Circulation. 2001;103:3142-3149
(Circulation. 2001;103:3142.)
© 2001 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
Evaluation of the Culprit Plaque and the Physiological Significance of Coronary Atherosclerotic Narrowings
Morton J. Kern, MD;
Bernhard Meier, MD
From the Department of Internal Medicine, Division of Cardiology, Saint
Louis University Health Sciences Center, Saint Louis, Mo (M.J.K.), and the
Division of Cardiology, Swiss Cardiovascular Center Bern, University Hospital,
Bern, Switzerland (B.M.).
Correspondence to Morton J. Kern, MD, Director, J.G. Mudd Cardiac Catheterization Laboratory, Saint Louis University Health Sciences Center, 3635 Vista Avenue at Grand Blvd, St. Louis, MO 63110. E-mail kernm{at}slu.edu
Key Words: plaque • atherosclerosis • imaging
 |
Introduction
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Clues to the
identification of a plaque as dangerous (ie, vulnerable
to sudden
activation and/or rupture) before it becomes the culprit
of a major,
potentially life-threatening event currently must
be gleaned from
studies examining plaques after the
fact.
1 2 Although
the risk of a given plaque causing a cardiac event,
in particular a
myocardial infarction, is closely related to
the severity of luminal
narrowing (complete occlusions excepted),
it is incorrect to focus
exclusively on the most conspicuous
stenoses, that is, the
angiographically significant (>70%
diameter narrowing) lesions that
compete with a larger number
of nonsignificant (<50% diameter
narrowing) and, at times,
inapparent lesions. Because the aggregate
risk of rupture associated
with many nonsignificant lesions (each with
an admittedly lower
individual potential) exceeds that of the fewer
significant
lesions, a myocardial infarction will more likely originate
from
a nonsignificant
lesion.
3
In addressing atherosclerotic plaques,
coronary interventionists strive to achieve the following 2
primary therapeutic goals: (1) the elimination of angina and (2) the
prevention of myocardial infarction and death. The first goal may be
readily achieved with revascularization, either by
percutaneous coronary interventions (PCI) or
coronary bypass surgery. Methods to identify and neutralize a
vulnerable plaque before it produces a coronary occlusion are
new and as-yet unproven, and the therapeutic approaches in some cases
are highly
controversial.4
To these ends, the interventionist is handicapped when
relying solely on contrast angiography to identify fine details of
coronary artery disease because lumenology has an inherent
inability to evaluate the vessel wall, atherosclerotic plaque
dimensions, composition, distribution, and morphology.
Arterial remodeling confuses the determination of the
severity of segmental or diffuse coronary artery disease,
because only an angiographically uninvolved lumen segment serves as a
"normal" reference for comparison. To move our understanding beyond
angiography, this review will discuss various current and potential
anatomic and physiological techniques to identify
whether a coronary plaque is truly a "culprit" lesion
(Table 1
).
|
Structure and Metabolism
of the Culprit Plaque
|
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To varying degrees, an atheromatous
lesion is comprised of a
lipid-rich core, a cap of fibrous tissue,
vascular smooth muscle
cells expressing collagen and elastin that
impart tensile strength
to an extracellular matrix, and inflammatory
cells (such as
macrophages) that produce various enzymes and
procoagulant
factors.
5 6
The fibrous cap, which is characterized by a single
endothelial cell layer, may be thinned and partially
eroded by both inflammatory (T-lymphocytes) and invading smooth muscle
cells. Abundant activated macrophages moving into the
plaque from the vasa vasorum produce proteolytic enzymes, such as
matrix metalloproteinases, that promote collagen degradation, which
leads to cap disruption and the thrombogenic surface activation
associated with acute coronary
syndromes.6
Other plaques (or other areas within the same plaque) have a
thick fibrous cap with a predominance of quiescent smooth muscle cells
securely separating the lumen from the distant lipid core. In this
plaque, activated macrophages account for 
25% of
the population of inflammatory and smooth muscle cells; this often
testifies to earlier plaque rupture with subsequent
healing.6 Stimulation of
intimal proliferation seems to be a plausible mechanism that stabilizes
coronary plaque.7
Smooth muscle cells engender new fibrous proteins to strengthen the
cap, regulate the synthesis of interstitial collagen, and
render the plaque less prone to rupture. Typically, a plaque may
simultaneously have quiescent (stable) and vulnerable
(unstable) regions at any given moment
(Figure 1). The vulnerability of a culprit plaque is thus
determined by the critical mass of the lipid core, the thickness of the
atheromatous fibrous cap, and the presence of an
increased population of inflammatory cells. The ability of a plaque to
limit blood flow is characterized by anatomic features (eg, lumen
cross-sectional area, orifice configuration, and lesion length)
impinging on and disrupting luminal blood flow.
