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    <title>JAMA Internal Medicine: Cardiology Topic Collection</title>
    <link>http://archinte.jamanetwork.com/</link>
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    <language>en-us</language>
    <pubDate>Wed, 15 May 2013 00:00:00 GMT</pubDate>
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      <title>Significance of First-Degree Atrioventricular Block in Acute Endocarditis—Quiz Case</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1656542</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Atallah P. </author>
      <description>&lt;span class="paragraphSection"&gt;A 64-year-old man with a history of congenital bicuspid aortic valve and bioprosthetic valve replacement presented with fever, chills, and dysuria. He was treated with ciprofloxacin as an outpatient for presumed urinary tract infection by his primary care physician. In the emergency center, his urinalysis result was positive. He was given intravenous ceftriaxone sodium and admitted for observation.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">724</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">724</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.3334a</prism:doi>
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    <item>
      <title>Significance of First-Degree Atrioventricular Block in Acute Endocarditis—Diagnosis</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1656543</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author />
      <description />
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">726</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">726</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.3334b</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1656543</guid>
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    <item>
      <title>Rapid Assessment of Cardiovascular Risk Among Users of Smoking Cessation Drugs Within the US Food and Drug Administration's Mini-Sentinel Program</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1672280</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Toh S, Baker MA, Brown JS, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;In June 2011, the US Food and Drug Administration (FDA) issued a Drug Safety Communication indicating that varenicline tartrate, a drug prescribed for smoking cessation, may increase the risk of certain cardiovascular events in individuals with cardiovascular disease. The finding was based on the FDA's review of a randomized placebo-controlled trial of 714 smokers. In July 2011, the FDA requested that the Mini-Sentinel program perform a rapid safety assessment of the drug.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">817</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">819</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.3004</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1672280</guid>
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    <item>
      <title>Use of Glucocorticoids and Risk of Venous Thromboembolism A Nationwide Population-Based Case-Control Study  Glucocorticoids and Risk of Venous Thromboembolism </title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1673744</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Johannesdottir SA, Horváth-Puhó E, Dekkers OM, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Importance&lt;/div&gt;Excess endogenous cortisol has been linked to venous thromboembolism (VTE) risk, but whether this relationship applies to exogenous glucocorticoids remains uncertain. Because the prevalence of glucocorticoid use and the incidence of VTE are high, an increased risk of VTE associated with glucocorticoid use would have important implications.&lt;div class="boxTitle"&gt;Background&lt;/div&gt;To examine the association between glucocorticoid use and VTE.&lt;div class="boxTitle"&gt;Design&lt;/div&gt;Population-based case-control study using nationwide databases.&lt;div class="boxTitle"&gt;Setting&lt;/div&gt;Denmark (population 5.6 million).&lt;div class="boxTitle"&gt;Participants&lt;/div&gt;We identified 38 765 VTE cases diagnosed from January 1, 2005, through December 31, 2011, and 387 650 population controls included through risk-set sampling and matched by birth year and sex. The VTE diagnosis date for the case was the index date for cases and matched controls.&lt;div class="boxTitle"&gt;Exposure&lt;/div&gt;We classified individuals who filled their most recent glucocorticoid prescription 90 days or less, 91 to 365 days, and more than 365 days before the index date as present, recent, and former users, respectively. Present users were subdivided into new (first-ever prescription 90 days or less before the index date) and continuing users (others).&lt;div class="boxTitle"&gt;Main Outcomes and Measures&lt;/div&gt;We used conditional logistic regression adjusted for VTE risk factors to estimate incidence rate ratios (IRRs) and 95% CIs for glucocorticoid users vs nonusers.&lt;div class="boxTitle"&gt;Results&lt;/div&gt;Systemic glucocorticoids increased VTE risk among present (adjusted IRR, 2.31; 95% CI, 2.18-2.45), new (3.06; 2.77-3.38), continuing (2.02; 1.88-2.17), and recent (1.18; 1.10-1.26) users but not among former users (0.94; 0.90-0.99). The adjusted IRR increased from 1.00 (95% CI, 0.93-1.07) for a prednisolone-equivalent cumulative dose of 10 mg or less to 1.98 (1.78-2.20) for more than 1000 to 2000 mg, and to 1.60 (1.49-1.71) for doses higher than 2000 mg. New use of inhaled (adjusted IRR, 2.21; 95% CI, 1.72-2.86) and intestinal-acting (2.17; 1.27-3.71) glucocorticoids also increased VTE risk.&lt;div class="boxTitle"&gt;Conclusions and Relevance&lt;/div&gt;The risk of VTE is increased among glucocorticoid users. Although residual confounding may partly explain this finding, we consider a biological mechanism likely because the association followed a clear temporal gradient, persisted after adjustment for indicators of severity of underlying disease, and existed also for noninflammatory conditions. Hence, our observations merit clinical attention.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">743</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">752</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.122</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1673744</guid>
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    <item>
