening hyaline cartilage. Examination of the coronary arteries revealed complete occlusion of the left anterior descending and left circumflex artery lumina by tumor emboli composed of glistening white chondromyxoid material. Histopathology confirmed the presence of mature hyaline cartilage and chondromyxoid material in tumor emboli. The individual died due to severe coronary insufficiency and sudden cardiac arrest secondary to complete luminal occlusion of the left anterior descending and left cir...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347180</comments>
            <pubDate>Fri, 26 Nov 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347180</guid>        </item>
        <item>
            <title>A rare cardiac neoplasm: case report of cardiac epithelioid angiosarcoma</title>
            <link>http://www.medworm.com/index.php?rid=5196226&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001419%2Fabstract%3Frss%3Dyes</link>
            <description>We report a case of an epithelioid angiosarcoma that involved the right atrium and aorta of a 47-year-old male. The patient presented with atrial fibrillation and presyncopal spells. Following clinical evaluation, including computed tomography scan and trans-esophageal echocardiography, the neoplasm was surgically removed. It was a poorly differentiated malignant neoplasm composed of medium-sized epithelioid cells with a moderate amount of amphophilic cytoplasm. Immunohistochemical staining, including positive staining for CK22, AE1/AE3, melan-A, vimentin, and CD31, indicated the neoplasm was best categorized as an epithelioid angiosarcoma. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196226</comments>
            <pubDate>Wed, 17 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196226</guid>        </item>
        <item>
            <title>Post-myocardial infarction left ventricular myocyte remodeling: are there gender differences in rats?</title>
            <link>http://www.medworm.com/index.php?rid=5196225&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001420%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: This study demonstrates that post-myocardial infarction changes in LV function and myocyte remodeling are remarkably similar in young adult male and female rats. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196225</comments>
            <pubDate>Wed, 17 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196225</guid>        </item>
        <item>
            <title>The response to valve injury. A paradigm to understand the pathogenesis of heart valve disease</title>
            <link>http://www.medworm.com/index.php?rid=4782359&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001432%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Human heart valve diseases have become an important topic in cardiovascular pathology and medicine. These diseases have different etiologies and manifestations. However, the most common ones including calcific aortic stenosis have histopathological features that are best characterized as a “response to tissue injury” similar to ones seen in numerous tissues and organs. The valve interstitial cell is the prevalent cell type in the valve and is likely the master cell which ultimately regulates cell and molecular repair processes within the valve that involve autocrine and paracrine processes as well as interactions with the matrix components of the valve. This presentation explores the concept of “response to tissue injury” in understanding the pathogenesis of calcific aort...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782359</comments>
            <pubDate>Mon, 15 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782359</guid>        </item>
        <item>
            <title>Histiocytoid cardiomyopathy: does it exist in the fetal-age group?</title>
            <link>http://www.medworm.com/index.php?rid=5347181&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001444%2Fabstract%3Frss%3Dyes</link>
            <description>A 20-week-old female fetus was identified to have Down's syndrome by amniocentesis in a 37-year-old primigravida. Fluorescent in situ hybridization analysis result for trisomy 21 was positive. Fetal echocardiography was done antenatally which was unremarkable. Elective abortion was carried out and the fetus was sent for autopsy and histopathology examination. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347181</comments>
            <pubDate>Tue, 09 Nov 2010 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347181</guid>        </item>
        <item>
            <title>Primary valvular lipomatous hamartoma: a case report and a collective review of the literature</title>
            <link>http://www.medworm.com/index.php?rid=5347178&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001407%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cardiac valvular tumors are very infrequent lesions constituting about 10% of the primary cardiac neoplasms. Among the valvular tumors, lipomatous hamartoma represents a very rare and distinct pathological entity. Retrieval of the literature reveals only eight reported cases, and there is lack of information regarding their clinical features. Herein, we describe a patient with a mass on the tricuspid valve detected incidentally and diagnosed to be a “lipomatous hamartoma.” To obtain a better understanding of the nature of these unusual lesions, we reviewed the literature and presented their clinicoanatomical characteristics together with diagnostic and therapeutic approaches. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347178</comments>
            <pubDate>Mon, 01 Nov 2010 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347178</guid>        </item>
        <item>
            <title>Isolated thoracic aortitis: clinicopathological and immunohistochemical study of 11 cases</title>
            <link>http://www.medworm.com/index.php?rid=5347174&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001389%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Isolated thoracic aortitis (ITA) is diagnosed in a variable proportion of patients operated on for dilation/aneurysm of ascending aorta. The etiopathogenesis of ITA remains unclear.We studied 11 cases of ITA in order to determine the role of IgG4-mediated immune responses in its pathogenesis.The series included nine women and two men aged 52–79 years. All patients developed aortic incompetence due to dilation/aneurysm of ascending aorta. None of the patients had a history of IgG4-related disease neither did they develop features of such disease during the follow-up period. The microscopic findings included the presence of lymphoplasmacellular fibrosing infiltrate of varied intensity involving the adventitia and media of aorta. This inflammation was associated with severe medial...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347174</comments>
            <pubDate>Mon, 01 Nov 2010 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347174</guid>        </item>
        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=4160039&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001481%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160039</comments>
            <pubDate>Mon, 01 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160039</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4160038&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071000147X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160038</comments>
            <pubDate>Mon, 01 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160038</guid>        </item>
        <item>
            <title>Endomyocardial nodular calcification as a cause of heart failure</title>
            <link>http://www.medworm.com/index.php?rid=5196224&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001201%2Fabstract%3Frss%3Dyes</link>
            <description>We present an intriguing case of massive myocardial calcification of the left ventricle in a young patient with restrictive cardiomyopathy and progressive heart failure who required transplantation. The patient's history and clinical presentation did not reveal the etiology of the myocardial calcification. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196224</comments>
            <pubDate>Wed, 20 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196224</guid>        </item>
        <item>
            <title>Overexpression of scavenger receptor LOX-1 in endothelial cells promotes atherogenesis in the ApoE−/− mouse model</title>
            <link>http://www.medworm.com/index.php?rid=5347176&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001365%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: These results demonstrate that up-regulation of LOX-1 promotes atherogenesis, highlighting LOX-1 function as a target for intervention. In addition, this study further demonstrated the inhibitory function of LOXIN. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347176</comments>
            <pubDate>Wed, 13 Oct 2010 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347176</guid>        </item>
        <item>
            <title>Endomyocardial biopsy—when and how?</title>
            <link>http://www.medworm.com/index.php?rid=5196214&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001225%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Endomyocardial biopsy is a commonly performed useful procedure utilized for the evaluation of cardiac tissue. Biopsy may be used to monitor transplant rejection, but it has many other applications including the evaluation of myocarditis, cardiomyopathy, chest pain, arrhythmia, and secondary involvement by systemic diseases. Drug toxicity may be evaluated and neoplasms may be biopsied. Recent developments include advances in myocardial and viral molecular biology and advances in image or electrophysiology guided biopsy. The utility of endomyocardial biopsy is reviewed with consideration of these advances. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196214</comments>
            <pubDate>Sun, 10 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196214</guid>        </item>
        <item>
            <title>Cardiac fibroma in adults</title>
            <link>http://www.medworm.com/index.php?rid=5020462&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001341%2Fabstract%3Frss%3Dyes</link>
            <description>We present the case of a 61-year-old woman with nonspecific symptoms who on investigation and treatment had a fibroma of the right ventricular free wall. She underwent surgical resection of the mass and is doing well. The literature pertaining to cardiac fibromas in adults is reviewed and discussed. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020462</comments>
            <pubDate>Sun, 10 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020462</guid>        </item>
        <item>
            <title>Extremely rare case of primary cardiac chondroma in a patient presenting with acute pulmonary edema</title>
            <link>http://www.medworm.com/index.php?rid=5347177&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001353%2Fabstract%3Frss%3Dyes</link>
            <description>We describe the case of a patient presenting with acute pulmonary edema with the incidental echocardiographic finding of a large left atrial tumor that was histopathologically diagnosed as primary cardiac chondroma. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5347177</comments>
            <pubDate>Mon, 04 Oct 2010 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5347177</guid>        </item>
        <item>
            <title>Expression of allograft inflammatory factor-1 (AIF-1) in acute cellular rejection of cardiac allografts</title>
            <link>http://www.medworm.com/index.php?rid=5196223&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001195%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: AIF-1 was expressed in both CMCs and MNCs in hearts with various adverse conditions including but not limited to heart transplantation. In cardiac transplantation, AIF-1 was associated with the severity of cardiac allograft rejection and Quilty B lesions, which could predict subsequent increases in rejection grade. Thus, AIF-1 shows promise that it can be a potential biomarker for cardiac allograft rejection. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196223</comments>
            <pubDate>Sun, 19 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196223</guid>        </item>
        <item>
            <title>Sex differences play a role in cardiac endoplasmic reticulum stress (ERS) and ERS-initiated apoptosis induced by pressure overload and thapsigargin</title>
            <link>http://www.medworm.com/index.php?rid=5196213&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071000116X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Excessive endoplasmic reticulum stress (ERS) triggers myocardial apoptosis. Sex differences appear to be an important determinant in the occurrence of stress and apoptosis through many pathways, but the roles of sex differences in the cardiac ERS and ERS-initiated apoptosis are largely unknown. In the present study, we investigated the in vivo role of sex differences in the cardiac ERS and apoptosis elicited by ascending aortic banding surgery or thapsigargin (Thap) injection using male and female C57BL/6 JAX mice. The surgery significantly increased the expression levels of cardiac glucose-regulated protein (GRP)78 and CCAAT/enhancer binding protein homology protein (CHOP) protein, increased the myocardial apoptosis and decreased the sarcoplasmic reticulum Ca2+-ATPase isoform (S...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196213</comments>
