(Circulation. 1997;95:1791-1798.)
© 1997 American Heart Association, Inc.
Articles |
Contribution of Inadequate Arterial Remodeling to the Development of Focal Coronary Artery Stenoses
An Intravascular Ultrasound Study
From the Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, The Washington Hospital Center, Washington, DC.
Correspondence to Martin B. Leon, MD, Director of Research, Washington Cardiology Center, Washington Hospital Center 4B-1, 110 Irving St, Washington, DC 20010.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background Adaptive remodeling occurs to compensate for the accumulation of atherosclerotic plaque. Lumen reduction depends on the relative rates of plaque deposition and adaptive remodeling responses. Intravascular ultrasound permits detailed, high-quality, cross-sectional imaging of the coronary arteries in vivo.
Methods and Results Preintervention intravascular
ultrasound was used to study 603 focal, new, nonostial significant
coronary artery stenoses in patients with chronic stable angina.
Measurements of the target lesion of the external elastic membrane
(EEM), lumen, and plaque plus media (P&M; P&M=EEM-Lumen)
cross-sectional areas (CSAs) were compared with a proximal reference
segment (most normal-looking cross section within 10 mm proximal
to the lesion but distal to any side branch). Inadequate remodeling was
defined as lesion/reference EEM CSA that exceeded the upper limits of
normal arterial tapering (lesion/reference EEM CSA ratio 
0.78 or a
21% reduction in EEM CSA per 10-mm length). Overall, the
lesion/reference EEM CSA ratio was 1.00±0.22; 15% of lesions had
inadequate remodeling, and 37% of the 603 lesions had less plaque than
expected. This represented a lesion-specific response. The only
predictor of inadequate remodeling was the arc of superficial lesion
calcium.
Conclusions Inadequate remodeling is present in at least 15% of chronic, focal, new coronary arterial stenoses in patients with stable angina. The magnitude of arterial remodeling appears to be a lesion-specific response.
Key Words: ultrasonics • coronary disease • stenosis
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Adaptive remodeling of the wall of diseased arterial segments occurs to compensate for the accumulation of atherosclerotic plaque.1 2 On average, lumen compromise is delayed until the atherosclerotic lesion occupies more than an estimated 40% to 50% of the potential area within the internal elastic lamina (40% to 50% CSN). This compensatory mechanism has been noted in primates with diet-induced atherosclerosis3 and in human coronary arteries, in which it has been seen pathologically and in vivo with high-frequency epicardial echocardiography4 and IVUS.5 6 7 8 9 The development of angiographically detectable coronary artery disease is thought to depend on (1) relative rates of plaque deposition and adaptive remodeling or (2) ultimate failure of the remodeling response.
IVUS permits detailed cross-sectional imaging of the coronary arteries in vivo. The normal coronary artery architecture, the major components of the atherosclerotic plaque, and the changes that occur in coronary arterial dimensions and anatomy with the atherosclerotic disease process can be studied in vivo in a manner previously not possible using any other modality.10 11 We hypothesized that there may be a spectrum of remodeling responses to plaque accumulation and that in some target lesions, inadequate arterial remodeling may contribute to the development of focal, hemodynamically significant coronary artery stenoses.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Lesion and Patient Population
The Washington Cardiology Center IVUS database, which contains 2684 native vessel lesions, was probed to identify 603 lesions in 550 patients with chronic stable angina that met the following strict criteria: (1) high-quality IVUS images of the target lesion and of a proximal reference segment before intervention, (2) new lesion presentation, (3) nonostial native vessel lesion location, (4) absence of side branches between the center of the lesion and the proximal reference segment, (5) lesion severity significant enough to warrant intervention, (6) focal stenosis and absence of ectasia or angular segments on angiography, and (7) target-lesion or reference-segment calcification that did not preclude quantitative assessment of IVUS arterial CSA. There were 454 males and 96 females with a mean patient age of 61±11 years. Target-lesion location was left main artery in 12 patients, left anterior descending in 268, left circumflex in 103, and right coronary in 220.
Clinical Demographics
The hospital charts of all patients were reviewed independently
by a registered nurse to obtain clinical demographics and laboratory
results. Risk factors for coronary artery disease that were tabulated
included diabetes mellitus (medication-dependent only), hypertension
(medication-dependent only), and hypercholesterolemia
(medication-dependent or serum cholesterol 
240 mg/dL).
Angiographic Analysis
All cineangiograms were analyzed with the use of a
computer-assisted, automated edge-detection algorithm (ARTREK,
Quantitative Cardiac Systems) by a core laboratory that was blinded to
the ultrasound findings. With the outer diameter of the contrast-filled
catheter used as the calibration, the minimal lumen diameter in
diastole before intervention was measured from multiple projections,
and the results from the "worst" view were recorded. The
reference-segment diameter was averaged from user-defined, 5-mm-long,
angiographically normal segments proximal and distal to the lesion but
between any major side branches. Lesion length was measured as the
distance (in millimeters) from the proximal shoulder to the distal
shoulder in the projection with the least amount of foreshortening. A
focal stenosis had a length 10 mm. For the purposes of this
study, ostial lesions were within 3 mm of the coronary ostia or
<3 mm distal to a major proximal side branch. An eccentric target
lesion appeared to have three times as much plaque on one side of the
lesion as on the other. Calcification was identified as readily
apparent radiopacities within the vascular wall at the site of the
stenosis. An angular segment contained a bend >45° within 5 mm
of the lesion. Ectasia was a lumen >20% larger than the user-defined
reference segments. These represent standard qualitative and
quantitative analyses and definitions that have been published
previously.12
IVUS Imaging Protocol
All IVUS imaging studies were performed before any intervention
and only after administration of 200 µg of intracoronary
nitroglycerin. The IVUS studies were performed by use of one of two
commercially available systems. The first system
(InterTherapy/Cardiovascular Imaging Systems Inc) incorporated a
single-element, 25-MHz transducer and an angled mirror mounted on the
tip of a flexible shaft that was rotated at 1800 rpm within a 3.9F
short, monorail, polyethylene imaging sheath to form planar
cross-sectional images in real time. The second system (Cardiovascular
Imaging Systems Inc) incorporated a single-element, 30-MHz beveled
transducer within either a 2.9F long, monorail imaging catheter having
a common distal lumen design (the distal lumen alternatively
accommodates the imaging core or the guidewire, but not both) or a 3.2F
short, monorail imaging catheter. With both systems, the transducer was
withdrawn automatically at 0.5 mm/s to perform the imaging
sequence. The use of a motorized transducer pullback device and
sheath-based imaging catheters permitted the transducer to move at the
same speed as the proximal end of the imaging core. The IVUS catheter
was advanced 10 mm distal to the lesion, the video recorder
turned on, the transducer pullback device activated, and the entire
artery imaged to the aorto-ostial junction. IVUS studies were recorded
on 0.5-in high-resolution super VHS tape for off-line analysis.
