(Circulation. 1997;96:475-483.)
© 1997 American Heart Association, Inc.
Articles |
Remodeling of Human Coronary Arteries Undergoing Coronary Angioplasty or Atherectomy
From the Department of Cardiology, Kokura Memorial Hospital, Kitakyushu, Japan (T.K., S.K., T.T., H.Y., Y.N., H.Y., N.H., H.N., M.N.), and the Intravascular Ultrasound Imaging Laboratory, Washington Hospital Center, Washington, DC (G.S.M., J.J.P, M.B.L).
Correspondence to Takeshi Kimura, MD, 1-1 Kifune-machi, Kokurakita-ku, Kitakyushu, 802, Japan.
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Abstract |
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Background Recently, long-term constriction of the vessel has been suggested as an alternative mechanism of restenosis after coronary angioplasty.
Methods and Results To understand remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy, serial intravascular ultrasonographic examinations were performed at preintervention and postintervention examinations and at 24 hours, 1 month, and 6 months. Complete serial data were obtained in 61 lesions (balloon angioplasty, 35 lesions; directional atherectomy, 26 lesions). Lumen area improved from 6.81±2.24 mm2 after intervention to 8.22±2.79 mm2 at 1 month (P=.0001) and decreased to 4.88±2.86 mm2 at 6 months (P=.0001). Vessel area enlarged from 17.32±5.35 mm2 after intervention to 19.39±5.33 mm2 at 1 month (P=.0001) and decreased to 16.33±5.54 mm2 at 6 months (P=.0001). Plaque+media area increased significantly from postintervention examination to 24 hours (10.51±4.38 versus 10.96±4.49 mm2, P=.0008) and from 24 hours to 6 months (10.96±4.49 versus 11.45±4.45 mm2, P=.03). Changes in lumen area in each study interval correlated more closely with changes in vessel area than with changes in plaque+media area. Restenotic lesions compared with nonrestenotic lesions had a greater decrease in the vessel area between 1 month and 6 months (-4.33±2.73 versus -2.49±2.15 mm2, P=.006) and greater increase in the plaque+media area both within 24 hours (0.84±1.22 versus 0.27±0.38 mm2, P=.04) and between 24 hours and 6 months (1.19±2.19 versus 0.18±1.46 mm2, P=.04).
Conclusions Remodeling after coronary angioplasty or atherectomy was characterized by early adaptive enlargement and late constriction of the vessel.
Key Words: remodeling • angioplasty • vessels
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Introduction |
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Restenosis remains a major limitation to coronary angioplasty.1 2 3 4 5 Studies in animals6 7 8 and necropsy studies in humans9 10 11 suggested that neointimal hyperplasia ensues in response to injury by angioplasty, resulting in restenosis when hyperplastic responses become excessive. Recently, studies in animals suggested that arterial remodeling might be a major contributing factor to the development of restenosis.12 13 14 Using serial intravascular ultrasonography, Mintz et al suggested that the predominant mechanism responsible for late lumen loss is remodeling rather than tissue growth.15 Mintz et al15 also reported that remodeling was bidirectional. In their study, 22% of the vessels enlarged from postintervention examination to 6-month follow-up. Therefore, remodeling could be defined as changes in total vessel area from postintervention examination to the follow-up time point.16 17 18 Constrictive remodeling could be defined as a decrease in total vessel area and adaptive remodeling as an increase in total vessel area. To understand remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy, we designed a study providing serial intravascular ultrasonographic and quantitative angiographic examination with predetermined time intervals after coronary intervention.
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Methods |
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Study Patients
From December 1993 through February 1995, 74 patients (79 lesions) undergoing coronary intervention at Kokura Memorial Hospital were screened for entry into the Serial Ultrasound REstenosis (SURE) study. During this time interval, 2151 patients underwent coronary intervention in 2984 lesions. The screening criteria used for the study was generally based on suitability for the intravascular ultrasonographic study. Focal lesions located in proximal segments of nontortuous coronary arteries were selected to ensure safety in performing repeated intravascular ultrasonography. Lesions without fluoroscopic calcification were preferred to make accurate ultrasonographic measurement of the vessel area. Primary lesions were preferentially enrolled. Therefore, this patient series did not represent the entire population treated during the same time interval. The study protocol consisted of quantitative angiographic and intravascular ultrasonographic examination before and after intervention and at 24 hours, 1 month, and 6 months after balloon angioplasty or directional atherectomy. All the patients gave informed consent for the procedure and the follow-up protocol, which were approved by the institutional review board. Among 74 patients (79 lesions), 8 patients (9 lesions) were excluded from the study because of technical failure of intravascular ultrasonography (in one lesion), need for stent implantation (in 5 lesions), and extensive calcification at the lesion site making ultrasonographic measurement unreliable (in 3 lesions). Sixty-six patients (70 lesions) were enrolled for the follow-up study. The 24-hour study was performed in all patients (19±4 hours after the procedure). Six patients refused the study at 1 month. In 3 other patients, the study at 6 months was not performed because of intercurrent target lesion revascularization (in 1 patient) and sudden death (in 2 patients). Therefore, complete serial study was performed in 57 patients with 61 lesions (87%). The intervals from intervention to 1- and 6-month studies were 37±8 and 181±32 days, respectively. There was no complication related to any intravascular ultrasonographic examination.
