Featured IAS
Commentaries
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of IAS.
COMMENTARIES
POSTED IN SEPTEMBER 2009
Is the Consumption of Light Cigarettes a Valid
Alternative to Smoking Cessation?
Authors: Damiano Baldassarre, Ph.D.
Cigarette smoking is a formidable enemy of
health. WHO estimates that tobacco use may cause the death
of 5 million people in 2008, and that by 2030, the number
of deaths related to the tobacco epidemic could exceed
annually 8 million – more than tuberculosis, HIV/AIDS,
and malaria combined [1]. Cigarette consumption grew from
only a few billion per year in 1900 to present values of
approximately 5.5 trillion worldwide.
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Experimental Data Support a Role of Macrophage
Specific Expression of MBL in Atherosclerosis
Authors: Robert A. Matthijsen, M.D. and Wim. A. Buurman,
Ph.D.
Recently, the concept in which different
elements of the innate immune system mediate atherosclerosis
gained support [1,2]. Accumulating evidence suggests that
inflammation participates centrally during all stages of
atherosclerosis development, from the initial lesion to
end-stage complications. Early atheromatous plaques demonstrate
increased vascular cell adhesion molecule (V-CAM1), P-selectin
and E-selectin expression, mediating local adhesion and
sequestration of circulating leucocytes and monocytes into
the arterial intima [3].
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Behavior of In Vivo Oxidized LDL Can Offer New Insights
into Mechanisms for Atherosclerosis Development
Authors: Hiroyuki Itabe* and Rina Kato
The latest progress in cardiovascular disease
(CVD) research is the understanding of the oxidized low
density lipoprotein (OxLDL) behavior in vivo during atherogenesis.
It is well established that OxLDL is a strong marker of
CVD [1,2]. The presence of OxLDL in macrophage-enriched
atherosclerotic lesions was demonstrated immunohistochemically
by using anti-OxLDL monoclonal antibodies [3-6]. Measurement
of plasma OxLDL levels revealed that patients with CVD
have increased OxLDL levels compared to healthy subjects
[7,8]. From these observations, it is hypothesized that
OxLDL plays a role in the development of atherosclerotic
lesions. However, the behavior of OxLDL in vivo during
atherogenesis remains unclear.
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New-onset Occlusive Coronary Atherosclerosis as a Cause of Acute or Subacute
Decompensation of Chronic Stable Non-ischemic Dilated Cardiomyopathy
Authors:Carl V. Leier, MD and Philip F. Binkley, MD, MPH
The latest progress in cardiovascular disease
(CVD) research is the understanding of the oxidized low
density lipoprotein (OxLDL) behavior in vivo during atherogenesis.
It is well established that OxLDL is a strong marker of
CVD [1,2]. The presence of OxLDL in macrophage-enriched
atherosclerotic lesions was demonstrated immunohistochemically
by using anti-OxLDL monoclonal antibodies [3-6]. Measurement
of plasma OxLDL levels revealed that patients with CVD
have increased OxLDL levels compared to healthy subjects
[7,8]. From these observations, it is hypothesized that
OxLDL plays a role in the development of atherosclerotic
lesions. However, the behavior of OxLDL in vivo during
atherogenesis remains unclear.
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Vitamin E-Modulated ROS Generation and ROS-Related Diseases
Authors: Yukiko K. Nakamura and Stanley T. Omaye
Despite results of earlier prospective, in
vitro, and animal studies [1-5], clinical trials have failed
to show beneficial effects of vitamin E, in particular
a-tocopherol, on cardiovascular disease (CVD) [5-7]. The
contradiction may be attributed to: 1) genetic and/or behavioral
factors associated with risk for CVD [5], including polymorphisms
in genes involved in lipid metabolism [8], 2) interaction
with other dietary antioxidants [9], 3) needs to optimize
physiological concentrations and duration of a-tocopherol
supplementation [10,11], 4) no animal models that mimic
perfectly human atherosclerosis [4], and 5) intervention
at a relatively late stage of CVD [1].
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Fetuin-A and Progression
of Atherosclerosis in Hemodialysis Patients
Authors: Giovanni Pertosa, M.D.
