<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.onlinepcd.com/?rss=yes"><title>Progress in Cardiovascular Diseases</title><description>Progress in Cardiovascular Diseases RSS feed: Current Issue. 
 Each issue of  Progress in Cardiovascular Diseases  comprehensively covers a single topic in the understanding and treatment 
of disorders of the heart and circulation. Some issues include special articles, definitive reviews that capture the state of the art 
in the management of particular clinical problems in cardiology.   
 
 Recent Topics   
 
 The Myths Surrounding Diastolic Heart 
Failure 
Guest Editor:  Dirk L. Brutsaert 
 
Hypertension 
Guest Editor:  Franz Messerli 
 
Resynchronization Therapy 
Guest 
Editor:  Jonathan S. Steinberg 
 
Atrial Fibrillation 
Guest Editor:  Albert L. Waldo 
 
Diastolic Heart Failure 
Guest Editor: 
 Michael R. Zile 
 
Troponins 
 
Drug Class Effects 
Guest Editor:  James A. Reiffel 
 
Chest Pain Units 
Guest Editors:  Ezra 
A. Amsterdam and J. Douglas Kirk</description><link>http://www.onlinepcd.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:issn>0033-0620</prism:issn><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:publicationDate>January 2010</prism:publicationDate><prism:copyright> © 2009 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009001091/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009001078/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000991/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000863/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000966/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000942/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS003306200900098X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000930/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000929/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009001005/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009000978/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS0033062009001108/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinepcd.com/article/PIIS003306200900111X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009001091/abstract?rss=yes"><title>Masthead</title><link>http://www.onlinepcd.com/article/PIIS0033062009001091/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0033-0620(09)00109-1</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009001078/abstract?rss=yes"><title>Kenneth L. Baughman, MD, 1946-2009</title><link>http://www.onlinepcd.com/article/PIIS0033062009001078/abstract?rss=yes</link><description></description><dc:title>Kenneth L. Baughman, MD, 1946-2009</dc:title><dc:creator>Rodney H. Falk, Uri Elkayam</dc:creator><dc:identifier>10.1016/j.pcad.2009.12.001</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>In Memoriam</prism:section><prism:startingPage>261</prism:startingPage><prism:endingPage>261</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000991/abstract?rss=yes"><title>Cardiomyopathy: The Importance of Recognizing the Uncommon Diagnosis</title><link>http://www.onlinepcd.com/article/PIIS0033062009000991/abstract?rss=yes</link><description>The distinction between a sound cardiologist and an excellent cardiologist is the ability of the latter to recognize and diagnose the unusual. In this issue, a group of experts reviews a spectrum of unusual cardiomyopathies, any or all of which may present to the general cardiologist. Myocarditis, reviewed by Blauwet and Cooper, runs the gamut of severity from mild to life-threatening and may mimic a whole spectrum of cardiovascular disease. Although the classic presentation with acute onset heart failure, electrocardiographic changes, and arrhythmia suggests an immediately apparent diagnosis, the authors clearly describe the more subtle ways in which myocarditis may present, as well as the difficulties in precisely defining a diagnosis.</description><dc:title>Cardiomyopathy: The Importance of Recognizing the Uncommon Diagnosis</dc:title><dc:creator>Rodney H. Falk, Uri Elkayam</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.009</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>262</prism:startingPage><prism:endingPage>263</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000863/abstract?rss=yes"><title>Left Ventricular Noncompaction</title><link>http://www.onlinepcd.com/article/PIIS0033062009000863/abstract?rss=yes</link><description>Abstract: According to the World Health Organization classification of cardiomyopathies, left ventricular noncompaction is still an unclassified cardiomyopathy. In 2006, the American Heart Association classified this entity as a primary cardiomyopathy of genetic origin. In 2008, the European Society of Cardiology updated the classification scheme similar to the World Health Organization classification. At present, there is no consensus on the diagnostic criteria, and diagnosis is based on the morphologic features identified by cardiac imaging studies or at autopsy. Due to lack of standardization of the diagnostic criteria and little awareness of this condition among clinicians, the true prevalence of this disease is not clear. There is no specific therapy for this condition. However, it seems prognosis is much better than initially reported. The current status of diagnosis, prognosis, and management of isolated noncompaction in adults is discussed in this review.