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Figure 1. Atheromatous lesion displaying a lipid-rich core (A) separated from the lumen (L) by a single layer of endothelium (arrow, unstable plaque area). In other areas, there is a thick fibrous cap (F, stable plaque area). The dark staining represents CD68-positive inflammatory macrophages.
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Plaque Anatomy: Use of
Intracoronary Catheter-Based Sound and Light
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Catheter-based techniques transmitting ultrasound or
light can
uniquely visualize the atherosclerotic plaque in vivo.
Intravascular
ultrasound (IVUS) imaging, which is superior to
angiography,
provides 2D cross-sectional tomographic views and, when
digitally
reconstructed, can display 3D images of the artery and
plaque.
In addition to improved measurements of lumen plaque and vessel
area
(and volume), plaque constituents such as calcification, fibrous
tissue,
thrombus, and plaque fractures or dissections are readily
identified
and, in most cases, well
differentiated.
8
Because of its limited resolution (>100 µm even for 40
MHz systems) and the confounding influences of surrounding tissues,
IVUS is currently of little use in determining the instability of
subendothelial plaque
components.9 The fibrous cap
thickness and protruding fractures can only be visualized with
difficulty.8 In contrast,
arterial calcifications, associated more with stable than
unstable syndromes,10 are
easily observed, even with low-frequency IVUS imaging.
Echocardiographically identified vulnerable plaques
seem to be associated with negative remodeling after plaque rupture.
Ward et al11 reviewed data
indicating that true arterial vessel size by IVUS rather
than plaque area has a more dynamic role in arterial lumen
remodeling and subsequent plaque stability.
Newer catheter-based modalities use ultrasound
radiofrequency signals to gauge the elastic properties of the
atherosclerotic plaque and different histological
components of the
plaque.12 13 By
using ultrasound radiofrequency data from arterial tissue
during diastole and systole, elastograms or "strain"
plaque images can be constructed; these will identify hard and soft
tissue component regions. In vitro studies report differentiating
lipid-rich from fibrous regions within atherosclerotic
plaques.12 Similarly, IVUS
radiofrequency signal analysis can differentiate an
atherosclerotic lipid core from surrounding vascular tissue using 30
MHz IVUS catheter signals digitized at 500 MHz from atherosclerotic
coronary artery specimens in
vitro.13 IVUS elastography
and radiofrequency tissue analysis provide unique
characterizations of plaque without the need for additional
catheters.
|
Angioscopy, Optical Coherence Tomography, and
Raman Spectroscopy
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Using projected light through thin, flexible glass
fibers, angioscopy
catheters can be inserted into a coronary
artery and, after
blocking blood flow, can visualize the
arterial surface in color
through saline irrigation. Color
visualization permits separation
of red and/or white thrombus from
yellow lipid-rich plaques
in patients with acute coronary
syndromes. Because of technical
limitations and lack of clinical
enthusiasm, angioscopy never
achieved widespread use, despite
observations that angioscopic
thrombosis at the culprit lesions after
PCI was related to adverse
clinical
outcomes.
