Circulation. 2006;114:1133
(Circulation. 2006;114:1133.)
© 2006 American Heart Association, Inc.
Issue Highlights
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FAMILIAL SUDDEN DEATH IS AN IMPORTANT RISK FACTOR FOR PRIMARY VENTRICULAR FIBRILLATION: A CASE-CONTROL STUDY IN ACUTE MYOCARDIAL INFARCTION PATIENTS, by Dekker et al.
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and
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HOW SUDDEN IS SUDDEN CARDIAC DEATH? by Müller et al.
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Sudden death is most commonly due to coronary artery disease
in Western nations, but approximately half occur in patients
who either do not have recognized heart disease or have a low
risk profile. Two studies in this issue provide the basis for
potential strategies to improve sudden death prevention in this
population. Studying patients with acute myocardial infarction,
Dekker et al found that ventricular fibrillation was associated
with a family history of sudden death, supporting a genetic
susceptibility to ventricular fibrillation during ischemia.
Müller and colleagues used emergency teams responding to
cardiac arrest victims to obtain interviews from bystanders.
They found that cardiac arrest was often preceded by a substantial
period of symptoms. These studies emphasize the potential importance
of educating populations to the significance of their family
history, and recognizing and responding to symptoms of heart
disease as a strategy to reduce sudden cardiac death. See p
1140 and
1146.
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IDENTIFICATION OF THE OXIDIZED LOW-DENSITY LIPOPROTEIN SCAVENGER RECEPTOR CD36 IN PLASMA: A NOVEL MARKER OF INSULIN RESISTANCE, by Handberg et al.
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The macrophage scavenger receptor CD36 promotes the uptake of
oxidized low-density lipoprotein, foam cell formation, and atherosclerosis.
Insulin resistance is also associated with increased expression
of macrophage CD36. In this issue of
Circulation, Handberg and
colleagues have identified for the first time a soluble form
of CD36 in plasma that also appears to be a marker of metabolic
syndrome. Similar to other soluble receptors, such as soluble
intercellular adhesion molecule-1 or P-selectin, the authors
propose that soluble CD36 might represent a potential surrogate
marker of atherosclerosis. See p
1169.
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5-METHYLTETRAHYDROFOLATE RAPIDLY IMPROVES ENDOTHELIAL FUNCTION AND DECREASES SUPEROXIDE PRODUCTION IN HUMAN VESSELS: EFFECTS ON VASCULAR TETRAHYDROBIOPTERIN AVAILABILITY AND ENDOTHELIAL NITRIC OXIDE SYNTHASE COUPLING, by Antoniades et al.
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It has become increasingly clear that endothelial dysfunction
is an important contributor to the development of atherosclerosis
and the clinical manifestations of cardiovascular disease. Considerable
data from animal models indicate that defects in nitric oxide
production are a key component of endothelial dysfunction. Data
from human samples, however, are needed to substantiate these
findings. In this issue, Antoniades et al present a human study
demonstrating a favorable impact of folic acid on endothelial
function. This study fills an important gap in knowledge and
provides insight into the putative mechanisms whereby folate
may have cardiovascular effects. See p
1193.
Visit http://circ.ahajournals.org:
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Images in Cardiovascular Medicine
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An Unusual Explanation for Episodic Dyspnea. See p
e485.
Rheumatic Myocarditis Masquerading as Left Ventricle Tumor. See p e487.
Unmasking of the Brugada Syndrome Phenotype During the Acute Phase of Amiodarone Infusion. See p e489.
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Book Review
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ESC Textbook of Cardiovascular Medicine. See p
e492.
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Correspondence
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See p
e495.
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