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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.amjmed.com/?rss=yes"><title>The American Journal of Medicine</title><description>The American Journal of Medicine RSS feed: Current Issue.    
 The American Journal of Medicine  - "The Green Journal" -  publishes original clinical research of interest to physicians in internal 
medicine, both in academia and community-based practice.  The American Journal of Medicine  is the official journal of The Association 
of Professors of Medicine, a prestigious group comprised of chairs of departments of internal medicine at more than 125 medical schools 
across the country. Each issue carries useful reviews as well as seminal articles of immediate interest to the practicing physician, 
including peer-reviewed, original scientific studies that have direct clinical significance, and position papers on health care issues, 
medical education, and public policy.  The journal's ISI factor - the international measure of cited manuscripts and scientific impact 
- is fourteenth in the world among all general medical journals.
  
 The  AJM  publishes studies performed by multi-center groups 
in the various disciplines of medicine, including clinical trials and cohort studies from large patient populations, specifically: 

 
 Phase I, phase II, and phase III studies performed under the auspices of groups such as general clinical research centers, cooperative 
oncology groups, and the like.   
 Reports of patients with common presentations or diseases, especially studies that delineate 
the natural history and therapy of important conditions.  
 Reviews oriented to the practicing internist and  diagnostic puzzles, 
complete with images from a variety of specialties. 
 Careful physiological or pharmacological studies that explain normal function 
or the body's response to disease.  
 Analytic reviews such as meta-analyses and decision analyses that use a formal structure 
to summarize an important field.  
 
   </description><link>http://www.amjmed.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:issn>0002-9343</prism:issn><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:publicationDate>May 2012</prism:publicationDate><prism:copyright> © 2012 Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000708/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431100948X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009478/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009491/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431100996X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009004/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009922/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009223/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311006577/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009120/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010254/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311004815/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000691/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431200006X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009934/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000149/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311006462/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000095/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431100653X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009910/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009958/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311008989/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000150/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311008977/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000162/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311008953/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000174/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000083/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431200071X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311008564/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431200191X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001933/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000708/abstract?rss=yes"><title>Changing US and World Demographics: Consequences for the Practice of Medicine</title><link>http://www.amjmed.com/article/PIIS0002934312000708/abstract?rss=yes</link><description>Demographics is a field of study in which statistical characteristics of a population are followed over a period of time. Commonly, demographic data are used in analyses involving fields such as sociology, public policy, and marketing. Characteristics that are followed often include gender, age, survival, a variety of disabilities, urbanization, socioeconomic factors, educational level, and many other variables. Demographic changes in a population can have major consequences for healthcare delivery and planning. For example, if the population in a specific country demonstrates a demographic trend for increasing numbers of geriatric individuals, this will have a major impact on the demand for inpatient hospital and rehabilitation services because this age group has a high rate of use for such services.</description><dc:title>Changing US and World Demographics: Consequences for the Practice of Medicine</dc:title><dc:creator>Joseph S. Alpert</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.006</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>427</prism:startingPage><prism:endingPage>428</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431100948X/abstract?rss=yes"><title>Thrombolytics and Vena Cava Filters Decrease Mortality in Patients with Unstable Pulmonary Embolism</title><link>http://www.amjmed.com/article/PIIS000293431100948X/abstract?rss=yes</link><description>