14
Optical coherence tomography (OCT) uses a beam of coherent
infrared laser light directed and reflected within the tissue to create
a detailed tissue image with an extraordinary high resolution (2 to 30
µm). It easily differentiates lipid from water-based tissues and
precisely quantifies fibrous cap thickness, despite a penetration depth
of only 1 to 2 mm.15
Compared with IVUS, OCT provides more detailed information to
differentiate intima, plaque, and lipid
pools.16 Like angioscopy,
successful clinical application must overcome the low penetration depth
and the blood absorbance of signal light.
Reflected laser light from tissues can also be
analyzed using spectral modeling by a spectrometer. Specific
spectral characteristics, called Raman spectra, identify chemical
alterations in atherosclerotic
tissue.17 Raman spectra can
differentiate nonatherosclerotic, noncalcified plaque from calcified
plaque within coronary arteries. Like OCT, the penetration
depth of Raman spectroscopy is only 1.0 to 1.5 mm, but this is
sufficient to examine tissue beneath fibrous caps and within the
atheromatous core. Raman spectroscopy is limited by
strong image artifact from background fluorescence and the
absorbance of the laser light by blood. Unlike IVUS or OCT, however,
Raman spectroscopy provides no information on plaque configuration and
thus would likely be coupled with IVUS, angioscopy, or OCT
catheters.
|
Activated Plaque Physiology:
Catheter-Based Thermography
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The inflammation and activation of macrophages
in acute ischemic
syndromes promote plaque rupture, thrombosis,
and vasoconstriction
and are associated with increased temperature
within an atheroma.
Casscells et
al
18 showed a temperature
rise of up to 2.2°C
in macrophage-rich areas in freshly
obtained carotid endarterectomy
specimens,
confirming a significant correlation between macrophage
density
and local temperature. In human atherosclerotic coronary
arteries,
a 3F thermography catheter demonstrated thermal
heterogeneity
with a spatial resolution of 0.5 mm
in the coronary arteries
of 20% of patients with stable
angina, 40% of those with unstable
angina, and 67% of those with
acute myocardial
infarction.
19 No thermal
heterogeneity was seen in arterial
specimens from
control subjects. Thermography may identify regions
likely to
activate in the near-term and could support early
intervention
or verify stabilization after mechanical or
pharmacological
therapy.
|
Coronary Physiology: Use of Sensor
Guidewire–Based Pressure and Flow
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In addition to the anatomic limitations of angiography,
the
lack of physiological correlations for
angiographically intermediate-severe
stenoses (40% to 70%)
facilitated the emergence of sensor-tipped
angioplasty guidewire-based
coronary physiological measurements
as
important clinical
tools.
20
The principles supporting the use of pressure and flow for
culprit plaque assessment arise from the rheology of epicardial blood
flow. An epicardial coronary artery stenosis produces
resistance to blood flow with a proportionately increasing pressure
loss occurring as a quadratic function of increasing flow.
Coronary flow resistance varies according to the lesion length
and morphology (entrance/exit angles, length, eccentricity, and luminal
topography), as well as the status of the microvasculature. In
addition, because net coronary flow is the result of a complex
system involving both conduit and microvascular bed resistances,
attempts to establish reliable physiological
correspondence from only quantitative anatomic variables (either
IVUS or angiography) generally failed to predict the functional
response of flow through a given stenosis
accurately.
Sensor-tipped angioplasty-style guidewires delivered to
regions distal to a culprit stenosis can measure
post-stenotic absolute coronary vasodilatory reserve
(CVR), relative CVR (rCVR), and pressure-derived fractional flow
reserve (FFR;
Figure 2). These measurements, now in common use for both
clinical and research
purposes,20 21
provide an enhanced understanding of the separate functions of the
epicardial, microvascular, and collateral coronary
circulation.22 For example,
the impact of diffuse coronary artery disease, compared with a
focal stenosis, on coronary flow can be separated using
CVR and FFR. rCVR, the ratio of the target CVR to CVR in an
angiographically normal reference artery, examines the status of the
microvascular bed. During PCI, CVR and FFR relationships may identify
coronary dissection, emboli, or diffuse microvascular
constriction, offering clinicians a complete functional description of
the results of coronary
interventions23 and leading
to appropriate therapy for best outcomes.