            <pubDate>Sun, 19 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196213</guid>        </item>
        <item>
            <title>Left ventricular mesenchymal hamartoma, a new hamartoma of the heart</title>
            <link>http://www.medworm.com/index.php?rid=5196217&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001171%2Fabstract%3Frss%3Dyes</link>
            <description>We report a 22-year-old female with a primary left ventricle tumor composed of multiple mature mesenchymal tissues, including mature cardiac myocytes, smooth muscle, fibroblasts, fat, blood vessels including a hemangioma like area, and nerve fibers. The various elements were disorganized, but well differentiated, and showed little mitotic activity, which are features suggestive of a hamartoma. Unlike a cardiac fibroma, which may entrap myocardium at the periphery of the lesion, the present case demonstrated all tissue elements throughout the tumor mass. We suggest that this lesion is sufficiently different from those hamartomas previously described to warrant a new designation, for which we propose the title cardiac mesenchymal hamartoma. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196217</comments>
            <pubDate>Thu, 16 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196217</guid>        </item>
        <item>
            <title>Sudden infant and perinatal unexplained death: are we moving forward yet?</title>
            <link>http://www.medworm.com/index.php?rid=5196216&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001183%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Autonomic nervous system and cardiac conducting system dysfunctions have been proposed to be implied in the pathogenesis of sudden infant death syndrome (SIDS). However, most clinicians and even pathologists lack experience with detailed examination of the brainstem and cardiac conducting system and may not recognize lesions within those systems that potentially could be crucial factors in the sudden unexpected perinatal and infant death. Recent anatomical, pathological, and bacteriological studies in SIDS confirm that the multidisciplinary approach provides the best approach to the challenging problems of SIDS and sudden unexplained perinatal death. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196216</comments>
            <pubDate>Thu, 16 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196216</guid>        </item>
        <item>
            <title>Current status of the role of stem cells in myocardial biology and repair</title>
            <link>http://www.medworm.com/index.php?rid=5196215&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001213%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The purpose of this article is to present an analysis of current knowledge and understanding of the role of stem cells in myocardial biology and myocardial repair following injury. This rapidly evolving field has assumed relevance for the understanding, diagnosis, and treatment of heart failure. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196215</comments>
            <pubDate>Wed, 15 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196215</guid>        </item>
        <item>
            <title>Adiponectin gene expression and adipocyte diameter: a comparison between epicardial and subcutaneous adipose tissue in men</title>
            <link>http://www.medworm.com/index.php?rid=5196220&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001158%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Adipocytes in epicardial fat are smaller than those in peritoneal and subcutaneous fat. Adipocyte size, both in epicardial and in subcutaneous fat, is positively related with insulin resistance, shows negative association with local adiponectin gene expression, and is decreased in subjects with coronary artery disease.Adiponectin gene expression is significantly lower in epicardial- than in subcutaneous fat. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196220</comments>
            <pubDate>Wed, 08 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196220</guid>        </item>
        <item>
            <title>Survey of current practice related to grading of rejection in cardiac transplant recipients in North America</title>
            <link>http://www.medworm.com/index.php?rid=5196210&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001134%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: There is appreciable variability in the system(s) used for reporting rejection among North American cardiac transplant centers. Understanding the reasons behind this variability will be crucial for the optimization of future grading systems for cardiac allograft rejection. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196210</comments>
            <pubDate>Mon, 06 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196210</guid>        </item>
        <item>
            <title>Infective endocarditis of the Dacron patch—a report of 13 cases at autopsy</title>
            <link>http://www.medworm.com/index.php?rid=5196222&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001110%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Correction of simple or complex congenital cardiac defects offers new substrates for organisms to colonize resulting in infective endocarditis, which are often difficult to treat. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196222</comments>
            <pubDate>Thu, 02 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196222</guid>        </item>
        <item>
            <title>Extracellular matrix remodeling and cell phenotypic changes in dysplastic and hemodynamically altered semilunar human cardiac valves</title>
            <link>http://www.medworm.com/index.php?rid=5196221&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001146%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Introduction: Congenital cardiac valve disease is common, affecting ∼1% of the population, with substantial morbidity and mortality, but suboptimal treatment options. Characterization of the specific matrix and valve cell phenotypic abnormalities in these valves could lend insight into disease pathogenesis and potentially pave the way for novel therapies.Methods: Thirty-five human aortic and pulmonic valves were categorized based on gross and microscopic assessment into control valves (n=21); dysplastic valves, all except one also displaying hemodynamic changes (HEMO/DYSP, n=6); and hemodynamically altered valves (HEMO, n=8). Immunohistochemistry was performed on valve sections and flow cytometry on valvular interstitial cells.Results: While both hemodynamically altered aortic ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196221</comments>
            <pubDate>Thu, 02 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196221</guid>        </item>
        <item>
            <title>Sudden death due to myocardial metastasis of lingual squamous cell carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5020456&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001122%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cardiac metastases are rare events encountered in pathological practice but with often dramatic fatal outcome. Among malignancies associated with cardiac involvement, we would like to draw the attention of clinicians about lingual squamous cell carcinoma by reporting a sudden cardiac death in a 57-year-old woman without prior symptom and considered in remission 1 month before her death. The forensic autopsy led to the diagnosis emphasizing its role in epidemiology and public health. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020456</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020456</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3947877&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001274%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947877</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947877</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3947876&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001262%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947876</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947876</guid>        </item>
        <item>
            <title>Targeted intracellular catalase delivery protects neonatal rat myocytes from hypoxia-reoxygenation and ischemia-reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=5196212&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001092%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: (1) Catalase-SKL increased myocyte extracellular catalase content and activity and dramatically increased resistance to hydrogen peroxide-induced oxidation; (2) catalase-SKL protects against both hypoxia–reoxygenation and ischemia reperfusion; (3) catalase-SKL may represent a new therapeutic approach to protect hearts against myocardial hypoxia–reoxygenation or ischemia reperfusion. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196212</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196212</guid>        </item>
        <item>
            <title>Immunohistochemical properties in the patients with Buerger's disease—possible role of plasminogen activator inhibitor-1 for preservation of vessel wall architecture</title>
            <link>http://www.medworm.com/index.php?rid=5196211&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001109%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: In Buerger's disease, PAI-1 was strongly expressed around the internal elastic lamina, while both uPA and MMP-3 were slightly recognized on vessel walls. These findings could be one of the reasons the general architecture of vessel walls in Buerger's disease is preserved. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196211</comments>
            <pubDate>Thu, 12 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196211</guid>        </item>
        <item>
            <title>Screening for sudden death in the athlete</title>
            <link>http://www.medworm.com/index.php?rid=4160021&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001079%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Sudden death in the athlete is a rare occurrence, yet there is evidence that screening may reduce this tragedy. Pre-participation screening programs differ between the United States and Italy. The causes of sudden death in this young, athletic population are reviewed, as are each program's merits and pitfalls. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160021</comments>
            <pubDate>Thu, 12 Aug 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160021</guid>        </item>
        <item>
            <title>Sudden cardiac death secondary to demonstrated reperfusion ventricular fibrillation in a woman with Takotsubo cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=5020459&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000785%2Fabstract%3Frss%3Dyes</link>
            <description>We present the case of a 52-year-old woman who presented with angina diagnosed with Takotsubo cardiomyopathy on the basis of both noninvasive (electrocardiography, echocardiography) and invasive (angiography) exams. At discharge, a Holter monitor was fitted to the patient. During the recording the patient faced sudden cardiac death. The analysis of the Holter traces allowed some speculations on the mechanism of this unexpected arrhythmic death. The cause of the fatal ventricular fibrillation appears to be the fast reperfusion following a short occlusion of an epicardial coronary artery. This case highlights the epicardial vasospasm as an important pathogenic mechanism of the syndrome and the possible usefulness of diagnostic tests able to elicit the spasm susceptibility and guide a more ta...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020459</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020459</guid>        </item>
        <item>
            <title>Transcriptional regulation of heart valve development and disease</title>
            <link>http://www.medworm.com/index.php?rid=4782356&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710001080%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Aortic valve disease is estimated to affect 2% of the United States population. There is increasing evidence that aortic valve disease has a basis in development, as congenital valve malformations are prevalent in patients undergoing valve replacement surgery. In fact, a number of genetic mutations have been linked to valve malformations and disease. In the initial stages of aortic valve pathogenesis, the valvular interstitial cells become activated, undergo cell proliferation, and participate in extracellular matrix remodeling. Many of these cell properties are shared with mesenchymal progenitor cells of the normally developing valves and bones. Historically, valve calcification was thought to be a passive process reflecting end-stage disease. However, recent evidence describes ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782356</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782356</guid>        </item>
