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(Circulation. 2001;103:604.)
© 2001 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
From the Cleveland Clinic Foundation, Cleveland, Ohio (S.E.N.), and Stanford University, Palo Alto, Calif (P.Y.).
Correspondence to Steven E. Nissen, MD, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail nissens{at}ccf.org
Abstract
AbstractIntravascular
ultrasound (IVUS) is a valuable adjunct to angiography, providing new
insights in the diagnosis of and therapy for coronary disease.
Angiography depicts only a 2D silhouette of the lumen, whereas IVUS
allows tomographic assessment of lumen area, plaque size, distribution,
and composition. The safety of IVUS is well documented, and the
assessment of luminal dimensions represents an important application of
this modality. Comparative studies show the greatest disparities
between angiography and ultrasound after mechanical interventions. In
young subjects, normal intimal thickness is typically
0.15 mm. With
IVUS, lipid-laden lesions appear hypoechoic, fibromuscular lesions
generate low-intensity echoes, and fibrous or calcified tissues are
echogenic. Calcium obscures the underlying wall (acoustic shadowing).
The extent and severity of disease by angiography and ultrasound are
frequently discrepant. Arterial remodeling refers to changes in
vascular dimensions during the development of atherosclerosis. At
diseased sites, the external elastic membrane may actually shrink in
size, contributing to luminal stenosis. The interpretation of IVUS
relies on simple visual inspection of acoustic reflections to determine
plaque composition. However, different tissue components may look quite
similar, and artifacts may adversely affect ultrasound images. IVUS
commonly detects occult disease in angiographically "normal" sites.
In ambiguous lesions, ultrasound permits lesion quantification,
particularly for left main coronary disease. IVUS has emerged as the
optimal method for the detection of transplant vasculopathy. An
important potential application of ultrasound is the identification of
atheromas at risk of rupture. The mechanisms of action of
interventional devices have been elucidated using IVUS, and ultrasound
is used by some operators to select the most suitable interventional
device. IVUS-derived residual plaque burden is the most useful
predictor of clinical outcome. In restenosis after balloon angioplasty,
negative remodeling is a major mechanism of late lumen loss. IVUS is
not routinely used for stent optimization, and there is no consensus
regarding optimal procedural end points. Ultrasound has proven useful
in evaluating brachytherapy. New and emerging applications for IVUS are
continuing to evolve, particularly in atherosclerosis
regression-progression trials.
Key Words: ultrasonics imaging stents
Contrast angiography is still the most important imaging method used to guide therapy for coronary disease. In recent years, intravascular ultrasound (IVUS) has evolved as a valuable adjunct to angiography, providing insights that are significantly altering conventional paradigms in diagnosis and therapy.1 2 3 4 5 6 The contributions of ultrasound originate principally from 2 key features, its tomographic perspective and its ability to directly image the vessel wall. Whereas angiography depicts only a 2D silhouette of the lumen, ultrasound allows precise tomographic measurement of lumen area and plaque size, distribution and, to some extent, composition. Despite the independent value of IVUS, this technique should be considered supplemental to angiography, not a comprehensive alternative. This review describes the rationale, technique, and interpretation of IVUS imaging in diagnostic and therapeutic applications. We will emphasize the impact of ultrasound in understanding atherosclerotic coronary disease and its management.
Rationale for Ultrasound Imaging
Limitations of Angiography
Although angiography has endured for >40 years as the
predominant method used to define coronary anatomy, many studies have
challenged the accuracy and reproducibility of this
technique.7 8 9 10 11 12 13
The visual interpretation of angiograms exhibits significant observer
variability and correlates poorly with post-mortem examination.
Angiography depicts arteries as a planar silhouette of the
contrast-filled lumen. Any arbitrary angiographic projection can
misrepresent the true extent of luminal narrowing. Mechanical
interventions may increase luminal irregularity, impairing the accuracy
of angiography.14 An
assessment of lesion severity requires the measurement of luminal
diameter within the lesion and an uninvolved "normal" segment.
However, necropsy studies demonstrate that disease is usually diffuse,
with no truly normal segment. Angiography is also confounded by outward
remodeling of the vessel wall, which may conceal early atherosclerosis.
Although remodeled lesions may not restrict blood flow, retrospective
studies demonstrate that nonobstructive lesions represent the most
common substrate for acute coronary syndromes.
Advantages of Ultrasound
Several characteristics inherent to ultrasound imaging
offer potential advantages in the evaluation of coronary disease. The
tomographic orientation of ultrasound enables a visualization of the
full circumference of the vessel wall, not just two surfaces.
Angiographic vessel or stenosis sizing requires calibration to correct
for radiographic magnification. However, ultrasound devices use an
electronically generated scale, with measurements performed using
direct planimetry. The tomographic perspective of ultrasound enables an
assessment of vessels that are difficult to image by angiography,
including diffusely diseased segments, ostial or bifurcation stenoses,
eccentric plaques, and angiographically foreshortened vessels. Finally,
the penetrating nature of ultrasound provides unique images of the
atherosclerotic plaque, not merely the lumen.
Equipment and Technique
Ultrasound Catheters
The equipment required to perform intracoronary
ultrasound consists of 2 major components, a catheter incorporating a
miniaturized transducer and a console containing the electronics
necessary to reconstruct the image. High ultrasound frequencies are
used, typically centered at 20 to 50 MHz and providing excellent
theoretical resolution. At 30 MHz, the wavelength is 50 µm, yielding
a practical axial resolution of
150 µm. Determinants of lateral
resolution are more complicated and depend on imaging depth, which
average 250 µm at typical coronary diameters. Current catheters range
from 2.6 and 3.5 French (0.87 to 1.17 mm) and can be placed through a
6-French guiding catheter.
Two different approaches to transducer design have
emerged: mechanically rotated devices and multielement electronic
arrays. Mechanical probes use a drive cable to rotate a single
piezoelectric transducer at 1800 rpm, yielding 30 images per second. In
electronic systems, multiple transducer elements (currently up to 64)
in an annular array are activated sequentially to generate the image.
Multielement designs typically result in catheters that are easier to
set up and use, whereas mechanical probes have traditionally offered
superior image quality, although these differences have narrowed in
recent years. Imaging studies are usually recorded on videotape,
although one system permits digital recording of
60 seconds with
permanent archiving on a recordable CD-ROM.
Examination Technique
Standard techniques for intracoronary catheter delivery
are used for intravascular examination. Heparin and intracoronary
nitroglycerin are routinely administered, and the coronary artery is
subselectively cannulated. The operator advances or retracts the
imaging device over the wire, recording images on videotape or CD for
subsequent analysis. Many centers use a motorized pullback device to
withdraw the catheter at a constant speed (between 0.25 and 1 mm/s;
most frequently, 0.5 mm/s). However, a single pullback, even when
controlled by a motor, may be insufficient for a complete diagnostic
examination. Side branches visualized by angiography or ultrasound are
useful landmarks to facilitate interpretation and comparisons in
sequential examinations.
Safety of Coronary Ultrasound
The safety of intracoronary ultrasound is well
documented.15 16
Studies report complication rates varying from 1% to 3%; the
complication most frequently reported is transient spasm, which
responds rapidly to intracoronary nitroglycerin. The major complication
rate (dissection or vessel closure) is <0.5%. Nearly all major
complications occur in patients undergoing intervention rather than
diagnostic imaging. Examination of vessels previously imaged by IVUS
compared with noninstrumented vessels shows no accelerated progression
of atheroma at 1 year of follow-up. Despite the favorable safety
profile, subselective coronary instrumentation always carries a
potential risk of vessel injury. Accordingly, only operators
experienced in intracoronary catheter manipulation should perform
intravascular imaging.
Image Interpretation and Measurements
Lumen Appearance and Measurements
At frequencies >20 to 25 MHz, flowing blood exhibits a
characteristic pattern of echogenicity, observed as finely textured
echoes moving in a swirling pattern
(Figure 1
). Blood "speckle" can assist image
interpretation; for example, it can help confirm the communication
between a dissection plane and the lumen. The pattern of blood
echogenicity depends on blood flow velocity; it shows increased
intensity and a more coarse texture when flow is reduced. Blood speckle
is also more prominent at higher imaging frequencies, which may
interfere with delineation of the blood-tissue interface. This
phenomenon has so far limited IVUS imaging devices to frequencies <40
to 45 MHz, although automatic methods of blood noise reduction may
substantially reduce the problem in the future.
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Assessment of luminal dimensions affects many therapeutic decisions and represents an important application for IVUS. Lumen area is determined by planimetry of the leading edge of the blood-intima acoustic interface. Because of the speckled nature of ultrasound, individual video frames may not contain a continuous intimal leading edge. Accordingly, a review of moving images is routinely performed to assist edge detection by "filling-in" a discontinuous border. Comparisons of ultrasound luminal measurements with angiography usually show a close correlation for vessels without atherosclerosis. However, for diseased arteries, investigators report only a moderate correlation (r=0.7 to 0.8) and a standard error >0.5 mm.3 5 17
Comparative studies show the greatest disparities between angiography and ultrasound after mechanical interventions.18 In this setting, the shape of the lumen may be extremely complex, with plaque fissures or deep wall dissections.14 18 Accordingly, the reduced correlation between IVUS and angiography is probably explained by an irregular, noncircular cross-sectional profile, which cannot be adequately depicted by angiography.13 Extraluminal channels contribute little to blood flow, raising the question of whether such structures should be included in tracing the luminal contour. A commonly applied approach distinguishes the true lumen area from the "dissection area." Lumen eccentricity is often reported using a variety of indices that compare minimal and maximal lumen dimensions.