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Figure 2. Diagrammatic definitions of CVR, FFR, and rCVR. A theoretically normal artery is drawn behind the stenotic artery. CFR is determined by maximal stenosis flow (QSmax) divided by stenosis artery flow at rest (QSrest). FFR is determined by maximal stenosis flow (QSmax) divided by maximal theoretical normal artery flow (QNmax). rCVR is determined by maximal stenosis flow (QSmax) divided by maximal normal adjacent artery flow (QN'max).
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Absolute and Relative Coronary Flow
Reserve
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Absolute CVR (the ratio of hyperemic to
basal flow) measures
the capacity of the dual system of
coronary artery and supplied
vascular bed to achieve maximal
oxygen supply in response to
a given hyperemic stimulation and
is only of value when normal.
To determine whether an abnormal CVR
reflects abnormal stenosis
physiology, the ratio of the CVR in
the target vessel to that
in an angiographically normal reference
vessel (rCVR) can be
used. rCVR assumes that global myocardial reserve
(ie, the microcirculation)
is uniformly responsive and distributed,
nullifying the confounding
effects of hemodynamics and
the microcirculation. Normal CVR
in young patients using IVUS
demonstrated that normal arteries
have values that commonly exceed 3.0.
The values for CVR associated
with nonobstructed coronary
arteries in patients with chest
pain syndromes and transplanted hearts
and in normal arteries
in patients with obstructive coronary
artery disease elsewhere
are 2.8±0.6, 3.1±0.9, and 2.5±0.95,
respectively.
24 In patients
with coronary artery disease, target artery CVR
values
associated with negative ischemic testing are generally
>2.0.
20 rCVR values
associated with unobstructed postangioplasty and
stent results are
>0.80.
25 26
CVR in unobstructed arteries in different patients may
be highly variable due to the multiple factors that can alter
either basal or hyperemic flow. To improve the assessment of
CVR, Wieneke et al27
measured CVR in 141 patients in 242 unobstructed coronary
arteries. On the basis of a regression model, individual CVR values
obtained at different basal average peak velocities could be
transformed and corrected for patient age, relating them to a mean
basal average peak velocity (BAPV) of 15 cm/s and age of 55 years
[CVRcorrected=2.85xCVRmeasuredx10a,
where a=(0.48xlogBAPV) +(0.0025xage)-1.16]. The
transformation by the correction formula showed that only patients with
diabetes had a significant decrease in the traditional CVR and
corrected CVR, whereas hypertension and current smoking had no
influence on corrected CVR. Use of the corrected CVR standardizes for
variations in basal average peak velocity and patient age and may
discriminate between intrinsic and extracardiac factors impairing
CVR.
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Pressure-Derived FFR
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Reducing regional tissue perfusion below the
ischemic threshold
(ie, the level needed to meet myocardial
oxygen demand) produces
myocardial dysfunction. Myocardial perfusion is
directly dependent
on the coronary "driving" pressure
associated with vascular
resistances at the 3 major control points
(R
1=epicardial,
R
2=arteriolar,
and
R
3=intramyocardial capillary resistance) in the
coronary
circulation. The myocardial perfusion pressure (aortic
pressure,
left ventricular pressure, or right atrial
pressure) is reduced
when an epicardial stenosis produces
increased resistance to
flow. Resistance translates energy loss into
pressure loss distal
to the stenosis in proportion to the flow
rate. If the more
distal R
2 and
R
3 myocardial bed resistances are stimulated to
maximal
hyperemia and remain constant, then the
post-stenotic hyperemic
coronary artery
pressure represents the maximal achievable perfusion
available
in that vessel.