        <item>
            <title>Primary cardiac undifferentiated sarcoma: role of intraoperative imprint cytology and frozen section of two cases</title>
            <link>http://www.medworm.com/index.php?rid=5020454&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000992%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Primary cardiac tumors are very rare, and a vast majority of such malignant tumors are sarcomas. Associated symptoms are usually vague and nonspecific resulting in a late diagnosis and poorer prognosis. Most cardiac sarcomas have been reported in autopsy series. Although echocardiography may help make a diagnosis of a cardiac sarcoma, histopathological confirmation is quintessential. Presented here are two cases of patients who underwent successful surgery for the removal of a cardiac tumor, along with echocardiographic, cytological, and histopathological findings as well as a compact literature review. In both patients, the masses were on the surface of the mitral valve, and intraoperative evaluation of frozen sections and imprint cytology were indicative of a “probably malign...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020454</comments>
            <pubDate>Thu, 29 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020454</guid>        </item>
        <item>
            <title>Timing of bone marrow cell therapy is more important than repeated injections after myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=5020451&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000980%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Bone marrow cell treatment has been proposed as a therapy for myocardial infarction, but the optimal timing and number of injections remain unknown.Methods: Myocardial infarction was induced in mice followed by ultrasound-guided injection of mouse bone marrow cells at different time points post myocardial infarction (Days 3, 7, and 14) as monotherapy and at Days 3+7 as “double” therapy and at Days 3+7+14 as “triple” therapy. Controls received saline injections at Day 3 and Days 3+7+14. Left ventricular ejection fraction was evaluated post myocardial infarction prior to any therapy and at Day 28. Hearts were analyzed at Day 28 for infarct size and survival of donor cells.Results: Left ventricular ejection fraction decreased from 55.3±0.9% to 37.6±0.6% (P (Sou...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020451</comments>
            <pubDate>Thu, 29 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020451</guid>        </item>
        <item>
            <title>Clear cells in the atrioventricular valves of infants with severe human mucopolysaccharidosis (Hurler syndrome) are activated valvular interstitial cells</title>
            <link>http://www.medworm.com/index.php?rid=5196218&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000761%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Severe mucopolysaccharidosis type I (Hurler syndrome) is an autosomal recessive lysosomal storage disease of childhood that results in accumulation of glycosaminoglycans within cardiac valves and consequent valve dysfunction. Valve thickening in mucopolysaccharidosis type I (Hurler syndrome) is due, in part, to the presence of glycosaminoglycan-laden cells (the so-called “clear” or “Hurler” cells) within the valve that remain largely unstudied with respect to identity, origin, and function. We hypothesized that the “clear” or “Hurler” cells within the atrioventricular valves from individuals with untreated mucopolysaccharidosis type I are activated valvular interstitial cells.Methods: We performed routine and immunohistochemical staining on atrioventri...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196218</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196218</guid>        </item>
        <item>
            <title>Pathology of explanted polytetrafluoroethylene vascular grafts</title>
            <link>http://www.medworm.com/index.php?rid=5020452&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000773%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Interstitial calcification is frequently found within explanted polytetrafluoroethylene grafts and is associated with graft disruption. These findings suggest that calcification of polytetrafluoroethylene biomaterials may play a role in eventual graft failure. A better understanding of the process of polytetrafluoroethylene graft calcification may lead to novel therapies that aid in the prevention of polytetrafluoroethylene vascular graft failure. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020452</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020452</guid>        </item>
        <item>
            <title>Dr. Groven M. Hutchins</title>
            <link>http://www.medworm.com/index.php?rid=4295560&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071000075X%2Fabstract%3Frss%3Dyes</link>
            <description>Dr. Grover M. Hutchins died on April 27, 2010, following an accident while traveling abroad with his wife Loretta Hutchins. He was 77. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295560</comments>
            <pubDate>Fri, 09 Jul 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295560</guid>        </item>
        <item>
            <title>Sudden coronary death in children</title>
            <link>http://www.medworm.com/index.php?rid=4160020&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000736%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Coronary disease is an uncommon cause of severe morbidity and death in the young. The great majority of lesions are congenital, and anomalous origins and courses of the coronary arteries are the most common groups of diseases in the age group. Intimal proliferation and coronary arteritis are even less common causes of death in this age population. For this review, we retrospectively studied cases of coronary cardiac death in children and adolescents, from 2004 to 2007, from a statewide medical examiner's office. There were 197 natural deaths in children ages ≤16 years and 58 deaths from sudden infant death syndrome. Of these, the largest group of deaths showed no morphologic abnormalities and was attributed to arrhythmias. The next largest group of deaths comprised complex cong...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160020</comments>
            <pubDate>Fri, 09 Jul 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160020</guid>        </item>
        <item>
            <title>What a pity the master cannot admire his pupil's work: the autopsy of the anatomist Antonio Cocchi (1695–1758) performed by his pupil Saverio Manetti</title>
            <link>http://www.medworm.com/index.php?rid=5020455&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000712%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antonio Cocchi (1695–1758) was a physician, sanitary administrator, and Professor of Anatomy at the University of Florence. Wide-ranging in his interests, he was also a philologist, botanist, and a cultured traveler through 18th-century Europe.After Cocchi died, his pupil Saverio Manetti (1723–1785) reported in a private letter on the state of health of his renowned master the circumstances of his death and the autopsy findings. In an endeavour to determine the cause of death, Manetti accurately described the symptoms and clinical signs preceding the exitus of Antonio Cocchi and related them to the autopsy results. Interestingly, his lifestyle habits, past medical history, and family diseases were all considered when making the diagnosis. This handling of the matter clearly p...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020455</comments>
            <pubDate>Thu, 08 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020455</guid>        </item>
        <item>
            <title>iNOS induction and PARP-1 activation in human atherosclerotic lesions: an immunohistochemical and ultrastructural approach</title>
            <link>http://www.medworm.com/index.php?rid=5020450&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000748%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Our data imply the possibility of a significant role for cross-talk between inducible nitric oxide synthase and poly(ADP-ribose) polymerase-1 in human atherosclerotic lesions. We conclude that the prooxidant milieu of the plaque might exert damaging effects on mitochondria via a poly(ADP-ribose) polymerase-1-mediated mechanism since the absence of the enzyme results in a corresponding lack of changes in mitochondrial morphology. The present report may open avenues for further researches that could have important therapeutic consequences for the treatment of atherosclerosis and its clinical sequelae. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020450</comments>
            <pubDate>Thu, 08 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020450</guid>        </item>
        <item>
            <title>Idiopathic massive myocardial calcification: a case report and review of the literature</title>
            <link>http://www.medworm.com/index.php?rid=4465425&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000633%2Fabstract%3Frss%3Dyes</link>
            <description>We report a rare case of massive myocardial calcification in a 42-year-old male who presented with symptoms of congestive heart failure and arrhythmia. Myocardial calcification is most commonly associated with myocardial infarction or, less commonly, hypercalcemia. This case is particularly unusual due to the lack of any known predisposing risk factors, including normal coronary arteries, normal renal function, and normal serum calcium levels. Alternative etiologies are discussed accompanied by a review of the literature. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465425</comments>
            <pubDate>Mon, 05 Jul 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465425</guid>        </item>
        <item>
            <title>Perivascular mantle cell lymphoma affecting a temporal artery—a highly unusual cause of temporal headache</title>
            <link>http://www.medworm.com/index.php?rid=5020457&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000724%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: This report describes a highly unusual histological and clinical scenario of peri-temporal artery Mantle cell lymphoma causing temporal headache from peripheral nerve and artery side branch involvement by the lymphoma immediately adjacent to the temporal artery. We propose that involvement of a temporal artery by lymphoma be considered in the differential diagnosis, in patients with an established diagnosis of lymphoma, if presenting with “temporal arteritis” type headache symptoms. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020457</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020457</guid>        </item>
        <item>
            <title>Early obstruction of decellularized xenogenic valves in pediatric patients: involvement of inflammatory and fibroproliferative processes</title>
            <link>http://www.medworm.com/index.php?rid=5020453&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000670%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Early obstruction of decellularized Matrix P plus valve is associated with massive inflammatory reaction and exaggerated fibrotic scaring around porcine conduit wall. Detailed studies will be necessary to determine factors that contribute to remnant immunogenicity of decellularized grafts. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020453</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5020453</guid>        </item>
        <item>
            <title>Why the diameter of sinusoidal fenestrae unlikely matters for lipoprotein metabolism and atherosclerosis susceptibility</title>
            <link>http://www.medworm.com/index.php?rid=4782361&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000700%2Fabstract%3Frss%3Dyes</link>
            <description>In their Letter to the Editor, Le Couteur et al. provide a series of interesting comments on our manuscript entitled “The diameter of liver sinusoidal fenestrae is not a major determinant of lipoprotein levels and atherosclerosis in cholesterol-fed rabbits” . We thank them for their ad hoc analysis. Here, we provide a detailed response to their specific comments. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782361</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782361</guid>        </item>
        <item>
            <title>Fenestrations and lipoproteins</title>
            <link>http://www.medworm.com/index.php?rid=4782360&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000682%2Fabstract%3Frss%3Dyes</link>
            <description>In their recent article, Jacobs et al. 