Normal Arterial Appearance
Studies performed in vivo or using excised,
pressure-distended vessels have characterized the appearance of normal
coronary
arteries.19 20 21 22 23
An ultrasound reflection is generated at a tissue interface if there is
an abrupt change in acoustic impedance. In the normal artery, 2 such
interfaces are usually observed, one at the border between blood and
the leading edge of the intima and a second at the external elastic
membrane (EEM), which is located at the media-adventitia border
(Figure 1
). The tunica media is relatively sonolucent and, in
good-quality images, it can be visualized as a distinct, relatively
sonolucent layer. The trailing edge of the intima is poorly defined and
cannot be used reliably for measurements. The outer border of the
adventitia is also indistinct, merging imperceptibly into the
surrounding tissues. In normal arteries, the intima is thin, consisting
mostly of endothelial cells and connective tissue, with a relatively
small difference in impedance from blood. In 30% to 50% of normal
coronary arteries, the thin intima reflects ultrasound poorly, so it is
not visualized as a separate layer. This finding has led some observers
to propose that a trilaminar wall represents evidence of early
atherosclerosis.23 In young
subjects, the reported normal value for intimal thickness is typically
0.15±0.07
mm.5 19 23
Most investigators use 0.25 to 0.50 mm as the upper limit of
normal.
Characterization of Atherosclerosis
Ultrasound provides a unique method for studying the
morphology of atherosclerosis in vivo. Studies have compared the
ultrasound appearance of plaques to histology in freshly explanted
human
arteries.20 21 22
Lipid-laden lesions appear hypoechoic, fibromuscular lesions generate
low-intensity or "soft" echoes, and fibrous or calcified tissues
are relatively echogenic. Lipid-laden or fibromuscular lesions may
exhibit a prominent echogenic fibrous cap, although most fibrous caps
are too thin to be resolved by IVUS. Calcium obstructs ultrasound
penetration, obscuring the underlying vessel wall (acoustic shadowing;
Figure 2
). The angle subtended by the calcified arc is often
used to quantify the severity of calcification. Ultrasound imaging has
shown significantly higher sensitivity than fluoroscopy in the
detection of coronary
calcification.24 25
Target lesion calcification is detected by ultrasound in 70% to 80%
of patients undergoing intervention, whereas fluoroscopy detects
calcium in 10% to 35%. The arc of calcium measured by ultrasound is
usually greater in patients with angiographically visible
calcification.
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Atheroma Measurements
Ultrasound atheroma measurements are obtained from
leading edge to leading edge, a standard approach that has been
validated in echocardiography. Atheroma area is determined by
planimetry of the intimal leading edge and EEM, thereby including the
media in measurements. The rationale for this convention arises from
several phenomena. First, the media is not always distinguished as a
sonolucent layer, whereas the EEM represents a reliable boundary.
Second, the location of the trailing edge of the intima is confounded
by the spread of the ultrasound signal into the media (called
blooming). Atheroma area measurements performed in this fashion
correlate closely with
histology.20 21 22
However, calcium-induced acoustic shadowing can obscure a large portion
of the EEM, requiring interpolation with a reduction in accuracy. In
the literature, the vague term "vessel area" is sometimes
substituted for "EEM area."
The percentage of the EEM area occupied by atheroma is often calculated, and this parameter is often referred to as "percent area stenosis," "plaque area stenosis" or, simply, "plaque burden." It should be realized, however, that this measurement is not equivalent to angiographic percent stenosis, which represents an expression of luminal narrowing at the lesion relative to a reference segment. Some laboratories routinely measure maximum atheroma thickness, which is defined as the longest distance between the intimal leading edge and the EEM. The difference between maximum and minimum thickness represents a measure of plaque eccentricity. The circumferential extent of disease is also commonly classified by determining whether abnormal intimal thickening is present throughout the 360° arterial circumference. The longitudinal extent of disease is also commonly reported; it is defined as "diffuse" if the intimal thickness is abnormal at every site within the segment.26
Discrepancies With Angiography
The extent and severity of disease by angiography and
ultrasound are frequently
discrepant.13 The percentage
of stenosis determined by ultrasound is usually substantially greater
than that determined by angiography. This phenomenon is a consequence
of 2 major factors, the diffuse nature of atherosclerosis affecting the
angiographically "normal reference sites" and adaptive enlargement
of the EEM, which maintains a constant lumen during early
atherosclerosis
(Figure 3
). Studies have demonstrated a significant
discordance between angiography and ultrasound in assessing plaque
distribution, highlighting the inaccuracy inherent in determining
plaque location from a projected 2D silhouette of the
lumen.27 IVUS demonstrates
that the majority of plaques are eccentrically located, a phenomenon
with important implications for guiding coronary interventions,
particularly for selective plaque removal techniques such as
directional atherectomy.
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Arterial Remodeling
The term arterial remodeling refers to changes in
vascular dimensions during the development of atherosclerosis
(Figure 4
). This phenomenon was initially described from
necropsy specimens by Glagov et
al,28 who reported a
positive correlation between EEM and atheroma area. At lesions with a
stenosis <40%, an increase in arterial size "overcompensated" for
plaque accumulation, resulting in an increase in lumen area. At
advanced lesions, remodeling was less evident and lumen size was
reduced. The authors hypothesized that this phenomenon represented a
compensatory mechanism to preserve lumen size. IVUS provides
cross-sectional areas of the lumen, atheroma, and EEM, allowing the in
vivo study of remodeling. Ultrasound studies show a correlation between
EEM and plaque area and confirm overcompensation in early
disease.29 30
Although the exact mechanism of remodeling remains uncertain, this
phenomenon helps explain the underestimation of the disease severity by
angiography and may influence the assessment of the true vessel size in
guiding coronary interventions.
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IVUS studies have demonstrated a new dimension to arterial
remodeling: negative remodeling or arterial
shrinkage31 32
(Figure 5
). At diseased sites, the EEM may actually shrink in
size, contributing to luminal stenosis. However, it is important to
realize that when remodeling is defined by comparing lesion to
reference EEM areas, there is an inherent assumption that the reference
EEM area represents the original vessel size. Studies of
atherosclerotic coronary arteries demonstrate that angiographic
reference segments are invariably diseased by ultrasound. Therefore,
these reference segments are probably remodeled and may not provide an
accurate measure of vessel size. Recently, negative remodeling has been
implicated in restenosis after mechanical
intervention.33 34
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Recent and intriguing IVUS studies have examined the relationship between remodeling and clinical presentation in patients with coronary artery disease.35 In unstable patients, both EEM and plaque areas were significantly larger than the corresponding measurements in stable patients. Positive remodeling seems to be significantly more prevalent in the unstable group and negative remodeling more prevalent in the stable group.
Limitations of IVUS
Although contemporary ultrasound devices produce
remarkably detailed views of the vessel wall, interpretation must rely
on simple visual inspection of acoustic reflections to determine plaque
composition. The echogenicity and texture of different tissue
components may exhibit comparable acoustic properties and therefore
appear quite similar. A sonolucent luminal mass of tissue may represent
intracoronary thrombus, while a nearly identical appearance may result
from an atheroma with a high lipid content. Thus, IVUS is accurate in
determining the thickness and echogenicity of vessel wall structures,
but it is not consistently able to provide actual histology. Validated
methods do not yet exist for objective or automated classification of
atheromatous lesions. Although promising, radiofrequency analysis is
not yet reliable enough for routine clinical applications.
Artifacts may adversely affect ultrasound images,
including "ring-down" artifacts produced by acoustic oscillations
in the piezoelectric transducer that obscure the near field, resulting
in an acoustic catheter size larger than its physical
size.36 Geometric distortion
can result from imaging in an oblique plane (not perpendicular to the
long axis of the vessel). An important artifact, "non-uniform
rotational distortion," arises from uneven drag on the drive cable of
the mechanical style catheters, resulting in cyclical oscillations in
rotational speed, observed as visible distortion of the image. The
physical size of ultrasound catheters (currently
1.0 mm) constitutes
an important limitation in imaging severe
stenoses.
Diagnostic Applications
Angiographically Normal Coronary
Vessels
Angiographically normal coronary arteries are
encountered in
10% to 15% of patients undergoing catheterization
for suspected coronary disease. IVUS commonly detects occult disease in
these
patients.13 37 38
However, no short- or long-term studies have determined whether disease
detected exclusively by ultrasound portends a worse prognosis than
"true normal" angiography. If any luminal irregularity is present
by angiography, ultrasound will usually demonstrate disease at most
other examined sites.13 The
prevalence of disease at angiographically normal sites confirms the
finding, previously reported from necropsy studies, that coronary
disease is usually diffuse, not focal, and that angiography frequently
underestimates disease
burden.12
Angiographically Indeterminate Lesions
Despite improvements in x-ray equipment, angiographers
still commonly encounter lesions that elude accurate characterization,
despite thorough examination using multiple radiographic projections.
In ostial and bifurcation lesions, the stenosis may be obscured by
overlapping contrast-filled structures. Intermediate stenoses
(angiographic severity ranging from 40% to 75%) are particularly
problematic in patients whose symptomatic status is difficult to
assess. In ambiguous lesions, ultrasound provides a tomographic
perspective, independent of the radiographic projection, that often
permits lesion quantification. In 2 large prospective series,
intracoronary ultrasound changed the management strategy (primarily
decisions to perform or defer interventions or choice of interventional
device) in
20% of examinations performed immediately before
coronary
intervention.39 40
In both studies, however, the selection of patients for ultrasound may
have resulted in an overestimation of the true impact of intravascular
imaging on clinical decision-making.