   SEE RELATED ARTICLES pp. 465, 471, and 478.</description><dc:title>Thrombolytics and Vena Cava Filters Decrease Mortality in Patients with Unstable Pulmonary Embolism</dc:title><dc:creator>James E. Dalen</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.023</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>429</prism:startingPage><prism:endingPage>430</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009478/abstract?rss=yes"><title>Caveat Promisor: The Potential Pitfalls of Clinical Guarantees</title><link>http://www.amjmed.com/article/PIIS0002934311009478/abstract?rss=yes</link><description>In George Bernard Shaw's acerbic depiction of the medical profession, an unscrupulous physician reveals that “just two words” had brought him financial success: “Cure Guaranteed.” It is common knowledge that such an advertising scheme would be considered unethical. The American Medical Association (AMA) Code of Ethics prohibits outcome-contingent treatment fees as “creating unrealistic expectations of medicine and false promises to consumers.” Elsewhere, AMA policy reaffirms that “the results of medical services cannot be guaranteed.”</description><dc:title>Caveat Promisor: The Potential Pitfalls of Clinical Guarantees</dc:title><dc:creator>Charles G. Kels, Lori H. Kels</dc:creator><dc:identifier>10.1016/j.amjmed.2011.08.030</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Commentary</prism:section><prism:startingPage>431</prism:startingPage><prism:endingPage>432</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009491/abstract?rss=yes"><title>Salt and Hypertension: Is Salt Dietary Reduction Worth the Effort?</title><link>http://www.amjmed.com/article/PIIS0002934311009491/abstract?rss=yes</link><description>Abstract: 
In numerous epidemiologic, clinical, and experimental studies, dietary sodium intake has been linked to blood pressure, and a reduction in dietary salt intake has been documented to lower blood pressure. In young subjects, salt intake has a programming effect in that blood pressure remains elevated even after a high salt intake has been reduced. Elderly subjects, African Americans, and obese patients are more sensitive to the blood pressure-lowering effects of a decreased salt intake. Depending on the baseline blood pressure and degree of salt intake reduction, systolic blood pressure can be lowered by 4 to 8 mm Hg. A greater decrease in blood pressure is achieved when a reduced salt intake is combined with other lifestyle interventions, such as adherence to Dietary Approaches to Stop Hypertension. A high salt intake has been shown to increase not only blood pressure but also the risk of stroke, left ventricular hypertrophy, and proteinuria. Adverse effects associated with salt intake reduction, unless excessive, seem to be minimal. However, data linking a decreased salt intake to a decrease in morbidity and mortality in hypertensive patients are not unanimous. Dietary salt intake reduction can delay or prevent the incidence of antihypertensive therapy, can facilitate blood pressure reduction in hypertensive patients receiving medical therapy, and may represent a simple cost-saving mediator to reduce cardiovascular morbidity and mortality.
</description><dc:title>Salt and Hypertension: Is Salt Dietary Reduction Worth the Effort?</dc:title><dc:creator>Tiberio M. Frisoli, Roland E. Schmieder, Tomasz Grodzicki, Franz H. Messerli</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.023</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Reviews</prism:section><prism:startingPage>433</prism:startingPage><prism:endingPage>439</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431100996X/abstract?rss=yes"><title>Evidence-based Use of Statins for Primary Prevention of Cardiovascular Disease</title><link>http://www.amjmed.com/article/PIIS000293431100996X/abstract?rss=yes</link><description>Abstract: 
Three-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, commonly known as statins, are widely available, inexpensive, and represent a potent therapy for treating elevated cholesterol. Current national guidelines put forth by the Adult Treatment Panel III recommend statins as part of a comprehensive primary prevention strategy for patients with elevated low-density lipoprotein cholesterol at increased risk for developing coronary heart disease within 10 years. Lack of a clear-cut mortality benefit in primary prevention has caused some to question the use of statins for patients without known coronary heart disease. On review of the literature, we conclude that current data support only a modest mortality benefit for statin primary prevention when assessed in the short term (&lt;5 years). Of note, statin primary prevention results in a significant decrease in cardiovascular morbidity over the short and long term and a trend toward increased reduction in mortality over the long term. When appraised together, these data provide compelling evidence to support the use of statins for primary prevention in patients with risk factors for developing coronary heart disease over the next 10 years.
</description><dc:title>Evidence-based Use of Statins for Primary Prevention of Cardiovascular Disease</dc:title><dc:creator>C. Michael Minder, Michael J. Blaha, Aaron Horne, Erin D. Michos, Sanjay Kaul, Roger S. Blumenthal</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.013</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-03-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-03-05</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Reviews</prism:section><prism:startingPage>440</prism:startingPage><prism:endingPage>446</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009004/abstract?rss=yes"><title>Amiodarone-associated Optic Neuropathy: A Critical Review</title><link>http://www.amjmed.com/article/PIIS0002934311009004/abstract?rss=yes</link><description>Abstract: 
Although amiodarone is the most commonly prescribed anti-arrhythmic drug, its use is limited by serious toxicities, including optic neuropathy. Current reports of amiodarone-associated optic neuropathy identified from the Food and Drug Administration's Adverse Event Reporting System and published case reports were reviewed. A total of 296 reports were identified: 214 from the Adverse Event Reporting System, 59 from published case reports, and 23 from adverse events reports for patients enrolled in clinical trials. Mean duration of amiodarone therapy before vision loss was 9 months (range 1-84 months). Insidious onset of amiodarone-associated optic neuropathy (44%) was the most common presentation, and nearly one third were asymptomatic. Optic disk edema was present in 85% of cases. Following drug cessation, 58% had improved visual acuity, 21% were unchanged, and 21% had further decreased visual acuity. Legal blindness (&lt;20/200) was noted in at least one eye in 20% of cases. Close ophthalmologic surveillance of patients during the tenure of amiodarone administration is warranted.
</description><dc:title>Amiodarone-associated Optic Neuropathy: A Critical Review</dc:title><dc:creator>Rod S. Passman, Charles L. Bennett, Joseph M. Purpura, Rashmi Kapur, Lenworth N. Johnson, Dennis W. Raisch, Dennis P. West, Beatrice J. Edwards, Steven M. Belknap, Dustin B. Liebling, Mathew J. Fisher, Athena T. Samaras, Lisa-Gaye A. Jones, Katrina-Marie E. Tulas, June M. McKoy</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.020</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-03-02</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-03-02</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Reviews</prism:section><prism:startingPage>447</prism:startingPage><prism:endingPage>453</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009922/abstract?rss=yes"><title>Improving the Preventive Care of Asplenic Patients</title><link>http://www.amjmed.com/article/PIIS0002934311009922/abstract?rss=yes</link><description>Asplenia and hyposplenia increase the risk of fulminant sepsis by a variety of organisms. Vaccination against encapsulated bacteria and early administration of empiric antibiotics for febrile illnesses can reduce the risk of sepsis.</description><dc:title>Improving the Preventive Care of Asplenic Patients</dc:title><dc:creator>Hans S. Kim, Gila Kriegel, Mark D. Aronson</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.009</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-03-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-03-05</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical effectiveness</prism:section><prism:startingPage>454</prism:startingPage><prism:endingPage>456</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009223/abstract?rss=yes"><title>From the Outside Looking In</title><link>http://www.amjmed.com/article/PIIS0002934311009223/abstract?rss=yes</link><description>One cannot overstate the value of a detailed skin examination in the diagnosis of systemic disorders, including infectious diseases. This precept was demonstrated in the present case.</description><dc:title>From the Outside Looking In</dc:title><dc:creator>Yasbanoo Moayedi, Paul E. Bunce, Shachar Sade, Danny Ghazarian, Wayne L. Gold</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.021</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-23</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-23</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Diagnostic dilemma</prism:section><prism:startingPage>457</prism:startingPage><prism:endingPage>460</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311006577/abstract?rss=yes"><title>Nonspecific but Significant</title><link>http://www.amjmed.com/article/PIIS0002934311006577/abstract?rss=yes</link><description>Vague signs should not be overlooked, as they can on occasion, hint at a dire diagnosis. A 24-year-old serviceman complained about mild lower-back pain about 1 year before admission to our hospital. Initially, he visited an orthopedist, and plain radiography of the lateral thoracic and lumbar spine was performed. Several small irregularly-shaped calcifications located over the peritoneal region were interpreted as a nonspecific finding ().</description><dc:title>Nonspecific but Significant</dc:title><dc:creator>Yu-Guang Chen, Woei-Yau Kao, Shih-Hung Tsai</dc:creator><dc:identifier>10.1016/j.amjmed.2011.08.004</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Images in radiology</prism:section><prism:startingPage>461</prism:startingPage><prism:endingPage>464</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009120/abstract?rss=yes"><title>Thrombolytic Therapy in Unstable Patients with Acute Pulmonary Embolism: Saves Lives but Underused</title><link>http://www.amjmed.com/article/PIIS0002934311009120/abstract?rss=yes</link><description>Abstract: 
Background: 
Data are sparse and inconsistent regarding whether thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism. We tested the hypothesis that thrombolytic therapy reduces case fatality rate in such patients.

