(Circulation. 1997;96:1470-1476.)
© 1997 American Heart Association, Inc.
Articles |
From the Division of Cardiology (H.L., T.N., M.C.F., N.L.E., S.W.T., R.J.S.), Cedars-Sinai Medical Center, Los Angeles, Calif, and the Department of Cardiology (H.B.), Huddinge University Hospital, Stockholm, Sweden.
Correspondence to Robert J. Siegel, MD, Division of Cardiology, Room 5335, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048.
| Abstract |
|---|
|
|
|---|
Methods and Results Cross-sectional dimensions of coronary arteries in 65 patients were measured with the use of intravascular ultrasound. A total of 104 arterial segments were studied, of which 88 had atherosclerosis; 16 served as nonatherosclerotic control segments. Three features of atherosclerotic arterial segments were classified: (1) plaque formation, (2) lumen shape, and (3) shape of arterial external elastic lamina. With our intravascular ultrasoundbased three-level classification system, we identified three patterns that accounted for 89% of all atherosclerotic arterial segments: (1) concentric plaque with a circular lumen and a circular external elastic lamina (n=17), (2) eccentric plaque with a circular lumen and an oval external elastic lamina (n=35), and (3) eccentric plaque with an oval lumen and a circular external elastic lamina (n=26). A circular lumen was preserved in 66% of all atherosclerotic arterial segments. Arterial segments with a circular lumen in the presence of an eccentric plaque had a significantly larger lumen area than the other two main groups (P<.05).
Conclusions With our intravascular ultrasoundbased classification, we provided information regarding the local remodeling response in the coronary artery wall. In a majority of cases, a circular lumen is maintained. Failure of this highly localized response to be operative may contribute to the development of stenotic lesions at a specific site in the artery.
Key Words: plaque atherosclerosis arteries ultrasonics
| Introduction |
|---|
|
|
|---|
The purpose of this study was therefore to use IVUS to study the shape of the arterial lumen and the artery itself associated with different atherosclerotic plaque morphologies in native human coronary arteries.
| Methods |
|---|
|
|
|---|
300° of the total
circumference of the artery. Exclusion criteria were (1) intervention
in the artery before intravascular imaging and (2) marked eccentricity
of the IVUS imaging catheter within the coronary artery being
studied. One hundred three patients were excluded because an
intervention was performed in the artery before intravascular imaging.
The remaining 73 patients had stable angina pectoris and underwent
diagnostic coronary angiography for evaluation of
the severity of coronary atherosclerosis. All
patients were considered for percutaneous transluminal
coronary angioplasty. Eight patients did not have
arterial segments on IVUS fulfilling the inclusion
criteria. The control and study groups are described in Table 1
|
IVUS System
The IVUS imaging system consisted of an imaging catheter
(Sonicath, Boston Scientific Corp) and an SONOS Intravascular System
imaging console (Hewlett-Packard). The imaging catheter has a 30-MHz
single-piezoelectric crystal transducer mechanically rotating at 1800
rpm within a 3.5F monorail over-the-wire catheter sheath.
Imaging Procedure
The right or left femoral artery was punctured by Seldinger
technique, an 8F or a 9F arterial introducer sheath was
advanced retrograde over a guide wire, and the sheath was placed in the
femoral artery. After angiography, the imaging catheter was introduced
through an 8F to 9F coronary guiding catheter over a 0.014-in
guide wire. The imaging catheter was advanced across the angiographic
lesion to the distal portion of the artery under fluoroscopic guidance,
and IVUS imaging was performed during the slow pullback (1 mm/s)
of the imaging catheter. X-ray fluoroscopy was used to confirm the
coaxiality of the imaging catheter at a region of interest in the
coronary artery. IVUS images were recorded on 0.5-in
Super-VHS videotape for subsequent review and quantitative
analysis.
Image Analysis
IVUS images were analyzed off-line with an SONOS
Intravascular System. The most stenotic cross section or the
closest (either distal or proximal) cross section fulfilling the
inclusion criteria within the area of the angiographic lesion was
targeted for analysis. A second or third cross section was
selected for analysis only if a different shape/pattern was
observed. The EEL of the artery was defined as the outer border of the
sonolucent zone adjacent to the echo-dense adventitia, as previously
described.7 8 9 Images recorded with an imaging catheter
that was markedly eccentric within the arterial lumen were
not considered acceptable to avoid errors due to possible image
distortions related to nonuniform transducer
rotation.10 11 Of the 73 patients analyzed, 61 had
at least one arterial segment meeting the inclusion and
exclusion criteria of this study, and an additional 4 patients
exhibited a segment without atherosclerosis.