 have provided an elegant set of experiments from which they conclude that fenestration diameter does not influence circulating lipoprotein concentrations and, hence, is unlikely to influence atherosclerosis. Fenestrations are pores in the liver sinusoidal endothelial cell with a diameter 50 to 200 nm. Fraser et al. 
 and Wisse et al 
 postulated that some lipoproteins traverse the fenestrations and, hence, that the diameter of fenestrations impacts on the concentration of circulating lipoproteins. In particular, it was hypothesized that because the average diameter of fenestrations is about 100 nm, their major influence will be on the blood levels of chylomicron remnants (diameter, 50–150 nm) and, hence, postprandial hypertriglyceridemia 
. It sho...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782360</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782360</guid>        </item>
        <item>
            <title>Introduction to congenital heart disease articles in Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=3947860&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000694%2Fabstract%3Frss%3Dyes</link>
            <description>Congenital heart disease is common and causes substantial consequences for patients, their families, their communities and the health care system. Congenital heart defects occur in nearly 1% of live births and comprise at least 18 distinct types (most commonly ventricular septal defect, tetralogy of Fallot, transposition of the great arteries, and atrioventricular septal defect). They range in severity from minute holes between chambers, which may resolve spontaneously, to major malformations that can require multiple surgical procedures (frequently in the first years of life) and may result in death in infancy, childhood, or as a young adult. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947860</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947860</guid>        </item>
        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=3734769&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000827%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734769</comments>
            <pubDate>Wed, 30 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734769</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3734768&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000815%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734768</comments>
            <pubDate>Wed, 30 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734768</guid>        </item>
        <item>
            <title>Smooth muscle cells in porcine vein graft intimal hyperplasia are derived from the local vessel wall</title>
            <link>http://www.medworm.com/index.php?rid=4782363&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000621%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The majority of neointimal SMC in the IH seen after interposition vein grafting derive from the engrafted local vessel wall. These are the first results from a clinically relevant large animal model that confirm data from rodent models. They have implications for the utility of therapeutic stem cells in this type of intimal hyperplasia. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782363</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782363</guid>        </item>
        <item>
            <title>Single measurement of troponin T for early prediction of infarct size, congestive heart failure, and pulmonary hypertension in an animal model of myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=4782362&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000645%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Early prediction of infarct size and of the subsequent development of congestive heart failure (CHF) and pulmonary hypertension (PH) would be useful in therapeutic trials using the rat myocardial infarction (MI) model.Methods: A total of 194 rats were subjected to MI or sham surgery, and plasma cardiac troponin T (cTnT) was measured 24 h after surgery in rats. Echocardiography was performed after 2 and 5 weeks. Hemodynamic and morphometric parameters were evaluated 5 weeks after MI.Results: cTnT had strong positive correlations with left ventricular (LV) wall motion abnormalities at 2 and 5 weeks (R=.85 and .89; P (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782362</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782362</guid>        </item>
        <item>
            <title>Association between AT C573T polymorphism and cardiovascular risk factors in myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=4782355&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000499%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: There is a relationship between the C573T polymorphism and the pathogenesis of myocardial infarction that seems to be due to its relationship with some risk factors. However, given the multifactorial nature of this pathology, further studies are needed to confirm the evidence that we report herein. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782355</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782355</guid>        </item>
        <item>
            <title>Phenotypic modulation and turnover of bone marrow-derived cells after myocardial infarction in rats</title>
            <link>http://www.medworm.com/index.php?rid=4782354&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000487%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: These results suggest that BMCs recruited to the heart underwent phenotypic modulation to a fibroblastic cell type and turnover within 2 weeks after MI without differentiating into cardiomyocytes or endothelial cells, and that although the number of BMCs in the infarcted myocardium decreased over time, the rate of turnover remained relatively constant during the chronic phase of MI. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782354</comments>
            <pubDate>Mon, 31 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782354</guid>        </item>
        <item>
            <title>Anatomical and pathophysiological classification of congenital heart disease</title>
            <link>http://www.medworm.com/index.php?rid=3947861&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000359%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Congenital heart diseases (CHD) consist of defects of the cardiac architecture which interfere with the venous drainage, septation of the cardiac segments and their sequences and regular function of the valve apparatuses. In the normal heart the segments are disposed in such a way to allow deoxygenated venous blood to go to the lungs through the pulmonary artery and the oxygenated venous blood to go to the systemic organs through the aorta without mixing. Small and great circulations are in sequence, with no communication to each other. Establishing the sequence of cardiac segments is the prerequisite for planning a surgical repair. We propose a pathyphysiological classification of CHD based upon the clinical consequence of structural defects on the physiology of blood circulatio...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947861</comments>
            <pubDate>Wed, 12 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947861</guid>        </item>
        <item>
            <title>Table of Contents</title>
            <link>http://www.medworm.com/index.php?rid=3550139&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000530%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550139</comments>
            <pubDate>Fri, 30 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550139</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3550138&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000529%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550138</comments>
            <pubDate>Fri, 30 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550138</guid>        </item>
        <item>
            <title>Opposing roles of PARP-1 in MMP-9 and TIMP-2 expression and mast cell degranulation in dyslipidemic dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=4465423&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000426%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The present study demonstrates that PARP-1 gene deletion exerts protective effects against HF diet-induced dilated cardiomyopathy by maintaining increased expression of TIMP-2. With additional protective effects against cell death and inflammation, PARP-1 deficiency preserves cardiac tissue homeostasis. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465423</comments>
            <pubDate>Fri, 30 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465423</guid>        </item>
        <item>
            <title>Does inducible NOS have a protective role against hypoxia/reoxygenation injury in rat heart?</title>
            <link>http://www.medworm.com/index.php?rid=4295563&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000189%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The inhibition of iNOS raises the peroxidative and apoptotic level in the hypoxic heart indicating that this isoform may have a protective effect on this organ against hypoxia/reoxygenation injuries, and challenging the conventional wisdom that iNOS is deleterious under these conditions. These findings could help in the design of new treatments based on NO pharmacology against hypoxia/reoxygenation dysfunctions. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295563</comments>
            <pubDate>Mon, 26 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295563</guid>        </item>
        <item>
            <title>Sudden death due to isolated right ventricular infarction: a case report</title>
            <link>http://www.medworm.com/index.php?rid=4295558&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000463%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: On the basis of morphologic and microscopic data, the cause of death was determined to be an isolated RVI. The autopsy findings of both right and left ventricular hypertrophy associated with a nondominant right coronary artery thrombosis were observed. In cases like this, the authors would like to underline the importance of a complete postmortem examination and a full pathological approach. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295558</comments>
            <pubDate>Mon, 26 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295558</guid>        </item>
        <item>
            <title>Survey of North American pathologist practices regarding antibody-mediated rejection in cardiac transplant biopsies</title>
            <link>http://www.medworm.com/index.php?rid=4782352&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000451%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: We found wide variation in pathologists' practices regarding hAMR diagnosis. A consensus document regarding hAMR is needed to better align our collective protocols, understand this disease process and to optimize patient care. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782352</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782352</guid>        </item>
        <item>
            <title>Alan George Rose: 1940–2009: in memoriam</title>
            <link>http://www.medworm.com/index.php?rid=3734757&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071000044X%2Fabstract%3Frss%3Dyes</link>
            <description>Professor Alan Rose was a graduate of the University of Cape Town, qualifying first as a medical doctor and then, in 1968, as an anatomical pathologist. At that time, he was a pathologist involved with cardiac research in association with the Barnard brothers. This research culminated in the world's first heart transplant, and Alan Rose ultimately conducted the autopsy on the recipient. So a famous and productive career in cardiovascular pathology was launched. His interest and contributions to the field of cardiovascular pathology grew exponentially and in a short time he was recognized as a pioneer, innovator, and major player in this area. His international reputation burgeoned, and he was invited to speak at several meetings overseas. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734757</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734757</guid>        </item>
        <item>