Left Main Coronary Disease
Assessment of left main coronary disease by angiography
represents a particularly difficult clinical
problem.8 Three major
anatomic factors impair angiographic left main evaluation. Aortic cusp
opacification or "streaming" of contrast may obscure the ostium,
the short length of the vessel may leave no normal segment for
comparison, and the distal left main artery may be concealed by
bifurcation or trifurcation. Ultrasound can help overcome these
confounding factors.41 The
ultrasound transducer is placed distal to the left main vessel, and a
slow pullback to the aorta is performed with the guiding catheter
disengaged. There is no consensus regarding the cross-sectional area at
which the left main obstruction is considered critical. However, a
stenosis area >50% or an absolute area <9
mm2 have been proposed as criteria for left
main stenosis severity requiring
revascularization.
Transplant Coronary Artery Disease
Coronary disease represents the major cause of death in
the first year after transplantation. This disease is often clinically
silent because the heart is denervated and ischemia by functional
testing does not usually occur until the disease is
advanced.42 43 44
Although angiography is been performed annually for surveillance, the
diffuse nature of the disease often impairs
detection.45 IVUS has
emerged as the optimal method for early
detection.46 Disease by
angiography is present in 10% to 20% of patients at 1 year and
50% by 5
years.47 48 The
prevalence of arteriopathy detected by ultrasound is much higher;
abnormal intimal thickening is seen by IVUS in 50% of patients by 1
year.26 48 49
The definition of abnormal intimal thickness is controversial
because the categorical classification of a continuous variable,
intimal thickness, into normal or abnormal is inherently arbitrary.
Most ultrasound studies define the threshold for transplant
vasculopathy as an intimal thickness >0.5 mm.
Despite the young donor age, conventional
atherosclerosis is frequently present in donor hearts. In one study,
atherosclerotic lesions were detected in 56% of patients at a mean
donor age of 32 years.50
However, the natural history of donor lesions after transplantation is
largely unknown. In the first year after transplantation, progression
of donor disease occurred in 42% of patients. A case report
documenting regression of donor lesions has also been published.
Ultrasound studies have demonstrated an association between the
severity of disease by ultrasound and clinical outcome, with an
increased incidence of death, myocardial infarction or
retransplantation in those with more severe
disease.51 52
Rapidly progressive intimal thickening (
0.5 mm increase) in the first
year after transplantation has major negative prognostic significance.
Intravascular imaging has been used to evaluate therapies for
transplant vasculopathy, including statin drugs, ACE inhibitors, and
calcium blockers.
Unstable Plaque and Thrombi
An important potential application of intracoronary
ultrasound is the identification of atheromas at risk of rupture. Acute
coronary syndromes frequently develop in territories with minimally
diseased vessels rather than high-grade
stenoses.53 The histology of
unstable plaques usually reveals a lipid-laden atheroma with a thin
fibrous cap (Figure 6
). Preliminary ultrasound reports have associated
echolucent, presumably lipid-laden, plaques with acute coronary
syndromes.54 Positive
remodeling has also been associated with an unstable clinical
presentation34
(Figure 7
). Intraluminal thrombi at ruptured or fissured
plaques are considered the hallmark of acute coronary syndromes. Small
studies have attempted to define the ultrasound appearance of
thrombi.55 56
However, IVUS is still unreliable in differentiating acute thrombi from
echolucent plaques because of the similar echogenicity and texture of
lipid-laden tissue, loose connective tissue, and stagnant blood.
Ultrasound is less reliable than angioscopy for the diagnosis of
thrombi in vitro.57
Radiofrequency analysis has shown some promise in differentiating
between thrombus and
atheroma.58
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Interventional Applications
A number of new devices have been added to the interventional armamentarium over the last decade. The mechanisms of action of these devices and their interaction with different plaque morphologies have been largely elucidated using IVUS. Although IVUS has played a pivotal role in understanding the effects of interventional devices, the precise clinical role for ultrasound during intervention has, for the most part, not been well defined in large-scale clinical trials.
Preinterventional Imaging
Ultrasound is used by some operators to select the
device most suitable for a specific patient or lesion. The process of
device selection depends on several factors, most commonly measurements
of atheroma severity, plaque distribution, depth and extent of
calcification, and the presence of thrombi or dissections.
Single-center studies have reported that ultrasound imaging frequently
influences the operators appreciation of target lesion severity,
morphology, and the optimal approach to
therapy.40 However, in these
studies, patients were not randomized, allowing for bias in the
selection of more complex cases, emphasizing the contributions of
ultrasound examination. The impact of ultrasound-triggered
modifications of strategy on outcome remains to be
determined.
Guidance for Angioplasty and
Atherectomy
In the early 1990s, studies were initiated to determine
whether intravascular imaging could predict clinical and angiographic
outcome after intervention. The goal of these investigations was to
determine whether some morphological features, such as the presence or
extent of dissection, or morphometric features (eg, lumen size or
plaque burden) were related to restenosis. The first multicenter trial,
Post-IntraCoronary Treatment Ultrasound Result Evaluation
(PICTURE), showed no
statistically significant predictors of outcome in a relatively small
cohort (250 patients) using early generation
equipment.59 Single-center
studies, however, identified residual plaque burden as an independent
predictor of outcome in multivariable
analysis.60 To examine this
issue more completely, phase II of the Guidance by Ultrasound Imaging
for Decision Endpoints (GUIDE) trial enrolled 524 patients undergoing
angioplasty and/or atherectomy. Among the angiographic and ultrasound
variables, ultrasound-derived residual percent plaque burden was the
most powerful predictor of clinical outcome, with a risk ratio of
1.7.61 However, the
long-term clinical impact of differences in angiographic result has not
been established.
The first trial to directly address the outcome of ultrasound guidance of balloon angioplasty was the Clinical Outcomes With Ultrasound Trial (CLOUT), in which IVUS imaging was performed after obtaining a satisfactory angiographic result. If vessel remodeling at the lesion or involvement of the reference segment was apparent on ultrasound, a larger balloon size was used. After IVUS, the balloon-to-artery ratio increased from 1.12 to 1.30, resulting in an increase in angiographic minimal lumen diameter from 1.95 to 2.21 mm.62 Several subsequent studies addressed the clinical outcome of IVUS-guided balloon sizing. In 2 single-center, nonrandomized studies of aggressive balloon sizing (based on the media-to-media dimension determined by IVUS), rates of major events and revascularization were similar to stenting.63 64 In these studies, stents were used as a backup strategy if aggressive angioplasty resulted in dissection (a strategy that has been called provisional stenting).
Although balloon angioplasty has been available for
many years, the mechanisms of lumen gain have been difficult to
elucidate using angiography. Ultrasound demonstrates plaque fracture
and arterial wall dissection much more often than angiography, with
some form of disruption seen in between 50% and 75% of cases. Vessel
wall stretching represents another potential mechanism of lumen gain;
this is most evident when the angioplasty is performed on soft
echolucent
plaques65 66 67
(Figure 8
). Plaque compression was originally suggested
as a mechanism for lumen gain. However, recent in vivo
ultrasound studies have disproved any significant contribution of
compression, demonstrating "axial redistribution" rather than
compression of the plaque at angioplasty
sites.68
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In the setting of directional coronary atherectomy, IVUS can facilitate lesion selection, demonstrating the presence of significant calcification, which is an important predictor of procedural failure.69 In particular, ultrasound imaging can identify superficial calcium, which is associated with poor tissue retrieval. The most striking finding from IVUS studies of directional atherectomy is the substantial residual plaque burden after an atherectomy in which the angiographic result seems to be good.69 Several studies have addressed the issue of more aggressive plaque removal on the basis of ultrasound imaging. In the Optimal Atherectomy Restenosis Study (OARS), ultrasound guidance yielded a target lesion revascularization rate of 17.8% and an angiographic restenosis rate of 28.9% at 6 months. However, these results failed to reach statistical significance compared with balloon angioplasty with stent backup.70 In the Adjunctive Balloon Angioplasty After Coronary Atherectomy Study (ABACAS), ultrasound-guided atherectomy provided a trend to lower restenosis rates than angioplasty (23.6% versus 19.6%), but this trend did not achieve statistical significance.71 In contrast, the Stent versus Directional Coronary Atherectomy Randomized Trial (START) demonstrated a significant reduction in restenosis in a group receiving aggressive IVUS-guided atherectomy (16%) compared with stenting (33%).72
IVUS imaging in the context of high-speed rotational atherectomy has confirmed the principle of differential cutting (selective removal of less compliant plaque material, most notably calcium)73 As in the case of directional atherectomy, IVUS demonstrates a large residual plaque burden after rotablation. Measurement of the true vessel size by ultrasound may allow safe use of larger burrs, with a greater lumen gain and less residual plaque burden.74
Mechanisms of Restenosis
For the first 15 years of interventional cardiology,
investigators believed that the predominant mechanism of restenosis
after angioplasty and atherectomy was intimal proliferation. Ultrasound
studies in the peripheral vessels by Pasterkamp and
colleagues31 presented the
first indication that negative remodeling, or localized shrinkage of
the vessel, was a major mechanism of late lumen loss. Mintz et
al32 studied 212 native
coronary arteries in patients undergoing repeat catheterization for
recurrent symptoms or research protocols after coronary interventions.
