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What is plaque?
We track it. We try to control
it, stop it, reverse it.
But what exactly is plaque? What is the importance of “vulnerable”
plaque?
Atherosclerotic plaque; if we were unable to
identify and measure plaque, there would be no Track Your Plaque
program. In other words, without the ability to detect, quantify,
and track coronary plaque, there would be no need for our program or
any effort to try and exert control over this thing.
If we couldn’t measure and track it, we would have to resign
ourselves to the old way of doing things in heart disease: Wait for
warning signs to appear like chest pain, heart attack, or death. Or,
we could rely on crude “risk factors” like cholesterol that suggest
the possibility of heart disease. Or, we could perform tests of
blood flow like stress tests in the hopes of uncovering heart
disease in the nick of time, before catastrophe strikes.
Thankfully, we can measure plaque, or at least an indirect
“dipstick” for plaque—calcium.
Despite the criticisms CT heart scans have had to endure, it remains
the best—safest, most precise, least radiation exposure, least
expensive—way to track coronary atherosclerotic plaque.
So let’s take a closer look at this thing that absorbs so much of
our attention.
Atherosclerotic plaque: An ingredient list
In our younger years, we all shared smooth,
thin-walled arteries feeding the heart, free of plaque.
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Normal artery |
As years pass, various injuries are imposed on the artery lining,
such as high shear stress (high blood pressure); direct injury (from
toxins such as those from smoking, small LDL cholesterol particles,
or triglyceride-containing lipoproteins); direct insertion of
undesirable particles like lipoprotein(a); and modification of
proteins through glycation that develops when blood sugar is
increased. Day-after-day, week-after-week injury ignites
inflammatory processes within the artery wall. Inflammatory white
blood cells migrate into the wall (the intima), producing more
inflammation and releasing enzymes that degrade and weaken plaque
structure. The process feeds upon itself, accelerating with any
source of ongoing injury that further flame the fires of
inflammation.
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In its earliest years, plaque might be evident simply as thickened
lining of the artery, composed mostly of structural fibrous tissue.
But, as more and more fatty products accumulate in the artery wall,
the artery becomes progressively more “fibrofatty.”
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Early fibrous plaque. Small speckles of calcium may
accumulate (not shown) |
The “soft” and “hard” (calcific) elements of plaque grow as more
inflammatory cells invade and die. Destructive enzymes that digest
and weaken fibrous tissues also leave behind a trail of debris.
Years of this process leads to fatty accumulations (sometimes called
“lipid pools,” visualized by invasive tools like intracoronary
ultrasound) can be detected.
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In parallel with these processes, little deposits of calcium,
similar to the mineral deposited in bone, accumulate. Calcium is
microscopic at first. It then accumulates in small “pebbles” and
grows along with plaque. Eventually, calcium can accumulate in large
“plates,” sometimes even extending through 180-degree or greater
arcs of plaque circumference, a phenomenon that tends to occur in
advanced disease. (Whether or not calcium plays a role in inciting
more plaque growth, or whether it is simply a plaque component that
accumulates passively, is controversial, though the growing
appreciation for the enormous influence of vitamins D3 and K2 are
fueling the argument that calcium plays an active role.)
Calcium, of course, because it grows along with total
atherosclerotic plaque, provides the basis for CT heart scan
quantification of plaque. Calcium volume parallels total plaque
volume, comprising approximately 20%.
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As plaque grows, calcium becomes visible (white).
Fatty debris also accumulates (yellow) sometimes forming a
"pool." The artery increase in diameter due to
remodeling. |
Along with plaque accumulation, a process of “remodeling” (the
so-called “Glagov phenomenon”) of the artery results in various
degrees of artery enlargement or constriction. It is not clear why
some people develop enlargement, while others develop constriction,
even with the same amount of plaque lining the artery wall. People
with diabetes, however, do tend to develop constriction more so than
non-diabetics. Areas of arteries that enlarge are more likely to
develop concentrations of softer elements like tissue and cellular
debris and visible accumulations of fatty debris.