Cardiovascular disease (CVD) is the leading
cause of mortality in patients with chronic kidney disease
(CKD), at a risk that is 10- to 20-fold higher than in
the age- and sex-matched general population [1]. The development
of atherosclerotic CVD seems to begin early in the course
of CKD, as demonstrated by the Second National Health and
Nutrition Examination Survey [2]. One of the potentially
life-threatening cardiovascular consequences of uremia
is the presence of vascular calcification [3], a form of
heterotopic mineralization predictive of cardiovascular
mortality both common and severe in CKD [4].
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Systemic Lupus Erythematosus: Atherosclerotic Risk and the Link to Cholesterol
Transport
Authors: Allison B. Reiss, M.D.
Premature atherosclerotic cardiovascular
disease (ASCVD) in systemic lupus erythematosus (SLE, lupus)
is a major public health concern. The incidence of cardiovascular
events including angina and myocardial infarction (MI)
is significantly increased in SLE patients and the mortality
rate for MI in SLE patients is ten times greater than in
age-matched controls [1]. Up to 30% of deaths in SLE patients
are due to coronary artery disease [2]. Acute MI and cerebrovascular
accidents are greater than 8 times more common and CHF
is 11 times more common in young women with SLE than in
non-SLE young women [3].
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Circadian Clock Gene Polymorphisms Link to Hypertension
and Type 2 Diabetes
Authors: Timo Partonen, M.D.
Individuals may be more or less sensitive
to the effects of light due to a change in the average
level of illumination [1,2], so that following increased
daytime bright-light exposure they tend to become less
sensitive to light and after exposure to dimmer light more
sensitive. This may affect signal transduction downstream
of the retina of the eye and subsequently downstream of
the suprachiasmatic nucleus of anterior hypothalamus in
which the principal circadian clock is located.
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Chemical Basis to Suggest That Antioxidants May Not Be Suitable For the Prevention
of Human Atherosclerosis
Authors: Sampath Parthasarathy
The low density lipoprotein oxidation hypothesis
was put forward to explain the accumulation of lipids in
macrophages and the formation of fatty streak lesions.
Since the inception of the original hypothesis, practically
every step in the atherogenic process has been reported
to be influenced by components of oxidized low density
lipoprotein (Ox-LDL).
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Osteoporosis Is Pathophysiologically Related To Atherosclerosis
Authors: Toru Yamaguchi
Although osteoporosis and atherosclerosis
are traditionally viewed as separate entities that increase
in prevalence with aging, accumulating evidence indicates
that similar pathophysiological mechanisms lead to them.
Arterial calcification, like osteogenesis, involves a complex
interaction of various cells that produce matrix vesicles
and subsequent mineralization. Previous studies have shown
that bone-associated proteins, such as osteocalcin (OC),
Gla protein, osteopontin, osteoprotegerin, and receptor-activated
nuclear factor-kappa B ligand (RANKL), were found in atherosclerotic
arteries [1-3], suggesting that these proteins could be
directly associated with vascular diseases.
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The Effect of Diabetes on the Progression of Coronary Atherosclerosis and Arterial
Remodeling: Insights from Intravascular Ultrasound (IVUS)
Authors: Andrea J. Lavoie and Stephen J. Nicholls
Diabetes mellitus is a serious disease with
potentially devastating cardiovascular complications. In
1985 an estimated 30 million people worldwide were diagnosed
with diabetes; in 2000 that number climbed to over 150
million and is projected to reach over 380 million by 2025
[1].
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Renin-Angiotensin System (RAS) Blockade: A Promising Therapeutic Approach to
Reduce Atherosclerotic Inflammation
Authors: Fabrizio Montecucco, M.D. and François
Mach, M.D.
The renin-angiotensin system (RAS) has been classically
described as an endocrine axis whose active metabolite
(angiotensin II) is produced through
the cleavage cascade of the hepatic precursor angiotensinogen. Mainly
circulating renin (highly specific proteases released
by the kidney), converts angiotensinogen
into the decapeptide angiotensin I that in turn is converted by the angiotensin-converting
enzyme (ACE) into angiotensin II [1]. Chronic angiotensin II activation
can promote cardiovascular disease development through hemodynamic effects
and up-regulation of inflammatory cytokines and growth factors.
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