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(Circulation. 1997;96:468-474.)
© 1997 American Heart Association, Inc.
Articles |
Late Regression of the Dilated Site After Coronary Angioplasty
A 5-Year Quantitative Angiographic Study
From Green Lane Hospital, Epsom, Auckland, New Zealand.
Correspondence to Dr John Ormiston, Cardiac Investigation Rooms, Green Lane Hospital, Epsom, Auckland 1003, New Zealand.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background Limited data are available on the changes that occur at the dilated site late after coronary angioplasty. The aim of this study was to evaluate with quantitative angiography the natural history of changes that occur in the dilated segment between "early" (
6 months) and "late" (5 years) follow-up
after angioplasty.
Methods and Results Of 127 consecutive patients (174
lesions) with successful angioplasty, 125 underwent early angiography.
Three patients subsequently died, and 24 underwent
revascularization surgery or repeated angioplasty,
giving a study-eligible population of 98 patients. Quantitative
angiographic analysis was performed before and immediately
after angioplasty and at early and late follow-up in the study
population of 84 patients (115 lesions), which was 86% of
study-eligible patients. Mean lesion diameter stenosis
decreased from 36.3±14.2% at early to 29.6±13.5% at late follow-up
(P<.0001). No lesion developed late restenosis by
the 50% diameter loss criterion. Late regression was related to
stenosis severity at early angiography (r=-.58,
P<.001). Subgroups at early angiography of 40% to 49%
stenosis and 
50% stenosis showed significant
regression at late angiography.
Conclusions Lesion regression at the dilated site is common late after angioplasty. The more severe a stenosis is at early angiography, the more likely the chance that there will be late regression. A strategy of watchful waiting may be appropriate for patients with restenotic lesions of borderline severity.
Key Words: restenosis • angioplasty • atherosclerosis • prognosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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We have observed that lesion regression occurs at the dilated site in some patients late after coronary angioplasty. Experimental studies in a number of species report that the myointimal thickening response to injury reaches a maximum within a few months and then, in the absence of further injury, regresses.1 2 3 4
Although it is well known from clinical and angiographic studies5 6 7 8 9 10 11 12 13 14 that restenosis is uncommon beyond 6 months after angioplasty, there is little quantitative angiographic information on the natural history of the restenotic process in the treated segment beyond this time. Late angiographic studies have been limited by small numbers of subjects, visual assessment of stenosis severity, low repeated angiography rates, or exclusion of those restenotic lesions managed conservatively.5 7 9 10 12 15 16
The purpose of this observational study was to determine, with a high
angiographic follow-up rate in a large cohort of consecutive
angioplasty patients who have not had subsequent
revascularization, the changes that occur at the
dilated site between "early" (6 months) and "late" (5
years) follow-up after intervention. This study sheds light on the
restenotic process and may help guide clinical management.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Population
During the initial experience of coronary angioplasty at Green Lane Hospital (December 1981 through July 1986), early angiography at
6 months after the procedure was performed as routine
clinical practice. To determine the long-term results after
angioplasty, a prospective follow-up protocol was devised that included
repeated angiography 5 years after angioplasty. Patients with a
successful angioplasty to de novo native vessel lesions who had
undergone early angiography and who were free from death or target
vessel revascularization by either angioplasty or
bypass graft surgery were eligible. Of the study-eligible patients,
those with both early and late angiography constituted the study
population (Table 1
). Patients with restenosis
treated conservatively were eligible for late follow-up. The study
protocol was approved by our institutional ethics committee, and all
patients gave written informed consent.
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Angioplasty Procedure
Angioplasty was performed through the femoral route. In the
early patients, 9F guide catheters and fixed-wire angioplasty balloons
were used; subsequently, 8F guide catheters and over-the-wire balloons
were used. Heparin 10 000 IU was routinely administered at the start
of the procedure, with an additional 5000 IU each procedural hour
thereafter. Procedural success was defined as <50% residual
coronary diameter stenosis as measured by ruler from a
Tagarno-magnified angiographic image and freedom from myocardial
infarction, surgical revascularization, or death
during the admission for angioplasty.