Angiographic Analysis
Quantitative angiographic analysis was performed with
the Cardiovascular Angiography Analysis System
II.19 Minimal luminal diameter, interpolated reference
diameter, and diameter stenosis were calculated by the
computer. The measurement was performed in two angiographic views and
the average values were calculated in each study.
Initial and follow-up studies were performed in the same angiographic
projections using the same cineangiographic machines.
Intracoronary injection of 5 mg of isosorbide dinitrate was
performed before each study. 8F guiding catheters free of contrast
medium were filmed at the center of the image and were used for
calibration. The diameter of the catheter tip used in each study was
measured by a caliper. Reproducibility of quantitative angiographic
analysis in our laboratory was detailed
elsewhere.20 Restenosis was defined as
stenosis of 
50% observed at 6-month follow-up.
Intravascular Ultrasonographic Analysis
The intravascular ultrasonographic imaging system used in this
study incorporated a single-element, 30-MHz beveled transducer within
either a 2.9F or a 3.2F imaging catheter
(Cardiovascular Imaging Systems Inc). In all studies
the transducer was withdrawn at 0.5 mm · s with the use of
a motorized pullback device. A complete ultrasonographic imaging run
was performed from beyond the target lesion to the aortoostial
junction. Studies were recorded on [1/2]-in high-resolution s-VHS
videoptape for off-line analysis.
Measurements of cross-sectional area by intravascular ultrasonography have been validated previously.21 With the use of computerized planimetry, the vessel area and lumen area were measured. The plaque+media area was calculated as vessel area minus lumen area. The vessel area was defined as the area within the border between the hypoechoic media and the echoreflective adventitia. When atherosclerotic tissue encompassed the ultrasound catheter, the lumen was assumed to be the same physical size as the catheter. To minimize the influence of vessel size, relative (vessel, lumen, and plaque+media) areas were calculated as (absolute areas-1 · vessel area at preintervention examination)x100. Quantitative measurements were performed independently at both Washington Hospital Center and Kokura Memorial Hospital. The anatomic slices selected for serial analysis of the lesion site had an axial location within the target lesion at the smallest lumen area at 6-month follow-up (in the Washington analysis) and at the smallest lumen area at preintervention study (in the Kokura analysis). Average values of the two centers were calculated and considered to represent the geometry of the lesion. The reference segment (selected from the preintervention study) was the most normal-looking cross section within 10 mm proximal to the lesion but distal to any major side branch.
Identification of the same anatomic slices throughout the serial studies was performed as follows. The anatomic slice with the smallest lumen was identified first; the distance from this slice to the closest axial landmark then was measured using seconds or frames of videotape. In general, the axial landmarks were within 10 mm of the image slice. Finally, this distance was used to identify the corresponding anatomic slices throughout the serial studies. Vascular and perivascular markings such as small side branches, venous structures, and calcific and fibrotic deposits were used to confirm proper identification of the image slices. The accuracy and reproducibility of intravascular ultrasound length measurements with the use of a motorized transducer pullback device were previously validated in human coronary arteries.22 The reproducibility of sequential intravascular ultrasonographic measurements was also previously validated.15
Statistical Analysis
Values are expressed as mean±SD. Paired numerical data obtained
by serial study were compared by the paired t test and other
continuous variables by the unpaired t test. Linear
regression analysis was used to assess the interobserver
variability of quantitative ultrasonographic measurements and
correlation among vessel area, lumen area, and plaque+media area. All
tests of significance were two tailed, and probability values of <.05
were considered to indicate statistical
significance.23
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Results |
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Patient and Lesion Characteristics
The baseline characteristics of the patients and the lesions that completed the serial study are shown in Table 1
. Calcification was
identified in 13% of lesions by angiography in contrast to 64% by
ultrasonography. However, extensive calcification with calcific arc of
180° was noted in only 12% of lesions. Furthermore, by an effort
to avoid calcification for cross-sectional measurements, only one
lesion had calcific arc of 180° in the analyzed cross
sections.