            <title>Cardiovascular pathology: maturation of a discipline and the Society for Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=3734746&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000438%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: This communication briefly summarizes the maturation of Cardiovascular Pathology, both as a subspecialty of Pathology and as an academic discipline, and the founding and contributions of the Society for Cardiovascular Pathology. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734746</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734746</guid>        </item>
        <item>
            <title>Quo Vadis? The Society for Cardiovascular Pathology over the next 25 years and beyond</title>
            <link>http://www.medworm.com/index.php?rid=3734745&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000475%2Fabstract%3Frss%3Dyes</link>
            <description>Those engaged in medicine, pathology, and biomedical science have experienced major developments, advances, opportunities, and challenges in a milieu of ever increasing pace of change in these fields commencing with the second half of the 20th century and continuing into the start of the current millennium. It was during this period of exciting and rapid technologic, diagnostic and therapeutic progress that the Society for Cardiovascular Pathology (SCVP) was founded 25 years ago. This signal event consolidated the maturation, significance and importance of the scientific discipline and clinical subspecialty of cardiovascular pathology. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734745</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734745</guid>        </item>
        <item>
            <title>Calcification after myocardial infarction is independent of amniotic fluid stem cell injection</title>
            <link>http://www.medworm.com/index.php?rid=4465424&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000360%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Ischemic heart disease remains one of the most common causes of mortality in developed countries. Recently, stem cell therapy is being considered for treating ischemic heart diseases. On the other hand, there has been evidence of chondro-osteogenic mass formation after stem cell injection in the heart. In a recent publication, Chiavegato et al. (J Mol Cell Cardiol. 42 (2007) 746–759) has suggested that amniotic fluid-derived stem (AFS) cells cause chondro-osteogenic masses in the infarcted heart. The goal of the current study was to further examine the formation of such masses, specifically, the role of AFS cells in this process. Our results confirm the presence of similar bone-like masses in the left ventricular wall of infarcted rats; however, this phenomenon occurred indepen...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465424</comments>
            <pubDate>Mon, 12 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465424</guid>        </item>
        <item>
            <title>Sudden cardiac death with normal heart: molecular autopsy</title>
            <link>http://www.medworm.com/index.php?rid=4160017&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000323%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Several culprits may be identified at postmortem in sudden death (SD) victims, including coronary artery, myocardial, valve, conduction system, and congenital heart diseases. However, particularly in young people, the heart can be found grossly and histologically normal in a not-so-minor amount of cases (the so-called unexplained SD or “mors sine materia”) and inherited ion channel diseases are implicated (long and short QT syndromes, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia). These channelopathies are due to defective genes encoding for proteins of sodium and potassium ion channels at the sarcolemma level or for receptors regulating intracellular calcium release at the sarcoplasmic reticulum level. Postmortem investigation may still represe...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160017</comments>
            <pubDate>Mon, 12 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160017</guid>        </item>
        <item>
            <title>Can sudden cardiac death be prevented?</title>
            <link>http://www.medworm.com/index.php?rid=4160019&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000372%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Hypertrophic cardiomyopathy is regarded as the most common cause of sudden cardiac death in young people (including trained athletes). Introduction of implantable cardioverter-defibrillators to the hypertrophic cardiomyopathy patient population represents a new paradigm for clinical practice and perhaps the most significant advance in the management of this disease to date. Implantable defibrillators offer the only proven protection against sudden death by virtue of effectively terminating ventricular tachycardia/fibrillation and, in the process, altering the natural history of hypertrophic cardiomyopathy and providing the potential opportunity of normal or near-normal longevity for many patients. However, targeting the most appropriate candidates for prophylactic device therapy ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160019</comments>
            <pubDate>Fri, 09 Apr 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160019</guid>        </item>
        <item>
            <title>Dr. William D. Edwards: 2008 SCVP Distinguished Achievement Award recipient</title>
            <link>http://www.medworm.com/index.php?rid=3734750&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000414%2Fabstract%3Frss%3Dyes</link>
            <description>William D. Edwards is the Society for Cardiovascular Pathology 2008 Distinguished Achievement awardee. He received a BA in Chemistry from the University of Kansas. His medical school training was at the same University, and he subsequently completed pathology training at the University of Kansas, University of Cincinnati, and the University of Minnesota. The last was with Dr. Jesse Edwards at the United Hospital, Miller Division, in St. Paul, MN, USA. He has worked at the Mayo Clinic Rochester MN since 1978. Currently, he is Professor in Pathology and cross-appointed in cardiology. He is Medical Director of autopsy pathology, Director of the Mayo Tissue Registry, and Director of the Cardiovascular Pathology Fellowship Training Program. His role as a teacher and a diagnostic cardiovascular ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734750</comments>
            <pubDate>Thu, 08 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734750</guid>        </item>
        <item>
            <title>Postoperative pathology of congenital heart disease</title>
            <link>http://www.medworm.com/index.php?rid=3947862&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000335%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The evaluation of congenitally malformed hearts that have been subjected to operative and nonoperative interventions includes not only a categorization of the underlying anomalies and various procedures but also an assessment of interventional complications, postprocedural changes in chamber, valvular, and vascular sizes, presence of ischemia or fibrosis, presence of cardiac or extracardiac infections, and evidence of regression or progression of hypertensive pulmonary vascular disease. Input from clinicians or surgeons may be helpful, but biases should be avoided. Referral of cardiopulmonary specimens to experienced pathologists may also be considered. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947862</comments>
            <pubDate>Wed, 07 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947862</guid>        </item>
        <item>
            <title>L. Maximilian Buja, M.D., 2009 SCVP Distinguished Achievement Award recipient</title>
            <link>http://www.medworm.com/index.php?rid=3734749&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000396%2Fabstract%3Frss%3Dyes</link>
            <description>L. Maximilian Buja, M.D., has recently been appointed as Executive Director of the Houston Academy of Medicine-Texas Medical Center Library, while continuing as a Professor of Pathology and Laboratory Medicine at The University of Texas Medical School at Houston. He previously was Executive Vice President for Academic Affairs at The University of Texas Health Science Center at Houston, a position he assumed in July 2003 after serving as Dean of The University of Texas Medical School at Houston from April 1996. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734749</comments>
            <pubDate>Wed, 07 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734749</guid>        </item>
        <item>
            <title>Dr. Bruce McManus, 2010 SCVP Distinguished Achievement Award recipient</title>
            <link>http://www.medworm.com/index.php?rid=3734748&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000402%2Fabstract%3Frss%3Dyes</link>
            <description>Dr. Bruce McManus is a professor in the Department of Pathology and Laboratory Medicine at the University of British Columbia, Vancouver, Canada. Since 2006, he has been the director of the James Hogg iCAPTURE Center of Cardiovascular and Pulmonary Research at St. Hall's Hospital–Providence Health Care, Vancouver, British Columbia, Canada. In September 2007, Dr. McManus was appointed inaugural director of the newly launched Providence Heart and Lung Institute at St. Paul's Hospital. Dr. McManus has served as the inaugural scientific director of the Institute of Circulatory and Respiratory Health, Canadian Institutes of Health Research (CIHR). (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734748</comments>
            <pubDate>Thu, 01 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734748</guid>        </item>
        <item>
            <title>Silver for the Society for Cardiovascular Pathology—SCVP Turns 25</title>
            <link>http://www.medworm.com/index.php?rid=3734744&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000384%2Fabstract%3Frss%3Dyes</link>
            <description>It is 25 years since the inception of the society in 1985! Conceived in a conference room on the 6th floor of the Medical Sciences Building at the University of Toronto, the Society was officially born the following year at the United States and Canadian Academy of Pathology (USCAP) meeting. Since then, the Society has flourished. Educationally, it has been achieving its aims and goals, meeting annually at the USCAP and holding symposia of its own, and in conjunction with the USCAP. In the early years, the Society had an additional meeting at the American Heart Association. However, this was not very productive and was soon canceled. In the last 3 years, the Society has been putting on its own additional symposia on the Saturday evening preceding the USCAP annual meeting. These have covere...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734744</comments>
            <pubDate>Thu, 01 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734744</guid>        </item>
        <item>
            <title>PTX3 expression in the heart tissues of patients with myocardial infarction and infectious myocarditis</title>
            <link>http://www.medworm.com/index.php?rid=4295564&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000347%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Thus, neutrophils are an early source of pentraxin 3 in acute myocardial infarction and presumably other inflammatory heart disorders. Subsequently, in acute myocardial infarction and infectious myocarditis, pentraxin 3 is produced by macrophages, the endothelium, and, to a lesser extent, myocardiocytes, and localized in the interstitium. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295564</comments>
            <pubDate>Wed, 31 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295564</guid>        </item>
        <item>
            <title>Professor Alan George Rose (1940–2009), the cardiovascular pathologist from Cabo de Buena Esperanza</title>
            <link>http://www.medworm.com/index.php?rid=3734756&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488071000030X%2Fabstract%3Frss%3Dyes</link>
            <description>In 1992, when the chair of the Jesse E. Edwards Cardiac Registry fell vacant, I was invited to be the reviewer of the application of Dr. Alan G. Rose, Chairman of the Department of Pathology at the University of Cape Town, known to me only from the literature as the cardiac pathologist of the Groote Schuur Hospital in Cape Town, where the first heart transplantation was performed in 1967 by Christian Barnard. He had the curriculum vitae of a scholar! (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734756</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734756</guid>        </item>