At follow-up, there was a decrease in EEM area and an increase in
plaque area at the target lesion. Interestingly, >70% of lumen loss
was attributable to the decrease in EEM area, whereas the neointimal
area accounted for only 23% of the loss. Moreover, the change in lumen
area correlated more strongly with the change in EEM area than with the
change in plaque area. For lesions with an increase in EEM area at
follow-up (47% of segments studied), there was no change or an actual
gain in lumen area and a reduction in angiographic restenosis (26%
versus 62%;
P<0.0001).32
These observations have provided a key insight into the reduction of restenosis observed with stenting. Unlike the restenotic response to angioplasty or atherectomy, which is a mixture of arterial remodeling and neointimal growth, stent restenosis is primarily due to neointimal proliferation. In serial ultrasound studies, late lumen loss correlated strongly with the degree of in-stent neointimal growth (r=0.98).75 76 The amount of intimal proliferation has been shown to correlate with the pre-stent plaque burden.77 78 In a serial study using IVUS of stented coronary segments, no significant change occurred in the area bound by stent struts, indicating that stents can resist the arterial remodeling process.75 This phenomenon, combined with the greater initial lumen expansion accomplished with stenting, results in a lower net restenosis rate than that with angioplasty or atherectomy.
Guidance for Stenting
In part because of this reduction in restenosis, use of
stents for percutaneous revascularization has increased exponentially
over the last 10 years. More refined stents and developments in
adjuvant pharmacological therapy have improved both short- and
long-term results. IVUS imaging has played a pivotal role in
understanding and optimizing the benefits of stent therapy.
During the initial clinical experience with stent
implantation, acute thrombosis was the most feared complication,
limiting application to a relatively narrow subset of patients and
leading to the routine use of warfarin. The pioneering observations of
Columbo et al,79 based on
IVUS, dramatically changed clinical practice. These investigators
demonstrated that deployment with conventional balloon pressures
resulted in a high incidence of incomplete expansion and apposition. In
a pivotal series, these investigators used ultrasound imaging to guide
high-pressure dilatation, achieving full expansion and complete stent
apposition in 96% of 359 consecutive but nonrandomized patients
(Figure 9
). Patients with optimal expansion received
antiplatelet therapy using aspirin and ticlopidine but no warfarin.
These technical modifications resulted in outstanding clinical
outcomes. The incidence of acute and subacute stent thrombosis was
<1%, and target vessel revascularization for symptomatic restenosis
at 6 months was 13%.
|
The concept of high-pressure stent implantation disseminated quickly, and larger trials demonstrated the safety of stent implantation using high pressures and antiplatelet therapy alone (without IVUS guidance).80 81 Consistent with these later trials, IVUS is not routinely used for stent optimization today, although there is great variability in its application from center to center, and conflicting evidence exists concerning the impact of IVUS on long-term freedom from restenosis. In a retrospective analysis of 315 lesions treated by high-pressure stenting, additional ultrasound-triggered inflations improved in-stent lumen area by >25% in 83 lesions (26%).82 Because in-stent restenosis is determined by the degree of intimal hyperplasia, it is a reasonable hypothesis that larger lumens should translate into lower rates of clinically significant restenosis.
Four multicenter trials have directly addressed the question of whether the increased lumen areas resulting from ultrasound guidance actually lead to a significant reduction in restenosis. In the nonrandomized Can Routine Ultrasound Influence Stent Expansion (CRUISE) study, 8 centers were assigned to ultrasound and 10 centers to angiographic guidance with a blinded ultrasound examination at the end of the procedure.83 The ultrasound-guided group achieved a 0.9 mm larger stent area, which translated into a 38% lower rate of target vessel revascularization, from 14.9% to 8.9%. A randomized study, the Optimal Coronary Ultrasound trial (OPTICUS), showed no significant difference in ultrasound versus angiographic guidance.84 However, critics of this trial have suggested that the statistical power of OPTICUS was borderline and there was less difference in minimal stent dimensions between the IVUS and angiographically-guided groups than has been seen in the other trials. A third trial (Restenosis after IVUS-guided Stenting [RESIST]), conducted in France, enrolled 155 patients and showed only a trend toward a reduction in the restenosis rate (6.3% relative reduction, which was not statistically significant) in IVUS-treated patients.85 A larger randomized trial, Angiography Versus IVUS-Directed Stent Deployment (AVID), has recently completed follow-up.86 This trial randomized 759 patients with native and vein graft disease to IVUS versus angiographic guidance. Overall, there was a trend for improved 12-month target lesion revascularization rates in all groups with IVUS guidance, but this did not achieve statistical significance (8% versus 12%). A statistically significant difference in favor of IVUS guidance was seen in vessels <3.25 mm, in more severe lesions and, particularly, in saphenous vein grafts.
Currently, there is no strict consensus regarding
optimal ultrasound procedural end points for stent implantation. Most
operators strictly advocate complete apposition of the stent struts to
the wall, because of the risk of thrombosis caused by protrusion of
stents into the blood field. The extent of stent expansion required for
optimal results remains controversial. Suggested relative stent
expansion criteria, which compare the minimal stent area to that of the
reference segments, include
90% or 100% of the distal and
80% or
90% of the average reference lumen
areas.87 Several groups have
demonstrated that restenosis decreases as a function of increasing
absolute postprocedure minimal stent area. An ultrasound analysis has
demonstrated that the degree of in-stent neointimal hyperplasia is
independent of the achieved stent lumen
size.88 This explains the
higher restenosis rates in smaller vessels and inadequately expanded
stents, in which the acute lumen gain is not adequate to accommodate
for tissue proliferation, resulting in significant late loss and
restenosis. A target minimal stent area >7 or 8
mm2 is applied in some laboratories as a
shorthand criterion for identifying an optimal result (although, of
course, the threshold will actually vary with the size of the vessel).
Some laboratories aim at reaching a lumen symmetry index >0.7,
determined as the minor in-stent diameter divided by the major
diameter. Other investigators have advocated more extensive stenting to
cover reference segment disease or dissections detected by IVUS.
Interestingly, the expansion, apposition, and symmetry end points are
not achieved in most cases.
In addition to evaluating stent expansion and strut apposition, ultrasound imaging may be useful in identifying reference segment disease or dissections that require additional interventions. The presence of significant peristent flow, limiting lesions, or dissections has been linked to a higher likelihood of stent thrombosis.89 Such findings are often angiographically occult, either not detectable at all or appearing as areas of vague haziness.90 The extent of neointimal hyperplasia at the stent margins has been linked to preexisting reference segment disease.91
Several studies have demonstrated the benefits of intravascular imaging before the implantation of coronary stents. In heavily calcified lesions, stenting results in a relatively small and asymmetrical acute lumen gain.92 In ostial lesions, ultrasound can identify whether the lesion involves the "true" ostium or if it spares first 1 or 2 mm. When stents are used to treat dissections, ultrasound often reveals the involvement of a longer vessel segment than appreciated angiographically. This is particularly relevant in cases of bailout stenting for threatened abrupt closure, where a residual dissection in the vicinity of the stent may increase the risk of stent thrombosis.
Percutaneous treatment of stent restenosis is a
challenging task. Balloon angioplasty results are satisfactory in focal
renarrowing but disappointing in diffuse stent restenosis. Ultrasound
imaging may prove very helpful in the management of these cases, often
revealing that the stent expansion was inadequate at the initial
procedure, and proper balloon sizing may lead to an improved lumen area
(Figure 10
). In adequately expanded stents, ultrasound-guided
use of debulking devices such as rotational atherectomy or laser
ablation has been advocated. Ultrasound imaging helps determine whether
the site of maximum tissue growth has occurred within the stent or in
the adjacent reference segment near the stent border. This is
particularly valuable with radiolucent stents, where precise
angiographic localization is problematic. However, it should be noted
that the various approaches suggested for the treatment of stent
restenosis have been studied in relatively small numbers of patients.
Larger randomized studies are needed to determine the optimal strategy
for the treatment of these difficult cases.
|
IVUS and Brachytherapy
Ultrasound has proven useful in clarifying the
mechanisms of benefit and refining the techniques in brachytherapy.
Ultrasound studies demonstrate that radiation has the potential to
inhibit profoundly neointimal proliferation within a stent. In the
nonstented segments, studies suggest that radiation initiates a process
of vessel expansion (a type of positive remodeling). These effects are
strongly influenced by the dose delivered to the media or adventitia,
which is dependent on the thickness and composition of the atheroma and
the position of the catheter in the lumen. Current research is
examining whether an ultrasound imagebased dosing algorithm will be
required to optimize therapeutic benefit. Ultrasound has already
demonstrated the potential for radiation to accelerate restenosis at
the edges of the treatment region, where the dosing falls off ("candy
wrapper effect";
Figure 11
).
|
Future Directions
The use of IVUS in the United States is in a phase of slow growth, with an average of 5% to 8% of coronary interventions currently being performed with IVUS guidance (mostly for stent optimization). IVUS use in Europe is considerably less than that in the United States and, in Japan, use is considerably higher, reflecting differing reimbursement rates and practice patterns. Technical developments in both catheters and systems are continuing with several companies, focusing on catheter deliverability, ease of use, and image quality.
New and creative areas of IVUS-guided therapy are being tested. Ultrasound provides the guidance modality for the so-called PICAB procedure (percutaneous in-situ coronary artery bypass), in which a conduit is created between a proximal coronary vessel and a coronary vein, providing a new source of oxygenated blood to ischemic myocardium. New combined imaging/stent delivery and imaging/atherectomy catheters are under development.