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In 35 lesions treated by balloon angioplasty, the mean balloon size was 3.19±0.29 mm for vessels 2.77±0.41 mm in diameter. In 26 lesions treated by directional atherectomy, adjunctive balloon angioplasty was performed in 12 lesions. In all lesions, a 7F device was used, resulting in retrieval of 16.3±8.3 mg of tissue.
Serial Angiographic Result
Minimal luminal diameter improved from 1.02±0.27 mm
before intervention to 2.16±0.43 mm after intervention
(P=.0001) and did not change at 24 hours (2.15±0.47
mm, P=.71 versus after intervention) (Table 2). Significant improvement of
minimal luminal diameter was noted between 24 hours and 1 month
(2.15±0.47 mm at 24 hours; 2.29±0.48 mm at 1 month;
P=.0008). A marked decrease of minimal luminal diameter was
observed between 1 and 6 months (2.29±0.48 mm at 1 month;
1.65±0.56 mm at 6 months; P=.0001). Minimal luminal
diameter measured by angiography and lumen area by ultrasonography
revealed a consistent time course (Fig 1). At 6 months,
restenosis was documented in 19 lesions (31.1%), with target
lesion revascularization in 15 lesions
(24.6%).
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) and lumen area by ultrasonography (
). Minimal
luminal diameter measured by angiography and lumen area by
ultrasonography revealed consistent time course up to 6 months.
Significant improvement of lumen was observed between 24 hours and 1
month and marked renarrowing between 1 month and 6 months.
P<.001 for comparison between the points linked by
brackets.
Serial Intravascular Ultrasonographic Result
Vessel area increased from 15.45±5.24 mm2
before intervention to 17.32±5.35 mm2 after
intervention (P=.0001) and plaque+media area decreased from
13.37±5.04 mm2 before intervention to
10.51±4.38 mm2 after intervention
(P=.0001) (Table 3). At 24 hours, both vessel
area (17.32±5.35 mm2 after intervention;
17.89±5.38 mm2 at 24 hours; P=.002) and
plaque+media area (10.51±4.38 mm2 after intervention;
10.96±4.49 mm2 at 24 hours; P=.0008)
increased significantly, with no change in lumen area (6.81±2.24
mm2 after intervention; 6.93±2.53 mm2 at
24 hours; P=.37). Between 24 hours and 1 month, vessel area
increased significantly (17.89±5.38 mm2 at 24 hours;
19.39±5.33 mm2 at 1 month; P=.0001).
Enlargement of the vessel resulted in significant improvement of lumen
area in this interval (6.93±2.53 mm2 at 24 hours;
8.22±2.79 mm2 at 1 month; P=.0001).
Between 1 and 6 months, vessel area decreased significantly
(19.39±5.33 mm2 at 1 month; 16.33±5.54
mm2 at 6 months; P=.0001). Constriction of
the vessel resulted in marked lumen loss in this interval
(8.22±2.79 mm2 at 1 month; 4.88±2.86
mm2 at 6 months; P=.0001). Plaque+media area
increased significantly from 24 hours to 6 months (10.96±4.49
mm2 at 24 hours; 11.45±4.45 mm2 at 6
months; P=.03). These observations were also true after
correction for vessel size (Table 3). A case showing typical biphasic
remodeling after directional coronary atherectomy is
illustrated in Fig 2.
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Serial changes in the lumen area closely paralleled changes in the
vessel area (Fig 3). Changes
in the lumen area in each interval correlated closely with changes in
the vessel area (Fig 4).
Changes in the lumen area did not correlate with changes in the
plaque+media area in the intervals between postintervention study and
24 hours (r=.07, P=.58) and between 24 hours and
1 month (r=.04, P=.76). Between 1 and 6 months, a
decrease in the lumen area correlated only weakly with an increase in
the plaque+media area (r=.26, P=.04).
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Reference segment measurements paralleled lesion site measurements
(Table 3
). Angiographic reference diameter also showed early
enlargement and late constriction (Table 2).
Quantitative analysis of intravascular ultrasonography,
independently performed at two centers, revealed excellent agreement
(Table 2). The differences in the measurements were 0.09±1.71
mm2 for the vessel area, 0.21±0.98 mm2
for the lumen area, and 0.13±1.73 mm2 for the
plaque+media area. Correlation coefficients were .95 for the vessel
area, .95 for the lumen area, and .93 for the plaque+media area. Most
importantly, the time course of the changes in the vessel, lumen, and
plaque+media area was consistent by both analyses.