Atherosclerosis was considered to be present if the
maximal thickness of the echogenic endoluminal layer was >0.3 mm,
the sonolucent zone thickness was >0.2 mm, or
both.7 9 Plaque morphology was described as fibrous if
less echo dense or fibrocalcific if more echo dense than the
adventitia, according to previously described criteria.7 8
The plaque was defined as concentric if the degree of
atherosclerosis was evenly distributed around the full
circumference of the lumen. An eccentric atherosclerotic plaque was
defined by three criteria: (1) marked wall thickening involving
180° of the lumen, (2) a thickest walltoopposite wall thickness
ratio of
1.5, and (3) thickest wall plus opposite wall being greater
than the perpendicular wall1 plus wall2 (Fig 1
). Wall thickness was measured as the
distance from the EEL to the lumen-intimal border. As illustrated in
Fig 1
, lumen diameters were measured along a line through the center of
the lumen and the thickest portion of the arterial wall and
as the maximum perpendicular diameter of the lumen. Artery diameters
were measured from EEL to EEL along the same lines. Lumen and
arterial diameter ratios were calculated as the diameter
along the line including the thickest portion of the wall compared with
the perpendicular diameter. To assess the arterial
lumen area (mm2), the lumen-intimal border was traced. The
area within this border and the area within the EEL were determined by
the computerized planimetry function in the SONOS intravascular imaging
console (Fig 2
).
|
|
Because a reliable delineation of the internal elastic lamina with IVUS is not feasible in atherosclerotic arteries, we used arterial wall area to indicate the degree of atherosclerosis.12 Arterial wall area was calculated as EEL area minus luminal area. Percent area stenosis was calculated as (artery wall area/EEL area)x100.
The definition of lumen and arterial shape was based on the assumption that the nonatherosclerotic artery would present with a circular lumen and artery, resulting in diameter ratios close to 1. To establish a variation of this measure using the present IVUS technique, with application of the inclusion and exclusion criteria, and using the definitions of this study, the diameter ratios were calculated in the 16 arterial segments without atherosclerosis.7 9 A ratio outside ±1.96 SDs of the ratios derived from our control group was considered to represent an oval lumen or artery.
Geometric Form Index
An independent form index indicative of "roundness" was
measured using a Micro-Plan II Image Analysis System
(Laboratory Computer Systems) to describe the degree of asymmetry of a
circumference. With this device, the contours of the cross section of
the lumen and the EEL (representing the shape of the
arterial outer circumference) were traced from photographs
of each of the 104 segments. This form index is a dimensionless ratio
of the enclosed area (A) to the perimeter (P) normalized so that for a
perfect circle the index is 1, and for a line, it is 0. The
relationship is expressed as Form Index=4/P2. A form index
outside ±1.96 SDs of the indexes derived from our control group was
considered to represent an oval lumen or artery. The greater
the deviation from 1, the less circular and more oval was the
artery.
Classification of Atherosclerotic Coronary Arteries
The IVUS definitions of plaque formation and the lumen and EEL
diameter ratios were subsequently used to describe the cross section of
the atherosclerotic artery segments. Each plaque was classified as
concentric or eccentric. Lumen and arterial shape were
classified as circular or oval, creating eight possible combinations.
The same classification was applied using the geometric form index for
lumen and artery symmetry.
Reproducibility of IVUS Measurements
Mean intraobserver and interobserver variabilities of
cross-sectional area determinations by planimetry in our laboratory
were 2.6±1.9% and 2.4±2.6%, respectively. Mean intraobserver and
interobserver variabilities of lumen diameter determinations were
1.7±2.0% and 2.2±1.7%, respectively.
Statistical Analysis
Data are given as mean±SD. Differences between groups in
continuous variables were tested with one-way ANOVA with Fisher's
Protected LSD as posthoc test. A
2 test followed
by Fisher's exact test was used for categorical data for comparison
between groups. Correlations between variables were tested with
linear regression. A value of P<.05 was considered
significant.
| Results |
|---|
|
|
|---|
1 segment that could be evaluated
according to the protocol. We found a positive correlation between wall
area and EEL area (r=.82; P<.001; n=104).
