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Circulation
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Circulation. 2007;116:1213
doi: 10.1161/CIRCULATIONAHA.107.185630
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(Circulation. 2007;116:1213.)
© 2007 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.
 


*    INCREASED ENDOPLASMIC RETICULUM STRESS IN ATHEROSCLEROTIC PLAQUES ASSOCIATED WITH ACUTE CORONARY SYNDROME, by Myoishi et al.
 
It is now widely appreciated that plaque rupture is an important component of the acute coronary syndrome. Cells in the vascular wall may become injured or dysfunctional and, as a consequence, contribute to the genesis of plaque rupture. In this issue, Myoishi and colleagues report on a particular type of cell injury response in the setting of acute coronary syndrome. In particular, they found that cells in rupture-prone areas of plaque exhibited features of endoplasmic reticulum stress. This stress response is an ancient cellular reaction to misfolded proteins, designed to prevent cells from continued protein production when they are in a dysfunctional state. The article by Myoishi et al elucidates important potential mechanisms whereby oxidized cholesterol may contribute to cellular dysfunction (via endoplasmic reticulum stress) that is ultimately manifest as plaque rupture. See p 1226.


*    PROGNOSTIC VALUE OF VERY LOW PLASMA CONCENTRATIONS OF TROPONIN T IN PATIENTS WITH STABLE CHRONIC HEART FAILURE, by Latini et al.
 
Blood levels of cardiac troponins are sensitive and specific markers of myocardial injury that are routinely used for the diagnosis of acute myocardial infarction. Troponin levels may also be elevated in some patients with heart failure, but blood levels are shown to be much lower compared with patients with acute myocardial infarction when currently available assays are used. In this issue of Circulation, Latini and colleagues report results of an investigation in which they measured circulating troponin T in 4053 patients with heart failure using a high-sensitivity troponin (hsTnT) assay. Whereas circulating troponins were detectable in 10% of the patients with heart failure when conventional assays were used, 90% of the patients had . . . [Full Text of this Article]


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