Using coronary pressure measured at constant and
minimal myocardial resistances (ie, maximal hyperemia), Pijls
et al28 derived an estimate
of the percentage of normal (ie, in the theoretical absence of the
stenosis) coronary blood flow expected to go through a
stenotic artery and called it the FFR. The FFR, calculated as
the ratio of the post-stenotic or distal coronary
pressure to aorta pressure (as the pressure in an unobstructed artery,
ie, the theoretical normal artery pressure) obtained at sustained
minimal resistance (ie, maximal hyperemia), reflects both
antegrade and collateral myocardial perfusion rather than merely
trans-stenotic pressure loss (ie, a stenosis pressure
gradient). Because it is calculated only at peak hyperemia, FFR
is further differentiated from CVR by being largely independent of
basal flow, driving pressure, heart rate, systemic blood pressure, or
status of the
microcirculation.29 The FFR,
but not the resting pressure or hyperemic pressure gradient, is
strongly related to provokable myocardial ischemia (FFR<0.75)
established by rigorous comparisons to different clinical stress
testing modalities in patients with stable
angina.21
The major concern in interpreting absolute CVR, rCVR, or FFR
is the impact of microcirculatory flow impairment. In patients with a
nonuniform microcirculation, such as those with myocardial infarction,
neither absolute CVR nor rCVR can identify the lesion-specific nature
of flow impairment because the target vessel microcirculation is
presumed to be abnormal. Likewise, in other patients, when the CVR is
severely blunted (eg, in severe hypertrophy, diabetes, or
hypertension), the discriminatory capacity using rCVR may not permit
accurate assessment of a stenosis. In patients with 3-vessel
coronary artery disease, there may be no suitable reference
vessel, invalidating the use of rCVR. A lesion in these situations is
best assessed by FFR. In patients with abnormal microcirculation, it
can be argued that a normal FFR indicates the conduit resistance is not
a major contributing factor to perfusion impairment and that focal
conduit enlargement (eg, stenting) would not restore normal perfusion.
Caution should be applied in extending the current
physiological criteria to patients with
microvascular disease, acute or remote myocardial infarction, and
unstable angina. Ischemic threshold values for rCVR are under
review.
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Physiological Techniques
Differentiating Focal From Diffuse
Atherosclerosis
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A diffusely diseased atherosclerotic coronary
artery can be
viewed as a series of branching units diverting and
gradually
distributing flow along the longitudinally narrowing conduit
length.
The perfusion pressure gradually diminishes along the artery.
In
this artery, CVR is also reduced but is not associated with
a focal
stenotic pressure loss. Thus, mechanical therapy directed
at a
presumed culprit plaque to reverse such abnormal physiology
would be
ineffective in restoring normal coronary perfusion
(Figure
3
).
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Figure 3. FFR measurements in a patient with both focal and diffuse coronary artery disease. A, Coronary angiogram demonstrating severe (>90%) proximal left anterior descending coronary artery stenosis. FFR is determined by distal coronary pressure (Pd; 34 mm Hg) divided by mean aortic pressure (Pa; 90 mm Hg) and is 0.38. B, After successful coronary stenting, CVR by Doppler velocity is only 1.5. C, FFRs after stenting immediately distal to the stent and far distally in the left anterior descending artery are 0.95 and 0.41, respectively. D, Pressure wire pullback from distal to proximal left anterior descending artery shows gradual pressure recovery associated with diffuse disease.
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By measuring coronary velocity and reserve,
quantitative angiographic coronary dimensions, and branch
lengths (to estimate regional left ventricular mass) in 59
patients, Anderson et al30
found that resting blood flow velocity varied inversely with the ratio
of lumen area (A) to regional mass (M). Resting average peak velocity
increased 27±16, 33±11, and 37±20 cm/s, respectively
(P=0.06), in patients with
minimal, mild, or moderate disease. Coronary artery disease in
the left anterior descending coronary artery could be
categorized as minimal, mild, or moderate based on the area/mass ratios
in these 3 groups (8.7±4, 8.5±6.2, and 5.6±0.03
mm2/100 g, respectively;
P<0.04), indicating that a
potentially insufficient lumen dimension exists for a given perfusion
field in patients with diffuse, mild, or moderate coronary
atherosclerosis. Such findings would likely influence
decisions toward mechanical revascularization or
continued medical therapy.