Balloon Angioplasty Versus Directional Coronary
Atherectomy
Since significantly larger vessels were treated by directional
atherectomy, serial changes were analyzed by indexing to
relative vessel, lumen, and plaque+media area. Early increase and late
decrease of relative vessel area were similarly observed in both groups
(Table 4). Although we could
not find any differences in interval changes of relative vessel, lumen,
and plaque+media area between the two groups, our samples are obviously
underpowered to make this kind of subgroup analysis.
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Restenotic Lesions Versus Nonrestenotic Lesions
Increase in the vessel area at 1 month was similar between 19
lesions with restenosis and 42 lesions without
restenosis (Table 5).
However, decrease in the vessel area between 1 and 6 months was
significantly greater in the restenotic lesions
(-4.33±2.73 mm2 in the restenotic lesions;
-2.49±2.15 mm2 in the nonrestenotic lesions;
P=.006), resulting in greater lumen loss in this interval
(-5.04±1.72 mm2 in the restenotic lesions;
-2.57±2.23 mm2 in the nonrestenotic lesions;
P=.0001).
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Regarding the changes in the plaque+media area, greater increase was observed in the restenotic lesions within 24 hours (0.84±1.22 mm2 in the restenotic lesions; 0.27±0.38 mm2 in the nonrestenotic lesions; P=.04) and between 24 hours and 6 months (1.19±2.19 mm2 in the restenotic lesions; 0.18±1.46 mm2 in the nonrestenotic lesions; P=.04).
Net Changes During 6 Months of Follow-up
The lumen area decreased from 6.81±2.24 mm2
after intervention to 4.88±2.86 mm2 at 6 months.
Decrease in the vessel area (-0.99±2.58 mm2) and
increase in the plaque+media area (0.94±1.91 mm2)
almost equally contributed to late lumen loss. However, the change in
the lumen area correlated more strongly with the change in the vessel
area (r=.72, P=.0001) than with the change in the
plaque+media area (r=.34, P=.0008). The change in
the vessel area and change in the plaque+media area also were
significantly correlated (r=.42, P=.0008) (Fig 5).
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In 19 lesions (31.1%), there was a net increase in total vessel area from postintervention study to 6-month follow-up. Restenosis rate was not different between the two groups with or without vessel enlargement (26.3% versus 33.3%, P=.58). However, late lumen loss assessed by quantitative coronary angiography was significantly less in lesions with vessel enlargement (-0.29±0.63 versus -0.61±0.55 mm, P=.05).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Remodeling of human coronary arteries was originally described by Glagov et al.24 As a challenge to the traditional injury-proliferation hypothesis of restenosis, a concept called remodeling was proposed from various sources. In the hypercholesterolemic rabbit model, Kakuta et al13 reported that the degree of vessel enlargement is more important than intimal area in determining the long-term lumen size. Using similar animal models, Post et al12 and Lafont et al14 demonstrated that long-term constriction of the vessel did occur and that constrictive remodeling rather than neointimal-medial growth might dominate the response to angioplasty. However, in the atherosclerotic rabbit model, Gertz et al25 reported that constrictive remodeling is not the principal pathogenetic process in restenosis.
Using serial intravascular ultrasonography, Mintz et al15 suggested that the predominant mechanism responsible for late lumen loss is constrictive remodeling rather than tissue growth. Di Mario et al26 reported that constrictive remodeling was the main operative mechanism of lumen dimension after balloon angioplasty but not after directional atherectomy. In an analysis of 36 restenotic lesions, Braden et al27 concluded that the predominant mechanism of late lumen loss was an increase in plaque area rather than constrictive remodeling. We could not explain the reason why results from intravascular ultrasonographic studies were not consistent regarding the role of constrictive remodeling. However, considering the bidirectional nature of arterial remodeling, the small sample size in these two studies might be misleading.
In this study, remodeling after coronary angioplasty or atherectomy was characterized by early (within 24 hours, and 24 hours to 1 month) enlargement of the vessel and late (1 month to 6 months) constriction of the vessel. In addition, significant increase in the plaque+media area was observed both within 24 hours and from 24 hours to 6 months.
