Circulation. 2007;116:359
doi: 10.1161/CIRCULATIONAHA.107.183537
(Circulation. 2007;116:359.)
© 2007 American Heart Association, Inc.
Issue Highlights
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BURDEN AND PROGNOSTIC IMPORTANCE OF SUBCLINICAL CARDIOVASCULAR DISEASE IN OVERWEIGHT AND OBESE INDIVIDUALS, by Ingelsson et al.
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Subclinical cardiovascular disease can be assessed using several
routinely available tests that can measure atherosclerotic burden
and target organ damage. The extent of subclinical disease in
obesity and its prognostic importance has not been investigated
systematically. In this issue of
Circulation, Ingelsson and
colleagues used data from 5 tests (electrocardiography, echocardiography,
carotid ultrasound, ankle-brachial pressure, urinary albumin
excretion) performed in the community-based Framingham Heart
Study sample. The authors report a higher cross-sectional prevalence
of subclinical disease in overweight and obese individuals (compared
with those with a normal body mass index), and in those with
increased waist circumference compared with those with a normal
waist circumference. On prospective follow-up, the risk of overt
cardiovascular disease was higher in overweight and obese individuals
with evidence of subclinical disease, as compared with individuals
without subclinical disease. These data suggest that overweight
and obesity are associated with a high prevalence of subclinical
disease, which in part contributes to the increased risk of
overt cardiovascular disease in individuals with excess adiposity.
See p
375.
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PREDICTION OF MODE OF DEATH IN HEART FAILURE: THE SEATTLE HEART FAILURE MODEL, by Mozaffarian et al.
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Therapeutic strategies to treat symptomatic heart failure are
directed toward improving prognosis. Clinicians are very aware
that the risk of death and other complications of heart failure
vary considerably The Seattle Heart Failure Model incorporates
commonly available clinical features, laboratory measurements,
and medications used to provide some quantization of this nonhomogeneous
risk. In this issue of
Circulation, Mozaffarian and colleagues
use information from several clinical trials and registries
to evaluate the Seattle Heart Failure Model score to assess
mode of death in over 10 000 ambulatory patients with symptomatic
heart failure. With over 2000 deaths at an annualized rate of
approximately 12%, there was a relatively greater increase in
the proportion of deaths attributed to progressive pump failure
versus sudden, unanticipated heart failure in those with higher
scores. The authors appropriately conclude that such information
warrants further study and may facilitate decision making regarding
improvements in recommendations for implantable cardioverter-defibrillators.
See p 392 (editorial p
360).
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MAST CELL STABILIZATION REDUCES HEMORRHAGE FORMATION AND MORTALITY AFTER ADMINISTRATION OF THROMBOLYTICS IN EXPERIMENTAL ISCHEMIC STROKE, by Strbian et al.
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Although thrombolysis is an established effective treatment
of ischemic stroke, hemorrhagic complications and reperfusion
injury limit the outcome of patients after this intervention.
Mast cells are known to increase ischemic and hemorrhagic brain
edema, possibly because of the release of vasoactive, proteolytic,
and fibrinolytic mediators upon degranulation. In a mouse model
of cerebral ischemia and reperfusion, the authors investigated
this question and found that application of a tissue plasminogen
activator, a commonly used treatment strategy in these patients,
induces strong mast cell degranulation. Similarly, postischemic
administration of a tissue plasminogen activator markedly increased
hemorrhagic edema formation, an effect that was significantly
reduced by pretreatment of the animals with the mast cell stabilizor,
cromoglycate. These results were confirmed in genetically modified
mast cell–deficient mice, suggesting that degranulation
of these cells is involved in this major complication, as well
as in stroke. Further, the potential clinical relevance of these
results is interesting, as neurological outcome was improved
and mortality reduced in this experimental animal model. Overall,
these results point to new treatment modalities in acute stroke
using mast cell stabilizers, such as cromoglycate or other molecules,
in a relevant clinical setting. See p 411 (editorial p
363).
Visit http://circ.ahajournals.org:
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Images in Cardiovascular Medicine
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Apicoaortic Valve–Containing Conduit in a Patient With
Relapsing Prosthetic Endocarditis. See p
e88.
Isolated Left Ventricular Noncompaction Enhanced by Echocontrast Agent. See p e90.
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Correspondence
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See p
e92.
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Circulation 2007 116: 360-362.
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Tissue Plasminogen Activator–Induced Reperfusion Injury After Stroke Revisited
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Isolated Left Ventricular Noncompaction Enhanced by Echocontrast Agent
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Circulation 2007 116: e90-e91.
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Letter by O’Rourke Regarding Articles, "Prevalence of Long-QT Syndrome Gene Variants in Sudden Infant Death Syndrome," "Cardiac Sodium Channel Dysfunction in Sudden Infant Death Syndrome," and "Contribution of Long-QT Syndrome Genes to Sudden Infant Death Syndrome: Is It Time to Consider Newborn Electrocardiographic Screening?"
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Burden and Prognostic Importance of Subclinical Cardiovascular Disease in Overweight and Obese Individuals
- Erik Ingelsson, Lisa M. Sullivan, Caroline S. Fox, Joanne M. Murabito, Emelia J. Benjamin, Joseph F. Polak, James B. Meigs, Michelle J. Keyes, Christopher J. O’Donnell, Thomas J. Wang, Ralph B. D’Agostino, Philip A. Wolf, and Ramachandran S. Vasan
Circulation 2007 116: 375-384.
[Abstract]
[Full Text]
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