        <item>
            <title>Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation</title>
            <link>http://www.medworm.com/index.php?rid=4295565&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000311%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Brugada syndrome is a disease known to cause ventricular fibrillation with a structurally normal heart and is linked to SCN5A gene mutation. However, the mechanism by which ventricular fibrillation develops in cases of Brugada-type electrocardiogram without SCN5A mutation has remained unclear. Recently, oxidative stress has been implicated in the pathophysiology of cardiac arrhythmia. We also investigated oxidative stress levels in the myocardia of patients with Brugada-type electrocardiogram.Methods: Endomyocardial biopsy samples were obtained from 68 patients with Brugada-type electrocardiogram (66 males and two females). We performed histological and immunohistochemical analyses for CD45, CD68, and 4-hydroxy-2-nonenal-modified protein, which is a major lipid peroxi...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295565</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295565</guid>        </item>
        <item>
            <title>Expression of hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN4) is increased in hypertrophic cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=4465420&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000232%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Higher HCN4 mRNA levels in the HCM hearts suggest that up-regulation of HCN4 gene expression might be responsible for ventricular arrhythmia that leads to sudden death. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465420</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465420</guid>        </item>
        <item>
            <title>Histopathologic correlates of myocardial improvement in patients supported by a left ventricular assist device</title>
            <link>http://www.medworm.com/index.php?rid=4782353&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000281%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Left ventricular assist device-removal patients had less hypertrophy and fibrosis overall than did nonremoval patients. These findings may help identify patients with a higher probability of left ventricular assist device removal and myocardial recovery. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4782353</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4782353</guid>        </item>
        <item>
            <title>Ventricular septal defect complicating acute myocardial infarction—still an unsolved problem in the invasive treatment era</title>
            <link>http://www.medworm.com/index.php?rid=4465417&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000244%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Post-acute myocardial infarction (AMI) ventricular septal defect (VSD) is a rare but catastrophic complication. The aim of study was to delineate the incidence and risk factors of VSD in patients after AMI treated with successful primary percutaneous coronary intervention (pPCI).Methods and results: In the years 2004–2006, a total of 1835 patients with AMI underwent successful pPCI in our hospital. Thirteen patients (0.71%) developed VSD after pPCI. Mean time of occurrence of VSD was 24.46±9.32 h. Patients with VSD had longer time from the AMI onset to pPCI vs. patients without VSD (7.77±2.83 vs. 4.49±4.45, P 70 years (OR=4.66; P=.007), female gender (OR=5.73; P=.004), anterior infarction (OR=3.86; P=.04), single-vessel CAD (OR=3.74; P=.03), body mass index (BMI)...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465417</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465417</guid>        </item>
        <item>
            <title>Ischemic myocardial injuries after cardiac malformation repair in infants may be associated with oxidative stress mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=4295566&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000293%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: The diversity of the lesions observed in these hearts seemed to indicate a large spectrum of cell damage due to inadequate myocardial perfusion, especially when these infants underwent surgery. Oxidative mechanisms could be a common mediator in the pathogenesis of myocardial injuries, mediated by peroxidation of the membrane phospholipids and resulting in changes in the permeability of the cell membrane, cell death, and intracellular calcium overload. Furthermore, an immature and often hypertrophied myocardium may promote unfavorable conditions, leading to heart failure and a lethal outcome. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295566</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295566</guid>        </item>
        <item>
            <title>Statin treatment of hypercholesterolemic-induced aortic valve sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4465416&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000207%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: In established AVS, the cellular response to statin therapy does not result in full regression of the sclerotic process. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465416</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465416</guid>        </item>
        <item>
            <title>Animal models of abdominal aortic aneurysm and their role in furthering management of human disease</title>
            <link>http://www.medworm.com/index.php?rid=4465421&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000025%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Abdominal aortic aneurysm is a common degenerative disorder associated with sudden death due to aortic rupture. Current therapy is limited to open surgical repair of the aorta or endovascular placement of covered stents to exclude the abdominal aortic aneurysm from the circulation. A number of different animal models have been developed in order to study abdominal aortic aneurysm in an effort to advance current management deficiencies. Large animal models have been mostly used to assist in developing novel methods to surgically treat abdominal aortic aneurysms. Small animal models, particularly those developed in rodents, have been employed to further the understanding of the mechanisms involved in abdominal aortic aneurysm in order to identify potential new medical treatments. I...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465421</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465421</guid>        </item>
        <item>
            <title>Aortic aneurysms in systemic lupus erythematosus: a meta-analysis of 35 cases in the literature and two different pathogeneses</title>
            <link>http://www.medworm.com/index.php?rid=4295561&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000190%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Two principal patterns emerged from this analysis. One was the fatal nonatherosclerotic thoracic aneurysm which was associated with cystic medial degeneration and probably due to vasculitis. The other was atherosclerotic abdominal aneurysm which was complicated by long-term steroid treatment and it showed a relatively favorable prognosis. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295561</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295561</guid>        </item>
        <item>
            <title>The Society for Cardiovascular Pathology celebrating 25 disruptively exciting years</title>
            <link>http://www.medworm.com/index.php?rid=3734747&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000268%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: It was 25 years ago when the Society for Cardiovascular Pathology was first organized. The Society has since devoted itself to the advancement of understanding about heart and blood vessel disorders, especially their diagnosis, and for the improvement of prevention, management, and treatment. In this 25 year span, the Society has accomplished many goals and met its initial commitments as an organization, dedication to education and learning, and to collegiality. With the many exciting steps the Society has taken in the first 25 years, it is sure to move to new and significantly transformative endeavours in the coming decades. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734747</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734747</guid>        </item>
        <item>
            <title>Congenital stridor and wheezing as harbingers of the del22q11.2 syndrome presenting cardiovascular malformations of right aortic arch, aberrant left subclavian artery, Kommerell's diverticulum, and left ligamentum arteriosum</title>
            <link>http://www.medworm.com/index.php?rid=4465422&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000220%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A complete vascular ring composed of right aortic arch, aberrant left subclavian artery with Kommerell's diverticulum, and left ligamentum arteriosum was diagnosed by barium esophagography, echocardiography, angiography, and multidetector computed tomography of chest in an 18-day-old male neonate who presented with remarkable inspiratory stridor, expiratory wheezing, postprandial vomiting, and dysphagia since birth, and survived surgical division of the left ligamentum arteriosum, resection of the Kommerell's diverticulum, and reimplanation of the left subclavian artery to the left common carotid artery. Cytogenetic analysis and fluorescence in situ hybridization study of his blood revealed chromosome 22q11.2 deletion, with a karyotype of 46,XY.ish del(22)(q11.2 q11.2). A constel...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465422</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465422</guid>        </item>
        <item>
            <title>Aneurysms in the arteries of the upper extremity in a Kenyan population</title>
            <link>http://www.medworm.com/index.php?rid=4295567&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000256%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Aneurysms of the upper extremity arteries are not uncommon in the Kenyan population. They occur more commonly in individuals aged 50 years and less, and although most of them are traumatic, atherosclerosis constitutes a significant proportion. Prudent management of risk factors is recommended. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295567</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295567</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3228686&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000062%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228686</comments>
            <pubDate>Tue, 02 Feb 2010 14:01:16 +0100</pubDate>
            <guid isPermaLink="false">3228686</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3228685&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000050%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228685</comments>
            <pubDate>Tue, 02 Feb 2010 14:01:16 +0100</pubDate>
            <guid isPermaLink="false">3228685</guid>        </item>
        <item>
            <title>Primary malignant mesothelioma of the pericardium</title>
            <link>http://www.medworm.com/index.php?rid=4465419&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880710000219%2Fabstract%3Frss%3Dyes</link>
            <description>We report a case of a 66-year-old man who presented with shortness of breath, right shoulder pain, and peripheral edema of the lower limbs. A large pericardial effusion was seen on echocardiography, which was drained but the patient died the following day. A malignant tumor was found on autopsy and a final diagnosis of primary malignant pericardial mesothelioma was made following histopathological examination. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465419</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465419</guid>        </item>
        <item>
            <title>The infarcted cardiac microenvironment cannot selectively promote embryonic stem cell differentiation into cardiomyocytes</title>