Methods: 
In-hospital all-cause case fatality rate according to treatment was determined in unstable patients with pulmonary embolism who were discharged from short-stay hospitals throughout the United States from 1999 to 2008 by using data from the Nationwide Inpatient Sample. Unstable patients were in shock or ventilator dependent.

Results: 
Among unstable patients with pulmonary embolism, 21,390 of 72,230 (30%) received thrombolytic therapy. In-hospital all-cause case fatality rate in unstable patients with thrombolytic therapy was 3105 of 21,390 (15%) versus 23,820 of 50,840 (47%) without thrombolytic therapy (P&lt;.0001). All-cause case fatality rate in unstable patients with thrombolytic therapy plus a vena cava filter was 505 of 6630 (7.6%) versus 4260 of 12,850 (33%) with a filter alone (P&lt;.0001). Case fatality rate attributable to pulmonary embolism in unstable patients was 820 of 9810 (8.4%) with thrombolytic therapy versus 1080 of 2600 (42%) with no thrombolytic therapy (P&lt;.0001). Case fatality rate attributable to pulmonary embolism in unstable patients with thrombolytic therapy plus vena cava filter was 70 of 2590 (2.7%) versus 160 of 600 (27%) with a filter alone (P&lt;.0001).

Conclusion: 
In-hospital all-cause case fatality rate and case fatality rate attributable to pulmonary embolism in unstable patients was lower in those who received thrombolytic therapy. Thrombolytic therapy resulted in a lower case fatality rate than using vena cava filters alone, and the combination resulted in an even lower case fatality rate. Thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.
</description><dc:title>Thrombolytic Therapy in Unstable Patients with Acute Pulmonary Embolism: Saves Lives but Underused</dc:title><dc:creator>Paul D. Stein, Fadi Matta</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.015</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-13</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>465</prism:startingPage><prism:endingPage>470</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010254/abstract?rss=yes"><title>Case Fatality Rate with Pulmonary Embolectomy for Acute Pulmonary Embolism</title><link>http://www.amjmed.com/article/PIIS0002934311010254/abstract?rss=yes</link><description>Abstract: 
Background: 
There are insufficient data to assess the potential role of pulmonary embolectomy in patients with acute pulmonary embolism.

Methods: 
In-hospital all-cause case fatality rate with pulmonary embolectomy was assessed from the Nationwide Inpatient Sample from 1999 through 2008.

Results: 
Among unstable patients (in shock or ventilator-dependent), case fatality rate with embolectomy was 380 of 950 (40%). Among stable patients, case fatality rate was lower: 690 of 2820 (24%) (P &lt;.0001). Case fatality rate in unstable patients was 39% in 1999-2003 and 40% in 2004-2008 (not significant), and in stable patients it was 27% in 1999-2003 and 23% in 2004-2008 (P=.01). Case fatality rates were lower in patients with a primary diagnosis of pulmonary embolism and even lower in patients with a primary diagnosis who had none of the comorbid conditions listed in the Charlson Index. Within each stratified group, patients with vena cava filters had a lower case fatality rate.

Conclusions: 
Case fatality rate in unstable patients who underwent pulmonary embolectomy remained at 39%-40% from 1999-2003 to 2004-2008, and in stable patients it decreased only from 27% to 23%. Case fatality rates were lower in those with fewer comorbid conditions and in those who received a vena cava filter. Our data reflect average outcome in the US. It may be that experienced surgeons and an aggressive multidisciplinary team could obtain a lower case fatality rate.
</description><dc:title>Case Fatality Rate with Pulmonary Embolectomy for Acute Pulmonary Embolism</dc:title><dc:creator>Paul D. Stein, Fadi Matta</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.003</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>471</prism:startingPage><prism:endingPage>477</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311004815/abstract?rss=yes"><title>Impact of Vena Cava Filters on In-hospital Case Fatality Rate from Pulmonary Embolism</title><link>http://www.amjmed.com/article/PIIS0002934311004815/abstract?rss=yes</link><description>Abstract: 
Background: 
The effects of vena cava filters on case fatality rate are not clear, although they are used increasingly in patients with pulmonary embolism. The purpose of this investigation is to determine categories of patients with pulmonary embolism in whom vena cava filters reduce in-hospital case fatality rate.

Methods: 
In-hospital all-cause case fatality rate according to the use of vena cava filters was determined in patients with pulmonary embolism discharged from short-stay hospitals throughout the United States using data from the Nationwide Inpatient Sample.

Results: 
In-hospital case fatality rate was marginally lower in stable patients who received a vena cava filter: 21,420 of 297,700 (7.2%) versus 135,240 of 1,712,800 (7.9%) (P&lt;.0001). Filters did not improve in-hospital case fatality rate if deep venous thrombosis was diagnosed in stable patients. A few stable patients (1.4%) received thrombolytic therapy. Such patients who received a vena cava filter had a lower case fatality rate than those who did not: 550 of 8550 (6.4%) versus 2950 of 19,050 (15%) (P&lt;.0001). Unstable patients who received thrombolytic therapy had a lower in-hospital case fatality rate with vena cava filters than those who did not: 505 of 6630 (7.6%) versus 2600 of 14,760 (18%) (P&lt;.0001). Unstable patients who did not receive thrombolytic therapy also had a lower in-hospital case fatality rate with a vena cava filter: 4260 of 12,850 (33%) versus 19,560 of 38,000 (51%) (P&lt;.0001).

