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Circulation. 2006;114:529

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(Circulation. 2006;114:529.)
© 2006 American Heart Association, Inc.

Issue Highlights


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    PERFORMANCE OF TOP-RANKED HEART CARE HOSPITALS ON EVIDENCE-BASED PROCESS MEASURES, by Williams et al.
 
The US News & World Report annual publication of "America’s Best Hospitals" attracts considerable attention each year, but the validity of the ranking is not known. Investigators from the Joint Commission on Accreditation of Healthcare Organizations sought to determine how ranked and unranked hospitals compared on the publicly reported quality-of-care measures for patients admitted with acute myocardial infarction and heart failure. Williams and colleagues compare 41 ranked hospitals and 733 unranked hospitals with respect to their performance on 6 acute myocardial infarction and 4 heart failure process measures. The study determined if the ranked hospitals, in aggregate, performed better and then investigated how well the ranking discriminated between hospitals by their performance. The results provide important information about the value of this popular system. See p 558.


*    INHIBITION OF UROKINASE-TYPE PLASMINOGEN ACTIVATOR OR MATRIX METALLOPROTEINASES PREVENTS CARDIAC INJURY AND DYSFUNCTION DURING VIRAL MYOCARDITIS, by Heymans et al.
 
The mechanisms by which viral myocarditis leads to cardiac injury and failure are not fully understood. In this issue of Circulation, Heymans et al examined the role of the proteinases urokinase-type plasminogen activator (uPA) and matrix metalloproteinases (MMPs) in mediating cardiac inflammation, injury, and subsequent failure during coxsackievirus-B3 induced myocarditis. The expression and activity of uPA and MMP-9 was increased in mice 7 days after infection with coxsackievirus-B3. In mice with deletion of uPA or inhibition of MMPs by adenoviral gene overexpression of tissue inhibitor of metalloproteinases-1, there was decreased cardiac inflammation and reduced myocardial necrosis, decreased cardiac fibrosis at 35 days, and prevention of cardiac dilatation and dysfunction. These data implicate these proteinases in the pathogenesis of viral myocarditis and . . . [Full Text of this Article]


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