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The Future: Assessing the Culprit Plaque With
Positrons, Magnets, and Bubbles
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The obvious advantages of noninvasive means to assess
the culprit
plaque have expedited the dramatic growth in positron
emission
tomography (PET),
31
MRI,
32 MRI and
angiography,
33 and
microbubble
contrast echocardiographic
imaging.
34 PET and MRI
techniques
can discriminate between flow impairment due to focal,
localized
obstructions compared with diffuse disease. Similarly, the
use
of microbubble contrast echocardiography is
emerging as a means
to assess the microcirculatory responses to
flow-limiting stenoses,
collateral function, and myocardial
viability. A full discussion
of this field may be found
elsewhere.
34
PET Scanning
For lesions of intermediate severity, PET-derived CVR
correlates well with intracoronary Doppler
CVR.35 Abnormal
PET-determined coronary reserve in angiographically normal
territories seems to represent early functional abnormalities
of vascular reactivity or possible diffuse atherosclerotic involvement
by demonstrating a graded longitudinal perfusion deficit from base to
apex during hyperemic
stress.36 Coupled with
quantitative coronary angiographic assessment of diffuse
disease37 and confirmed by
PET-derived longitudinal perfusion gradients, decisions for a vigorous
antiatherosclerotic risk factor reduction program over difficult or
marginally indicated mechanical revascularization
can be
facilitated.38
MRI
Current whole-body MRI at 1.5 Tesla is
limited by a resolution >400 µm. A catheter-based magnet coil
positioned within the target vessel can resolve atherosclerotic tissue
images to 120 to 300 µm, with an 80% concordance of plaque size and
intimal thickness to pathological
examination.39 The
high-resolution 9T MRI (spatial resolution, 100 µm) permits
examination of serial responses of atherosclerotic pathology to
pharmacological and mechanical
therapies40
(Figure 4).
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Figure 4. A, MRI of a plaque with an intact, thick fibrous cap (uniform dark band between the bright lumen and great plaque core). B, MRI of a plaque with intact, thin fibrous cap in which dark band adjacent to the lumen is absent. Reprinted with permission from reference 32.
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Phase-contrast MRI has a high correlation
(r>0.89) with invasive CVR
determinations.33 In 17
patients with recurrent chest pain 3 months after successful PCI, a
phase-contrast MRI-CVR value 
2 had 100% sensitivity and 82%
specificity for detecting luminal diameter narrowing >70%,
respectively.33 After acute
myocardial infarction and reperfusion therapy directed at the
microcirculation, the potential to quantify coronary flow
restoration will likely have substantial therapeutic
implications.41
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Clinical Outcomes Related to Catheter-Based
Anatomic and Physiological Data
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The new modalities of OCT, Raman spectroscopy, and
thermography
have yet to be clinically applied. Longitudinal studies
relating
the IVUS characterization of a vulnerable plaque to clinical
outcomes
have not yet been performed. Large cross-sectional IVUS lumen
areas
after stenting are associated with reduced
restenosis.
42
Complete
and full stent strut apposition to the vessel wall (by IVUS)
is
associated with reduced subacute thrombosis; however,
complete
stent strut apposition may not occur in 30% to 40% of
angiographically-guided
cases.
43 For lesions of
uncertain physiological significance, IVUS lumen
cross-sectional
areas <3 to 4 mm
2 are
associated with abnormal CVR and FFR
in most patients, supporting an
objective indication for
intervention
44 45
(Figure 5
).
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Figure 5. Left, Left main (LM) coronary artery narrowing (arrow) in a 44-year-old man with mild dyspnea. Top right, IVUS measurements. Mean luminal areas (MLA) are 3.9 and 9.8 mm2, respectively. Bottom right, FFR across the lesion was 0.69. This lesion is both anatomically and physiologically significant.
