(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.
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Abstract |
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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
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Introduction |
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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.
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Methods |
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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.
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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.
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Results |
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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.
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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.
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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).
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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).
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Discussion |
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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.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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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.
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