http://select.nytimes.com/mem/tnt.html?emc=tnt&tntget=2006/11/27/business
/27heart.html&tntemail1=yIn
This is a premium article so I just offer a taste.
Below also is more from Wikipedia, the free encyclopedia
Quest to Improve Heart Therapies, Plaque Gets a Fresh Look
By BARNABY J. FEDER
Published: November 27, 2006
Most people have of a clear image of how atherosclerosis, popularly
known as hardening of the arteries, causes a heart attack ‹ fatty
deposits called plaque build up in a coronary artery until the day the
blood flow that sustains the heart is blocked.
If only they were right. In reality, severe coronary artery blockages
almost always cause chest pain known as angina and other symptoms as
they form. But among those who suffer heart attacks, half of the men and
two-thirds of the women report never experiencing a warning symptom. And
autopsies of such victims frequently show blood clots jammed into
arteries that have been only modestly narrowed.
Standard atherosclerosis therapies include bypass surgery to route blood
around blockages, angioplasty and stenting to clear blockages from
inside the artery, and drugs like statins that reduce cholesterol levels
to slow the formation of plaque. But they have not been enough to
prevent 200,000 to 500,000 American deaths annually from what doctors
refer to as coronary artery disease.
As a result, many researchers have turned their attention from
atherosclerosis in general to the tendency of some patients to develop a
form of plaque prone to inflammation and rupture, which can spill a stew
of cells into the bloodstream that can incite rapid clotting. Such
plaques have been called ³vulnerable² plaque.
But little is known about how such plaques form and even less about how
long they last or what makes them rupture. ³Figuring out who is going to
have plaque rupture would be the Holy Grail of cardiology,² said Dr.
Deepak L. Bhatt, a leading research cardiologist at the Cleveland Clinic
Foundation.
The broadest effort yet to do that will be announced today by a
consortium pledging to invest $30 million over four years in an
international plaque research program that will be overseen by Dr.
Valentin Fuster, a cardiologist at Mount Sinai Medical Center in New
York.
Large Snip. Copy right respect.
........................
Vulnerable plaque
From Wikipedia, the free encyclopedia
A vulnerable plaque is an atheromatous plaque which is particularly
prone to produce sudden major problems, such as a heart attack or stroke.
Generally an atheroma becomes vulnerable if it grows more rapidly and
has a thin cover separating it from the bloodstream inside the arterial
lumen. Tearing of the cover is called plaque rupture.
Because artery walls typically enlarge in response to enlarging plaques,
these plaques do not usually produce much stenosis of the artery lumen.
Therefore, they are not detected by cardiac stress tests or angiography,
the tests most commonly performed clinically with the goal of predicting
susceptibility to future heart attack.
In many cases, a vulnerable plaque has a thin fibrous cap and a large
and soft lipid pool underlying the cap. These characteristics together
with the usual hemodynamic pulsating expansion during systole and
elastic recoil contraction during diastole contribute to a high
mechanical stress zone on the fibrous cap of the atheroma, making it
prone to rupture. Increase hemodynamic stress correlates with increased
rates of major cardiovascular events associated with exercise,
especially exercise beyond levels the individual does routinely.
The most frequent cause of a cardiac event following rupture of a
vulnerable plaque is blood clotting on top of the site of the ruptured
plaque that blocks the lumen of the artery, thereby stopping blood flow
to the tissues the artery supplies.
Upon rupture, atheroma tissue debris may spill into the blood stream;
these debris are often too large (over 5 micrometers) to pass on through
the capillaries downstream. In this, the usual situation, the debris
obstruct smaller downstream branches of the artery resulting in
temporary to permanent end artery/capillary closure with loss of blood
supply to, and death of the previously supplied tissues. A severe case
of this can be seen during angioplasty in the slow clearance of injected
contrast down the artery lumen. This situation is often termed
non-reflow.
Additionally, atheroma rupture may allow bleeding from the lumen into
the inner tissue of the atheroma making the atheroma size suddenly
increase and protrude into the lumen of the artery producing lumen
narrowing or even total obstruction.
Because vulnerable plaques are not revealed by either cardiac stress
testing or coronary angiography, the tests most commonly performed
clinically with the goal of testing susceptibility to future heart
attack, several medical research efforts, starting in the early to
mid-1990s, have worked on using intravascular ultrasound IVUS),
thermography,(near-infrared spectroscopy) careful clinical follow-up and
other methods, to predict these lesions and the individuals most prone
to future heart attacks. These efforts remain largely research with no
useful clinical methods to date (2006).
Repeated atheroma rupture and healing is one of the mechanisms, perhaps
the dominant one, which creates artery stenosis.
.......................................
Retrieved from "http://en.wikipedia.org/wiki/Vulnerable_plaque"
Categories: Cardiology | Neurology
€ This page was last modified 00:43, 22 October 2006. All text is
available under the terms of the GNU Free Documentation License. (See
Copyrights for details.)
€ Wikipedia® is a registered trademark of the Wikimedia Foundation,
Inc.
€ Privacy policy About Wikipedia Disclaimers

Signature
S Jersey USA Zone 5 Shade
http://www.ocutech.com/ High tech Vison aid
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.
aria - 27 Nov 2006 19:28 GMT
Here is a link to the full text:
http://www.nytimes.com/2006/11/27/business/27heart.html?ei=5087%0A&em=&en=527be2
84f490403e&ex=1164776400&pagewanted=all#
aria
> http://select.nytimes.com/mem/tnt.html?emc=tnt&tntget=2006/11/27/business
> /27heart.html&tntemail1=yIn
[quoted text clipped - 38 lines]
> Valentin Fuster, a cardiologist at Mount Sinai Medical Center in New
> York.
