Circulation. 2007;116:1213
doi: 10.1161/CIRCULATIONAHA.107.185630
(Circulation. 2007;116:1213.)
© 2007 American Heart Association, Inc.
Issue Highlights
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INCREASED ENDOPLASMIC RETICULUM STRESS IN ATHEROSCLEROTIC PLAQUES ASSOCIATED WITH ACUTE CORONARY SYNDROME, by Myoishi et al.
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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.
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PROGNOSTIC VALUE OF VERY LOW PLASMA CONCENTRATIONS OF TROPONIN T IN PATIENTS WITH STABLE CHRONIC HEART FAILURE, by Latini et al.
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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 detectable troponin
levels using the hsTnT assay. The authors report that higher
hsTnT was a marker of greater severity of heart failure, was
associated with greater risk of adverse outcomes, and added
incremental value to prediction models for death. These data
demonstrate the prognostic utility of measurement of circulating
troponins at levels that are not detectable with conventional
assays, emphasizing the potential importance of the hsTnT assay.
See p
1242.
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DISTINCT DOWNREGULATION OF C-TYPE NATRIURETIC PEPTIDE SYSTEM IN HUMAN AORTIC VALVE STENOSIS, by Peltonen et al.
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Once thought to be a passive process, calcification and subsequent
degeneration of the aortic valve leading to aortic stenosis
is now conceptualized as an actively regulated process, with
some similarities to atherosclerosis. In this issue of
Circulation,
Peltonen and colleagues examine whether components of the natriuretic
peptide system may be involved in the process of aortic valve
calcification. They find that evidence of 3 natriuretic peptides
(ANP, BNP, and CNP), as well as their processing enzymes and
their receptors, could be identified in aortic valve tissue.
Moreover, in valves from patients with aortic stenosis, they
demonstrate downregulation of gene expression of CNP, its processing
enzyme furin, and target receptors NPR-B and NPR-A. These data
suggest that the natriuretic system may play a role in the progression
of nonrheumatic aortic valve stenosis, opening up a potential
therapeutic approach. See p
1283.
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Cardiology Patient Page
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Natural Bypasses Can Save Lives. See p
e340.
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Images in Cardiovascular Medicine
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Cardiac Tamponade With Fibrin Strands Leading to the Diagnosis
of Systemic Lupus Erythematosus. See p
e342.
Retroperitoneal Hematoma After Inferior Vena Cava Filter Insertion. See p e345.
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Correspondence.
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See p
e346.
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