The ability of ultrasound to quantify precisely the extent of intramural atherosclerotic plaque is currently being exploited through a series of regression-progression trials that are currently underway. These include the Reversal of Atherosclerosis with Lipitor (REVERSAL) trial (600 patients), which is comparing 2 lipid-lowering regimens (expected completion, 2002), and the Norvasc for Regression of Manifest Atherosclerotic Lesions (NORMALISE) trial (750 patients), which is comparing amlodipine, enalapril, and placebo (expected completion, 2003). In both studies, IVUS measurements represent the primary end points of the trials. Such studies avoid the inherent limitations of angiographic regression trials and have the potential to define a new standard for the evaluation of drug therapy to limit the progression of atherosclerosis.
Footnotes
Dr Paul Yock receives grant support from and serves on the scientific advisory boards of various manufacturers of intravascular ultrasound equipment.
References
1. Yock PG, Linker DT, Angelsen BA. Two-dimensional intravascular ultrasound: technical development and initial clinical experience. J Am Soc Echocardiogr. 1989;2:296304.[Medline] [Order article via Infotrieve]
2. Hodgson JM, Graham SP, Savakus AD, et al. Clinical percutaneous imaging of coronary anatomy using an over-the-wire ultrasound catheter system. Int J Card Imaging. 1989;4:187193.[Medline] [Order article via Infotrieve]
3.
Nissen SE,
Grines CL, Gurley JC, et al. Application of a new phased-array
ultrasound imaging catheter in the assessment of vascular dimensions:
in vivo comparison to cineangiography.
Circulation. 1990;81:660666.
4.
Tobis JM,
Mallery J, Mahon D, et al. Intravascular ultrasound imaging of human
coronary arteries in vivo: analysis of tissue characterizations with
comparison to in vitro histological specimens.
Circulation. 1991;83:913926.
5.
Nissen SE,
Gurley JC, Grines CL, et al. Intravascular ultrasound assessment of
lumen size and wall morphology in normal subjects and patients with
coronary artery disease.
Circulation. 1991;84:10871099.
6. Arnett EN, Isner JM, Redwood CR, et al. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med. 1979;91:350356.
7.
Grodin CM,
Dydra I, Pastgernac A, et al. Discrepancies between cineangiographic
and post-mortem findings in patients with coronary artery disease and
recent myocardial revascularization.
Circulation. 1974;49:703709.
8.
Isner JM,
Kishel J, Kent KM. Accuracy of angiographic determination of left main
coronary arterial narrowing.
Circulation. 1981;63:10561061.
9.
Vlodaver Z,
Frech R, van Tassel RA, et al. Correlation of the antemortem coronary
angiogram and the postmortem specimen.
Circulation. 1973;47:162168.
10.
Zir LM,
Miller SW, Dinsmore RE, et al. Interobserver variability in coronary
angiography. Circulation. 1976;53:627632.
11. Galbraith JE, Murphy ML, Desoyza N. Coronary angiogram interpretation: interobserver variability. JAMA. 1981;240:20532059.
12. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol. 1979;44:3944.[Medline] [Order article via Infotrieve]
13.
Topol EJ,
Nissen SE. Our preoccupation with coronary luminology: the dissociation
between clinical and angiographic findings in ischemic heart
disease. Circulation. 1995;92:23332342.
14. Waller BF. "Crackers, breakers, stretchers, drillers, scrapers, shavers, burners, welders, and melters": the future treatment of atherosclerotic coronary artery disease? A clinical-morphologic assessment. J Am Coll Cardiol. 1989;13:969987.[Abstract]
15.
Hausmann D,
Erbel R, Alibelli-Chemarin MJ, et al. The safety of intracoronary
ultrasound: a multicenter survey of 2207 examinations.
Circulation. 1995;91:623630.
16. Batkoff BW, Linker DT. Safety of intracoronary ultrasound: data from a Multicenter European Registry. Cathet Cardiovasc Diagn. 1996;38:238241.[Medline] [Order article via Infotrieve]
17.
Tobis JM,
Mallery JA, Gessert J, et al. Intravascular ultrasound cross-sectional
arterial imaging before and after balloon angioplasty in vitro.
Circulation. 1989;80:873882.
18.
Honye J,
Mahon DJ, Jain A, et al. Morphological effects of coronary balloon
angioplasty in vivo assessed by intravascular ultrasound imaging.
Circulation. 1992;85:10121025.
19. St Goar FG, Pinto FJ, Alderman EL, et al. Intravascular ultrasound imaging of angiographically normal coronary arteries: an in vivo comparison with quantitative angiography. J Am Coll Cardiol. 1991;18:952958.[Abstract]
20. Gussenhoven EJ, Essed CE, Lancee CT, et al. Arterial wall characteristics determined by intravascular ultrasound imaging: an in vitro study. J Am Coll Cardiol. 1989;14:947952.[Abstract]
21.
Potkin BN,
Bartorelli AL, Gessert JM, et al. Coronary artery imaging with
intravascular high-frequency ultrasound.
Circulation. 1990;81:15751585.
22. Nishimura RA, Edwards WD, Warnes CA, et al. Intravascular ultrasound imaging: in vitro validation and pathologic correlation. J Am Coll Cardiol. 1990;16:145154.[Abstract]
23.
Fitzgerald
PJ, St. Goar FG, Connolly AJ, et al. Intravascular ultrasound imaging
of coronary arteries. Is three layers the norm?
Circulation. 1992;86:154158.
24. Mintz GS, Douek P, Pichard AD, et al. Target lesion calcification in coronary artery disease: an intravascular ultrasound study. J Am Coll Cardiol. 1992;20:11491155.[Abstract]
25. Tuzcu EM, Berkalp B, De Franco AC, et al. The dilemma of diagnosing coronary calcification: angiography versus intravascular ultrasound. J Am Coll Cardiol. 1996;27:832838.[Abstract]
26. Tuzcu EM, DeFranco AC, Goormastic M, et al. Dichotomous pattern of coronary atherosclerosis 1 to 9 years after transplantation: insights from systematic intravascular ultrasound imaging. J Am Coll Cardiol. 1996;27:839846.[Abstract]
27.
Mintz GS,
Popma JJ, Pichard AD, et al. Limitations of angiography in the
assessment of plaque distribution in coronary artery disease: a
systematic study of target lesion eccentricity in 1446 lesions.
Circulation. 1996;93:924931.
28. Glagov S, Weisenberg E, Zarins C, et al. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:13711375.[Abstract]
29. Hermiller JB, Tenaglia AN, Kisslo KB, et al. In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol. 1993;71:665668.[Medline] [Order article via Infotrieve]
30.
Losordo DW,
Rosenfield K, Kaufman J, et al. Focal compensatory enlargement of human
arteries in response to progressive atherosclerosis: in vivo
documentation using intravascular ultrasound.
Circulation. 1994;89:25702577.
31.
Pasterkamp
G, Wensing PJ, Post MJ, et al. Paradoxical arterial wall shrinkage may
contribute to luminal narrowing of human atherosclerotic femoral
arteries. Circulation. 1995;91:14441449.
32.
Mintz GS,
Kent KM, Pichard AD, et al. Contribution of inadequate arterial
remodeling to the development of focal coronary artery stenoses: an
intravascular ultrasound study.
Circulation. 1997;95:17911798.
33.
Mintz GS,
Popma JJ, Pichard AD, et al. Arterial remodeling after coronary
angioplasty: a serial intravascular ultrasound study.
Circulation. 1996;94:3543.
34.
Kimura T,
Kaburagi S, Tamura T, et al. Remodeling of human coronary arteries
undergoing coronary angioplasty or atherectomy.
Circulation. 1997;96:475483.
35.
Shoenhagen
P, Ziada K, Kapadia SR, et al. Extent and direction of arterial
remodeling in stable versus unstable coronary syndromes: an
intravascular ultrasound study.
Circulation. 2000;101:598603.
36. ten Hoff H, Korbijn A, Smith TH, et al. Imaging artifacts in mechanically driven ultrasound catheters. Int J Card Imaging. 1989;4:195199.[Medline] [Order article via Infotrieve]
37.
Erbel R, Ge
J, Bockisch A, et al. Value of intracoronary ultrasound and Doppler in
the differentiation of angiographically normal coronary arteries: a
prospective study in patients with angina pectoris.
Eur Heart J. 1996;17:880889.
38. Mintz GS, Painter JA, Pichard AD, et al. Atherosclerosis in angiographically "normal" coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:14791485.[Abstract]
39. Lee DY, Eigler N, Luo H, et al. Effect of intracoronary ultrasound imaging on clinical decision making. Am Heart J. 1995;129:10841093.[Medline] [Order article via Infotrieve]
40. Mintz GS, Pichard AD, Kovach JA, et al. Impact of preintervention intravascular ultrasound imaging on transcatheter treatment strategies in coronary artery disease. Am J Cardiol. 1994;73:423430.[Medline] [Order article via Infotrieve]
41. Hermiller JB, Buller CE, Tenaglia AN, et al. Unrecognized left main coronary artery disease in patients undergoing interventional procedures. Am J Cardiol. 1993;71:173176.[Medline] [Order article via Infotrieve]
42. Stark RP, McGinn AL, Wilson RF. Chest pain in cardiac-transplant recipients: evidence of sensory reinnervation after cardiac transplantation. N Engl J Med. 1991;324:17911794.[Medline] [Order article via Infotrieve]
43. Mairesse GH, Marwick TH, Melin JA, et al. Use of exercise electrocardiography, technetium-99 m-MIBI perfusion tomography, and two-dimensional echocardiography for coronary disease surveillance in a low-prevalence population of heart transplant recipients. J Heart Lung Transplant. 1995;14:222229.[Medline] [Order article via Infotrieve]
44. Smart FW, Ballantyne CM, Cocanougher B, et al. Insensitivity of noninvasive tests to detect coronary artery vasculopathy after heart transplant. Am J Cardiol. 1991;67:243247.[Medline] [Order article via Infotrieve]
45. Dressler FA, Miller LW. Necropsy versus angiography: how accurate is angiography? J Heart Lung Transplant. 1992;11:S56S59.[Medline] [Order article via Infotrieve]
46.