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The great bulk of time required for plaque growth is a silent
process, yielding no symptoms, nor other perceptible phenomena. From
here, plaque can follow different paths.
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A vulnerable plaque. All plaque components
continue to grow. The lipid pool is separated from the
blood by a thin layer of fibrous tissue, the "fibrous cap." |
Continued growth—Plaque continues to grow, both cross-sectionally
(outward and inward) and longitudinally (along the length of the
artery). Regions of poor flow can develop simply due to restriction
of blood flow, resulting in symptoms like breathlessness and chest
discomfort, or reduced coronary flow detected by stress testing.
“Vulnerable” plaque—Some, but not all, areas of plaque develop
features that have been associated with potential for plaque
“rupture,” or the sudden eruption of the plaque surface that exposes
the tissue ordinarily covered by the artery lining (intima). This
provokes blood clot formation and heart attack. Much research has
focused on what makes a plaque “vulnerable,” though there has been
little insight gained into why some plaques assume a “vulnerable”
form, while others do not. The typical vulnerable plaque contains a
large “pool” of semi-liquid fatty material, representing the debris
of inflammatory blood cells that have died, with an overlying
fibrous “cap,” the thin barrier between lipid pool and coronary
blood flow. |
These two different paths overlap to a great degree and can occur in
the same artery and in the same person. However, each path can show
itself in different ways. While gradual, continued growth generally
results in warning symptoms that can provide time for appropriate
action, it’s the rupture of the vulnerable plaque that poses the
greatest—and unpredictable—danger. Thus, research efforts have
recently focused on techniques to identify features of
vulnerability.
Among the techniques that have emerged to identify the presence or
potential for vulnerable plaques are:
- C-reactive protein (CRP) and other inflammatory measures—CRP is a
blood markers for inflammation associated with greater risk for
cardiovascular events. CRP levels ≥3.0 mg/dl are clearly associated
with heightened risk for plaque rupture; the higher the CRP, the
greater the risk. An ideal CRP level is ≤1.0 mg/dl, perhaps as low
as <0.5 mg/dl. However, though CRP and related measures (IL-6, MMP,
etc.) have proven helpful, they are limited in practical usefulness.
Heart attacks still occur with low CRPand heart attacks don’t
necessarily occur with high CRP. High CRP levels also afford no
insight into when rupture might occur. Nonetheless, in large
populations, greater inflammation and higher CRP is associated with
greater risk for heart attack.
- Vulnerability markers—In addition to CRP, blood markers like
phospholipase A2 (PLAC), myeloperoxidase (an inflammatory cell
enzyme), oxidized LDL, and other inflammatory and oxidative measures
have captured some attention, but share the same practical
limitations of CRP.
- Plaque morphology—This simply means that plaques are studied and
characterized, looking for the features of “vulnerability,” such as
the lipid pool and thin fibrous cap. However, this requires
intravascular ultrasound (IVUS) of all three coronary arteries, an
approach that is invasive, very expensive, and poses some dangers
(heart attack from tear of the artery lining consequent to the
trauma induced by the ultrasound imaging catheter). CT coronary
angiography and MRI may prove to be useful techniques to study
plaque composition. However, resolution (imaging accuracy) and, in
the case of CT angiography, radiation exposure, limit application
for these purposes.
- Other intravascular techniques—Beyond visualization of artery wall
composition through IVUS, there are invasive catheter-based
techniques like optical coherence tomography, a form of
high-resolution IVUS that yields greater plaque detail but is
limited by interference from blood and limited signal penetration
into the artery wall; intracoronary thermography that measures
temperature distribution within plaque, looking for “hot spots,” or
regions of inflammation that generate heat; and near-infrared
spectroscopy, based on the principle that different tissue types
absorb and reflect varying amounts of near-infrared wavelength light
that is detectable by a device inserted into the artery. All of
these methods remain experimental, and all require insertion of
devices into the coronary arteries.
From the Track Your Plaque experience, we would add:
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Copyright 2008, Track Your Plaque.
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