Conclusion: 
At present, it seems prudent to consider a vena cava filter in patients with pulmonary embolism who are receiving thrombolytic therapy and in unstable patients who may not be candidates for thrombolytic therapy. Future prospective study is warranted to better define in which patients a filter is appropriate.
</description><dc:title>Impact of Vena Cava Filters on In-hospital Case Fatality Rate from Pulmonary Embolism</dc:title><dc:creator>Paul D. Stein, Fadi Matta, Daniel C. Keyes, Gary L. Willyerd</dc:creator><dc:identifier>10.1016/j.amjmed.2011.05.025</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-06</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-06</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>478</prism:startingPage><prism:endingPage>484</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000691/abstract?rss=yes"><title>Exercise Is Associated with a Reduced Incidence of Sleep-disordered Breathing</title><link>http://www.amjmed.com/article/PIIS0002934312000691/abstract?rss=yes</link><description>Abstract: 
Background: 
The effect of exercise on sleep-disordered breathing is unknown. While diet and weight loss have been shown to reduce the severity of sleep-disordered breathing, it is unclear whether exercise has an independent effect.

Methods: 
A population-based longitudinal epidemiologic study of adults measured the association between exercise and incidence and severity of sleep-disordered breathing. Hours of weekly exercise were assessed by 2 mailed surveys (1988 and 2000). Sleep-disordered breathing was assessed by 18-channel in-laboratory polysomnography at baseline and at follow-up.

Results: 
Associations were modeled using linear and logistic regression, adjusting for body mass index, age, sex, and other covariates. Hours of exercise were associated with reduced incidence of mild (odds ratio 0.76, P=.011) and moderate (odds ratio 0.67, P=.002) sleep-disordered breathing. A decrease in exercise duration also was associated with worsening sleep-disordered breathing, as measured by the apnea-hypopnea index (β=2.368, P=.048). Adjustment for body mass index attenuated these effects.

Conclusions: 
Exercise is associated with a reduced incidence of mild and moderate sleep-disordered breathing, and decreasing exercise is associated with worsening of sleep-disordered breathing. The effect of exercise on sleep-disordered breathing appears to be largely, but perhaps not entirely, mediated by changes in body habitus.
</description><dc:title>Exercise Is Associated with a Reduced Incidence of Sleep-disordered Breathing</dc:title><dc:creator>Karim M. Awad, Atul Malhotra, Jodi H. Barnet, Stuart F. Quan, Paul E. Peppard</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.025</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>485</prism:startingPage><prism:endingPage>490</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431200006X/abstract?rss=yes"><title>Determinants of High-Sensitivity Troponin T Among Patients with a Noncardiac Cause of Chest Pain</title><link>http://www.amjmed.com/article/PIIS000293431200006X/abstract?rss=yes</link><description>Abstract: 
Background: 
It is unknown to what extent noncardiac causes, including renal dysfunction, may contribute to high-sensitivity cardiac troponin T levels.

Methods: 
In an observational international multicenter study, we enrolled consecutive patients presenting with acute chest pain to the emergency department. Of 1181 patients enrolled, 572 were adjudicated by 2 independent cardiologists to have a noncardiac cause of chest pain. Multiple linear regression analyses were used to determine the important predictors of log-transformed high-sensitivity cardiac troponin T. Kaplan-Meier curve was used to assess the prognostic significance of high-sensitivity cardiac troponin T&gt;0.014 μg/L (99th percentile).

Results: 
A total of 88 patients (15%) had high-sensitivity cardiac troponin T&gt;0.014 μg/L. Less than 50% of cardiac troponins could be explained by known cardiac or noncardiac diseases. In decreasing order of importance, age, estimated glomerular filtration rate, hypertension, previous myocardial infarction, and chronic kidney disease (adjusted r2 0.44) emerged as significant factors in linear regression analysis to predict high-sensitivity cardiac troponin T. High-sensitivity cardiac troponin T was best explained by a linear curve with age as≤0.014 μg/L. Patients with high-sensitivity cardiac troponin T levels&gt;0.014 μg/L were at increased risk for all-cause mortality (hazard ratio 3.0; 95% confidence interval, 0.8-10.6; P=.02) during follow-up.

Conclusion: 
Among the known covariates, age and not renal dysfunction is the most important determinant of high-sensitivity cardiac troponin T. Because known cardiac and noncardiac factors, including renal dysfunction, explain less than 50% of high-sensitivity cardiac troponin T levels among patients with a noncardiac cause of chest pain, unknown or underestimated cardiac involvement during the acute presenting condition seems to be the major cause of elevated high-sensitivity cardiac troponin T.
</description><dc:title>Determinants of High-Sensitivity Troponin T Among Patients with a Noncardiac Cause of Chest Pain</dc:title><dc:creator>Affan Irfan, Raphael Twerenbold, Miriam Reiter, Tobias Reichlin, Claudia Stelzig, Michael Freese, Philip Haaf, Willibald Hochholzer, Stephan Steuer, Stefano Bassetti, Christa Zellweger, Heike Freidank, Federico Peter, Isabel Campodarve, Christophe Meune, Christian Mueller</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.031</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>491</prism:startingPage><prism:endingPage>498.e1</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009934/abstract?rss=yes"><title>Nature Versus Nurture in Gout: A Twin Study</title><link>http://www.amjmed.com/article/PIIS0002934311009934/abstract?rss=yes</link><description>Abstract: 
Background: 
Gouty arthritis (gout) is the most common inflammatory arthritis in the United States and several other countries. Some rare forms of gout have a known genetic basis, but the relative importance of genetic factors on the risk for the lifetime prevalence of gout is not clear.