      <title>High-Sensitivity Cardiac Troponin T Levels and Secondary Events in Outpatients With Coronary Heart Disease From the Heart and Soul Study High-Sensitivity Cardiac Troponin T Levels </title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1675872</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Beatty AL, Ku IA, Christenson RH, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Importance&lt;/div&gt;Levels of high-sensitivity cardiac troponin T (hs-cTnT) predict secondary cardiovascular events in patients with stable coronary heart disease.&lt;div class="boxTitle"&gt;Objectives&lt;/div&gt;To determine the association of hs-cTnT levels with structural and functional measures of heart disease and the extent to which these measures explain the relationship between hs-cTnT and secondary events.&lt;div class="boxTitle"&gt;Design&lt;/div&gt;We measured serum concentrations of hs-cTnT and performed exercise treadmill testing with stress echocardiography in a prospective cohort study of outpatients with coronary heart disease who were enrolled from September 11, 2000, through December 20, 2002, and followed up for a median of 8.2 years.&lt;div class="boxTitle"&gt;Setting&lt;/div&gt;Twelve outpatient clinics in the San Francisco Bay Area.&lt;div class="boxTitle"&gt;Participants&lt;/div&gt;Nine hundred eighty-four patients with stable coronary heart disease.&lt;div class="boxTitle"&gt;Main Outcomes and Measures&lt;/div&gt;Cardiovascular events (myocardial infarction, heart failure, or cardiovascular death), determined by review of medical records and death certificates.&lt;div class="boxTitle"&gt;Results&lt;/div&gt;Of 984 participants, 794 (80.7%) had detectable hs-cTnT levels. At baseline, higher hs-cTnT levels were associated with greater inducible ischemia and worse left ventricular ejection fraction, left atrial function, diastolic function, left ventricular mass, and treadmill exercise capacity. During follow-up, 317 participants (32.2%) experienced a cardiovascular event. After adjustment for clinical risk factors, baseline cardiac structure and function, and other biomarkers (N-terminal portion of the prohormone of brain-type natriuretic peptide and C-reactive protein levels), each doubling in hs-cTnT level remained associated with a 37% higher rate of cardiovascular events (hazard ratio, 1.37 [95% CI, 1.14-1.65]; P = .001).&lt;div class="boxTitle"&gt;Conclusions and Relevance&lt;/div&gt;In outpatients with stable coronary heart disease, higher hs-cTnT levels were associated with multiple abnormalities of cardiac structure and function but remained independently predictive of secondary events. These findings suggest that hs-cTnT levels may detect an element of risk that is not captured by existing measures of cardiac disease severity.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">763</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">769</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.116</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1675872</guid>
    </item>
    <item>
      <title>Reconstructing Angina: Cardiac Symptoms Are the Same in Women and Men</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1675875</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Kreatsoulas C, Shannon HS, Giacomini M, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;Coronary artery disease (CAD) is the leading cause of mortality in the Western world. The prevalence of angina and proportion of deaths from CAD is higher among women than men. Despite this, the perception that CAD is a man's disease prevails. Historic faulty assumptions in the construct of angina, failure to systematically include women in clinical studies, and differences in age-specific incidence rates have perpetuated this perception. As a result, the term typical angina has evolved to describe symptoms in men, whereas atypical angina is applied to women. This lack of clarity has been a source of controversy in understanding CAD in women.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">829</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">833</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.229</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1675875</guid>
    </item>
    <item>
      <title>Serotonin Reuptake Inhibitor Use, Depression, and Long-Term Outcomes After an Acute Coronary Syndrome: A Prospective Cohort Study</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687523</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Rieckmann N, Kronish IM, Shapiro PA, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;Depression is highly prevalent among patients with coronary heart disease. Selective serotonin reuptake inhibitors (SSRIs) are recommended as first-line antidepressant treatments for this population. Whereas there is a long-standing notion that SSRIs may improve cardiac disease prognosis by inhibiting platelet aggregation, SSRI use may also worsen prognosis by increasing bleeding or increasing the risk for arrhythmia.&lt;/span&gt;</description>
      <prism:startingPage xmlns:prism="prism">1</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">2</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.910</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687523</guid>
    </item>
    <item>
      <title>Waste and Harm in the Treatment of Mild Hypertension Waste and Harm in Treatment of Mild Hypertension </title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687525</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Heath I. </author>
      <description>&lt;span class="paragraphSection"&gt;The 2012 Cochrane Review on “Pharmacotherapy for Mild Hypertension” concluded that antihypertensive drugs used in the treatment of otherwise healthy adults with mild hypertension (systolic blood pressure [BP], 140-159 mm Hg, and/or diastolic BP, 90-99 mm Hg) have not been shown to reduce mortality or morbidity in randomized clinical trials. Will this landmark conclusion affect clinical practice and slow the inexorable expansion of disease categories? It certainly should because overdiagnosis and overtreatment are potent causes of both waste and harm and seem to be operating in the interests of the pharmaceutical industry rather than in those of the patients whom the industry claims to serve.&lt;/span&gt;</description>
      <prism:startingPage xmlns:prism="prism">1</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">2</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.970</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687525</guid>
    </item>
    <item>
      <title>In This Issue of JAMA Internal Medicine</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687651</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author />