            <link>http://www.medworm.com/index.php?rid=4465415&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001550%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Postinfarct congestive heart failure is one of the leading causes of morbidity and mortality in industrialized countries. It is controversial whether embryonic stem cells are feasible sources for in situ cardiac regeneration in infarcted hearts. In order to investigate whether the infarcted cardiac microenvironment could selectively promote embryonic stem cell differentiation into cardiomyocytes, we assessed the cardiac differentiation potential of mouse embryonic stem cells (mESCs) injected into normal (n=16) or acutely infarcted rat hearts (n=18). We found that the transplanted 4′,6-diamidino-2-phenylindole (DAPI)-labeled mESCs were able to survive and form stable intracardiac grafts both in normal and infarcted hearts, along with macrophages found specifically in the engraft...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465415</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465415</guid>        </item>
        <item>
            <title>Collagen stimulates discoidin domain receptor 1-mediated migration of smooth muscle cells through Src</title>
            <link>http://www.medworm.com/index.php?rid=4465414&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001586%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Type I collagen induces SMC migration through DDR1 and this is mediated via Src signaling. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465414</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465414</guid>        </item>
        <item>
            <title>DNA repair gene polymorphism is associated with the genetic basis of atherosclerotic coronary artery disease</title>
            <link>http://www.medworm.com/index.php?rid=4295562&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001562%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Atherosclerotic coronary artery disease (CAD) is a multifactorial process that appears to be caused by the interaction of environmental risk factors with multiple predisposing genes. It is nowadays accepted that increased levels of DNA damage induced by xenobiotics play an important role in the early phases of atherogenesis. Therefore, in this study, we focus on determining whether genetic variations in xenobiotic-metabolizing [glutathione-S-transferase theta 1 (GSTT1), glutathione-S-transferase mu 1 (GSTM1), cytochrome P450 IIEI (CYP2E1)] and DNA repair [X-ray cross-complementing group 1 (XRCC1)] genes might be associated with increased risk for CAD.Methods: A case-control study was conducted with 400 individuals who underwent subjected to coronary angiography. A tot...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295562</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295562</guid>        </item>
        <item>
            <title>Proteome changes in CaMKIIδC-overexpressing cardiac myocytes</title>
            <link>http://www.medworm.com/index.php?rid=4160034&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001525%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recent studies have demonstrated that the expression as well as the activity of Ca/calmodulin-dependent protein kinase IIδC (CaMKIIδC) is increased in heart failure. Transgenic overexpression of CaMKIIδC in mouse hearts results in severe dilated cardiomyopathy. So far, little is known about CaMKIIδC-induced changes in gene expression and proteome alteration. We hypothesize that proteome changes similar to those found in advanced heart failure can be assessed even after short term overexpression of CaMKIIδC in an in vitro culture model. Thus, we designed a study using a proteomic approach combined with adenovirus-mediated gene transfer of CaMKIIδC to identify early CaMKIIδC-induced changes in cardiac myocyte phenotype on proteome level. CaMKIIδC was overexpressed by adenov...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160034</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160034</guid>        </item>
        <item>
            <title>Remodeling of cardiac fibroblasts following myocardial infarction results in increased gap junction intercellular communication</title>
            <link>http://www.medworm.com/index.php?rid=4160033&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001549%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Fibroblasts isolated from infarcted hearts exhibited marked up-regulation of Cx43 protein expression and enhanced intercellular coupling. Exogenous administration of transforming growth factor-β (TGF-β) to fibroblast cultures from normal, non-operated hearts produced comparable up-regulation of Cx43, suggesting that increased intercellular communication between fibroblasts in infarct and peri-infarct regions may be secondary to activation of a TGF-β pathway. Unlike cardiac myocytes that down-regulate Cx43, presumably to limit intercellular transmission of biochemical mediators of ischemic injury, fibroblasts may up-regulate Cx43 to maintain electrical and metabolic coupling at a time when intercellular communication is compromised. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160033</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160033</guid>        </item>
        <item>
            <title>Atrial myocardial nox2 containing NADPH oxidase activity contribution to oxidative stress in mitral regurgitation: potential mechanism for atrial remodeling</title>
            <link>http://www.medworm.com/index.php?rid=4465418&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001574%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Results of this study demonstrate that membrane-bound nox2 containing NADPH oxidase activity and expression in the atrial myocardium is increased in patients with severe mitral regurgitation, possibly contributing to atrial remodeling in this clinical setting. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4465418</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4465418</guid>        </item>
        <item>
            <title>Cardiac infections: focus on molecular diagnosis</title>
            <link>http://www.medworm.com/index.php?rid=3550126&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001136%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The role of different types of infections in heart diseases is more important than commonly thought, with new and re-emerging infections (i.e., Mycobacterium tuberculosis).This review addresses the pathology of infective pericarditis, myocarditis, and endocarditis, mainly focusing on the significance of molecular techniques in the detection of infective agents. Molecular investigations represent important ancillary diagnostic tools and combined with other conventional approaches provide a more precise final diagnosis. A close collaboration and communication among cardiologists, cardiac surgeons, pathologists, and microbiologists is essential to ensure optimal diagnoses and management as well as a favorable impact on patient outcome. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550126</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550126</guid>        </item>
        <item>
            <title>AECVP and SCVP 2009 Recommendations for Training in Cardiovascular Pathology</title>
            <link>http://www.medworm.com/index.php?rid=3550119&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001537%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cardiovascular disease is of continuing importance as the result of a growing burden of risk factors in both developing and developed countries and the increasing number of elderly people worldwide. The recruitment and training of a new generation of Cardiovascular Pathologists is crucial to sustaining clinical excellence and to advancing our knowledge of cardiovascular disease. These pathologists will also have a key role in undergraduate and postgraduate training. In 2005 a task force of the Society for Cardiovascular Pathology published a document on the role of Cardiovascular Pathology as subspecialty of Anatomical Pathology (Pathological Anatomy). The 2005 report emphasized the need for a core curriculum and structured learning for residents and fellows in Cardiovascular Pat...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550119</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550119</guid>        </item>
        <item>
            <title>Primary cardiac tumors: a clinicopathologic evaluation of four cases</title>
            <link>http://www.medworm.com/index.php?rid=4295559&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001513%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: All four cases were sarcomas. A limited number of immunohistochemical markers can be used in order to define a specific line of differentiation. In this small study, three of the patients were offered orthotopic heart transplantation, and the survival times were generally longer than in most series. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295559</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295559</guid>        </item>
        <item>
            <title>Protein kinase G activity prevents pathological-level nitric oxide-induced apoptosis and promotes DNA synthesis/cell proliferation in vascular smooth muscle cells</title>
            <link>http://www.medworm.com/index.php?rid=4160032&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001355%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Protein kinase G (PKG), a recognized downstream mediator of nitric oxide, is a key regulator of cardiovascular physiology and pathology. High-level stimulation of cyclic guanosine monophosphate/PKG signaling using high concentrations of nitric oxide donors, mimicking pathological conditions, induces apoptosis in vascular smooth muscle cells. In contrast, we have found that PKG at basal and moderately elevated activity prevents both spontaneous and toxin-induced apoptosis in many other cells. We hypothesized that PKG's apoptosis-regulatory role in vascular smooth muscle cells depends on PKG activation levels [low/basal-level activation prevents apoptosis, whereas high-level activation (hyperactivation) causes apoptosis]. Furthermore, we hypothesized that, although PKG ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160032</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160032</guid>        </item>
        <item>
            <title>Immunohistochemical evaluation of three nitric oxide synthase isoforms in human saphenous vein exposed to different degrees of distension pressures</title>
            <link>http://www.medworm.com/index.php?rid=4160031&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488070900146X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The effect of short duration and different degrees of distension pressures was investigated by means of immunohistochemistry of the three nitric oxide synthase isoforms in the human saphenous vein conventionally harvested from 20 patients submitted to coronary artery bypass graft. The human saphenous vein distal portion was divided into four segments, each one allocated to a different group. In Group I (control group), the human saphenous vein segment was not exposed to distension pressure. In Groups II, III, and IV, the human saphenous vein segment was exposed to 100, 200, and 300 mmHg of distension pressure, respectively. The distension pressures were applied and maintained with Krebs solution for 15 s. The human saphenous vein of the control group presented endothelial nitric ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160031</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160031</guid>        </item>
        <item>
            <title>Adult congenital heart disease—challenges and opportunities for pathologists</title>
            <link>http://www.medworm.com/index.php?rid=3947863&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001331%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Adults living with congenital heart disease (CHD) are numerous, at a prevalence of about four per 1000 population. Many of these patients are now over the age of 40 years. Typically, these adult CHD patients have had or require one or more invasive interventions, and thus most of them have modified anatomy and physiology. Despite professional education programs aimed at cardiologists, surgeons, radiologists, pathologists, and others to improve awareness of “grown-up kids” with CHD, there is still a paucity of caregivers who feel competent with these patients. An appreciation by pathologists of the main types of clinically modified congenital lesions seen in adult patients with CHD is of great importance in terms of helping clinicians understand why patients ultimately die (of...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3947863</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3947863</guid>        </item>
        <item>
            <title>Molecular basis and diagnosis of both inherited and acquired cardiovascular diseases: introduction</title>