Methods: 
We performed a heritability analysis for hyperuricemia and gout among 514 unselected, all-male twin pairs who were a part of the National Heart, Lung, and Blood Institute twin study, a prospective observational cohort study. Statistical analyses were performed using structural equation models and maximum likelihood methods. The covariates used for adjustment in the structural equation models were identified using bivariate logistic regressions.

Results: 
The study population included 253 monozygotic (MZ) and 261 dizygotic (DZ) twin pairs, aged 48 (±3) years at baseline and followed for a mean of 34 years. The lifetime prevalence of gout did not differ between MZ and DZ twins. The concordance of hyperuricemia was 53% in MZ and 24% in DZ twin pairs (P&lt;.001). Models that quantified the relative contribution of genetic and environmental factors on phenotypic variance showed that individual variability in gout was substantially influenced by environmental factors shared between co-twins and not by genetic factors. In contrast, individual differences in hyperuricemia were influenced significantly by genetic factors.

Conclusion: 
Hyperuricemia is a genetic trait. Outside the context of rare genetic disorders, risk for gout is determined by the environment. This has implications for prevention and treatment approaches.
</description><dc:title>Nature Versus Nurture in Gout: A Twin Study</dc:title><dc:creator>Eswar Krishnan, Christina N. Lessov-Schlaggar, Ruth E. Krasnow, Gary E. Swan</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.010</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-23</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-23</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>499</prism:startingPage><prism:endingPage>504</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000149/abstract?rss=yes"><title>Chlorhexidine Bathing to Reduce Central Venous Catheter-associated Bloodstream Infection: Impact and Sustainability</title><link>http://www.amjmed.com/article/PIIS0002934312000149/abstract?rss=yes</link><description>Abstract: 
Background: 
Chlorhexidine bathing has been associated with reductions in healthcare-associated bloodstream infection. To determine the impact and sustainability of the effect of chlorhexidine bathing on central venous catheter-associated bloodstream infection, we performed a prospective, 3-phase, multiple-hospital study.

Methods: 
In the medical intensive care unit and the respiratory care unit of a tertiary care hospital and the medical-surgical intensive care units of 4 community hospitals, rates of central venous catheter-associated bloodstream infection were collected prospectively for each period. Pre-intervention (phase 1) patients were bathed with soap and water or nonmedicated bathing cloths; active intervention (phase 2) patients were bathed with 2% chlorhexidine gluconate cloths with the number of baths administered and skin tolerability assessed; post-intervention (phase 3) chlorhexidine bathing was continued but without oversight by research personnel. Central venous catheter-associated bloodstream infection rates were compared over study periods using Poisson regression.

Results: 
Compared with pre-intervention, during active intervention there were significantly fewer central venous catheter-associated bloodstream infections (6.4/1000 central venous catheter days vs 2.6/1000 central venous catheter days, relative risk, 0.42; 95% confidence interval, 0.25-0.68; P&lt;.001), and this reduction was sustained during post-intervention (2.9/1000 central venous catheter days; relative risk, 0.46; 95% confidence interval, 0.30-0.70; P&lt;.001). During the active intervention period, compliance with chlorhexidine bathing was 82%. Few adverse events were observed.

Conclusion: 
In this multiple-hospital study, chlorhexidine bathing was associated with significant reductions in central venous catheter-associated bloodstream infection, and these reductions were sustained post-intervention when chlorhexidine bathing was unmonitored. Chlorhexidine bathing was well tolerated and is a useful adjunct to reduce central venous catheter-associated bloodstream infection.
</description><dc:title>Chlorhexidine Bathing to Reduce Central Venous Catheter-associated Bloodstream Infection: Impact and Sustainability</dc:title><dc:creator>Marisa A. Montecalvo, Donna McKenna, Robert Yarrish, Lynda Mack, George Maguire, Janet Haas, Lawrence DeLorenzo, Norine Dellarocco, Barbara Savatteri, Addie Rosenthal, Anita Watson, Debra Spicehandler, Qiuhu Shi, Paul Visintainer, Gary P. Wormser</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.032</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research studies</prism:section><prism:startingPage>505</prism:startingPage><prism:endingPage>511</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311006462/abstract?rss=yes"><title>Systematic Review of Noncancer Presentations with a Median Survival of 6 Months or Less</title><link>http://www.amjmed.com/article/PIIS0002934311006462/abstract?rss=yes</link><description>Abstract: 
Purpose: 
We report on clinical indicators of 6-month mortality in advanced noncancer illnesses and the effect of treatment on survival.

Methods: 
The MEDLINE database was searched comprehensively to find studies evaluating survival for common advanced noncancer illnesses. We retrieved and evaluated studies that reported a median survival of ≤1 year and evaluated prognostic factors or effect of treatment on survival. We extracted data on presentations with median survivals of ≤6 months for heart failure, chronic obstructive pulmonary disease, dementia, geriatric failure to thrive, cirrhosis, and end-stage renal failure. Independent risk factors for survival were combined and included if their combination was associated with a 6-month mortality of ≥50%.

Results: 
The search identified 1000 potentially relevant studies, of which 475 were retrieved and evaluated, and 74 were included. We report the common clinical presentations that are consistently associated with a 6-month median survival. Even though advanced noncancer syndromes differ clinically, a universal set of prognostic factors signals progression to terminal disease, including poor performance status, advanced age, malnutrition, comorbid illness, organ dysfunction, and hospitalization for acute decompensation. Generally, a 6-month median survival is associated with the presence of 2-4 of these factors. With few exceptions, these terminal presentations are quite refractory to treatment.

