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A mechanism by which Omega-3s prevent CV events
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Susan
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PostPosted: Fri Jun 23, 2006 2:44 pm    Post subject: A mechanism by which Omega-3s prevent CV events Reply with quote

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"Omega-3 fatty acids enter plaque, resulting in increased stability and
less inflammation
One of the possible ways in which long-chain omega-3 fatty acids play a
role in decreasing cardiovascular events is by entering advanced
atherosclerotic plaques, resulting in a decreased expression of various
agents involved in plaque instability, as well as reducing plaque
inflammation. (International Symposium on Atherosclerosis.) [21 Jun]"




Susan
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William Wagner
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PostPosted: Fri Jun 23, 2006 3:19 pm    Post subject: Re: A mechanism by which Omega-3s prevent CV events Reply with quote

In article <4g2d2iF1in0e5U2@individual.net>,
Susan <nevermind@nomail.com> wrote:

Quote:
x-no-archive: yes


x-no-archive: yes


"Omega-3 fatty acids enter plaque, resulting in increased stability and
less inflammation
One of the possible ways in which long-chain omega-3 fatty acids play a
role in decreasing cardiovascular events is by entering advanced
atherosclerotic plaques, resulting in a decreased expression of various
agents involved in plaque instability, as well as reducing plaque
inflammation. (International Symposium on Atherosclerosis.) [21 Jun]"




Susan

Where can I find

"(International Symposium on Atherosclerosis.) [21 Jun]"

Thanks!

Bill

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and informative purposes. This material is distributed without profit.
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Susan
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Posts: 932

PostPosted: Fri Jun 23, 2006 3:30 pm    Post subject: Re: A mechanism by which Omega-3s prevent CV events Reply with quote

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William Wagner wrote:

Quote:
Where can I find

"(International Symposium on Atherosclerosis.) [21 Jun]"

Thanks!



Sorry! theheart.org


Susan
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William Wagner
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Joined: 29 Apr 2005
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PostPosted: Fri Jun 23, 2006 3:55 pm    Post subject: Re: A mechanism by which Omega-3s prevent CV events Reply with quote

In article <4g2fnmF1jj3n9U1@individual.net>,
Susan <nevermind@nomail.com> wrote:

Quote:
x-no-archive: yes

William Wagner wrote:

Where can I find

"(International Symposium on Atherosclerosis.) [21 Jun]"

Thanks!



Sorry! theheart.org


Susan

Omega-3 fatty acids enter plaque, resulting in increased stability and
less inflammation

June 21, 2006

Michael O'Riordan






Rome, Italy - One of the possible ways in which long-chain omega-3 fatty
acids play a role in decreasing cardiovascular events is by entering
advanced atherosclerotic plaques. According to the results of a new
study, investigators were able to show that the incorporation of
eicosapentaenoic acid (EPA) into advanced plaque was associated with a
decreased expression of various matrix metalloproteinases (MMPs)
involved in causing plaque instability, as well as with decreased plaque
inflammation.

These are results of the Omacor Carotid Endarterectomy Intervention
(OCEAN) study, presented here this week at the International Symposium
on Atherosclerosis by Dr Philip Calder (University of Southampton, UK).
"By increasing the availability of omega-3 fatty acids, they appear in
advanced atherosclerotic plaques, indicated in this study by the carotid
artery, and this results in lower numbers of macrophages, foam cells,
and T cells, as well as the lower expression of inflammatory markers,"
said Calder. "Histologically, this results in a plaque that appears to
be less inflamed and more stable. This may contribute to reduced
mortality in patients consuming omega-3 fatty acids, for example, in the
GISSI Prevenzione trial."

Less inflamed and more stable
Calder and his group previously published data in which surgical
patients were randomized to placebo, vegetable oil, and omega-3 fatty
acids. Patients supplemented with omega-3 fatty acids before surgery
were more likely to have stable plaques and less likely to have unstable
plaques, said Calder, noting that the more stable plaque contained more
EPA and docosahexaenoic acid (DHA) than unstable plaque. Patients
treated with omega-3 fatty acids also had lower macrophage infiltration
into the plaque with more EPA and DHA.
Presenting the OCEAN findings, Calder said that patients identified for
carotid endarterectomy were randomized to treatment with 2 g/day of
omega-3 fatty acids or placebo. Patients remained in the trial until
surgery, which, historically, was an average of 40 to 50 days after
first being identified for endarterectomy. After surgery, the
investigators obtained the plaque and studied the morphology, histology,
and cellular infiltration using immunohistochemistry, as well as the
expression of MMPs, cytokines, and adhesion molecules at the mRNA level.
In total, 112 patients were randomized to therapy, with 50 patients in
the placebo arm and 45 patients in the active-therapy arm completing the
study. Average patient age was 75 years and a majority were men.
Patients were typically overweight and former or current smokers and had
hypertension. Calder noted that lipid measurements were typically good,
likely because patients were well treated, with 85% taking statins and
80% taking aspirin.
Investigators report that EPA and DHA were rapidly taken up into the
plaque. There was a significant 100% increase in EPA content in the
plaque in patients supplemented with omega-3 fatty acids, but only a 10%
nonsignificant increase in the uptake of DHA in the atherosclerotic
plaque. The number of foam cells was significantly lower in those
treated with fatty acids vs those randomized to placebo.
Calder noted that a combined mean score, a composite summed measure that
includes the size of the lipid core, number of foam cells, and number of
macrophages in the plaque and the cap, as well as the overall density of
inflammation in the plaque and cap, was lower among patients treated
with omega-3 fatty acids. The mean score was significantly negatively
correlated with plaque EPA, he reported.
 
"In other words, the more EPA in the plaque, the less inflamed and more
stable it is," said Calder.
In addition, investigators measured mRNA levels for seven MMPs. Three of
the seven‹MMP-9, MMP-7, and MMP-12‹were significantly decreased in
patients supplemented with omega-3 fatty acids. Intercellular adhesion
molecule 1 (ICAM-1), an adhesion molecule involved in the recruitment of
monocytes into the vessel wall, and the inflammatory cytokine
interleukin-6 were also lower in patients taking fatty acids.

What does it all mean?
Dr Heiner Bucher (University Hospital Basel, Switzerland), who moderated
the session, told heartwire that the investigators should be commended
for taking advantage of delays in the healthcare system to carry out
this study. As noted by Calder, investigators were somewhat hindered, as
a delay of 40 to 50 days from the time of referral for surgery until the
procedure is the norm in the hospital. Instead, patients underwent
surgery 21 days after referral, limiting the amount of time they were on
omega-3 fatty acids.
Bucher called the study and its findings intriguing in that it attempts
to show a mechanistic benefit with omega-3 fatty acids, long shown to
have cardioprotective benefits in epidemiological and case-control
studies. He does, however, have reservations about the clinical
implications of such findings.
"We are moving now to surrogate end points, like carotid thickening and
plaque stabilization, but I still don't know how this translates into
clinical benefit," said Bucher. "The piece that we're missing is how
much of a decline in carotid thickening or improvement in plaque
stabilization results in hard clinical end points, like improved
survival or reduced cardiovascular events."




Source

1. Cawood AL, Ding R, Napper FL, et al. Long chain omega-3 fatty
acids enter advanced atherosclerotic plaques and are associated with
decreased inflammation and decreased inflammatory gene expression. 2006
International Symposium on Atherosclerosis; June 18-22, 2006; Rome,
Italy.
2.

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and informative purposes. This material is distributed without profit.
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