IVUS Analysis
Validation of plaque composition and measurements of EEM CSA,
lumen CSA, and P&M CSA by IVUS have been reported
previously.6 13 14 15 16 17 18 19 The EEM CSA, the area encompassed by
the ultrasonic media-adventitia border, is measured by tracing the
leading edge of the adventitia; this has been shown to be a
reproducible measure of total arterial CSA. The CSN has also been
called the plaque burden or the percent plaque area by other
investigators. Because media thickness cannot be measured accurately,
P&M CSA was used as a measure of atherosclerotic plaque, and P&M
thickness was used to calculate lesion eccentricity.18
Using computer planimetry, we measured lesion site EEM CSA and lumen
CSA. P&M CSA was calculated as EEM CSA-Lumen CSA. CSN was
calculated as P&M CSA/EEM CSA. The eccentricity index was
calculated as Maximum P&M Thickness/Minimum P&M Thickness. The
lesion site selected for analysis was the image slice with the smallest
lumen CSA; if there were several image slices with an equally small
lumen, the image slice with the largest EEM CSA and P&M CSA was
analyzed (Fig 1
). This method for selecting the lesion
site and for measuring the EEM, lumen, and P&M CSA has been used
extensively to study short- and long-term effects of angioplasty
procedures and has been published previously.20 21 22 23 24 25 26 In our
laboratory, the intraclass correlation coefficient is .99 for repeated
measurement of the EEM CSA, .96 for the lumen CSA, and .99 for the P&M
CSA; the interclass correlation coefficient considers both
between-lesion and within-lesion variability, is widely used as a
measure of interrater variability, and includes reproducibility of
image-slice selection.
|
Target-lesion plaque composition was assessed visually to identify calcium. Calcium produced bright echoes (brighter than the reference adventitia) with acoustic shadowing of deeper arterial structures. Calcium location was classified as superficial or deep depending on its location within the plaque. Superficial calcium was closer to the plaque-lumen border than to the media-adventitia interface; the largest total (superficial plus deep) arc of calcium and the arc of superficial calcium were measured (in degrees) with a protractor centered on the lumen.27
Although acoustic shadowing caused by lesion calcification made
identification of the EEM difficult at times, two types of
extrapolation were useful: (1) because the cross-sectional geometry of
the coronary artery was more or less circular, extrapolation of the
circumference of the EEM was possible if each calcific deposit did not
shadow >60° of the adventitial circumference; and (2) real-time
axial movement of the transducer just distal and proximal to a calcific
deposit (or to find the smallest circumferential arc of calcium within
a larger calcific deposit) helped to unmask and fill in contiguous
parts of the adventitia that were otherwise shadowed by that deposit.
These methods have been reported previously.20 21 22 In
addition, the subpopulation of 238 lesions containing 45° of
target-lesion calcium were analyzed separately.
Identification of a Comparable Reference Segment
Reference-segment EEM and lumen CSA and arc of reference-segment
calcium were measured, and the P&M CSA and percent CSN were calculated
as for the target lesion. The reference segment was the most
normal-looking cross section within 10 mm proximal to the lesion
but distal to any side branch (Fig 1
). This method of reference-segment
selection has been published previously.28 The use of the
motorized transducer pullback device was crucial because it limited the
axial distance between the target lesion and the reference segment to
10 mm. Motorized transducer pullback measurement of arterial
lengths has been validated in vivo.29
Comparison of Target Lesion With Reference Segment
Target-lesion EEM CSA was compared with the reference segment as
an index of arterial remodeling. Previous studies have determined the
"expected" degree of EEM CSA tapering over a 10-mm axial length
of artery. Although the degree of tapering was greater for the left
circumflex and left anterior descending arteries than for the right
coronary artery, in 146 arterial segments studied, the EEM CSA tapered
by 10±6% for each 10 mm of arterial length, but never by
>21%.30 Therefore, inadequate arterial remodeling was
defined as a lesion/reference EEM CSA 0.78.
In addition, the lesion P&M CSA was compared with the reference P&M CSA. If one assumes that there was a similar magnitude of remodeling at the lesion site and within the reference segment (in fact, there should be more adaptive remodeling at the lesion site) and if one allows for a normal amount of arterial tapering, the minimum expected P&M CSA at the lesion can be calculated as 0.9x[Reference P&M CSA+(Reference Lumen CSA-Lesion Lumen CSA)].
Statistics
Statistical analysis was performed with the use of StatView 4.02
(Abacus Concepts) or SAS (Statistical Analysis Systems, SAS Institute
Inc) software. Data are presented as mean±SD. Categorical data were
compared by use of 
2 analysis. Continuous
variables were compared by use of unpaired t tests or
regression analysis. A value of P.05 was considered to be
significant. Univariate and multivariate linear regression analyses
were used to identify clinical, angiographic, and ultrasonic predictors
of the ratio of target-lesion to reference-segment EEM CSA. Univariate
variables with a value of P<.2 were entered into the
multivariate models. Forward stepping was used to determine the best
predictors of the ratio of target-lesion to reference-segment EEM
CSA.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Overall, the lesion-site/reference-site EEM CSA ratio was 1.00±0.22 (Fig 2
), and the lesion/reference P&M CSA
ratio was 1.96±0.82 (Fig 3). Ninety-one target lesions
(15%) fit the definition of inadequate arterial remodeling
(lesion/reference EEM CSA ratio 0.78). These lesions were equally
distributed in all coronary arteries. Examples are shown in Figs 1 and 4. In addition, 37% of the 603 lesions had less plaque
than expected.
|
|
|
The clinical, angiographic, and IVUS results are shown in Table 1. In all of the lesions with inadequate arterial
remodeling, there was less plaque accumulation than expected, and
in 21% there was less plaque accumulation within the lesion than at
the proximal reference.
|
There was only a poor correlation between angiographic or IVUS indices
of lesion severity and IVUS indices of remodeling. The angiographic
diameter stenosis correlated poorly with the ratios of lesion/reference
EEM CSA (r=.133, P=.0059) or lesion/reference P&M
CSA (r=.096, P=.0469). The angiographic minimum
lumen diameter correlated poorly with the ratio of lesion/reference EEM
CSA (r=.128, P=.008) but not at all with the
ratio of lesion/reference P&M CSA (r=.055,
P=.2539). The IVUS percent CSN correlated poorly with the
ratio of lesion/reference EEM CSA (r=.204,
P<.0001) and with the ratio of lesion/reference P&M CSA
(r=.226, P<.0001). This indicated that lesion
severity was only weakly related to plaque accumulation or to the
magnitude of remodeling. The ratio of lesion/reference P&M CSA
correlated with the lesion/reference EEM CSA (r=.672,
P<.0001; Fig 5).
|
Determinants of Inadequate Arterial Remodeling
The univariate predictors of inadequate remodeling are shown in
Table 1. There were no patient-related predictors. Furthermore, when
multiple lesions in the same patient were compared, there was no
between-lesion correlation of the ratios of lesion/reference EEM CSA or
lesion/reference P&M CSA. This suggests that remodeling is a
lesion-specific response, not a patient-specific response.
When multivariate linear regression analysis was used, the only independent predictor of the ratio of target-lesion to reference-segment EEM CSA was the superficial arc of calcium.
Noncalcified Lesions
When the subgroup of 238 lesions with 45° of target-lesion
calcium were analyzed separately, the overall lesion/reference-site EEM
CSA ratio was 1.04±0.24. The results are shown in Table 2. There was no correlation between angiographic indices
of lesion severity and IVUS indices of remodeling. There was a weak
correlation between the IVUS lesion site percent CSN and both the
lesion/reference EEM CSA (r=.320, P<.0001) and
the lesion/reference P&M CSA (r=.230, P=.0003).