Conclusion: 
This systematic review summarizes prognostic factors common to advanced noncancer illness. There is little evidence at present that treatment prolongs survival at these terminal stages.
</description><dc:title>Systematic Review of Noncancer Presentations with a Median Survival of 6 Months or Less</dc:title><dc:creator>Shelley R. Salpeter, Esther J. Luo, Dawn S. Malter, Brad Stuart</dc:creator><dc:identifier>10.1016/j.amjmed.2011.07.028</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2011-10-25</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2011-10-25</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical research study</prism:section><prism:startingPage>512.e1</prism:startingPage><prism:endingPage>512.e16</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000095/abstract?rss=yes"><title>Why the (Un)Affordable Care Act Should Be Repealed and Replaced</title><link>http://www.amjmed.com/article/PIIS0002934312000095/abstract?rss=yes</link><description>As coauthors of Why ObamaCare Is Wrong for America, we strongly recommend that the Affordable Care Act of 2010 be repealed and replaced as soon as possible. The Affordable Care Act has become deservedly more unpopular since its enactment. It is too costly to finance, too difficult to administer, too burdensome on health care professionals, and too disruptive of existing health care arrangements that many Americans prefer. It will limit future economic growth, distort health care delivery, exacerbate already unsustainable entitlement spending, and erase any meaningful constitutional limits on the enumerated powers of the federal government. By relying on illusory formulaic reductions in future payments to physicians, on burdensome new reporting requirements, and on top-down restrictions on medical innovation, the Affordable Care Act will further jeopardize access to quality care.</description><dc:title>Why the (Un)Affordable Care Act Should Be Repealed and Replaced</dc:title><dc:creator>Tom Miller, James C. Capretta, Grace-Marie Turner</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.002</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Commentaries</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e4</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431100653X/abstract?rss=yes"><title>The Closing of St Vincent's Hospital in New York City: What Happened to the House Staff Orphans?</title><link>http://www.amjmed.com/article/PIIS000293431100653X/abstract?rss=yes</link><description>During a time when a significant percentage of the population is uninsured and the cost of medical care has become unmanageable, it is no surprise that hospitals have recently fallen prey to mounting debt and financial woes.</description><dc:title>The Closing of St Vincent's Hospital in New York City: What Happened to the House Staff Orphans?</dc:title><dc:creator>Elizabeth Zheng, William H. Frishman</dc:creator><dc:identifier>10.1016/j.amjmed.2011.08.002</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-13</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Commentaries</prism:section><prism:startingPage>e5</prism:startingPage><prism:endingPage>e6</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009910/abstract?rss=yes"><title>A True Positive Nasal Nodule</title><link>http://www.amjmed.com/article/PIIS0002934311009910/abstract?rss=yes</link><description>A 36-year-old previously healthy immigrant from the Punjab area of Pakistan presented to his family physician when he became aware of lymph node enlargement in his neck. He had no other symptoms, and physical examination confirmed cervical lymphadenopathy but was otherwise unremarkable, as was peripheral blood testing. Nevertheless, given the prevalence of tuberculosis in the patient's country of origin and a history of previous infective involvement of a family member, the patient was referred to the respiratory department of our hospital for further assessment and evaluation.</description><dc:title>A True Positive Nasal Nodule</dc:title><dc:creator>Christos Tziotzios, Robert Jackson, David Burden</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.026</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical communications to the editor</prism:section><prism:startingPage>e7</prism:startingPage><prism:endingPage>e8</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009958/abstract?rss=yes"><title>Metformin-associated Lactic Acidosis Masquerading as Ischemic Bowel</title><link>http://www.amjmed.com/article/PIIS0002934311009958/abstract?rss=yes</link><description>A 69-year-old male inpatient on the psychiatric ward developed abdominal pain, nausea, non-bloody emesis, and diaphoresis shortly after eating. His medical history included depression, coronary artery disease, diabetes mellitus, and dyslipidemia. His medications included clopidogrel, gabapentin, glipizide, lisinopril, metformin, metoprolol, omeprazole, rosuvastatin, and sertraline. He denied overdosing on any medications. His vital signs were a heart rate of 74 beats/min, temperature of 36.2°C, respiratory rate of 24 breaths/min, and blood pressure of 82/52 mm Hg. The examination revealed decreased bowel sounds, voluntary guarding, and tenderness to palpation in the lower abdomen, which appeared out of proportion to the physical examination. A rectal examination revealed impacted stool and a positive stool guaiac.</description><dc:title>Metformin-associated Lactic Acidosis Masquerading as Ischemic Bowel</dc:title><dc:creator>Chase S. Correia, Kirk A. Bronander</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.012</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-02-23</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-23</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Clinical communications to the editor</prism:section><prism:startingPage>e9</prism:startingPage><prism:endingPage>e9</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311008989/abstract?rss=yes"><title>Usefulness of Electrocardiography for Cardiovascular Screening in Collegiate Athletes</title><link>http://www.amjmed.com/article/PIIS0002934311008989/abstract?rss=yes</link><description>I read with interest the article by Magalski et al about the role of electrocardiography (ECG) and transthoracic echocardiography (TTE) for preparticipation screening of athletes. The authors elegantly report their results in one of the largest single cohorts of collegiate athletes undergoing a screening program that includes both ECG and TTE. Their 9.9% prevalence of distinctly abnormal ECG patterns is in line with our recent report on this field. We found 75 of 1220 athletes (6.14%) with abnormal ECG, who were referred for further screening using TTE to rule out structural abnormalities. One of the strongest points of Magalski et al's work is that TTE was performed systematically. However, their 0.2% rate of athletes disqualified is similar to our 0.16%, and the authors admitted a negligible incremental value of TTE. On the other hand, we found that none of the cases with abnormal history or physical examination revealed structural findings on TTE. Magalski et al pointed out how the addition of ECG resulted in higher sensitivity, as well as higher positive and negative predictive values. Therefore, I agree with the authors that: 1) preparticipation screening with history and physical examination is not enough; 2) routine TTE adds little incremental value; 3) routine ECG is probably the best approach to raise suspicion of underlying cardiac diseases, which helps in the selection of athletes who should undergo further diagnostic scrutiny.