The mean lumen diameter ratio calculated from the perpendicular lumen
diameters as illustrated in Fig 1
was 1.0±0.03 in the control
segments. With application of the IVUS definitions for symmetry
described in the methods, lumen diameter ratios between 0.9 and 1.1
were considered to represent circular lumens.
The degree of atherosclerosis was evenly distributed
around the full circumference of the lumen (concentric plaque) in 22%
(19 segments from 19 patients) of the 88 atherosclerotic artery
segments. All 19 had circular lumens. Eccentric plaques were found in
78% (69 artery segments from 52 of the 61 patients); 57% (39
segments) of these arterial segments with an eccentric
plaque exhibited circular lumens, and 43% (30 segments) had an oval
lumen shape (Fig 2
).
Average dimensions in the three shape categories described by plaque
formation and lumen shape are given in Table 2
. Because clear delineation of the EEL
requires visualization of
300° of the total arterial
circumference, the most stenotic atherosclerotic segments could
not be classified; this was due to acoustic shadowing and/or thinning
of the EEL. As a consequence, the mean area stenosis studied
ranged from 51.1±7.7% to 56.7±10.7% (Table 2
). EEL area, lumen
area, arterial wall area, and degree of area
stenosis based on the plaque and lumen shape analyses
of the atherosclerotic segments are illustrated in Fig 3
. Mean lumen diameter ratios were almost
identical in segments with concentric atherosclerosis
(lumen diameter ratio, 1.0±0.05) and arterial segments
with eccentric plaque and a circular lumen (lumen diameter ratio,
1.0±0.03), whereas consistent with the definition, the group
with an oval lumen had an altered lumen diameter ratio (0.8±0.08;
P values <.001) compared with the other groups.
Arterial segments with an eccentric plaque and a circular
lumen were further characterized by an oval artery compared with the
group with concentric atherosclerosis (artery diameter
ratio, 1.2±0.09 versus 1.0±0.04; P<.001) and the
arterial segments with an oval lumen (vessel ratio,
1.0±0.06; P<.001). The wall thickness ratio did not differ
between segments with eccentric plaques regardless of whether the lumen
was circular (mean wall thickness ratios, 2.7±1.02 and 2.8±1.15,
respectively). As expected, both groups differed from those with
segments with concentric plaques (ratio, 1.2±0.23;
P<.001). The coronary arterial segments
with an oval lumen also had a higher proportion of fibrocalcific
plaques (19 of 30) than did segments with concentric
atherosclerosis (2 of 19) and segments with eccentric
plaques and circular lumen (5 of 39) (P.001).
|
|
In 25 patients, more than one atherosclerosis-lumen
pattern was seen in the examined coronary artery. Eight
patients with concentric atherosclerosis also had a
segment in the imaged artery with eccentric
atherosclerosis and a circular lumen. Fifteen patients
exhibited eccentric plaques with segments with both circular and oval
lumens, and 2 patients had the three different patterns of
atherosclerosis lumen shape in the same
coronary artery (Fig 4
).
|
The proportion of left anterior descending, left circumflex, and right
coronary arteries did not differ among different plaque-lumen
combinations. The different groups were not distinguished by
differences in age, gender, localization of the segment in the
respective artery, relative localization of the segment to the maximum
stenosis in the artery, or maximum area stenosis in the
imaged artery (Table 1
).