Finally, the ratio of lesion/reference P&M CSA correlated with the
lesion/reference EEM CSA (r=.681, P<.0001).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The conventional concept of development and progression of a focal coronary artery stenosis in "stable" coronary artery disease is that there is a balance between plaque accumulation and adaptive remodeling until plaque accumulation outstrips the ability of the artery to compensate. Our findings suggest that there is a spectrum in the magnitude of arterial remodeling and that in some lesions, inadequate remodeling may contribute to the development of focal stenoses.
Definition of Inadequate Arterial Remodeling
First, the expected degree of arterial tapering was determined. In
a previous report, cross-sectional measurements in diseased coronary
arteries at fixed axial distances proximal and distal to a lesion site
were compared.30 The EEM CSA tapered an average of 10%
per 10 mm of axial arterial length; it never tapered by >21% per
10 mm.
Then, the magnitude of arterial remodeling was determined by comparing
the target lesion with a carefully selected proximal reference. A
lesion site with inadequate remodeling had to have an EEM CSA that was
significantly smaller than could be accounted for by arterial tapering
alone; the absolute cutoff was a lesion site EEM CSA 78% of the
proximal reference. Fifteen percent of lesions fit this definition.
This rigid definition tended to minimize the prevalence of inadequate
remodeling.
Patient and Lesion Selection
Patients and target lesions had to meet strict criteria to permit
the study of a homogeneous population and eliminate confounding factors
that would have produced erroneous evidence of inadequate arterial
remodeling. Most of the lesions in our IVUS database had to be excluded
from this analysis.
Only lesions studied before intervention were included. All angioplasty devices improve lumen dimensions in part by altering lesion geometry.20 21 23 24 25 Furthermore, the largest IVUS catheter used in the present study had a diameter of 1.3 mm. Although the ultrasound catheter may have caused a minor Dotter effect, at most there would have been a 1.3-mm2 increase in lesion-site EEM CSA; thus, crossing the lesion would not have exaggerated inadequate arterial remodeling. Similarly, only new lesions were included. Previously treated lesions and reference segments have undergone a long-term alteration in EEM and P&M CSA precluding even inferential analysis of new lesion geometry.30 31 32
Only lesions studied with the use of IVUS systems incorporating motorized transducer pullback were analyzed because of the importance of the axial relationship between the lesion site and the proximal reference segment. By routinely administering intracoronary nitroglycerin and by including only lesions having a minimum lumen CSA smaller than (or equal to) the imaging catheter, we minimized the confounding effects of arterial spasm. The imaging catheter "splinted" the vessel to prevent a vasospastic decrease in lumen and EEM CSA at the lesion site. Furthermore, in our experience, when an IVUS catheter causes vasospasm, it is diffuse (also involving the reference segment). Catheter-induced vasospasm at the proximal reference would have masked but not exaggerated the presence of inadequate remodeling.
Only patients with stable angina were included in the present study. The mechanism of lesion progression in unstable coronary artery syndromes is thought to be different from "stable" angina. Emerging evidence33 34 35 36 suggests that lesion progression in acute coronary syndromes follows recurrent minor fissuring of the most fatty atheromatous plaques with subsequent thrombus formation. The rapid increase in lesion plaque mass does not allow time for remodeling.37 38 39 40
Ostial lesions (including all lesions within 3 mm of a large proximal side branch) were excluded because of the lack of an appropriate proximal reference site for comparison. Distal reference sites could have been used except that crossing a significant stenosis with the ultrasound catheter would have caused underperfusion of the distal artery and a decrease in distal reference lumen and EEM CSA. Similarly, long lesions and arteries with severe diffuse disease were excluded because of the difficulties in identifying proper proximal reference segments. Lesions with ectasia were excluded because the abnormal reference-site EEM enlargement would have caused false-positive evidence of inadequate remodeling.
Angiographic Findings
Lesions with inadequate arterial remodeling had more ultrasonic
calcium and less angiographic calcium than lesions with adaptive
remodeling. A previous study explains this apparent
contradiction.27 IVUS detected target-lesion calcification
twice as often as did angiography. However, when multivariate analysis
was used, superficial IVUS calcium (not total IVUS calcium) was an
independent predictor of angiographic calcium. IVUS identifies only the
leading edge of the calcific deposit; it does not measure the thickness
of the calcium.13 14 16 19 Nevertheless, it is likely that
superficial calcium is thicker than deep wall calcium. Thus, the
thickness of the lesion-associated calcium (a surrogate for which is
superficial calcium) may be the most important determinant of
angiographic calcium detection. In lesions with inadequate arterial
remodeling, there is a reduction in P&M CSA and P&M thickness and
therefore in the maximum possible thickness of the superficial calcium
deposits.
Furthermore, the current analysis used individual image-slice measurements. The location and extent of calcium within the lesion may vary from frame to frame on IVUS study.
Previous Studies of Inadequate Arterial Remodeling
Using pathological analysis of human necropsy specimens and IVUS
of human femoral arteries in vivo, Pasterkamp et al41
demonstrated the presence of inadequate arterial remodeling in human
femoral arteries. They subsequently found that this influences the
mechanisms of lumen enlargement during percutaneous transluminal
angioplasty procedures.42 Most recently, these same
investigators have shown that remodeling in human femoral arteries
varies from segment to segment, similar to the observations of the
current study.43
Mechanisms of Inadequate Arterial Remodeling
The current study does not indicate whether this is an early event
(failed adaptive remodeling) or a late event (arterial shrinkage).
However, there are several possible explanations for this finding. (1)
Previous studies have shown greater amounts of fibrocalcific plaque
elements at the lesion site.5 44 45 Potentially, these
fibrocalcific elements, especially superficial calcification, may have
limited the adaptive response to plaque accumulation. (2)
Alternatively, maturing of the atherosclerotic plaque with a reduction
in lipid content, an increase in fibrosis and calcification, and
apoptosis may result in retraction of the atherosclerotic plaque, a
decrease in P&M CSA, and a subsequent decrease in EEM
CSA.46 However, when multivariate analysis was used,
inadequate remodeling correlated with the lesion arc of superficial
calcium. Because superficial calcium may be a marker of more
advanced atherosclerosis,28 36 44 47 48 49 50 51 52 inadequate
remodeling may represent a late event, ie, arterial shrinkage.
Implications
Some target lesions respond to vasodilators while others do not.
Inadequate remodeling may explain the failure of some lesions to
dilate. Similarly, such lesions may also have a less pronounced
vasoconstrictor response. Inadequate remodeling may also explain the
occasional finding of unexpectedly large lumen dimensions after
atheroablative device use. There may be a subpopulation of lesions that
undergo facilitated dilation when freed from their restrictive
superficial components (eg, superficial target-lesion calcium).
Target lesions with inadequate remodeling have a modest accumulation of atherosclerotic plaque; in fact, lesion-site plaque accumulation may be less than the reference. Thus, aggressive atheroablative therapy could result in an increased incidence of complications, including perforation and aneurysm formation. A more rational approach would be to limit atheroablative therapy and instead use balloon- and/or stent-induced vessel expansion or to downsize the atheroablative devices by measuring lesion media-to-media dimensions.