Pinto FJ,
Chenzbraun A, Botas J, et al. Feasibility of serial intracoronary
ultrasound imaging for assessment of progression of intimal
proliferation in cardiac transplant recipients.
Circulation. 1994;90:23482355.
47.
Uretsky BF,
Murali S, Reddy PS, et al. Development of coronary artery disease in
cardiac transplant patients receiving immunosuppressive therapy with
cyclosporine and prednisone.
Circulation. 1987;76:827834.
48. Gao SZ, Alderman EL, Schroeder JS, et al. Accelerated coronary vascular disease in the heart transplant patient: coronary arteriographic findings. J Am Coll Cardiol. 1988;12:334340.[Abstract]
49. Yeung AC, Davis SF, Hauptman PJ, et al. Incidence and progression of transplant coronary artery disease over 1 year: results of a multicenter trial with use of intravascular ultrasound: Multicenter Intravascular Ultrasound Transplant Study Group. J Heart Lung Transplant. 1995;14:S215S220.[Medline] [Order article via Infotrieve]
50.
Tuzcu EM,
Hobbs RE, Rincon G, et al. Occult and frequent transmission of
atherosclerotic coronary disease with cardiac transplantation: insights
from intravascular ultrasound.
Circulation. 1995;91:17061713.
51. Mehra MR, Ventura HO, Stapleton DD, et al. Presence of severe intimal thickening by intravascular ultrasonography predicts cardiac events in cardiac allograft vasculopathy. J Heart Lung Transplant. 1995;14:632639.[Medline] [Order article via Infotrieve]
52. Wiedermann JG, Wasserman HS, Weinberger JZ. Severe intimal thickening by intravascular ultrasonography predicts early death in cardiac transplant recipients. Circulation. 1994;90:I-93. Abstract.
53.
Little WC,
Constantinescu M, Applegate RJ, et al. Can coronary angiography predict
the site of a subsequent myocardial infarction in patients with
mild-to-moderate coronary artery disease?
Circulation. 1988;78:11571166.
54. Hodgson JM, Reddy KG, Suneja R, et al. Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. J Am Coll Cardiol. 1993;21:3544.[Abstract]
55.
Kearney P,
Erbel R, Rupprecht HJ, et al. Differences in the morphology of unstable
and stable coronary lesions and their impact on the mechanisms of
angioplasty: an in vivo study with intravascular ultrasound.
Eur Heart J. 1996;17:721730.
56. Bocksch W, Schartl M, Beckmann S, et al. Intravascular ultrasound imaging in patients with acute myocardial infarction. Eur Heart J. 1995;16(Suppl J):4652.
57.
Siegel RJ,
Ariani M, Fishbein MC, et al. Histopathologic validation of angioscopy
and intravascular ultrasound.
Circulation. 1991;84:109117.
58. Bridal SL, Fornes P, Bruneval P, et al. Parametric (integrated backscatter and attenuation) images constructed using backscattered radio frequency signals (2556 MHz) from human aortae in vitro. Ultrasound Med Biol. 1997;23:215229.[Medline] [Order article via Infotrieve]
59.
Peters RJ,
Kok WE, Di Mario C, et al. Prediction of restenosis after coronary
balloon angioplasty: Results of PICTURE (Post-IntraCoronary Treatment
Ultrasound Result Evaluation), a prospective multicenter intracoronary
ultrasound imaging study.
Circulation. 1997;95:22542261.
60. Mintz GS, Popma JJ, Pichard AD, et al. Intravascular ultrasound predictors of restenosis after percutaneous transcatheter coronary revascularization. J Am Coll Cardiol. 1996;27:16781687.[Abstract]
61. Fitzgerald PJ, Yock PG. Mechanisms and outcomes of angioplasty and atherectomy assessed by intravascular ultrasound imaging. J Clin Ultrasound. 1993;21:579588.[Medline] [Order article via Infotrieve]
62.
Stone GW,
Hodgson JM, St Goar FG, et al. Improved procedural results of coronary
angioplasty with intravascular ultrasound-guided balloon sizing: the
CLOUT Pilot Trial: Clinical Outcomes With Ultrasound Trial (CLOUT)
Investigators. Circulation. 1997;95:20442052.
63. Abizaid A, Pichard AD, Mintz GS, et al. Acute and long-term results of an intravascular ultrasound-guided percutaneous transluminal coronary angioplasty/provisional stent implantation strategy. Am J Cardiol. 1999;84:12981303.[Medline] [Order article via Infotrieve]
64. Schroeder S, Baumbach A, Haase KK, et al. Reduction of restenosis by vessel size adapted percutaneous transluminal coronary angioplasty using intravascular ultrasound. Am J Cardiol. 1999;83:875879.[Medline] [Order article via Infotrieve]
65.
Losordo DW,
Rosenfield K, Pieczek A, et al. How does angioplasty work? Serial
analysis of human iliac arteries using intravascular ultrasound.
Circulation. 1992;86:18451858.
66. Potkin BN, Keren G, Mintz GS, et al. Arterial responses to balloon coronary angioplasty: an intravascular ultrasound study. J Am Coll Cardiol. 1992;20:942951.[Abstract]
67. Braden GA, Herrington DM, Downes TR, et al. Qualitative and quantitative contrasts in the mechanisms of lumen enlargement by coronary balloon angioplasty and directional coronary atherectomy. J Am Coll Cardiol. 1994;23:4048.[Abstract]
68. Mintz GS, Pichard AD, Kent KM, et al. Axial plaque redistribution as a mechanism of percutaneous transluminal coronary angioplasty. Am J Cardiol. 1996;77:427430.[Medline] [Order article via Infotrieve]
69. Matar FA, Mintz GS, Pinnow E, et al. Multivariate predictors of intravascular ultrasound end points after directional coronary atherectomy. J Am Coll Cardiol. 1995;25:318324.[Abstract]
70.
Simonton
CA, Leon MB, Baim DS, et al. Optimal directional coronary
atherectomy: final results of the Optimal Atherectomy Restenosis Study
(OARS). Circulation. 1998;97:332339.
71.
Suzuki T,
Hosokawa H, Katoh O, et al. Effects of adjunctive balloon angioplasty
after intravascular ultrasound-guided optimal directional coronary
atherectomy: the result of Adjunctive Balloon Angioplasty After
Coronary Atherectomy Study (ABACAS).
J Am Coll Cardiol. 1999;34:10281035.
72.
Tsuchikane
E, Sumitsuji S, Awata N, et al. Final results of the STent versus
directional coronary Atherectomy Randomized Trial (START).
J Am Coll Cardiol. 1999;34:10501057.
73. Kovach JA, Mintz GS, Pichard AD, et al. Sequential intravascular ultrasound characterization of the mechanisms of rotational atherectomy and adjunct balloon angioplasty. J Am Coll Cardiol. 1993;22:10241032.[Abstract]
74. De Franco AC, Nissen SE, Tuzcu EM, et al. Incremental value of intravascular ultrasound during rotational coronary atherectomy. Cathet Cardiovasc Diagn. 1996;(Suppl):2333.
75. Painter JA, Mintz GS, Wong SC, et al. Serial intravascular ultrasound studies fail to show evidence of chronic Palmaz-Schatz stent recoil. Am J Cardiol. 1995;75:398400.[Medline] [Order article via Infotrieve]
76.
Hoffmann R,
Mintz GS, Dussaillant GR, et al. Patterns and mechanisms of in-stent
restenosis: a serial intravascular ultrasound study.
Circulation. 1996;94:12471254.
77.
Hoffmann R,
Mintz GS, Mehran R, et al. Intravascular ultrasound predictors of
angiographic restenosis in lesions treated with Palmaz-Schatz stents.
J Am Coll Cardiol. 1998;31:4349.
78.
Prati F, Di
Mario C, Moussa I, et al. In-stent neointimal proliferation correlates
with the amount of residual plaque burden outside the stent: an
intravascular ultrasound study.
Circulation. 1999;99:10111014.
79.
Colombo A,
Hall P, Nakamura S, et al. Intracoronary stenting without
anticoagulation accomplished with intravascular ultrasound guidance.
Circulation. 1995;91:16761688.
80.
Goods CM,
Al-Shaibi KF, Yadav SS, et al. Utilization of the coronary
balloon-expandable coil stent without anticoagulation or intravascular
ultrasound. Circulation. 1996;93:18031808.
81.
Karrillon
GJ, Morice MC, Benveniste E, et al. Intracoronary stent implantation
without ultrasound guidance and with replacement of conventional
anticoagulation by antiplatelet therapy: 30-day clinical outcome of the
French Multicenter Registry.
Circulation. 1996;94:15191527.
82. Allen KM, Undemir C, Shaknovich A, et al. Is there need for intravascular ultrasound after high pressure dilatation of Palmaz-Schatz stents. J Am Coll Cardiol. 1996;27:138A. Abstract.
83.
Fitzgerald
PJ, Oshima A, Hayase M, et al, for the CRUISE investigators. Final
results of the Can Routine Ultrasound Influence Stent Expansion
(CRUISE) study. Circulation. 2000;102:523530.
84. Mudra H, Macaya C, Zahn R, et al. Interim analysis of the "OPTimization with ICUS to reduce stent restenosis" (OPTICUS) trial. Circulation. 1998;98:I-363. Abstract.