The mean EEL diameter ratio in controls was 1.0±0.35; hence, EEL
diameter ratios between 0.9 and 1.1 were considered to define circular
arteries. The mean geometric form index was 1.0±0.02 for lumen and
1.0±0.02 for the EEL. Accordingly, form indexes of <0.95 defined an
oval lumen, and indexes of <0.95 defined an oval artery. The
respective criteria for eccentricity or concentricity of plaque and
symmetry of lumen and arterial circumference within the
external elastic lamina were subsequently applied for each
atherosclerotic arterial segment. The frequency
distributions of the resulting plaque-lumen-artery patterns are
presented in Fig 5
. These data
demonstrate that with the use of IVUS-derived diameter ratios to
describe shape, (1) 40% (n=35) had an eccentric plaque with a circular
lumen and an oval arterial circumference within the EEL,
(2) 30% (n=26) had an eccentric plaque with an oval lumen and a
circular EEL, (3) 19% (n=17) had a concentric plaque with a circular
lumen and a circular EEL, (4) 4.5% (n=4) had an eccentric plaque with
a circular lumen and EEL, (5) 4.5% (n=4) had an eccentric plaque with
an oval lumen and a circular EEL, and (6) 2% (n=2) had a concentric
plaque with a circular lumen and EEL. There were no segments with
concentric plaque with an oval lumen and a circular or oval EEL. With
application of the geometric form index criteria for shape, the
patterns found were restricted to the first four patterns: eccentric
plaque/circular lumen/oval EEL in 33% (n=29), eccentric plaque/oval
lumen/circular EEL in 33% (n=29), concentric plaque/circular
lumen/circular EEL in 22% (n=19), and eccentric plaque/oval lumen/oval
EEL in 12% (n=11).
|
| Discussion |
|---|
|
|
|---|
Description and Classification
In vivo, vessel segments with eccentric
atherosclerosis, selected according to our criteria, in
a majority of cases demonstrated a crescent-shaped plaque on the
cross-sectional images with a gradual thinning toward the normal
portion of the artery. There were no plaques bulging into the lumen.
Our findings are in accordance with histopathological findings when
methods using physiological pressure distention
during fixation of the artery are used.3
We developed a descriptive classification system defining the cross section of the artery in terms of concentricity or eccentricity of the atherosclerotic plaque, symmetry of the lumen, and symmetry of the arterial outer circumference of the EEL. Such a three-level classification system that theoretically describes eight classes of arteries has not been previously proposed. The definitions of lumen and EEL asymmetry were based on the assumption that normal arteries are circular. The definition of plaque eccentricity was designed to allow detection of local arterial wall remodeling in response to atherosclerotic plaque formation. This IVUS-based classification was found to be a simple tool to determine whether effective remodeling mechanisms were operative in the arterial wall. The vast majority of arterial segments with concentric plaques had circular lumens and circular EELs. Eccentric plaques were usually associated with either a circular lumen in combination with an oval EEL or with an oval lumen in combination with a circular artery. These three patterns accounted for 89% of all arterial segments. A circular lumen was preserved in 66% of atherosclerotic artery segments. Describing the cross section of the atherosclerotic artery on three levels may contribute to the understanding of the evolving distinctions between atherosclerotic burden and lumen stenosis derived from IVUS data. Our approach provides a simple method to distinguish among lumen changes, adaptive responses in the artery wall, and alterations in the plaque itself, which may prove to be fruitful in longitudinal studies on progression or regression of atherosclerosis. This system may also help investigators evaluate the results of an intervention in a given segment to identify atherosclerotic patterns optimal for a given intervention. The potential use of our system to improve the description of the atherosclerotic artery and its dynamic changes should therefore be considered by investigators in this field. For example, an analysis of the localized remodeling according to our model may help predict the acute recoil after balloon angioplasty as well as the predilection of an arterial segment for restenosis.
Highly Localized Remodeling of the Coronary Artery
Focusing on eccentric wall thickening (considered to reflect
eccentric plaque deposition) allowed an analysis of
compensatory mechanisms in a portion of the artery wall. We observed
preservation of a circular lumen in 57% of these arterial
segments. The maintenance of a circular lumen shape was
associated with an increase of the artery diameter along the line
through the maximum thickness of the eccentric plaque and the center of
the lumen. Notably, luminal area was significantly larger in
arterial segments with a preserved circular lumen despite a
strong overall correlation between EEL area and artery wall area. Also,
this group with a circular lumen had a slightly larger mean EEL area.
Consequently, the calculated area stenosis was less pronounced
in arterial segments with circular lumens than in
arterial segments with concentric
atherosclerosis as well as segments with eccentric
plaques and an oval lumen. The arterial segments were
otherwise comparable between groups. Our observations suggest that very
precise mechanisms capable of maintaining a virtually circular lumen
are operant in the majority of coronary artery segments with
eccentric atherosclerotic plaque deposition.
In contrast to the arterial segments with a circular lumen, an oval lumen was strongly associated with a round artery, suggesting inadequate remodeling. The failure to expand the artery wall at sites of these eccentric lesions may thus be an important determinant for development of plaques causing stenoses. In this instance, a given degree of atherosclerosis will result in a more narrowed lumen compared with an artery segment showing local expansion of the affected portion of the artery wall.