Using the current definition (based on the lesion/reference EEM CSA ratio), the presence of inadequate remodeling did not correlate with any of the clinical variables tested (eg, diabetes, patient age, or sex) and correlated only weakly with indices of lesion severity. Furthermore, when multiple lesions in the same patient were compared, remodeling appeared to be a lesion-specific response.
Limitations
The major limitations to this study are that this was not a
natural history study, and the presence of inadequate remodeling at the
lesion site was an artifact of the methodology and definitions used.
However, true natural history studies (using serial IVUS analysis for a
period of years or decades) are currently not practical, and
pathological studies demonstrating adaptive remodeling have also
studied lesions at a single time in the natural history of the
disease.
The methodology used in the present study was different from the pathology methods that first detected adaptive remodeling.1 2 53 However, the current methodology also showed adaptive remodeling in most arteries. The mean lesion/reference EEM CSA was 1.0. This means that in most arteries, adaptive remodeling at the lesion site counteracted normal arterial tapering. Also, the current methods are not dissimilar from the IVUS methods used by other investigators.41 Nevertheless, the findings in the present study were entirely dependent on systematic and reproducible analyses, a careful selection of lesion-site and reference-segment image slices, and a correct definition of "expected" arterial taper.
The definition of inadequate arterial remodeling in the current study would have been influenced by the degree of remodeling within the reference segment. In the overall cohort, greater plaque accumulation and adaptive remodeling of the reference segment could have artificially produced inadequate remodeling at the lesion site. However, in the subset of lesions containing minimal calcium, the reference-segment measurements were similar in both groups.
Different amounts of vascular tone (spasm from the catheter at the lesion site or preferential vasodilatation at the reference site) could also have artificially produced inadequate remodeling. However, 37% of the overall lesion cohort had less plaque than expected, and 21% of the lesions with inadequate remodeling had less plaque than the contiguous reference segment.
Conclusions
There is a spectrum of remodeling responses to plaque
accumulation. Inadequate remodeling is present in at least 15% of
chronic, focal, new coronary arterial stenoses in patients with stable
angina. This appears to be a lesion-specific response.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was supported in part by the Medlantic Research Institute and by the Cardiology Research Foundation, Washington, DC.
Received August 14, 1996; revision received November 26, 1996; accepted November 27, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Glagov S, Weisenberg E, Zarins CK, Stankunavicius K, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:1371-1375. [Abstract]
2.
Stiel GM, Stiel LSG, Schofer J, Donath K, Mathey
DG. Impact of compensatory enlargement of atherosclerotic
coronary arteries on angiographic assessment of coronary heart
disease. Circulation. 1989;80:1603-1609.
3.
Armstrong ML, Heistad DD, Marcus ML, Megan MB, Piegors
DJ. Structural and hemodynamic responses of peripheral arteries
of macaque monkeys to atherogenic diet.
Arteriosclerosis. 1985;5:336-346.
4. McPherson DD, Sirna SJ, Hiratzka LF, Thorpe L, Armstrong ML, Marcus ML, Kerber RE. Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis. J Am Coll Cardiol. 1991;17:79-86. [Abstract]
5. Hodgson JM, Reddy KG, Suneja R, Nair RN, Lesnefsky EJ, Sheehan HM. Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. J Am Coll Cardiol. 1993;21:35-44. [Abstract]
6.
Tobis JM, Mallery J, Mahon D, Lehmann K, Zalesky P,
Griffith J, Gessert J, Moriuchi M, McRae M, Dwyer ML, Greep N, Henry
WL. Intravascular ultrasound imaging of human coronary arteries
in vivo: analysis of tissue characterizations with comparison to in
vitro histological specimens. Circulation. 1991;83:913-926.
7. Rasheed Q, Nair R, Sheehan H, Hodgson JM. Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables. Am J Cardiol. 1994;73:753-758. [Medline] [Order article via Infotrieve]
8. Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR, Bashore TM, Stack RS, Davidson CJ. In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol. 1993;71:665-668. [Medline] [Order article via Infotrieve]
9.
Losordo DW, Rosenfield K, Kaufman J, Pieczek A, Isner
JM. Focal compensatory enlargement of human arteries in response
to progressive atherosclerosis: in vivo documentation using
intravascular ultrasound. Circulation. 1994;89:2570-2577.
10. Coy KM, Maurer G, Siegel RJ. Intravascular ultrasound imaging: a current perspective. J Am Coll Cardiol. 1991;18:1811-1823. [Abstract]
11. Nissen SE, Gurley JC, Booth DC, DeMaria AN. Intravascular ultrasound of the coronary arteries: current applications and future directions. Am J Cardiol. 1992;69:18H-29H. [Medline] [Order article via Infotrieve]
12. Popma JJ, Bashore TD. Qualitative and quantitative angiography. In: Topol E, ed. Textbook of Interventional Cardiology. Philadelphia, Pa: WB Saunders; 1994:1052-1068.
13.
Potkin BN, Bartorelli AL, Gessert JM, Neville R,
Almagor Y, Roberts WC, Leon MB. Coronary artery imaging with
intravascular high-frequency ultrasound.
Circulation. 1990;81:1575-1585.
14.
Nissen SE, Grines CL, Gurley JC, Sublett K, Haynie D,
Diaz C, Booth DC, DeMaria AN. Application of a new phased-array
ultrasound imaging catheter in the assessment of vascular dimensions:
in vivo comparison to cineangiography. Circulation. 1990;81:660-666.
15.
Tobis JM, Mallery JA, Gessert J, Griffith J, Mahon D,
Bessen M, Moriuchi M, McLeay L, McRae M, Henry WL. Intravascular
ultrasound cross-sectional arterial imaging before and after balloon
angioplasty in vitro. Circulation. 1989;80:873-882.
16. Nishimura RA, Edwards WD, Warnes CA, Reeder GS, Holmes DR Jr, Tajik AJ, Yock PG. Intravascular ultrasound imaging: in vitro validation and pathologic correlation. J Am Coll Cardiol. 1990;16:145-154. [Abstract]
17. Hodgson JM, Graham SP, Sarakus AD, Dame SG, Stephens DN, Dhillon PS, Brands D, Sheehan H, Eberle MJ. Clinical percutaneous imaging of coronary anatomy using an over-the-wire ultrasound catheter system. Int J Card Imaging. 1989;4:186-193.
18. Mallery JA, Tobis JM, Griffith J, Gessert J, McRae M, Moussabeck O, Bessen M, Moriuchi M, Henry WL. Assessment of normal and atherosclerotic arterial wall thickness with an intravascular ultrasound imaging catheter. Am Heart J. 1990;119:1392-1400. [Medline] [Order article via Infotrieve]
19. Gussenhoven EJ, Essed CE, Lancee CT, Mastik F, Frietman P, van Egmond FC, Reiber J, Bosch H, van Urk H, Roelandt J, Bom N. Arterial wall characteristics determined by intravascular ultrasound imaging: an in vitro study. J Am Coll Cardiol. 1989;14:947-952. [Abstract]
20. Kovach JA, Mintz GS, Pichard AD, Kent KM, Popma JJ, Satler LF, Leon MB. Sequential intravascular ultrasound characterization of the mechanisms of rotational atherectomy and adjunct balloon angioplasty. J Am Coll Cardiol. 1993;22:1024-1032. [Abstract]
21.
Mintz GS, Kovach JA, Javier SP, Pichard AD, Kent KM,
Popma JJ, Salter LF, Leon MB. Mechanisms of lumen enlargement
after excimer laser coronary angioplasty: an intravascular ultrasound
study. Circulation. 1995;92:3408-3414.
22. Mintz GS, Pichard AD, Popma JJ, Kent KM, Satler LF, Leon MB. Preliminary experience with adjunct directional coronary atherectomy following high-speed rotational atherectomy in the treatment of calcific coronary artery disease. Am J Cardiol. 1993;71:799-804. [Medline] [Order article via Infotrieve]
23. Potkin BN, Keren G, Mintz GS, Douek P, Pichard AD, Satler LF, Kent KM, Leon MB. Arterial responses to balloon coronary angioplasty: an intravascular ultrasound study. J Am Coll Cardiol. 1992;20:942-951. [Abstract]
24. Matar FA, Mintz GS, Farb A, Douek P, Pichard AD, Kent KM, Satler LF, Popma JJ, Keller MB, Pinnow E, Merritt AJ, Lindsay J Jr, Leon MB. The contribution of tissue removal to lumen improvement after directional coronary atherectomy. Am J Cardiol. 1994;74:647-650. [Medline] [Order article via Infotrieve]
25. Dussaillant GD, Mintz GS, Pichard AD, Kenneth KM, Satler LF, Popma JJ, Bucher TA, Griffin J, Leon MB. Mechanisms and acute and long term results of adjunctive directional atherectomy after rotational atherectomy. J Am Coll Cardiol. 1996;27:1390-1397. [Abstract]
26.
Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF,
Wong SC, Hong MK, Kovach JA, Leon MB. Arterial remodeling after
coronary angioplasty: a serial intravascular ultrasound study.
Circulation. 1996;94:35-43.
27. Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF, Chuang YC, Ditrano CJ, Leon MB. Patterns of calcification in coronary artery disease: a statistical analysis of intravascular ultrasound and coronary angiography in 1155 lesions. Circulation. 1995;91:1965-1969.
28. Mintz GS, Painter JA, Pichard AD, Kent KM, Satler LF, Popma JJ, Chuang YC, Bucher TA, Sokolowica LE, Leon MB. Atherosclerosis in angiographically `normal' coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:1479-1485. [Abstract]
29. Fuessl RT, Mintz GS, Pichard AD, Kent KM, Satler LF, Popma JJ, Leon MB. In vivo validation of intravascular ultrasound length measurements using a motorized transducer pullback device. Am J Cardiol. 1996;77:1115-1118. [Medline] [Order article via Infotrieve]
30. Javier SP, Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF, Leon MB. Intravascular ultrasound assessment of the magnitude and mechanism of coronary artery and lumen tapering. Am J Cardiol. 1995;75:177-180. [Medline] [Order article via Infotrieve]
31.
Post MJ, Borst C, Kuntz RE. The relative
importance of arterial remodeling compared with intimal hyperplasia in
lumen renarrowing after balloon angioplasty.
Circulation. 1994;89:2816-2821.
32.
Kakuta T, Currier JW, Haudenschild CC, Ryan TJ, Faxon
DP. Differences in compensatory vessel enlargement, not intimal
proliferation, account for restenosis after angioplasty in the
hypercholesterolemic rabbit. Circulation. 1994;89:2809-2815.
33. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med. 1992;326:242-250,310-318. [Medline] [Order article via Infotrieve]
34. Ambrose JA, Winters SL, Stern A, Eng A, Teichholz LE, Gorlin R. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol. 1985;5:609-616. [Abstract]
35. Ambrose JA, Tannenbaum MA, Alexopoulos D, Hjemdahl-Monsen CE, Leavy J, Weiss M, Borrico S, Gorlin R, Fuster V. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol. 1988;12:56-62. [Abstract]
36. Ross R. The pathogenesis of atherosclerosis: an update. N Engl J Med. 1986;314:488-500. [Medline] [Order article via Infotrieve]
37. Hackett D, Vervilghen J, Davies G, Maseri A. Coronary stenoses before and after acute myocardial infarction. Am J Cardiol. 1989;63:1517-1518. [Medline] [Order article via Infotrieve]
38. Davies M. A macroscopic and microscopic view of coronary thrombi. Circulation. 1990;82:1138-1146.
39. Tracy R, Devaney K, Kissling G. Characteristics of the plaque under a coronary thrombus. Virchows Arch (A). 1985;405:411-427.
40. Ip JH, Fuster V, Badimon L, Badimon J, Taubman MB, Chesebro JH. Syndromes of accelerated atherosclerosis: role of vascular injury and smooth muscle cell proliferation. J Am Coll Cardiol. 1990;15:1667-1687. [Abstract]
41.
Pasterkamp G, Wensing PJW, Post MJ, Hillen B, Mali
WPTM, Borst C. Paradoxical arterial wall shrinkage may
contribute to luminal narrowing of human atherosclerotic femoral
arteries. Circulation. 1995;91:1444-1449.
42. Pasterkamp G, Borst C, Gussenhoven EJ, Mali WPTM, Post MJ, The SHK, Reekers JA, vondenBerg FG. Remodeling of de novo atherosclerotic lesions in femoral arteries: impact on the mechanism of balloon angioplasty. Eur Heart J. 1995;16:19. Abstract.
43.
Pasterkamp G, Borst C, Post MJ, Mali WPTM, Wensing PJW,
Gussenhoven EJ, Hillen B. Atherosclerotic arterial remodeling in
the superficial femoral artery: individual variation in local
compensatory enlargement response. Circulation. 1996;93:1818-1825.
44.
Picano E, Landini L, Distante A, Benassi A, Sarnelli R,
L'Abbate A. Fibrosis, lipids, and calcium in human
atherosclerotic plaque. Circ Res. 1985;56:556-562.
45. Hodgson JM, Reddy KG, Suneja R, Sheehan HM, Lesnefsky EJ, Nair R. Intracoronary ultrasound plaque composition in non-lesional segments differs in unstable angina and stable angina patients: evidence from intracoronary ultrasound. J Am Coll Cardiol. 1992;19:79A. Abstract.
46. Geng YJ, Libby P. Evidence for apoptosis in human atheroma: co-localization with interleukin-1 beta converting enzyme. FASEB J. 1995;9:A855. Abstract.
47. Blankenhorn DH. Coronary arterial calcification: a review. Am J Med Sci. 1961;242:4-49.
48. Warburten RK, Tampas JP, Soule AB, Taylar HE III. Coronary artery calcification: its relationship to coronary artery stenosis and myocardial infarction. Radiology. 1968;91:109-115. [Medline] [Order article via Infotrieve]
49. Frink RJ, Achor RWP, Braun AL Jr, Kincaid OW, Brandenburg RO. Significance of calcification of the coronary arteries. Am J Cardiol. 1970;26:241-247. [Medline] [Order article via Infotrieve]
50. Stary HC. Evolution and progression of atherosclerotic lesions in coronary arteries of children and young adults. Atherosclerosis. 1989;9(suppl I):I-19-I-32.