The initial sponsors include Humana, a leading manager of health plans;
AstraZeneca and Merck, from the drug industry; and BG Medicine, a
start-up company in Waltham, Mass., formerly known as Beyond Genomics.
Royal Philips Electronics, which makes a variety of diagnostic machines
widely used to scan the heart, the arteries that supply it with blood
and other parts of the circulatory system, has participated in the
planning and is expected to join them.
The centerpiece of the research will be a study of 4,000 to 6,000
Humana patients with at least two known risk factors for heart attacks.
As the outcome for the patients becomes clear over the next few years,
researchers hope the profiles that emerge from the study will, in
hindsight, show patterns pointing directly to the high-risk patients
who actually suffered heart attacks. That in turn could help the
companies create new therapeutic products.
The payoff could be enormous for health care companies. Coronary
stents, which limit the symptoms of atherosclerosis and the damage from
heart attacks, but do not reduce the likelihood of future attacks, make
up a $6 billion market for device makers and produce some of the
biggest profit margins the industry has ever seen.
Drug makers have fared even better with statins, which partially reduce
the risk of new attacks and top $20 billion in worldwide sales.
“How we treat the disease is up for grabs,” said Andrew S. Plump,
who monitors early-stage research on warning signs and new medicines
for cardiovascular disease at Merck’s research center in Rahway, N.J.
The initiative spotlights the growing lineup of research projects and
technology investments that reflect competition between drug makers and
device companies over who can develop the safest, most effective and
cheapest products to combat atherosclerosis.
This summer, doctors financed by Abbott Laboratories finished enrolling
700 patients in a clinical study that is identifying the type and
location of plaque in coronary arteries. Researchers are using
ultrasound probes and other devices mounted at the end of long
catheters. The catheters are inserted into the thigh and pushed
carefully up into the coronary arteries, the same procedure used to
clear blockages in angioplasty and to implant stents.
There are some doubts, however, that better understanding of vulnerable
plaques will do much to improve preventive therapy, particularly that
with devices. Atherosclerosis attacks the entire circulatory system, so
skeptics predict that visions of stenting to reinforce thin-capped
reservoirs of dangerous plaque would lead to a losing game of medical
whack-a-mole — fixing one trouble spot, then finding many others.
“Multiple studies show that if you have one ruptured plaque, you have
many,” said Dr. Steven E. Nissen, a Cleveland Clinic cardiologist and
the current president of the American College of Cardiology.
Dr. Nissen said that a complex combination of genetics and
“vulnerable blood” — patients whose blood is prone to clotting
— probably interact with the plaque in ways that make focusing so
much research on rupture short-sighted. “There’s a lot of wishful
thinking in this field,” he said.
The research initiative being announced today will involve several
methods for probing arteries from outside the body. None of these are
novel, but the researchers hope to show that a standardized, simplified
diagnostic approach to using them could identify levels and types of
plaque relatively inexpensively.
BG Medicine’s blood analysis system will test samples for particular
proteins or other substances that are known or suspected markers of
developing atherosclerosis.
The study patients will also undergo computerized tomography X-ray
scans of their coronary arteries and ultrasound scans of their necks;
plaque buildup in the carotid arteries there has been linked to stroke.
A smaller group of the patients will also be scanned magnetically and
with a device known as a positron emission tomography scanner, or
P.E.T., that may provide more details on inflamed vessel walls.
Abbott said its study, which is to follow the patients for two to five
years, was costing tens of millions of dollars. The ultrasound scans
from inside the artery generate so much data that it takes four days to
log the initial information received on each patient, according to
Abbott.
The company inherited the study, and became a leading manufacturer of
stents and other catheter-based devices, when it acquired Guidant’s
vascular businesses this year.
“We may need to look at hundreds or thousands of plaques in each
artery,” said Dr. Gregg W. Stone of the Cardiovascular Research
Foundation who is lead investigator for the Abbott trial, adding that
the images had been acquired millimeter by millimeter in each
patient’s three major heart arteries.
At the least, Dr. Fuster said, the results from such research may one
day be used to motivate the highest-risk patients to follow practices
that do reduce risk — more exercise; better diets; daily use of
aspirin to thin the blood; and statins. But the long-range goal is to
find new products to interrupt the deadly progression.
“Cardiology is being transformed from reactive to proactive,” said
John M. Capek, president for cardiac therapies of Abbott’s vascular
division, envisioning a day when doctors will prevent heart attacks the
way dentists can help prevent tooth decay with a mix of devices and
drugs.
Some experts say there is no basis yet for such optimism. Even if the
research eventually provides a rudimentary early warning system for
heart attacks linked to plaque rupture, the health care industry might
be stumped about what to do with it. Since there is no information on
how quickly vulnerable plaques form, no one knows how often patients
must be screened. Nor is it known how often plaques heal themselves, or
how often they break without causing a damaging clot.
And many patients who do not fall into the high-risk categories also
suffer heart attacks. Screening all adults could make the early warning
system prohibitively expensive.
Scans from the battery of devices Philips is providing for the study
being announced today cost the average patient $2,000 or more, said
Paul H. Smit, senior vice president for strategy and business
development of Philips Medical Systems. Figuring out how to reduce that
total is an important practical element of the plaque research
> Large Snip. Copy right respect.
> ........................
> Vulnerable plaque
[quoted text clipped - 65 lines]
> Title 17 U.S.C. Section 107, and is strictly for the educational
> and informative purposes. This material is distributed without profit.