      <description />
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">722</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">722</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.51</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687651</guid>
    </item>
    <item>
      <title>Resumption of Warfarin Therapy After Gastrointestinal Tract Bleeding: Benefit or Bias?</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687667</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Filion KB, Assayag J, Azoulay L. </author>
      <description>&lt;span class="paragraphSection"&gt;It is with great interest that we read the article by Witt and colleagues, who examined the risk of thromboembolism, recurrent hemorrhage, and death in a retrospective cohort of warfarin users with gastrointestinal tract bleeding. Although no difference was observed in recurrent hemorrhage, the authors found that warfarin therapy resumption after gastrointestinal tract bleeding resulted in substantial decreases in thrombosis (adjusted hazard ratio [HR], 0.05; 95% CI, 0.01-0.58) and death (adjusted HR, 0.31; 95% CI, 0.15-0.62). In contrast, a participant-level meta-analysis estimated that oral anticoagulants reduce the rate of ischemic stroke in patients with atrial fibrillation by 52% (HR, 0.48; 95% CI, 0.37-0.63) but not death (HR, 0.93; 95% CI, 0.76-1.13) relative to aspirin.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">833</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">834</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.3763</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687667</guid>
    </item>
    <item>
      <title>Resumption of Warfarin Therapy After Gastrointestinal Tract Bleeding: Benefit or Bias?—Reply</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687668</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Witt DM, Delate T, Crowther MA. </author>
      <description>&lt;span class="paragraphSection"&gt;In reply&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">833</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">834</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.14</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687668</guid>
    </item>
    <item>
      <title>Routine Noninvasive Testing and Highly Sensitive Troponin Immunoassays</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687669</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Lippi G, Cervellin G. </author>
      <description>&lt;span class="paragraphSection"&gt;In a recent article published in this journal, Prasad et al reviewed the current practice of routine noninvasive testing in patients with chest pain admitted to the emergency department (ED). Although stress testing is currently recommended in those patients with nondiagnostic results of serial electrocardiograms and biomarkers, the definition of “negative cardiac biomarker findings” may be an important drawback in this approach. At the time when the American College of Cardiology/American Heart Association guidelines were released (ie, 2007), the designation of “nondiagnostic biomarker” was based on the so-called contemporary-sensitive troponin immunoassays, which generate measurable values in approximately 35% of a healthy population, at best. The recent development and gradual commercialization of the novel highly sensitive immunoassays represent a major breakthrough in the management of chest pain in the ED, considering that a large number of these patients have comorbidities that contribute to increase troponin concentration because of an increased turnover of myocardiocytes (eg, nonischemic heart injury) or impaired protein catabolism (eg, kidney disease). With this development, measurable troponin values can now be obtained in up to 96% of cases of a presumably healthy population, and thereby in virtually all subjects admitted to the ED.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">834</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">835</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.3773</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687669</guid>
    </item>
    <item>
      <title>Routine Noninvasive Testing and Highly Sensitive Troponin Immunoassays—Reply</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687670</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Prasad V, Cheung M, Cifu A. </author>
      <description>&lt;span class="paragraphSection"&gt;In reply&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">834</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">835</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.4089</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687670</guid>
    </item>
    <item>
      <title>New Oral Anticoagulants in Acute Coronary Syndromes: What Does a Meta-analysis Tell Us?</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687671</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Kwong JW, Yu C. </author>
      <description>&lt;span class="paragraphSection"&gt;We read with interest the meta-analysis by Komócsi et al, which reported that the use of factor Xa and direct thrombin inhibitors in patients receiving antiplatelet therapy after an acute coronary syndrome (ACS) was associated with a substantial increase in major bleeding and moderate reduction in ischemic events. However, there are a few issues we would like to highlight.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">835</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">836</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.78</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687671</guid>
    </item>
    <item>
      <title>New Oral Anticoagulants in Acute Coronary Syndromes: What Does a Meta-analysis Tell Us?—Reply</title>
      <link>http://archinte.jamanetwork.com/article.aspx?articleID=1687672</link>
      <pubDate>Mon, 13 May 2013 00:00:00 GMT</pubDate>
      <author>Komócsi A, Vorobcsuk A, Aradi D. </author>
      <description>&lt;span class="paragraphSection"&gt;In reply&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">173</prism:volume>
      <prism:number xmlns:prism="prism">9</prism:number>
      <prism:startingPage xmlns:prism="prism">835</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">836</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/jamainternmed.2013.424</prism:doi>
      <guid>http://archinte.jamanetwork.com/article.aspx?articleID=1687672</guid>
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