51. Atherosclerosis of the aorta and coronary arteries in five towns. Bull World Health Organ. 1976;53:485-645.
52.
Dinsmore RE, Lees RJ. Vascular calcification in
types II and IV hypercholesterolemia: radiographic appearance and
clinical significance. Am J Roentgenol. 1985;144:895-899.
53. Zarins CK, Weisenberg E, Kolettis G, Stankunavicius R, Glagov S. Differential enlargement of artery segments in response to enlarging atherosclerotic plaques. J Vasc Surg. 1988;7:386-394.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  Y. J. Hong, G. S. Mintz, S. W. Kim, S. Y. Lee, S. Y. Kim, T. Okabe, A. D. Pichard, L. F. Satler, R. Waksman, K. M. Kent, et al. Disease progression in nonintervened saphenous vein graft segments a serial intravascular ultrasound analysis. J. Am. Coll. Cardiol., April 14, 2009; 53(15): 1257 - 1264. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Jimenez-Quevedo, N. Suzuki, C. Corros, C. Ferrer, D. J. Angiolillo, F. Alfonso, R. Hernandez-Antolin, C. Banuelos, J. Escaned, C. Fernandez, et al. Vessel Shrinkage as a Sign of Atherosclerosis Progression in Type 2 Diabetes: A Serial Intravascular Ultrasound Analysis Diabetes, January 1, 2009; 58(1): 209 - 214. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. S. Mintz Diabetic Coronary Artery Disease: How Little We Know and How Little Intravascular Ultrasound Has Taught Us J. Am. Coll. Cardiol., July 22, 2008; 52(4): 263 - 265. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Pasterkamp and I. Hoefer The visualization of the remodelling paradox Eur. Heart J., July 2, 2008; 29(14): 1704 - 1705. [Full Text] [PDF]
|
|
|
|
 |
|
 I Sipahi, E M Tuzcu, K-W Moon, S J Nicholls, P Schoenhagen, J Zhitnik, T D Crowe, S Kapadia, and S E Nissen Do the extent and direction of arterial remodelling predict subsequent progression of coronary atherosclerosis? A serial intravascular ultrasound study Heart, May 1, 2008; 94(5): 623 - 627. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. O. Jensen, P. Thayssen, G. S. Mintz, M. Maeng, A. Junker, A. Galloe, E. H. Christiansen, S. K.S. Hoffmann, K. E. Pedersen, H. S. Hansen, et al. Intravascular ultrasound assessment of remodelling and reference segment plaque burden in type-2 diabetic patients Eur. Heart J., July 2, 2007; 28(14): 1759 - 1764. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. S. Chatzizisis, A. U. Coskun, M. Jonas, E. R. Edelman, C. L. Feldman, and P. H. Stone Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling: Molecular, Cellular, and Vascular Behavior J. Am. Coll. Cardiol., June 26, 2007; 49(25): 2379 - 2393. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. N. Mitchell and P. Libby Vascular Remodeling in Transplant Vasculopathy Circ. Res., April 13, 2007; 100(7): 967 - 978. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 J. R. Crouse III Thematic review series: Patient-Oriented Research. Imaging atherosclerosis: state of the art J. Lipid Res., August 1, 2006; 47(8): 1677 - 1699. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Hartmann, C. von Birgelen, G. S. Mintz, P. M.J. Verhorst, and R. Erbel Relation between baseline plaque burden and subsequent remodelling of atherosclerotic left main coronary arteries: a serial intravascular ultrasound study with long-term (>=12 months) follow-up Eur. Heart J., August 1, 2006; 27(15): 1778 - 1784. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Schoenhagen, E. M. Tuzcu, C. Apperson-Hansen, C. Wang, K. Wolski, S. Lin, I. Sipahi, S. J. Nicholls, W. A. Magyar, A. Loyd, et al. Determinants of Arterial Wall Remodeling During Lipid-Lowering Therapy: Serial Intravascular Ultrasound Observations From the Reversal of Atherosclerosis With Aggressive Lipid Lowering Therapy (REVERSAL) Trial Circulation, June 20, 2006; 113(24): 2826 - 2834. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Jimenez-Quevedo, M. Sabate, D. Angiolillo, F. Alfonso, R. Hernandez-Antolin, C. Banuelos, E. Bernardo, C. Ramirez, R. Moreno, C. Fernandez, et al. LDL-cholesterol predicts negative coronary artery remodelling in diabetic patients: an intravascular ultrasound study: reply Eur. Heart J., May 2, 2006; 27(10): 1257 - 1258. [Full Text] [PDF]
|
|
|
|
|
|
C. von Birgelen, M. Hartmann, G. S. Mintz, D. Bose, H. Eggebrecht, T. Neumann, M. Gossl, H. Wieneke, A. Schmermund, M. G. Stoel, et al. Remodeling Index Compared to Actual Vascular Remodeling in Atherosclerotic Left Main Coronary Arteries as Assessed With Long-Term (>=12 Months) Serial Intravascular Ultrasound J. Am. Coll. Cardiol., April 4, 2006; 47(7): 1363 - 1368. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. K. Reddy, S. K. G. Koshy, S. Wasson, E. E. Quan, S. Pagni, A. M. Roberts, I. G. Joshua, and S. C. Tyagi Adaptive-Outward and Maladaptive-Inward Arterial Remodeling Measured by Intravascular Ultrasound in Hyperhomocysteinemia and Diabetes Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2006; 11(1): 65 - 77. [Abstract] [PDF]
|
|
|
|
|
|
G A Rodriguez-Granillo, P W Serruys, H M Garcia-Garcia, J Aoki, M Valgimigli, C A G van Mieghem, E McFadden, P P T de Jaegere, and P de Feyter Coronary artery remodelling is related to plaque composition Heart, March 1, 2006; 92(3): 388 - 391. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Jimenez-Quevedo, M. Sabate, D. Angiolillo, F. Alfonso, R. Hernandez-Antolin, C. Banuelos, E. Bernardo, C. Ramirez, R. Moreno, C. Fernandez, et al. LDL-cholesterol predicts negative coronary artery remodelling in diabetic patients: an intravascular ultrasound study Eur. Heart J., November 1, 2005; 26(21): 2307 - 2312. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Achenbach, D. Ropers, U. Hoffmann, B. MacNeill, U. Baum, K. Pohle, T. J. Brady, E. Pomerantsev, J. Ludwig, F. A. Flachskampf, et al. assessment of coronary remodeling in stenotic and nonstenotic coronary atherosclerotic lesions by multidetector spiral computed tomography J. Am. Coll. Cardiol., March 3, 2004; 43(5): 842 - 847. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Sahara, H. Kirigaya, Y. Oikawa, J. Yajima, K. Ogasawara, H. Satoh, K. Nagashima, H. Hara, Y. Nakatsu, and T. Aizawa Arterial remodeling patterns before intervention predict diffuse in-stent restenosis: An intravascular ultrasound study J. Am. Coll. Cardiol., November 19, 2003; 42(10): 1731 - 1738. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. S. Mintz, A. Tinana, M.-K. Hong, C. W. Lee, J.-J. Kim, N. E. Fearnot, S.-W. Park, S.-J. Park, and N. J. Weissman Impact of Preinterventional Arterial Remodeling on Neointimal Hyperplasia After Implantation of (Non-Polymer-Encapsulated) Paclitaxel-Coated Stents: A Serial Volumetric Intravascular Ultrasound Analysis From the ASian Paclitaxel-Eluting Stent Clinical Trial (ASPECT) Circulation, September 16, 2003; 108(11): 1295 - 1298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.