</description><dc:title>Usefulness of Electrocardiography for Cardiovascular Screening in Collegiate Athletes</dc:title><dc:creator>Amelia Carro</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.018</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e11</prism:startingPage><prism:endingPage>e11</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000150/abstract?rss=yes"><title>The Reply</title><link>http://www.amjmed.com/article/PIIS0002934312000150/abstract?rss=yes</link><description>We thank Carro for the comments regarding our article and the review of additional data supporting incorporation of the electrocardiogram into pre-participation athletic screening programs in addition to the history and physical examination. We agree that accumulating evidence supports electrocardiogram (ECG) interpretation using athlete-specific criteria as described by Corrado et al and Uberoi et al to reduce false-positive findings.</description><dc:title>The Reply</dc:title><dc:creator>Anthony Magalski, Marcia McCoy, Michael L. Main</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.012</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e13</prism:startingPage><prism:endingPage>e13</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311008977/abstract?rss=yes"><title>Interleukin-10 and Acute Coronary Syndromes</title><link>http://www.amjmed.com/article/PIIS0002934311008977/abstract?rss=yes</link><description>We have read with interest the article by Cavusoglu et al about the relation of interleukin (IL)-10 and 5-year outcomes in 193 male patients with acute coronary syndromes. In this well-performed study, increased levels of IL-10 on admission were associated independently with increased risk of death and nonfatal myocardial infarction. The authors also reviewed some of the controversial results published in this field, and, because their article provides the longest follow-up to date, they state that their finding could tip the scales in favor of considering increased IL-10 as a predictor of poorer outcomes in acute coronary syndrome patients.</description><dc:title>Interleukin-10 and Acute Coronary Syndromes</dc:title><dc:creator>Hugo Guillermo Ternavasio-de la Vega, Miguel Marcos, José Manuel González-Buitrago, Cándido Martín Luengo</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.017</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e15</prism:startingPage><prism:endingPage>e15</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000162/abstract?rss=yes"><title>The Reply</title><link>http://www.amjmed.com/article/PIIS0002934312000162/abstract?rss=yes</link><description>We appreciate the interest in our work expressed by Ternavasio de la Vega et al. We agree that ST-segment elevation myocardial infarction (MI) and non-ST-segment elevation acute coronary syndrome (ACS) represent distinct clinical entities, and grouping them together in our analysis is a limitation of our study. We took this approach because of our small sample size. However, we do not believe that the failure to adjust for this distinction accounts for our findings related to interleukin (IL)-10. Furthermore, we do not see how the studies cited by the authors of the letter support their position. The study by Yip et al was limited to ST-segment elevation MI patients and, like our study, found that elevated levels of IL-10 were independently associated with adverse outcomes. The study by Mälarstig was restricted to non-ST-segment elevation ACS and similarly found that elevated levels of IL-10 were predictive of adverse outcomes. Thus, 2 different studies restricted to 2 distinct ACS subtypes are in accord with our study. Although 2 other studies restricted to patients with non-ST-segment elevation ACS, one by Heeschen et al and the other by Oemrawsingh et al, found low levels of IL-10 to be associated with adverse outcomes, it is noteworthy that these 2 studies represent analyses derived from the same database. Furthermore, the discrepancy among the 5 studies appears unrelated to the particulars of the ACS because the 2 studies that included patients with ST-segment elevation MI had concordant findings.</description><dc:title>The Reply</dc:title><dc:creator>Erdal Cavusoglu</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.004</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e17</prism:startingPage><prism:endingPage>e17</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311008953/abstract?rss=yes"><title>Anti-inflammatory Cytokines: A Wolf in Sheep's Clothing?</title><link>http://www.amjmed.com/article/PIIS0002934311008953/abstract?rss=yes</link><description>We read with great interest the recent article by Cavusoglu et al showing that despite in vivo and in vitro evidence for a “cardioprotective” role of interleukin (IL)-10, elevated baseline plasma levels of IL-10 were a strong and independent predictor of long-term adverse cardiovascular outcomes in patients with acute coronary syndrome. The study results, which are at odds with previous work in the literature, contribute to the debate about the prognostic usefulness of anti-inflammatory cytokine measurement in the clinical setting.</description><dc:title>Anti-inflammatory Cytokines: A Wolf in Sheep's Clothing?</dc:title><dc:creator>Dimitrios N. Tziakas, Georgios K. Chalikias, Juan Carlos Kaski</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.015</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e19</prism:startingPage><prism:endingPage>e19</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000174/abstract?rss=yes"><title>The Reply</title><link>http://www.amjmed.com/article/PIIS0002934312000174/abstract?rss=yes</link><description>We appreciate the interest expressed by Tziakas et al in our work. We agree with them that our findings should not be interpreted to mean that interleukin-10 is a proatherogenic marker. Indeed, we do not challenge the overwhelming body of scientific literature supporting a cardioprotective role for interleukin-10. In fact, in our discussion, we state that “increased levels of this anti-inflammatory marker may represent a compensatory or a counter-regulatory mechanism during a heightened inflammatory state, as occurs in acute coronary syndrome, and may therefore represent a surrogate (rather than causal) marker of increased risk.” Indeed, and to this point, our group has previously published on several other markers with similar and seemingly contradictory and counterintuitive observations, where there has been a discordance between the known in vitro biologic actions of a particular protein and its anticipated or expected prognostic utility in the clinical setting. Thus, this is not the first time that our group has presented data demonstrating that the direction of the association between the levels of a particular protein and prognosis is not simply a function of biological plausibility. Rather, it is far more likely that the direction and magnitude of the association reflect the interplay among multiple, competing, and heretofore unknown factors in a complex biological system, as in humans presenting with acute coronary syndrome. Clearly, it would be both naive and scientifically undisciplined to assume otherwise.</description><dc:title>The Reply</dc:title><dc:creator>Erdal Cavusoglu</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.005</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>e21</prism:startingPage><prism:endingPage>e21</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000083/abstract?rss=yes"><title>Unstable Shoes Increase Energy Expenditure of Obese Patients</title><link>http://www.amjmed.com/article/PIIS0002934312000083/abstract?rss=yes</link><description>Abstract: 
Background: 
Ergonomic unstable shoes, which are widely available to the general population, could increase daily non-exercise activity thermogenesis as the result of increased muscular involvement. We compared the energy expenditure of obese patients during standing and walking with conventional flat-bottomed shoes versus unstable shoes.