Factors Influencing the IVUS Assessment of Atherosclerosis
From histopathological descriptions of
atherosclerosis, it is known that the plaques usually
have irregular morphologies within the artery that involve varying
proportions of the circumference along the artery.2
Consequently, the cross-sectional description of the plaque is
dependent on the sampling site. However, in our study, there was no
systematic influence of sampling site, but the described highly
localized remodeling occurs in any location of any of the epicardial
coronary arteries.
There is no generally accepted definition of eccentric
atherosclerosis or plaque formation based on IVUS data,
and proportions of eccentric plaque in studied coronary
arteries are dependent on the definitions.13 In
pathological studies, distinctions have been drawn between lesions that
are "eccentric" (ie, associated with an arc of normal
arterial wall within the lesion) and those that are
"concentric" (ie, the atherosclerosis completely
encircles the coronary artery).14 Our definition
of eccentric plaques was designed to facilitate detection of local
compensatory mechanisms in the artery wall. The presence of a normal
arc of arterial wall was not necessary, but the bulk of the
atherosclerosis had to be contained within one
hemisphere of the artery. In our study, the wall thickness ratio was
set at
1.5 to include mild and moderate
atherosclerosis in which the postulated compensatory
mechanisms are expected to be fully operative.4 Moreover,
the strict imaging criteria for inclusion requiring clear delineation
of the EEL for
300° of the 360° of the arterial
circumference resulted in our evaluating early and intermediate stages
of atheroma formation.
Every classification is dependent on its definitions and methods. In our study, the higher proportion of a circular shape of the arterial circumference within the EEL with the form index compared with the IVUS-based diameter ratio probably reflects the fact that the perpendicular artery diameter used in the IVUS-based diameter ratio often does not represent the largest diameter of the artery in this direction. There is a possibility that an oblique imaging plane may have influenced our results. This problem has been minimized by (1) ensuring fluoroscopically that the imaging catheter was coaxial to the artery during the pull-back procedure and (2) using measurement ratios for our definitions of eccentric or concentric plaques that consequently are not influenced by the imaging plane. The diameter ratios for the lumen and EEL are equally influenced by the imaging plane. This ensures that a measured difference represents a true difference in shape between lumen and EEL circumferences. (3) We defined normality from the same patient cohort and with the same imaging and measurement procedure.
Study Limitations
The major limitation of our study relates to the potential
limitation associated with IVUS technology; imaging of the most severe
stenosis is limited by two factors: (1) the IVUS catheter is
3.5F and thus may not cross severe stenoses, and (2)
determination of the entire EEL at the site of the most severe
stenosis was not possible due to acoustic shadowing from plaque
calcification and/or disruption of the EEL. Thus, our findings are
currently applicable to mild and moderately severe atherosclerotic
stenoses.
Potential Mechanisms
The same individual may express compensatory remodeling or
lack of remodeling in different portions of the same
coronary artery (Fig 4
), as indicated by the 25 patients who
expressed more than one pattern of plaque-lumen interaction in the same
coronary artery. This particular finding favors the concept of
localized determinants for regional adaptation in an atherosclerotic
artery, such as responses to localized alterations in wall stress or
degradation of underlying media and adventitia, rather than systemic
factors.15 The outward bulging of the plaque and
underlying wall in a majority of our segments with an eccentric plaque
may be related to the focal nature of the destruction or degradation of
the media underlying the plaque as well as the mechanical effect of
intraarterial distention pressure at the site of a thinned
or absent (weakened) arterial media. This observation is in
agreement with previous pathological observations.2 16
Lack of localized compensatory enlargement was associated with a higher
proportion of fibrocalcific plaques. This observation may mirror a less
compliant plaque, which reduces a possible, generalized passive
pressuremediated wall expansion. This interpretation is compatible
with the concept of McPherson et al.17 However, if
calcification is a factor influencing the efficiency of artery wall
remodeling, it is likely to be only one of several possible mechanisms
for modulation of localized compensatory enlargement, as indicated by
the 11 noncalcified atherosclerotic segments presenting without
localized enlargement. In their study on 100 human and 328 monkey
arteries, Clarkson et al5 failed to detect any
interference by the degree of calcification on arterial
remodeling. In the portion of their study concerning human arteries,
eccentricity of the plaque did not influence medial status. An
endothelium-mediated flow-velocityrelated enlargement
of the uninvolved segment of the artery has been proposed as an
alternative explanation.4 A prominent role for locally
mediated endothelial effects has also been
advocated.15 Nevertheless, the exact mechanisms for
compensatory dilatation remain unknown, and tentative explanations are
purely speculative.