-K. Hong, G. S. Mintz, C. W. Lee, Y.-H. Kim, J.-W. Lee, J.-M. Song, K.-H. Han, D.-H. Kang, J.-K. Song, J.-J. Kim, et al. Intravascular ultrasound assessment of patterns of arterial remodeling in the absence of significant reference segment plaque burden in patients with coronary artery disease J. Am. Coll. Cardiol., September 3, 2003; 42(5): 806 - 810. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B E Bouma, G J Tearney, H Yabushita, M Shishkov, C R Kauffman, D DeJoseph Gauthier, B D MacNeill, S L Houser, H T Aretz, E F Halpern, et al. Evaluation of intracoronary stenting by intravascular optical coherence tomography Heart, March 1, 2003; 89(3): 317 - 320. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.C. Kaski Atheromatous plaque location and arterial remodelling Eur. Heart J., February 2, 2003; 24(4): 291 - 293. [Full Text] [PDF]
|
|
|
|
|
|
F Prati, E Arbustini, A Labellarte, L Sommariva, T Pawlowski, A Manzoli, A Pagano, M Motolese, and A Boccanelli Eccentric atherosclerotic plaques with positive remodelling have a pericardial distribution: a permissive role of epicardial fat?: A three-dimensional intravascular ultrasound study of left anterior descending artery lesions Eur. Heart J., February 2, 2003; 24(4): 329 - 336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. DeFranco Understanding the pathophysiology of the arterial wall: which method should we choose? Intra-vascular ultrasound Eur. Heart J. Suppl., September 1, 2002; 4(suppl_F): F29 - F40. [Abstract] [PDF]
|
|
|
|
 |
|
 C. Indolfi, D. Torella, C. Coppola, E. Stabile, G. Esposito, A. Curcio, A. Pisani, L. Cavuto, O. Arcucci, M. Cireddu, et al. Rat carotid artery dilation by PTCA balloon catheter induces neointima formation in presence of IEL rupture Am J Physiol Heart Circ Physiol, August 1, 2002; 283(2): H760 - H767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
I.-K. Jang, B. E. Bouma, D.-H. Kang, S.-J. Park, S.-W. Park, K.-B. Seung, K.-B. Choi, M. Shishkov, K. Schlendorf, E. Pomerantsev, et al. Visualization of coronary atherosclerotic plaques in patients using optical coherence tomography: comparison with intravascular ultrasound J. Am. Coll. Cardiol., February 20, 2002; 39(4): 604 - 609. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D Saito, T Oka, A Kajiyama, N Ohnishi, and T Shiraki Factors predicting compensatory vascular remodelling of the carotid artery affected by atherosclerosis Heart, February 1, 2002; 87(2): 136 - 139. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. P. Burke, F. D. Kolodgie, A. Farb, D. Weber, and R. Virmani Morphological Predictors of Arterial Remodeling in Coronary Atherosclerosis Circulation, January 22, 2002; 105(3): 297 - 303. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Okura, M. Hayase, S. Shimodozono, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Impact of pre-interventional arterial remodeling on subsequent vessel behavior after balloon angioplasty: a serial intravascular ultrasound study J. Am. Coll. Cardiol., December 1, 2001; 38(7): 2001 - 2005. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H. M. Hassan, I. M. Lang, M. Ignatescu, R. Ullrich, D. Bonderman, P. Wexberg, F. Weidinger, and H. D. Glogar Increased intimal apoptosis in coronary atherosclerotic vessel segments lacking compensatory enlargement J. Am. Coll. Cardiol., November 1, 2001; 38(5): 1333 - 1339. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 E. Lutgens, E. D. de Muinck, S. Heeneman, and M. J.A.P. Daemen Compensatory Enlargement and Stenosis Develop in ApoE-/- and ApoE*3-Leiden Transgenic Mice Arterioscler. Thromb. Vasc. Biol., August 1, 2001; 21(8): 1359 - 1365. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A M Varnava and M J Davies Relation between coronary artery remodelling (compensatory dilatation) and stenosis in human native coronary arteries Heart, August 1, 2001; 86(2): 207 - 211. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. von Birgelen, W. Klinkhart, G. S. Mintz, A. Papatheodorou, J.o. Herrmann, D. Baumgart, M. Haude, H. Wieneke, J. Ge, and R. Erbel Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study in vivo J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1864 - 1870. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. S. Mintz, S. E. Nissen, W. D. Anderson, S. R. Bailey, R. Erbel, P. J. Fitzgerald, F. J. Pinto, K. Rosenfield, R. J. Siegel, E. M. Tuzcu, et al. American College of Cardiology clinical expert consensus document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (ivus): A report of the american college of cardiology task force on clinical expert consensus documents developed in collaboration with the european society of cardiology endorsed by the society of cardiac angiography and interventions J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1478 - 1492. [Full Text] [PDF]
|
|
|
|
|
|
H. Okura, Y. Morino, A. Oshima, M. Hayase, M. R. Ward, J. J. Popma, R. E. Kuntz, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Preintervention arterial remodeling affects clinical outcome following stenting: an intravascular ultrasound study J. Am. Coll. Cardiol., March 15, 2001; 37(4): 1031 - 1035. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Nissen and P. Yock Intravascular Ultrasound : Novel Pathophysiological Insights and Current Clinical Applications Circulation, January 30, 2001; 103(4): 604 - 616. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Nakamura, H. Nishikawa, S. Mukai, M. Setsuda, K. Nakajima, H. Tamada, H. Suzuki, T. Ohnishi, Y. Kakuta, T. Nakano, et al. Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study J. Am. Coll. Cardiol., January 1, 2001; 37(1): 63 - 69. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Endo, H. Hirayama, O. Yoshida, T. Arakawa, T. Akima, T. Yamada, and M. Nanasato Arterial remodeling influences the development of intimal hyperplasia after stent implantation J. Am. Coll. Cardiol., January 1, 2001; 37(1): 70 - 75. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M A Costa, K Kozuma, A L Gaster, W J van der Giessen, M Sabaté, D P Foley, I P Kay, J M R Ligthart, P Thayssen, M J van den Brand, et al. Three dimensional intravascular ultrasonic assessment of the local mechanism of restenosis after balloon angioplasty Heart, January 1, 2001; 85(1): 73 - 79. [Abstract] [Full Text]
|
|
|
|
|
|
C von Birgelen, W Klinkhart, G S Mintz, H Wieneke, D Baumgart, M Haude, T Bartel, S Sack, J Ge, and R Erbel Size of emptied plaque cavity following spontaneous rupture is related to coronary dimensions, not to the degree of lumen narrowing. A study with intravascular ultrasound in vivo Heart, November 1, 2000; 84(5): 483 - 488. [Abstract] [Full Text]
|
|
|
|
|
|
M. R. Ward, G. Pasterkamp, A. C. Yeung, and C. Borst Arterial Remodeling : Mechanisms and Clinical Implications Circulation, September 5, 2000; 102(10): 1186 - 1191. [Full Text] [PDF]
|
|
|
|
|
|
A Jeremias, C Spies, N A Herity, E Pomerantsev, P G Yock, P J Fitzgerald, and A C Yeung Coronary artery compliance and adaptive vessel remodelling in patients with stable and unstable coronary artery disease Heart, September 1, 2000; 84(3): 314 - 319. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Alfonso Videodensitometric vs edge-detection quantitative angiography. Insights from intravascular ultrasound imaging Eur. Heart J., April 2, 2000; 21(8): 604 - 607. [PDF]
|
|
|
|
 |
|
 G. Pasterkamp, D. P.V de Kleijn, and C. Borst Arterial remodeling in atherosclerosis, restenosis and after alteration of blood flow: potential mechanisms and clinical implications Cardiovasc Res, March 1, 2000; 45(4): 843 - 852. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Schoenhagen, K. M. Ziada, S. R. Kapadia, T. D. Crowe, S. E. Nissen, and E. M. Tuzcu Extent and Direction of Arterial Remodeling in Stable Versus Unstable Coronary Syndromes : An Intravascular Ultrasound Study Circulation, February 15, 2000; 101(6): 598 - 603. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Mehran, G. Dangas, G. S. Mintz, A. J. Lansky, A. D. Pichard, L. F. Satler, K. M. Kent, G. W. Stone, and M. B. Leon Atherosclerotic Plaque Burden and CK-MB Enzyme Elevation After Coronary Interventions : Intravascular Ultrasound Study of 2256 Patients Circulation, February 15, 2000; 101(6): 604 - 610. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C von Birgelen, G S Mintz, E A de Vrey, P W Serruys, T Kimura, M Nobuyoshi, J J Popma, M B Leon, R Erbel, and P J de Feyter Preintervention lesion remodelling affects operative mechanisms of balloon optimised directional coronary atherectomy procedures: a volumetric study with three dimensional intravascular ultrasound Heart, February 1, 2000; 83(2): 192 - 197. [Abstract] [Full Text]
|
|
|
|
|
|
P C Smits, G Pasterkamp, M A Q. van Ufford, F D Eefting, P R Stella, P P T de Jaegere, and C Borst Coronary artery disease: arterial remodelling and clinical presentation Heart, October 1, 1999; 82(4): 461 - 464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Taylor, A. P. Burke, A. Farb, P. Yousefi, G. T. Malcom, J. Smialek, and R. Virmani Arterial remodeling in the left coronary system: The role of high-density lipoprotein cholesterol J. Am. Coll. Cardiol., September 1, 1999; 34(3): 760 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Gyongyosi, P Yang, A Hassan, F Weidinger, H Domanovits, A Laggner, and D Glogar Arterial remodelling of native human coronary arteries in patients with unstable angina pectoris: a prospective intravascular ultrasound study Heart, July 1, 1999; 82(1): 68 - 74. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Dangas, G. S. Mintz, R. Mehran, A. J. Lansky, R. Kornowski, A. D. Pichard, L. F. Satler, K. M. Kent, G. W. Stone, and M. B. Leon Preintervention Arterial Remodeling as an Independent Predictor of Target-Lesion Revascularization After Nonstent Coronary Intervention : An Analysis of 777 Lesions With Intravascular Ultrasound Imaging Circulation, June 22, 1999; 99(24): 3149 - 3154. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. C. Leertouwer, E. J. Gussenhoven, L. C. van Dijk, J. A. van Essen, J. Honkoop, J. Deinum, and P. M. T. Pattynama Intravascular Ultrasound Evidence for Coarctation Causing Symptomatic Renal Artery Stenosis Circulation, June 15, 1999; 99(23): 2976 - 2978. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nishioka, A. M. Amanullah, H. Luo, H. Berglund, C.-J. Kim, T. Nagai, N. Hakamata, S. Katsushika, A. Uehata, B. Takase, et al. Clinical validation of intravascular ultrasound imaging for assessment of coronary stenosis severity: Comparison with stress myocardial perfusion imaging J. Am. Coll. Cardiol., June 1, 1999; 33(7): 1870 - 1878. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. C Smits, G. Pasterkamp, P. P.T de Jaegere, P. J de Feyter, and C. Borst Angioscopic complex lesions are predominantly compensatory enlarged: an angioscopy and intracoronary ultrasound study Cardiovasc Res, February 1, 1999; 41(2): 458 - 464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Thome, L. W. Gimple, B. G. Bachhuber, C. A. McNamara, M. Ragosta, S. D. Gertz, E. R. Powers, G. K. Owens, J. E. Humphries, and I. J. Sarembock Early Plus Delayed Hirudin Reduces Restenosis in the Atherosclerotic Rabbit More Than Early Administration Alone : Potential Implications for Dosing of Antithrombin Agents Circulation, November 24, 1998; 98(21): 2301 - 2306. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Pasterkamp, A. H. Schoneveld, A. C. van der Wal, C. C. Haudenschild, R. J. G. Clarijs, A. E. Becker, B. Hillen, and C. Borst Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox J. Am. Coll. Cardiol., September 1, 1998; 32(3): 655 - 662. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Fuster, J. J. Badimon, and J. H Chesebro Atherothrombosis: mechanisms and clinical therapeutic approaches Vascular Medicine, August 1, 1998; 3(3): 231 - 239. [Abstract] [PDF]
|
|
|
|
|
|
B. J. G. L. de Smet, G. Pasterkamp, Y. J. van der Helm, C. Borst, and M. J. Post The Relation Between De Novo Atherosclerosis Remodeling and Angioplasty-Induced Remodeling in an Atherosclerotic Yucatan Micropig Model Arterioscler. Thromb. Vasc. Biol., May 1, 1998; 18(5): 702 - 707. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nishioka, H. Berglund, H. Luo, T. Nagai, R. J. Siegel, G. S. Mintz, and M. B. Leon How Should We Define Inadequate Coronary Arterial Remodeling? • Response Circulation, April 14, 1998; 97 (14): 1424 - 1425. [Full Text]
|
|
|
|
|
|
P. Libby Gene Therapy of Restenosis : Promise and Perils Circ. Res., February 23, 1998; 82(3): 404 - 406. [Full Text] [PDF]
|
|
|
|
|
|
C von Birgelen, G S Mintz, E A de Vrey, T Kimura, J J Popma, S G Airiian, M B Leon, M Nobuyoshi, P W Serruys, and P J de Feyter Atherosclerotic coronary lesions with inadequate compensatory enlargement have smaller plaque and vessel volumes: observations with three dimensional intravascular ultrasound in vivo Heart, February 1, 1998; 79(2): 137 - 142. [Abstract] [Full Text]
|
|
|
|
|
|
A. M. Varnava, P. G. Mills, and M. J. Davies Relationship Between Coronary Artery Remodeling and Plaque Vulnerability Circulation, February 26, 2002; 105(8): 939 - 943. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||