85.
Schiele F,
Meneveau N, Vuillemenot A, et al. Impact of intravascular ultrasound
guidance in stent deployment on 6-month restenosis rate: a multicenter,
randomized study comparing two strategieswith and without
intravascular ultrasound guidance: RESIST Study Group: REStenosis
after Ivus guided STenting. J Am Coll
Cardiol. 1998;32:320328.
86. Russo RJ, Nicosia A, Teirstein PS, for the AVID Investigators. Angiography versus intravascular ultrasound-directed stent placement. J Am Coll Cardiol. 1997;29:369A. Abstract.
87.
de Jaegere
P, Mudra H, Figulla H, et al. Intravascular ultrasound-guided optimized
stent deployment: Immediate and 6 months clinical and angiographic
results from the Multicenter Ultrasound Stenting in Coronaries Study
(MUSIC Study). Eur Heart
J. 1998;19:12141223.
88. Hoffmann R, Mintz GS, Pichard AD, et al. Intimal hyperplasia thickness at follow-up is independent of stent size: a serial intravascular ultrasound study. Am J Cardiol. 1998;82:11681172.[Medline] [Order article via Infotrieve]
89.
Schuhlen H,
Hadamitzky M, Walter H, et al. Major benefit from antiplatelet therapy
for patients at high risk for adverse cardiac events after coronary
Palmaz-Schatz stent placement: analysis of a prospective risk
stratification protocol in the Intracoronary Stenting and
Antithrombotic Regimen (ISAR) trial.
Circulation. 1997;95:20152021.
90. Ziada KM, Tuzcu EM, De Franco AC, et al. Intravascular ultrasound assessment of the prevalence and causes of angiographic "haziness" following high-pressure coronary stenting. Am J Cardiol. 1997;80:116121.[Medline] [Order article via Infotrieve]
91. Hoffmann R, Mintz GS, Kent KM, et al. Serial intravascular ultrasound predictors of restenosis at the margins of Palmaz-Schatz stents. Am J Cardiol. 1997;79:951953.[Medline] [Order article via Infotrieve]
92.
Hoffmann R,
Mintz GS, Popma JJ, et al. Treatment of calcified coronary lesions with
Palmaz-Schatz stents. An intravascular ultrasound study.
Eur Heart J. 1998;19:12241231.
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S.-J. Park, Y.-H. Kim, D.-W. Park, S.-W. Lee, W.-J. Kim, J. Suh, S.-C. Yun, C. W. Lee, M.-K. Hong, J.-H. Lee, et al. Impact of Intravascular Ultrasound Guidance on Long-Term Mortality in Stenting for Unprotected Left Main Coronary Artery Stenosis Circ Cardiovasc Intervent, June 1, 2009; 2(3): 167 - 177. [Abstract] [Full Text] [PDF] |
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M. U Farooq, A. Khasnis, A. Majid, and M. Y Kassab The role of optical coherence tomography in vascular medicine Vascular Medicine, February 1, 2009; 14(1): 63 - 71. [Abstract] [PDF] |
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H. F. Langer, R. Haubner, B. J. Pichler, and M. Gawaz Radionuclide imaging a molecular key to the atherosclerotic plaque. J. Am. Coll. Cardiol., July 1, 2008; 52(1): 1 - 12. [Abstract] [Full Text] [PDF] |
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M. E. Clouse, A. Sabir, C.-S. Yam, N. Yoshimura, S. Lin, F. Welty, P. Martinez-Clark, and V. Raptopoulos Measuring Noncalcified Coronary Atherosclerotic Plaque Using Voxel Analysis with MDCT Angiography: A Pilot Clinical Study Am. J. Roentgenol., June 1, 2008; 190(6): 1553 - 1560. [Abstract] [Full Text] [PDF] |
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J. J.P. Kastelein and E. de Groot Ultrasound imaging techniques for the evaluation of cardiovascular therapies Eur. Heart J., April 1, 2008; 29(7): 849 - 858. [Abstract] [Full Text] [PDF] |
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Y. Fukumoto, T. Hiro, T. Fujii, G. Hashimoto, T. Fujimura, J. Yamada, T. Okamura, and M. Matsuzaki Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution. J. Am. Coll. Cardiol., February 12, 2008; 51(6): 645 - 650. [Abstract] [Full Text] [PDF] |
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J. Horiguchi, M. Kiguchi, C. Fujioka, Y. Shen, R. Arie, K. Sunasaka, and K. Ito Radiation Dose, Image Quality, Stenosis Measurement, and CT Densitometry Using ECG-Triggered Coronary 64-MDCT Angiography: A Phantom Study Am. J. Roentgenol., February 1, 2008; 190(2): 315 - 320. [Abstract] [Full Text] [PDF] |
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J. Horiguchi, C. Fujioka, M. Kiguchi, Y. Shen, C. E. Althoff, H. Yamamoto, and K. Ito Soft and Intermediate Plaques in Coronary Arteries: How Accurately Can We Measure CT Attenuation Using 64-MDCT? Am. J. Roentgenol., October 1, 2007; 189(4): 981 - 988. [Abstract] [Full Text] [PDF] |
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A. Konig and V. Klauss Virtual histology Heart, August 1, 2007; 93(8): 977 - 982. [Abstract] [Full Text] [PDF] |
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S. K. Mehta, J. R. McCrary, A. D. Frutkin, W. J.S. Dolla, and S. P. Marso Intravascular ultrasound radiofrequency analysis of coronary atherosclerosis: an emerging technology for the assessment of vulnerable plaque Eur. Heart J., June 1, 2007; 28(11): 1283 - 1288. [Abstract] [Full Text] [PDF] |
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J. R Larsen, T. Tsunoda, E M. Tuzcu, P. Schoenhagen, M. Brekke, H. Arnesen, K. F Hanssen, S. E Nissen, and K. Dahl-Jorgensen Intracoronary ultrasound examinations reveal significantly more advanced coronary atherosclerosis in people with type 1 diabetes than in age- and sex-matched non-diabetic controls Diabetes and Vascular Disease Research, March 1, 2007; 4(1): 62 - 65. [Abstract] [PDF] |
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S. Waxman, F. Ishibashi, and J. E. Muller Detection and Treatment of Vulnerable Plaques and Vulnerable Patients: Novel Approaches to Prevention of Coronary Events Circulation, November 28, 2006; 114(22): 2390 - 2411. [Full Text] [PDF] |
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D. R. Elmaleh, A. J. Fischman, A. Tawakol, A. Zhu, T. M. Shoup, U. Hoffmann, A.-L. Brownell, and P. C. Zamecnik Detection of inflamed atherosclerotic lesions with diadenosine-5',5'''-P1,P4-tetraphosphate (Ap4A) and positron-emission tomography PNAS, October 24, 2006; 103(43): 15992 - 15996. [Abstract] [Full Text] [PDF] |
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M. Ferencik, R. C. Chan, S. Achenbach, J. B. Lisauskas, S. L. Houser, U. Hoffmann, S. Abbara, R. C. Cury, B. E. Bouma, G. J. Tearney, et al. Arterial Wall Imaging: Evaluation with 16-Section Multidetector CT in Blood Vessel Phantoms and ex Vivo Coronary Arteries Radiology, September 1, 2006; 240(3): 708 - 716. [Abstract] [Full Text] [PDF] |
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J. Hausleiter, T. Meyer, M. Hadamitzky, A. Kastrati, S. Martinoff, and A. Schomig Prevalence of Noncalcified Coronary Plaques by 64-Slice Computed Tomography in Patients With an Intermediate Risk for Significant Coronary Artery Disease J. Am. Coll. Cardiol., July 18, 2006; 48(2): 312 - 318. [Abstract] [Full Text] [PDF] |
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H. Li, K. Tanaka, B. Oeser, J. A. Kobashigawa, and J. M. Tobis Vascular remodelling after cardiac transplantation: a 3-year serial intravascular ultrasound study Eur. Heart J., July 2, 2006; 27(14): 1671 - 1677. [Abstract] [Full Text] [PDF] |
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S. J. Nicholls, E. M. Tuzcu, T. Crowe, I. Sipahi, P. Schoenhagen, S. Kapadia, S. L. Hazen, C.-C. Wun, M. Norton, F. Ntanios, et al. Relationship Between Cardiovascular Risk Factors and Atherosclerotic Disease Burden Measured by Intravascular Ultrasound J. Am. Coll. Cardiol., May 16, 2006; 47(10): 1967 - 1975. [Abstract] [Full Text] [PDF] |
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E. R. McVeigh Emerging Imaging Techniques Circ. Res., April 14, 2006; 98(7): 879 - 886. [Abstract] [Full Text] [PDF] |
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K. Sano, M. Kawasaki, Y. Ishihara, M. Okubo, K. Tsuchiya, K. Nishigaki, X. Zhou, S. Minatoguchi, H. Fujita, and H. Fujiwara Assessment of Vulnerable Plaques Causing Acute Coronary Syndrome Using Integrated Backscatter Intravascular Ultrasound J. Am. Coll. Cardiol., February 21, 2006; 47(4): 734 - 741. [Abstract] [Full Text] [PDF] |
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N. Nighoghossian, L. Derex, and P. Douek The Vulnerable Carotid Artery Plaque: Current Imaging Methods and New Perspectives Stroke, December 1, 2005; 36(12): 2764 - 2772. [Abstract] [Full Text] [PDF] |
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P. Raggi, A. Taylor, Z. Fayad, D. O'Leary, S. Nissen, D. Rader, and L. J. Shaw Atherosclerotic Plaque Imaging: Contemporary Role in Preventive Cardiology Arch Intern Med, November 14, 2005; 165(20): 2345 - 2353. [Abstract] [Full Text] [PDF] |