In conclusion, our IVUS-based classification system provides information regarding highly localized remodeling responses to plaque formation in vivo in human coronary arteries. A circular lumen was maintained in the majority of cases. Arterial segments with a failure of this mechanism to be operant may be prone to develop stenotic lesions. These data in themselves may have implications for ongoing follow-up and evaluation of the growth and development of atherosclerosis and their effect on vascular flow and reactivity.
| Acknowledgments |
|---|
Received February 25, 1997; revision received April 8, 1997; accepted April 13, 1997.
| References |
|---|
|
|
|---|
2. Glagov S, Zarins CK. Quantitating atherosclerosis: problems of definition. In: Bond MG, Insull W Jr, Glakov S, Chandeler AB, Cornhill JF, eds. Clinical Diagnosis of Atherosclerosis: Quantitative Methods of Evaluation. New York, NY: Springer-Verlag; 1983:11-35.
3. Thomas AC, Davies MJ. Post-mortem investigation and quantification of coronary artery disease. Histopathology. 1985;9:959-976.[Medline] [Order article via Infotrieve]
4. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:1371-1375.[Abstract]
5.
Clarkson TB, Prichard RW, Morgan MT, Petrick GS, Klein
KP. Remodeling of coronary arteries in human and
nonhuman primates. JAMA. 1994;271:289-294.
6. Nishioka T, Luo H, Eigler NL, Berglund H, Kim C-J, Siegel RJ. Contribution of inadequate compensatory enlargement to the development of human coronary artery stenosis-an in vivo intravascular ultrasound study. J Am Coll Cardiol. 1996;27:1571-1576.[Abstract]
7. Yamagishi M, Nissen SE, Booth DC, Gurley JC, Koyama J, Kawano S, DeMaria AN. Coronary reactivity to nitroglycerin: intravascular ultrasound evidence for the importance of plaque distribution. J Am Coll Cardiol. 1995;25:224-230.[Abstract]
8.
Tobis JM, Mallery J, Mahon D, Lehman 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 analyses of tissue characterizations with
comparison to in vitro histological specimens.
Circulation. 1991;83:913-926.
9.
Nissen SE, Gurley JC, Grines CL, Booth DC, McClure R,
Berk M, Fischer C, DeMaria AN. Intravascular ultrasound
assessment of lumen size and wall morphology in normal subjects and
patients with coronary artery disease.
Circulation. 1991;84:1087-1099.
10. Coy KM, Maurer G, Siegel RJ. Intravascular ultrasound imaging: a current perspective. J Am Coll Cardiol. 1991;18:1811-1823.[Abstract]
11. Chae J-S, Brisken AF, Maurer G, Siegel RJ. Geometric accuracy of intravascular imaging. J Am Soc Echocardiogr. 1992;5:577-587.[Medline] [Order article via Infotrieve]
12. Porter TR, Radio SJ, Anderson JA, Michels A, Xie F. Composition of coronary atherosclerotic plaque in intima and media affects intravascular ultrasound measurements of intimal thickness. J Am Coll Cardiol. 1994;23:1079-1084.[Abstract]
13.
Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF,
Chuang YC, DeFalco RA, Leon MB. 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;93:924-931.
14. Roberts WC. Coronary heart disease: a review of abnormalities observed in the coronary arteries. Cardiovasc Med. 1977;2:29-49.
15.
Gibbons GH, Dzau VJ. The emerging concept of
vascular remodeling. N Engl J Med. 1994;330:1431-1438.
16. Crawford T, Levine CI. Medial thinning in atheroma. J Pathol. 1953;66:19-23.
17. 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]
This article has been cited by other articles:
![]() |
R Krishna Kumar and K R Balakrishnan Influence of lumen shape and vessel geometry on plaque stresses: possible role in the increased vulnerability of a remodelled vessel and the "shoulder" of a plaque Heart, November 1, 2005; 91(11): 1459 - 1465. [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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |