Circulation. 2005;112:1677
(Circulation. 2005;112:1677.)
© 2005 American Heart Association, Inc.
Issue Highlights
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LEVELS OF HEMATOPOIESIS INHIBITOR N-ACETYL-SERYL-ASPARTYL-LYSYL-PROLINE PARTIALLY EXPLAIN THE OCCURRENCE OF ANEMIA IN HEART FAILURE, by van der Meer et al.
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There is evidence that inhibition of the renin-angiotensin system
is associated with the development of anemia in patients. Of
98 patients with heart failure who were treated with angiotensin-converting
enzyme (ACE) inhibitors, 10 had unexplained anemia. They were
compared to 10 without anemia. The anemic patients had lower
serum ACE activity; their serum inhibited proliferation of bone
marrowderived hematopoietic progenitor cells from healthy
donors; and their levels of hematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline
(Ac-SDKP), which is degraded by ACE, were higher. These preliminary
findings led the authors to propose that ACE inhibitors might
contribute to anemia by increasing the levels of Ac-SDKP. See
p
1743.
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SAFETY AND FEASIBILITY OF AUTOLOGOUS MYOBLAST TRANSPLANTATION IN PATIENTS WITH ISCHEMIC CARDIOMYOPATHY: FOUR-YEAR FOLLOW-UP, by Dib et al.
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Although there is increasing experience with myoblast transplantation
by direct intramyocardial injection in patients, little is known
about the long-term viability and function of the injected cells.
Dib et al provide follow-up for a mean of 27 months in 24 patients
who received autologous myoblast injections at the time of coronary
bypass surgery and at a mean of 9 months in 6 additional patients
who received injections at the time of left ventricular assist
device placement. There was PET evidence of increased glucose
uptake and echocardiographic evidence of improved cardiac function.
There was also histological evidence of myoblast survival in
4 of 6 patients studied 5 days to 6 months after injection.
Together, these observations support the feasibility of myoblast
transplantation and suggest that injected cells are viable for
up to several months. See p
1748.
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ARTERIAL DISTENSIBILITY IN ADOLESCENTS: THE INFLUENCE OF ADIPOSITY, THE METABOLIC SYNDROME, AND CLASSIC RISK FACTORS, by Whincup et al.
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Atherosclerosis develops from childhood, but the determinants
of this preclinical stage remain uncertain. Whincup and colleagues
examined the relations of classic coronary risk factors, adiposity,
and its associated metabolic disturbances to arterial distensibility
(a marker of early arterial disease) in 13- to 15-year-olds,
some of whom had previously been studied at ages 9 to 11 years.
Adiposity and its associated metabolic abnormalities had strong
and in many cases graded adverse relations to vascular function
in teenagers. The association between adiposity and distensibility
appeared stronger than the previously documented relationship
between blood cholesterol and distensibility. The combination
of classic risk factors, metabolic abnormalities, and C-reactive
protein appeared to explain at least a part of the relation
of adiposity on arterial distensibility. The findings are important
for understanding the determinants of early atherosclerosis
and could have major public health implications. See p
1789.
Visit http://www.circ.ahajournals.org:
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Images in Cardiovascular Medicine
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Extracardiac Unruptured Sinus of Valsalva, Coronary, and Intracranial
Aneurysms. See p
e146.
Encasement of the Heart by Calcific Constrictive Pericardium. See p e148.
Endovascular Treatment of a Giant Aortic Arch Aneurysm With a Triple-Branched Stent Graft. See p e151.
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Correspondence
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See p
e153.
Related Articles:
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Levels of Hematopoiesis Inhibitor N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Partially Explain the Occurrence of Anemia in Heart Failure
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[Abstract]
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Safety and Feasibility of Autologous Myoblast Transplantation in Patients With Ischemic Cardiomyopathy: Four-Year Follow-Up
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Extracardiac Unruptured Sinus of Valsalva, Coronary, and Intracranial Aneurysms
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[Extract]
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Encasement of the Heart by Calcific Constrictive Pericardium
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Circulation 2005 112: e148-e150.
[Extract]
[Full Text]
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Endovascular Treatment of a Giant Aortic Arch Aneurysm With a Triple-Branched Stent Graft
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[Extract]
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Circulation 2005 112: e153.
[Extract]
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