            <link>http://www.medworm.com/index.php?rid=3550124&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709000714%2Fabstract%3Frss%3Dyes</link>
            <description>The long wave of molecular biology, since the discovery of DNA and the processing of genetic information to protein synthesis followed by the introduction of polymerase chain reaction, with the ability to clone DNA and RNA, has influenced cardiovascular medicine with major clinical impact. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550124</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550124</guid>        </item>
        <item>
            <title>Arrhythmogenic right ventricular cardiomyopathy: new insights into mechanisms of disease</title>
            <link>http://www.medworm.com/index.php?rid=3550125&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001343%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Arrhythmogenic right ventricular cardiomyopathy is a primary heart muscle disorder characterized by the early occurrence of arrhythmias often out of proportion to the extent of structural remodeling and contractile derangement. Approximately 40% of patients with arrhythmogenic right ventricular cardiomyopathy have one or more mutations in genes encoding proteins in desmosomes, intercellular adhesion junctions which, in cardiac myocytes, reside within intercalated disks. Some desmosomal proteins fulfill roles both as structural proteins in cell–cell adhesion junctions and as signaling molecules in pathways mediated by Wnt ligands. Evidence is increasing that mutations in desmosomal proteins can perturb the normal balance of critical proteins in junctions and the cytosol which, i...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550125</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550125</guid>        </item>
        <item>
            <title>Aspergillus pancarditis manifesting as hospital-acquired infection: Report of two cases and review of literature</title>
            <link>http://www.medworm.com/index.php?rid=4160037&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001471%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Nosocomial cardiac infections are most often related to interventions performed within the preceding one to two months of hospital admission and usually affect the endocardium or prosthetic devices. These can be sometimes caused by fungi, especially the molds. This is a report of rare fungal pancarditis seen as hospital-acquired infection in two patients who were admitted in the intensive care unit for leptospirosis. The cardiac manifestation was part of systemic mycosis; mechanical ventilation, administration of steroids and hepatorenal failure were the risk factors. Incidentally, both the patients had underlying intrinsic cardiac disease. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160037</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160037</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3057821&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001392%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057821</comments>
            <pubDate>Sat, 05 Dec 2009 13:50:30 +0100</pubDate>
            <guid isPermaLink="false">3057821</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3057820&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001380%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057820</comments>
            <pubDate>Sat, 05 Dec 2009 13:50:30 +0100</pubDate>
            <guid isPermaLink="false">3057820</guid>        </item>
        <item>
            <title>The metamorphosis of myocardial infarction following coronary recanalization</title>
            <link>http://www.medworm.com/index.php?rid=3057810&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709000751%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The “metamorphosis” of acute myocardial infarction (AMI) in terms of pathological features and complications in the reperfusion era is herein discussed. Typically, the AMI following coronary artery recanalization is characterized by frequent subendocardial location, since a prompt coronary lumen recanalization is able to prevent the transmural progression of myocardial necrosis from the endocardium towards the epicardium. Transmural AMI may develop when recanalization occurs late (&gt;6 hours) or is not effective (persistent coronary occlusion). Moreover, reperfused AMI frequently appears reddish because of interstitial haemorrhage, which is thought to be caused by vascular cell damage with leakage of blood out of the injured vessels. Hemorrhage occurs always within the area of ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057810</comments>
            <pubDate>Sat, 05 Dec 2009 13:50:28 +0100</pubDate>
            <guid isPermaLink="false">3057810</guid>        </item>
        <item>
            <title>Common pathogenic features of atherosclerosis and calcific aortic stenosis: role of transforming growth factor-β</title>
            <link>http://www.medworm.com/index.php?rid=3734754&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001100%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Calcific aortic stenosis and atherosclerosis have been investigated separately in experimental in vitro and in vivo studies and in clinical studies. The similarities identified in both diseases suggest that similar pathogenic pathways are involved in both conditions. Most current therapeutic studies are focused on statins. The evidence suggests that statin effects on valves may, in large part, be independent of the lipid lowering effects of the drug. There are several molecules that play significant regulatory roles on the development and progression of valve sclerosis and calcification and on growth and complications of atherosclerotic plaques. The purpose of this review is to discuss the pathogenic features of the two conditions, highlight the important similarities, and then r...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734754</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734754</guid>        </item>
        <item>
            <title>Prosthetic valve endocarditis: clinicopathological correlates in 122 surgical specimens from 116 patients (1985–2004)</title>
            <link>http://www.medworm.com/index.php?rid=4295554&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001094%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Background: Few studies have documented the clinicopathological features of prosthetic valve endocarditis independently of native valve endocarditis.Study Design: Retrospective analysis of patients undergoing cardiac surgery for prosthetic valve endocarditis at our institution (1985–2004).Methods: Medical records and microscopic slides were reviewed from 116 patients for demographics, infecting organisms, comorbidities, and pathologic features.Results: Patients were 12–86 years old (mean, 59 years). Among 122 valves, 64% were from men and 67% were purely regurgitant. Aortic prosthetic valve endocarditis frequently affected men (76%); mitral prosthetic valve endocarditis often affected women (62%). Embolization occurred in 35% and heart failure in 32%. Prevalent predisposing c...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295554</comments>
            <pubDate>Fri, 20 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295554</guid>        </item>
        <item>
            <title>Causes and histopathology of ascending aortic disease in children and young adults</title>
            <link>http://www.medworm.com/index.php?rid=4295553&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001112%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: While extensive literature on the common causes of ascending aortic disease exists, there is a need for better histologic documentation of aortic pathology in rarer diseases. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295553</comments>
            <pubDate>Fri, 20 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295553</guid>        </item>
        <item>
            <title>Sally Patricia Allwork (June 14, 1938–July 12, 2009)</title>
            <link>http://www.medworm.com/index.php?rid=3734758&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS105488070900129X%2Fabstract%3Frss%3Dyes</link>
            <description>After a short illness of rapid onset, Sally Allwork passed away on the July 12, 2009. Sally achieved her ultimate position as a morphologist despite the lack of an initial traditional university education. Her mother was Italian in origin. She left school at the age of 16 after taking her 'O' level examinations. She became an Almoners' Clerk at The Central Middlesex Hospital, continuing her studies in the evenings so as to obtain the necessary qualifications to become a laboratory technician. She was appointed as a student technician at The Hammersmith Hospital and eventually achieved a position as a technician working in the operating rooms. It was there that she met her life-long mentor, Professor Hugh Bentall. Under his subsequent tutelage, she began to prepare homograft heart valves, b...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734758</comments>
            <pubDate>Fri, 20 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3734758</guid>        </item>
        <item>
            <title>Heterogeneity of atherosclerosis in mesenteric arteries and outgrowth remodeling</title>
            <link>http://www.medworm.com/index.php?rid=4160029&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001148%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Outgrowth remodeling occurred in both the SMA and the IMA. Less severe atherosclerosis in the IMA than in the SMA was associated with stronger signs of inflammation. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4160029</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4160029</guid>        </item>
        <item>
            <title>Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content</title>
            <link>http://www.medworm.com/index.php?rid=4295555&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001069%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Introduction: Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition.Methods: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms ( (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295555</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295555</guid>        </item>
        <item>
            <title>The heart in Fabry's disease</title>
            <link>http://www.medworm.com/index.php?rid=4295552&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001161%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Fabry's disease (FD) is a rare X-linked recessive genetic disorder that leads to premature mortality as a result of renal, cardiovascular, or cerebrovascular complications. FD is caused by a deficiency of α-galactosidase A (alpha-Gal A), due to mutations in the GLA gene. There is an inability to catabolize lipids which results in cellular accumulation of its most abundant substrate, globotriaosylceramide (Gb3), and other neutral glycosphingolipids in vascular endothelium and other tissues throughout the body. This progressive glycosphingolipid accumulation leads to life-threatening clinical sequelae in renal, cardiac, and cerebrovascular systems. In males who carry the mutation (1/40,000), severe multisystem disease develops in childhood or adolescence. Hemizygous male patients ...</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295552</comments>
            <pubDate>Wed, 18 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4295552</guid>        </item>
        <item>
            <title>The diameter of liver sinusoidal fenestrae is not a major determinant of lipoprotein levels and atherosclerosis in cholesterol-fed rabbits</title>
            <link>http://www.medworm.com/index.php?rid=4295556&amp;cid=s_35391_7_f&amp;fid=35391&amp;url=http%3A%2F%2Fwww.cardiovascularpathology.com%2Farticle%2FPIIS1054880709001057%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: The data presented in this study do not support the hypothesis that the diameter of fenestrae is an important determinant of chylomicron remnant levels, diet-induced hypercholesterolemia, and atherosclerosis in cholesterol-fed rabbits. (Source: Cardiovascular Pathology)</description>
            <author>Cardiovascular Pathology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4295556</comments>
            <pubDate>Mon, 16 Nov 2009 00:00:00 +0100</pubDate>
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