The early increase in plaque+media area could be explained by
thrombosis.28 Alternatively, if one of the mechanisms of
balloon angioplasty is axial redistribution of plaque,29
partial reversal of this phenomenon might explain early increase in
plaque+media area observed in a single-slice analysis. We
previously reported that a significant decrease in stenosis
diameter within 24 hours occurs in 
16% of patients.4
Also in the current study, we observed significant decrease in minimal
luminal diameter within 24 hours after balloon angioplasty but not
after directional atherectomy. Rodriguez et al30 reported
that coronary stenting decreased restenosis in lesions
with early lumen loss within 24 hours after coronary
angioplasty. Considering the efficacy of stents in preventing
restenosis in this group of patients, partial reversal of axial
plaque redistribution rather than thrombosis might be a major mechanism
of early increase in the plaque+media area. On the other hand, early
enlargement of the vessel observed at 24 hours could be partly
explained by release of vasospasm. Even after intracoronary
administration of nitrates, prolonged vasospasm could persist,
especially after use of bulky (eg, atherectomy) devices.
Further enlargement of the vessel at 1 month could be explained by the increase in the wall shear stress resulting from the augmented local flow after angioplasty.17 31 32 Release of the cicatrizing effects of the noncompliant plaque by angioplasty might increase coronary distensibility, allowing the vessel to distend in response to arterial pressure.33 This adaptive remodeling could also result from the response to early growth of neointimal tissue analogous to the original observation by Glagov et al.24 Adaptive remodeling explains why most patients are stable up to 1 or 2 months after coronary angioplasty even in the presence of extensive dissection and/or overtly suboptimal result.
The increase in the plaque+media area between 24 hours and 6 months, which would be an ultrasonographic index of intimal proliferation, was significantly greater in the restenotic lesions compared with the nonrestenotic lesions. Numerous reports of human necropsy studies demonstrating intimal hyperplasia as a mechanism of restenosis could not be dismissed easily.9 10 11 However, this study demonstrated that late constriction of the vessel is an additional important mechanism of restenosis. Between 1 and 6 months, when luminal renarrowing was most prevalent, constriction of the vessel contributed to lumen loss much more than the increase in plaque+media area. This late constriction of the vessel was significantly more prominent in restenotic lesions compared with nonrestenotic lesions.
Several mechanisms could be proposed to explain constriction of the vessel. This study clearly demonstrated that constriction of the vessel is a late event, that it follows early enlargement of the vessel, and therefore is distinct from early passive elastic recoil. Adventitial fibrosis could play an important role in constricting the vessel. Andersen et al34 reported impressive neoadventitial formation 3 weeks after angioplasty in a porcine coronary model. Scar contracture of the plaque could be another important mechanism of late constriction of the vessel. O'Brien et al35 demonstrated that transforming growth factor-ß, which is known to be a key mediator of tissue fibrois,36 was overexpressed in the fibrous connective tissue of restenotic coronary lesions. In this and other studies15 using serial intravascular ultrasonography, extreme decrease in the vessel area was often associated with a decrease in the plaque+media area, suggesting the presence of plaque retraction and/or apoptosis.37
In this study, remodeling of the reference segment was demonstrated to parallel the response of the lesion site. The reference segment was selected within 10 mm of the center of the lesion and therefore was inevitably influenced by the injury of interventional procedures. Results from this and a previous angiographic study4 as well as an animal study34 were consistent with the idea that remodeling has some axial length. Actually, we did measure two different sites at two different centers because we were not sure which anatomic slices should be measured; by measuring two different slices and averaging them, we were able to obtain a sense of overall lesion geometry.
This study has several important limitations. Accurate identification of the same anatomic cross section on serial studies is still a challenge for current methods of analysis of intravascular ultrasonography. Second, the number of restenotic lesions were relatively small. However, prospective enrollment of patients and a high rate of follow-up afforded enough statistical power to evaluate time course of arterial remodeling.
This study demonstrated that mechanisms of late lumen loss after coronary angioplasty were heterogeneous, with variable contribution of each mechanism depending on the time after the procedure. Intracoronary stents could reduce the rate of restenosis38 39 by eliminating early increase in the plaque+media area and late constriction of the vessel as well as by obtaining a larger lumen immediately after the procedure. However, this is at the expense of early compensatory enlargement and more prominent intimal hyperplasia. Future strategies to reduce restenosis should target prevention of late constrictive remodeling and enhancement of adaptive remodeling as well as suppression of intimal hyperplasia.
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Acknowledgments |
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We appreciate the efforts of the catheterization laboratory staff, collection of data by Yasue Tashima, and secretarial help of Tamami Shimizu.
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Footnotes |
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Reprint requests to Dr M. Nobuyoshi, Kokura Memorial Hospital, 1-1 Kifunemachi Kokura Kita-ku, Kitakyushu, 802, Japan.
Received November 18, 1996; revision received February 5, 1997; accepted February 11, 1997.
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