</description><dc:title>Left Ventricular Noncompaction</dc:title><dc:creator>Radha J. Sarma, Amar Chana, Uri Elkayam</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.001</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>264</prism:startingPage><prism:endingPage>273</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000966/abstract?rss=yes"><title>Myocarditis</title><link>http://www.onlinepcd.com/article/PIIS0033062009000966/abstract?rss=yes</link><description>Abstract: Myocarditis is an uncommon, potentially life-threatening disease that presents with a wide range of symptoms in children and adults. Viral infection is the most common cause of myocarditis in developed countries, but other etiologies include bacterial and protozoal infections, toxins, drug reactions, autoimmune diseases, giant cell myocarditis, and sarcoidosis. Acute injury leads to myocyte damage, which in turn activates the innate and humeral immune system, leading to severe inflammation. In most patients, the immune reaction is eventually down-regulated and the myocardium recovers. In select cases, however, persistent myocardial inflammation leads to ongoing myocyte damage and relentless symptomatic heart failure or even death. The diagnosis is usually made based on clinical presentation and noninvasive imaging findings. Most patients respond well to standard heart failure therapy, although in severe cases, mechanical circulatory support or heart transplantation is indicated. Prognosis in acute myocarditis is generally good except in patients with giant cell myocarditis. Persistent, chronic myocarditis usually has a progressive course but may respond to immunosuppression.</description><dc:title>Myocarditis</dc:title><dc:creator>Lori A. Blauwet, Leslie T. Cooper</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.006</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>274</prism:startingPage><prism:endingPage>288</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000942/abstract?rss=yes"><title>Alcoholic and Cocaine-Associated Cardiomyopathies</title><link>http://www.onlinepcd.com/article/PIIS0033062009000942/abstract?rss=yes</link><description>Abstract: Alcohol and cocaine use are associated with significant cardiovascular complications, including cardiomyopathy. The pathophysiologic mechanisms underlying the development of these toxic cardiomyopathies vary depending on the inciting agent but include direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. The typical patient with alcoholic cardiomyopathy is a long-term excessive alcohol consumer who is otherwise indistinguishable from other patients with nonischemic cardiomyopathy. The typical patient with cocaine cardiomyopathy is a young male smoker who presents with signs of adrenergic excess. Management of these patients is similar to that of patients with other forms of dilated cardiomyopathy, although β-blockers should be avoided in patients with cocaine-associated heart failure and benzodiazepines should be given in this setting to blunt adrenergic excess. Left ventricular function may improve dramatically with abstinence from alcohol or cocaine. Unfortunately, the rate of recidivism is high and left ventricular dysfunction and symptomatic heart failure often recurs.</description><dc:title>Alcoholic and Cocaine-Associated Cardiomyopathies</dc:title><dc:creator>Eric H. Awtry, George J. Philippides</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.004</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>289</prism:startingPage><prism:endingPage>299</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS003306200900098X/abstract?rss=yes"><title>Chagas Cardiomyopathy—Where Do We Stand After a Hundred Years?</title><link>http://www.onlinepcd.com/article/PIIS003306200900098X/abstract?rss=yes</link><description>Abstract: A hundred years from its description, Chagas cardiomyopathy remains a challenging disease. Although successful vector-control strategies have decreased the incidence of Chagas disease in several Latin American countries, both migration to urban areas and immigration have spread the disease worldwide; and now, blood transfusion, organ transplantation, and vertical transmission are a concern. The pathogenesis of Chagas cardiomyopathy involves complex host-parasite interactions, where low-grade but incessant systemic infection and triggered autoimmune reaction are the main mechanisms for its development, with the contribution of autonomic damage and microvascular disturbances. Chagas cardiomyopathy is the most important clinical presentation of Chagas disease and comprises a wide range of manifestations, including heart failure, arrhythmias, heart blocks, sudden death, thromboembolism, and stroke. Recently, simple clinical prognostic scores have been developed to identify high-risk patients and help with management. The treatment of Chagas cardiomyopathy focuses mostly on managing heart failure, arrhythmias, and thromboembolism. The role of specific antiparasitic therapy in the chronic form is not yet defined, and a randomized trial is now under way to address this crucial point. In this article, we review the main clinical aspects of Chagas cardiomyopathy and underscore some upcoming challenges for the appropriate control, diagnosis, and management of this complex disease.</description><dc:title>Chagas Cardiomyopathy—Where Do We Stand After a Hundred Years?</dc:title><dc:creator>Andréia Biolo, Antonio L. Ribeiro, Nadine Clausell</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.008</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>300</prism:startingPage><prism:endingPage>316</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000930/abstract?rss=yes"><title>Peripartum Cardiomyopathy in Africa: Challenges in Diagnosis, Prognosis, and Therapy</title><link>http://www.onlinepcd.com/article/PIIS0033062009000930/abstract?rss=yes</link><description>Abstract: Peripartum cardiomyopathy (PPCM) is a form of heart failure affecting women of childbearing age, which can be associated with considerable mortality and chronic debilitating disease. Most patients present with acute postpartal heart failure that resembles the clinical presentation of idiopathic dilated cardiomyopathy. Historically, patients with PPCM have shown high rates of rapid recovery, with 6-month recovery rates averaging at 50%. However, recent prospective long-term follow-up of patients with PPCM in developing societies suggest recovery occurring only well into the second year after diagnosis, and recovery is poorly predicted by baseline left ventricular function. Beyond any potentially inherent factors contributing to poorer outcomes of patients with PPCM in developing societies, prognosis in these settings will continue to lag behind as the challenges faced to optimizing diagnosis remain immense. New insights into the role of inflammatory, apoptotic, and other genetic pathways may improve prognosis through the early detection and more targeted treatment of PPCM.</description><dc:title>Peripartum Cardiomyopathy in Africa: Challenges in Diagnosis, Prognosis, and Therapy</dc:title><dc:creator>Kemi Tibazarwa, Karen Sliwa</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.003</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>317</prism:startingPage><prism:endingPage>325</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000929/abstract?rss=yes"><title>Anderson-Fabry Disease and the Heart</title><link>http://www.onlinepcd.com/article/PIIS0033062009000929/abstract?rss=yes</link><description>Abstract: Anderson-Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations of the GLA gene that encodes α-galactosidase A. The ensuing enzyme deficiency results in intracellular accumulation of neutral glycosphingolipids (primarily globotriaosylceramide) and progressive renal, cardiac, and cerebrovascular disease. Female carriers are at risk of developing disease, but this tends to be milder and more slowly progressive than in males. Left ventricular hypertrophy is the most common cardiac manifestation followed by conduction system disease, valve dysfunction, and arrhythmias. Management of cardiovascular symptoms and the prevention of complications rely on conventional pharmacologic and device-based therapies, but data on the effect of enzyme replacement therapy suggest that it has the potential to attenuate and possibly reverse some aspects of cardiac involvement.</description><dc:title>Anderson-Fabry Disease and the Heart</dc:title><dc:creator>Constantinos O'Mahony, Perry Elliott</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.002</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>326</prism:startingPage><prism:endingPage>335</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009001005/abstract?rss=yes"><title>Diagnosis and Management of Cardiac Sarcoidosis</title><link>http://www.onlinepcd.com/article/PIIS0033062009001005/abstract?rss=yes</link><description>Abstract: Cardiac sarcoidosis is an underdiagnosed disease that may be present in as many as 25% of patients with systemic sarcoidosis. Although most commonly recognized in patients with other manifestations of sarcoidosis, it may occur in isolation and its presence is often not appreciated. Cardiac sarcoidosis may present as asymptomatic left ventricular dysfunction, congestive heart failure, atrioventricular block, atrial or ventricular arrhythmia and sudden death. Although untested in clinical trials, early use of high-dose steroid therapy may halt or reverse cardiac damage. This article reviews the clinical manifestations, diagnosis and treatment of sarcoidosis, with an emphasis on new imaging techniques and therapies.</description><dc:title>Diagnosis and Management of Cardiac Sarcoidosis</dc:title><dc:creator>Simon W. Dubrey, Rodney H. Falk</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.010</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>336</prism:startingPage><prism:endingPage>346</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009000978/abstract?rss=yes"><title>Amyloid Heart Disease</title><link>http://www.onlinepcd.com/article/PIIS0033062009000978/abstract?rss=yes</link><description>Abstract: The systemic amyloidoses are an uncommon group of disorders characterized by the extracellular deposition of amyloid in one or more organs. Cardiac deposition, leading to an infiltrative/restrictive cardiomyopathy, is a common feature of amyloidosis. It may be the presenting feature of the disease or may be discovered while investigating a patient presenting with non-cardiac amyloidosis. In this article we review the features of cardiac amyloidosis and its varied manifestations. The need for a high index of suspicion and the critical importance of precise biochemical typing of the amyloid deposits is stressed in light of recent advances in therapy which can, when appropriately used, significantly improve prognosis.</description><dc:title>Amyloid Heart Disease</dc:title><dc:creator>Rodney H. Falk, Simon W. Dubrey</dc:creator><dc:identifier>10.1016/j.pcad.2009.11.007</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>347</prism:startingPage><prism:endingPage>361</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS0033062009001108/abstract?rss=yes"><title>Table of contents</title><link>http://www.onlinepcd.com/article/PIIS0033062009001108/abstract?rss=yes</link><description></description><dc:title>Table of contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0033-0620(09)00110-8</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A7</prism:startingPage><prism:endingPage>A7</prism:endingPage></item><item rdf:about="http://www.onlinepcd.com/article/PIIS003306200900111X/abstract?rss=yes"><title>List of recent issues</title><link>http://www.onlinepcd.com/article/PIIS003306200900111X/abstract?rss=yes</link><description></description><dc:title>List of recent issues</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0033-0620(09)00111-X</dc:identifier><dc:source>Progress in Cardiovascular Diseases 52, 4 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Progress in Cardiovascular Diseases</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>52</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0033-0620(09)X0007-1</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A8</prism:startingPage><prism:endingPage>A8</prism:endingPage></item></rdf:RDF>