Methods: 
Twenty-nine obese patients were asked to stand quietly and to walk at their preferred walking speed while wearing unstable or conventional shoes. The main outcome measures were metabolic rate of standing and gross and net energy cost of walking, as assessed with indirect calorimetry.

Results: 
Metabolic rate of standing was higher while wearing unstable shoes compared with conventional shoes (1.11±0.20 W/kg−1vs 1.06±0.23 W/kg−1, P=.0098). Gross and net energy cost of walking were higher while wearing unstable shoes compared with conventional shoes (gross: 4.20±0.42 J/kg−1/m−1vs 4.01±0.39 J/kg−1/m−1, P=.0035; net: 3.37±0.41 J/kg−1/m−1vs 3.21±0.37 J/kg−1/m−1; P=.032).

Conclusion: 
In obese patients, it is possible to increase energy expenditure of standing and walking by means of ergonomic unstable footwear. Long-term use of unstable shoes may eventually prevent a positive energy balance.
</description><dc:title>Unstable Shoes Increase Energy Expenditure of Obese Patients</dc:title><dc:creator>Nicola A. Maffiuletti, Davide Malatesta, Fiorenza Agosti, Alessandro Sartorio</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.001</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Brief observation</prism:section><prism:startingPage>513</prism:startingPage><prism:endingPage>516</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431200071X/abstract?rss=yes"><title>Accountability and Transparency in Graduate Medical Education Expenditures</title><link>http://www.amjmed.com/article/PIIS000293431200071X/abstract?rss=yes</link><description>Graduate medical education (GME) funding in the US supports over 110,000 residents and fellows each year. Funding is divided into direct medical expenditures (DME) (ie, salary and fringe) and indirect medical expenditures (a Medicare add-on to offset the extra cost teaching hospitals are thought to incur by having residents provide care). The passage of the Affordable Care Act combined with national and statewide fiscal shortfalls has caused the amount and administration of GME funding to come under greater scrutiny. The Medicare Payment Advisory Commission (MedPAC) has called for greater transparency in GME funding and recommends residency programs be held financially accountable for the training resulting from public funds. Recent discussions of the Joint Select Committee on Deficit Reduction (ie, the “Super Committee”) also have highlighted an opportunity to reduce GME payments as a mechanism to offset the nation's multi-trillion-dollar deficit.</description><dc:title>Accountability and Transparency in Graduate Medical Education Expenditures</dc:title><dc:creator>Saima I. Chaudhry, Sameer Khanijo, Andrew J. Halvorsen, Furman S. McDonald, Kavita Patel</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.007</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>APM perspectives</prism:section><prism:startingPage>517</prism:startingPage><prism:endingPage>522</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311008564/abstract?rss=yes"><title>Managing Chronic Pain with Nonopioid Analgesics: A Multidisciplinary Consult</title><link>http://www.amjmed.com/article/PIIS0002934311008564/abstract?rss=yes</link><description>
As detailed in this online CME activity (www.cmeaccess.com/AJM/ChronicPain04), determining pain mechanism is an important aspect guiding treatment selection for chronic musculoskeletal pain states. Although broad classifications provide a framework, any combination of mechanisms may be present in a chronic pain patient, and there is growing evidence that pain states generally considered nociceptive may also involve elements of augmented central nervous system pain processing. Nonopioid analgesics, including serotonin norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, and alpha-2-delta ligand anticonvulsants, are the treatments of choice for fibromyalgia and other central neuropathic pain states. Additionally, studies have now shown that certain SNRIs can be effective in treating “classic” nociceptive pain states, such as osteoarthritis, and also are effective for low back pain. In addition to considering biological mechanisms, chronic pain management also involves recognizing and evaluating the contribution of psychological and sociocultural factors that can influence pain chronicity and patient prognosis. A multimodal/multidisciplinary approach incorporating pharmacologic and nonpharmacologic therapy into a program that includes more than 1 discipline is important to improve outcomes in patients with chronic pain.
</description><dc:title>Managing Chronic Pain with Nonopioid Analgesics: A Multidisciplinary Consult</dc:title><dc:creator>Daniel Clauw, Bill H. McCarberg</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.003</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>CME multimedia activity</prism:section><prism:startingPage>S1</prism:startingPage><prism:endingPage>S1</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431200191X/abstract?rss=yes"><title>Masthead</title><link>http://www.amjmed.com/article/PIIS000293431200191X/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0002-9343(12)00191-X</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A4</prism:endingPage></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001933/abstract?rss=yes"><title>Contents</title><link>http://www.amjmed.com/article/PIIS0002934312001933/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0002-9343(12)00193-3</dc:identifier><dc:source>The American Journal of Medicine 125, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>125</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S0002-9343(12)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A9</prism:startingPage><prism:endingPage>A9</prism:endingPage></item></rdf:RDF>