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M. Y. Desai, S. Lai, C. Barmet, R. G. Weiss, and M. Stuber Reproducibility of 3D free-breathing magnetic resonance coronary vessel wall imaging Eur. Heart J., November 1, 2005; 26(21): 2320 - 2324. [Abstract] [Full Text] [PDF] |
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K. Imoto, T. Hiro, T. Fujii, A. Murashige, Y. Fukumoto, G. Hashimoto, T. Okamura, J. Yamada, K. Mori, and M. Matsuzaki Longitudinal Structural Determinants of Atherosclerotic Plaque Vulnerability: A Computational Analysis of Stress Distribution Using Vessel Models and Three-Dimensional Intravascular Ultrasound Imaging J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1507 - 1515. [Abstract] [Full Text] [PDF] |
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G. Romeo, L. Houyel, C.-Y. Angel, P. Brenot, J.-Y. Riou, and J.-F. Paul Coronary Stenosis Detection by 16-Slice Computed Tomography in Heart Transplant Patients: Comparison With Conventional Angiography and Impact on Clinical Management J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1826 - 1831. [Abstract] [Full Text] [PDF] |
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E. M. Tuzcu, S. R. Kapadia, R. Sachar, K. M. Ziada, T. D. Crowe, J. Feng, W. A. Magyar, R. E. Hobbs, R. C. Starling, J. B. Young, et al. Intravascular Ultrasound Evidence of Angiographically Silent Progression in Coronary Atherosclerosis Predicts Long-Term Morbidity and Mortality After Cardiac Transplantation J. Am. Coll. Cardiol., May 3, 2005; 45(9): 1538 - 1542. [Abstract] [Full Text] [PDF] |
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J. A. Ambrose and D. J. D'Agate Plaque rupture and intracoronary thrombus in nonculprit vessels: An eyewitness account J. Am. Coll. Cardiol., March 1, 2005; 45(5): 659 - 660. [Full Text] [PDF] |
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A.-A. Fassa, K. Wagatsuma, S. T. Higano, V. Mathew, G. W. Barsness, R. J. Lennon, D. R. Holmes Jr, and A. Lerman Intravascular ultrasound-guided treatment for angiographically indeterminate left main coronary artery disease: A long-term follow-up study J. Am. Coll. Cardiol., January 18, 2005; 45(2): 204 - 211. [Abstract] [Full Text] [PDF] |
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S. E. Nissen, E. M. Tuzcu, P. Schoenhagen, T. Crowe, W. J. Sasiela, J. Tsai, J. Orazem, R. D. Magorien, C. O'Shaughnessy, P. Ganz, et al. Statin Therapy, LDL Cholesterol, C-Reactive Protein, and Coronary Artery Disease N. Engl. J. Med., January 6, 2005; 352(1): 29 - 38. [Abstract] [Full Text] [PDF] |
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U. J. Schoepf, C. R. Becker, B. M. Ohnesorge, and E. K. Yucel CT of Coronary Artery Disease Radiology, July 1, 2004; 232(1): 18 - 37. [Abstract] [Full Text] [PDF] |
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J. L. Orford, A. Lerman, and D. R. Holmes Routine intravascular ultrasound guidance of percutaneous coronary intervention: A critical reappraisal J. Am. Coll. Cardiol., April 21, 2004; 43(8): 1335 - 1342. [Abstract] [Full Text] [PDF] |
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S. E. Nissen, E. M. Tuzcu, P. Schoenhagen, B. G. Brown, P. Ganz, R. A. Vogel, T. Crowe, G. Howard, C. J. Cooper, B. Brodie, et al. Effect of Intensive Compared With Moderate Lipid-Lowering Therapy on Progression of Coronary Atherosclerosis: A Randomized Controlled Trial JAMA, March 3, 2004; 291(9): 1071 - 1080. [Abstract] [Full Text] [PDF] |
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S. E. Nissen, T. Tsunoda, E. M. Tuzcu, P. Schoenhagen, C. J. Cooper, M. Yasin, G. M. Eaton, M. A. Lauer, W. S. Sheldon, C. L. Grines, et al. Effect of Recombinant ApoA-I Milano on Coronary Atherosclerosis in Patients With Acute Coronary Syndromes: A Randomized Controlled Trial JAMA, November 5, 2003; 290(17): 2292 - 2300. [Abstract] [Full Text] [PDF] |
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M. Naghavi, P. Libby, E. Falk, S. W. Casscells, S. Litovsky, J. Rumberger, J. J. Badimon, C. Stefanadis, P. Moreno, G. Pasterkamp, et al. From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part I Circulation, October 7, 2003; 108(14): 1664 - 1672. [Abstract] [Full Text] [PDF] |
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J. Barkhausen, W. Ebert, C. Heyer, J. F. Debatin, and H.-J. Weinmann Detection of Atherosclerotic Plaque With Gadofluorine-Enhanced Magnetic Resonance Imaging Circulation, August 5, 2003; 108(5): 605 - 609. [Abstract] [Full Text] [PDF] |
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B. D. MacNeill, H. C. Lowe, M. Takano, V. Fuster, and I.-K. Jang Intravascular Modalities for Detection of Vulnerable Plaque: Current Status Arterioscler. Thromb. Vasc. Biol., August 1, 2003; 23(8): 1333 - 1342. [Abstract] [Full Text] [PDF] |
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J. Genest and T. R. Pedersen Prevention of Cardiovascular Ischemic Events: High-Risk and Secondary Prevention Circulation, April 22, 2003; 107(15): 2059 - 2065. [Full Text] [PDF] |
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P. V. Oemrawsingh, G. S. Mintz, M. J. Schalij, A. H. Zwinderman, J. W. Jukema, and E. E.v.d. Wall Intravascular Ultrasound Guidance Improves Angiographic and Clinical Outcome of Stent Implantation for Long Coronary Artery Stenoses: Final Results of a Randomized Comparison With Angiographic Guidance (TULIP Study) Circulation, January 7, 2003; 107(1): 62 - 67. [Abstract] [Full Text] [PDF] |
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F. J. Schoen and R. F. Padera Jr. Cardiac Surgical Pathology Card. Surg. Adult, January 1, 2003; 2(2003): 119 - 185. [Full Text] |
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A. Nair, B. D. Kuban, E. M. Tuzcu, P. Schoenhagen, S. E. Nissen, and D. G. Vince Coronary Plaque Classification With Intravascular Ultrasound Radiofrequency Data Analysis Circulation, October 22, 2002; 106(17): 2200 - 2206. [Abstract] [Full Text] [PDF] |
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J. R. Guyton Clinical Assessment of Atherosclerotic Lesions: Emerging From Angiographic Shadows Circulation, September 10, 2002; 106(11): 1308 - 1309. [Full Text] [PDF] |
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J. A. Cabrera, D. Sanchez-Quintana, J. Farre, F. Navarro, J. M. Rubio, F. Cabestrero, R. H. Anderson, and S. Y. Ho Ultrasonic Characterization of the Pulmonary Venous Wall: Echographic and Histological Correlation Circulation, August 20, 2002; 106(8): 968 - 973. [Abstract] [Full Text] [PDF] |
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G. Rioufol, G. Finet, I. Ginon, X. Andre-Fouet, R. Rossi, E. Vialle, E. Desjoyaux, G. Convert, J.F. Huret, and A. Tabib Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome: A Three-Vessel Intravascular Ultrasound Study Circulation, August 13, 2002; 106(7): 804 - 808. [Abstract] [Full Text] [PDF] |
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P. Schoenhagen and S. Nissen Understanding coronary artery disease: tomographic imaging with intravascular ultrasound Heart, July 1, 2002; 88(1): 91 - 96. [Full Text] [PDF] |
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P J de Feyter and K Nieman New coronary imaging techniques: what to expect? Heart, March 1, 2002; 87(3): 195 - 197. [Full Text] [PDF] |
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B Chandrasekaran and A S Kurbaan Myocardial infarction with angiographically normal coronary arteries J R Soc Med, January 8, 2002; 95(8): 398 - 400. [Full Text] [PDF] |
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P. K. Shah and Z. S. Galis Matrix Metalloproteinase Hypothesis of Plaque Rupture: Players Keep Piling Up But Questions Remain Circulation, October 16, 2001; 104(16): 1878 - 1880. [Full Text] [PDF] |
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J. A. Beckman, J. Ganz, M. A. Creager, P. Ganz, and S. Kinlay Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses Arterioscler. Thromb. Vasc. Biol., October 1, 2001; 21(10): 1618 - 1622. [Abstract] [Full Text] [PDF] |
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R. Seabra-Gomes Is there a future for coronary physiological evaluation in clinical decision making? Eur. Heart J., September 2, 2001; 22(18): 1633 - 1635. [PDF] |
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Z. A. Fayad and V. Fuster Clinical Imaging of the High-Risk or Vulnerable Atherosclerotic Plaque Circ. Res., August 17, 2001; 89(4): 305 - 316. [Abstract] [Full Text] [PDF] |
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P. Schoenhagen, K. M. Ziada, D. G. Vince, S. E. Nissen, and E. M. Tuzcu Arterial remodeling and coronary artery disease: the concept of "dilated" versus "obstructive" coronary atherosclerosis J. Am. Coll. Cardiol., August 1, 2001; 38(2): 297 - 306. [Abstract] [Full Text] [PDF] |
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