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For outcomes related to physiological
measurements, threshold values (CVR<2.0 and FFR<0.75) associated with
inducible myocardial ischemia in patients with stable angina
have been reproduced by many centers with several different
techniques.20 In support of
a provisional stent strategy after balloon angioplasty alone, the
coupled criteria of CVR 
2.5 and 35% diameter stenosis (by
quantitative coronary angiography) were associated with a
6-month major adverse cardiac event rate
<20%.46 When FFR>0.90 was
achieved after balloon angioplasty alone, there was <15%
restenosis seen at 2 years
follow-up.47 A FFR>0.94
after Wiktor stent implantation was associated with complete stent
strut apposition in >80% of IVUS-documented
procedures.48
For clinical decision making, several studies have
demonstrated <10% lesion progression requiring intervention over 1 to
2 years of follow-up,20
supporting the safe deferment of intervention for intermediate lesions.
Table 2 summarizes catheter-based criteria for the
assessment of a culprit plaque.
|
The Future: Catheter-Based Culprit Plaque
Assessment and Plaque Sealing
|
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When coronary flow or pressure measurements
clearly identify
a hemodynamically significant
obstruction, the indication for
PCI is undisputed. However, many
interventionists are troubled
when confronted with a modest but
hemodynamically insignificant
plaque. The risk of an
untreated plaque causing a myocardial
infarction within the next 3
years increases from 2% to 15%
as stenosis severity increases
from
50% diameter narrowing to
90% to
98%.
49 Would such a lesion
(and patient) benefit from
mechanical disruption with subsequent plaque
stabilization?
The concept of mechanical disruption with plaque
stabilization, termed plaque sealing, has great intellectual and
clinical appeal but little current data to endorse its use. For
example, the risk of a significant restenosis varies from
10% for a mild lesion to 50% for a severe and complex
lesion49 50 and
might be balanced against the risk of myocardial infarction given that
acute PCI infarction is <2% and that balloon-dilated lesions that are
patent at 6 months have only a 0.7% risk of causing an infarction
during the next 7 years.50
Data to support such an approach will need to demonstrate that,
balanced against short-term complications and restenosis,
plaque sealing reduces the risk of a future infarction, reduces plaque
activation in the near and hopefully distant term, and favorably
influences the plaque’s natural history while incorporating PCI into
the diagnostic angiography, thus reducing additional
procedures, hospitalizations, and cost.
Figure 6 depicts a historically relevant patient example. In
the future, techniques assessing plaque vulnerability may lead to PCI
to augment medical therapies for mild, non–flow-limiting lesions
situated proximally in large
vessels.
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Figure 6. The first coronary angioplasty patient presented with atypical chest pain and a negative maximal exercise test 23 years after his initial coronary angioplasty, which was performed on September 16, 1977 in Zurich (a). The initially dilated site (old) looked pristine. There was a new, nonsignificant lesion (new). The FFR was normal across both the new and the old lesion (b and c). Toward the end of plaque sealing, a 3.5 mm balloon was inflated. The nonsignificant lesion (arrow in b) yielded between 4 and 6 bar (d). Because of the unsatisfactory results with a basically unchanged stenosis and an apparent dissection (circle in d), a 3.0x8 mm stent was placed (e). Panel f shows the entire vessel 23 years after balloon angioplasty (1) and immediately after plaque sealing for a new, nonsignificant lesion (2).
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Conclusion
|
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Compared with angiography, catheter-based
diagnostic (light,
sound, MRI, thermal, pressure, flow,
etc) modalities better
quantify the anatomic and
physiological features of a culprit
plaque, can
direct appropriate mechanical or medical therapies,
and potentially
reduce unnecessary or ineffective attempts to
restore normal
coronary blood flow. However, these modalities
come at a price
that must be weighed against the relative benefit
for improved
diagnostic information. Although theoretically
attractive,
preemptive PCI (sealing) of significant but non–flow-limiting
potential
culprit plaques must await further information from both
catheter-based
and noninvasive methods. Assessment of the culprit
plaque will
help achieve the ultimate goal of improving long-term
outcomes
in more patients with coronary artery disease at an
earlier
age.
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Acknowledgments
|
|---|
The authors thank Donna Sander for
manuscript preparation, Dr
Bernard de Bruyne and Dr Nico Pijls for
their FFR cases, and
Dr Paul Hauptman for manuscript
review.
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References
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Introduction
Structure and Metabolism
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