Circulation. 2006;114:359
(Circulation. 2006;114:359.)
© 2006 American Heart Association, Inc.
Issue Highlights
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INCREASED CARDIAC ADENYLYL CYCLASE EXPRESSION IS ASSOCIATED WITH INCREASED SURVIVAL AFTER MYOCARDIAL INFARCTION, by Takahashi et al.
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This mouse study will, as Takahashi and colleagues point out,
appear to be counter-intuitive in the light of generally accepted
clinical data that ß-blockade lessens adverse myocardial
infarction–associated events, mechanistically by decreased
formation of the second messenger, cyclic adenosine monophosphate
(cAMP). This model had cardiac-directed overexpression of adenylyl
cyclase, potentially increasing formation of cAMP, and thus
expected to worsen experimental myocardial infarction. In reality,
mouse mortality rate decreased, left ventricular dilation lessened,
and the ejection fraction rose. To explain these unexpected
data, the authors point out that (1) left ventricular remodeling
was improved and (2) there was increased sensitivity to calcium
of the calcium-uptake pump of the sarcoplasmic reticulum, thereby
improving calcium cycling and contractile function. According
to the view that there is subcellular compartmentation of cAMP
(see editorial by Leineweber et al, p 365), there might be different
functional end results according to exactly where and how cAMP
is formed and broken down. Theoretically, combined ß-blockade
and inhibitors of cAMP breakdown might be clinically tested
in very large infarcts. See p
388.
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DELETION OF P47phox ATTENUATES ANGIOTENSIN II–INDUCED ABDOMINAL AORTIC ANEURYSM FORMATION IN APOLIPOPROTEIN E–DEFICIENT MICE, by Thomas et al.
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The role of oxidative stress in vascular pathology is slowly
becoming clearer. In this issue of
Circulation, Thomas and colleagues
report on the role of nicotinamide adenine dinucleotide phosphate
oxidase in the formation of aortic aneurysms in a mouse model.
At one time, the nicotinamide adenine dinucleotide phosphate
oxidase enzyme was thought limited to neutrophils and its function
restricted to host defense. As this important article shows,
this enzyme system is now recognized as an important mediator
of vascular pathology. These data add aneurysm formation to
the list of vascular diseases that appear modulated by vascular
oxidative stress. See p
404.
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CAUSES OF PURE AORTIC REGURGITATION IN PATIENTS HAVING ISOLATED AORTIC VALVE REPLACEMENT AT A SINGLE US TERTIARY HOSPITAL (1993 TO 2005), by Roberts et al.
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Aortic regurgitation has multiple causes with the mechanism
of regurgitation being related either to primary valve dysfunction
or secondary to aortic root pathology. In this edition of
Circulation,
Roberts et al describe the cause of pure aortic regurgitation
in 268 patients having isolated aortic valve replacement. The
primary and secondary groups are nearly equally divided. A congenitally
malformed valve, with and without endocarditis, is the major
cause of pure aortic regurgitation in the valvar group. Examples
of the anatomic abnormalities of the valves are beautifully
demonstrated in the figures. Despite careful pathological evaluation,
the mechanism of regurgitation could not be established in 62%
of the patients in the secondary group. These patients tended
to be older and have a history of hypertension. This unique
pathological study provides an important perspective in the
modern era on the cause of pure aortic regurgitation. See p
422.
Visit http://circ.ahajournals.org:
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Clinician Update
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C-Reactive Protein as a Risk Predictor: Do Race/Ethnicity and
Gender Make a Difference? See p
e67.
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Images in Cardiovascular Medicine
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Progressive Myocardial Fibrosis in a Patient With Apical Hypertrophic
Cardiomyopathy Detected by Cardiovascular Magnetic Resonance.
See p
e75.
Tension Pneumopericardium in Hodgkin’s Disease.
See p e77.
Rapid Development of Multiple Pseudoaneurysms After Arterial Homograft Placement. See p e80.
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Correspondence
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See p
e82.
Related Articles:
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C-Reactive Protein as a Risk Predictor: Do Race/Ethnicity and Gender Make a Difference?
- Michelle A. Albert and Paul M Ridker
Circulation 2006 114: e67-e74.
[Extract]
[Full Text]
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Progressive Myocardial Fibrosis in a Patient With Apical Hypertrophic Cardiomyopathy Detected by Cardiovascular Magnetic Resonance
- R. Gebker, M. Neuss, I. Paetsch, and E. Nagel
Circulation 2006 114: e75-e76.
[Extract]
[Full Text]
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Tension Pneumopericardium in Hodgkin’s Disease
- Frank M.P. van Haren, Aernout Borstlap, and Norbert Foudraine
Circulation 2006 114: e77-e79.
[Extract]
[Full Text]
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Rapid Development of Multiple Pseudoaneurysms After Arterial Homograft Placement
- Michael Heise, Michael Werk, Inga Husmann, Robert Eisele, and Peter Neuhaus
Circulation 2006 114: e80-e81.
[Extract]
[Full Text]
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Letter by Schmermund and Erbel Regarding Article, "Coronary Artery Calcium: Should We Rely on This Surrogate Marker?"
- Axel Schmermund and Raimund Erbel
Circulation 2006 114: e82.
[Extract]
[Full Text]
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Deletion of p47phox Attenuates Angiotensin II–Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E–Deficient Mice
- Manesh Thomas, Dan Gavrila, Michael L. McCormick, Francis J. Miller, Jr, Alan Daugherty, Lisa A. Cassis, Kevin C. Dellsperger, and Neal L. Weintraub
Circulation 2006 114: 404-413.
[Abstract]
[Full Text]
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Causes of Pure Aortic Regurgitation in Patients Having Isolated Aortic Valve Replacement at a Single US Tertiary Hospital (1993 to 2005)
- William Clifford Roberts, Jong Mi Ko, Timothy Richard Moore, and William Hampton Jones, III
Circulation 2006 114: 422-429.
[Abstract]
[Full Text]
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Increased Cardiac Adenylyl Cyclase Expression Is Associated With Increased Survival After Myocardial Infarction
- Toshiyuki Takahashi, Tong Tang, N. Chin Lai, David M. Roth, Brian Rebolledo, Miho Saito, Wilbur Y.W. Lew, Paul Clopton, and H. Kirk Hammond
Circulation 2006 114: 388-396.
[Abstract]
[Full Text]
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INCREASED CARDIAC ADENYLYL...
DELETION OF P47phox ATTENUATES...