Coronary Angiography
Four coronary angiograms were recorded before and
immediately after angioplasty, at early follow-up, and at late
follow-up. Sublingual nitroglycerin was administered
before each follow-up angiogram but was not routine during the
angioplasty procedure. Orthogonal projections best demonstrating
the stenosed segment in the center of the frame and free of
foreshortening and superimposed radiopaque structures were identified
before angioplasty and repeated at follow-up angiography. Care was
taken to reproduce at follow-up angiography for each projection the
field size, rotation, angulation, image-intensifier height, and table
height. After angioplasty and at each follow-up angiogram, a 1-cm
calibration grid was filmed at the isocenter for each prospectively
chosen projection at each image-intensifier height. Calibration
with a well-defined structure at the radiographic isocenter
has a slightly higher accuracy and precision for computerized
quantitative angiography than calibration with the angiographic
catheter.17 18
Quantitative Angiographic Analysis
Quantitative coronary angiographic measurements were
made with the Cardiovascular Measurement System
(CMS-MEDIS Medical Imaging Systems).19 The 1-cm grid was
used in most cases for calibration, although in some patients a
nontapering portion of an angiographic catheter was used. The same
method of calibration (either grid or catheter) was used for the four
angiograms of each patient.
The maximum percent diameter stenosis, lesion minimum
luminal diameter, and corresponding automatically determined reference
diameter were computed (Fig 1). One technician formally
trained in the use of the CMS system analyzed the four
angiograms of each individual patient in one session to avoid
time-related changes. Analysis of cineframes in end
diastole, free of superimposed structures and
foreshortening, was performed blinded to the order of follow-up
cineangiograms.
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To determine changes that occur between early and late angiography in nondilated lesions and to estimate the possible effect of regression to the mean on the late regression of dilated lesions, a cohort of nondilated lesions from nontarget arteries of similar angiographic severity (at early angiography) was measured at both early and late time points.
Intraobserver Variability
To test intraobserver variability, the technician remeasured the
same images of stenosed segments in each of the four
cineangiograms of 19 randomly selected patients 2 months
later. From these data, mean signed differences between the repeated
measurements (accuracy) and the SDs of these differences (precision)
were calculated.20
Statistical Analysis
Repeated measures ANOVA was used to establish any significant
differences over time in percent diameter stenosis, lesion
minimum luminal diameter, and reference diameter in all lesions and in
the five subgroups on the basis of stenosis severity at early
angiography. Comparisons between specific groups were made with the
Bonferroni modification for multiple testing (SAS Statistics Package).
For other continuous variables, comparisons between times were
carried out by use of a paired t test with Bonferroni
modification. Categorical variables were compared by use of
Fisher's exact t test.
To determine the likely magnitude of regression to the mean as a mechanism of the apparent regression of the more severe early lesions, the mean, SD, and correlation coefficient of measurements from a cohort of 107 nondilated lesions in 39 patients were compared at early and late angiography.21
Continuous variables were expressed as mean±SD. Changes in individual lesion minimum luminal diameter were considered significant if the difference was greater than twice the group SD of repeated measurements (calculated from the intraobserver study).
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Of 127 consecutive patients with successful angioplasty of 174 de novo native vessel lesions, 125 patients had early angiography at a mean of 7.0 months (range, 1 to 13 months). There were 27 patients ineligible for late angiography because of repeated angioplasty to the same vessel (n=20), revascularization surgery (n=4), or death (n=3). The remaining 98 patients were study eligible. The study population was that cohort of 84 study-eligible patients who had early and late angiography (Table 1
). Late angiography was
performed at a mean of 4.5 years (range, 1.5 to 7.8 years) after
angioplasty. Of the 14 study-eligible patients who did not have late
angiography, 8 patients refused late angiography, all of whom were free
of angina, and 6 were lost to follow-up. This represents an
86% late angiography rate in study-eligible patients (Table 1).
Table 2 compares the baseline clinical and angiographic
characteristics of the study population of 84 patients who had both
early and late angiography with those of the 14 patients who had early
but not late angiography. There were no significant differences noted
between the two groups. Table 3 summarizes the clinical
characteristics at baseline and follow-up of the 84 study patients. The
reduction in serum cholesterol from baseline to late
follow-up was significant (P<.01).
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The mean minimum luminal diameter increased from 1.85±0.54 mm at
early to 2.10±0.62 mm at late follow-up (P<.0001).
There was a decrease in mean diameter stenosis from
36.3±14.2% at early to 29.6±13.5% (P<.0001) at late
follow-up (Table 4). The reference diameter did not
change significantly between early and late angiography.
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The diameter stenosis of the study group at early angiography (36.3±14.2%) was significantly less than that of the 24 patients who had repeated percutaneous intervention or who had revascularization surgery (67.0±21.5%, P<.001). Of the 20 patients who had repeated angioplasty, the median time from early angiography to repeated intervention was 11 days (range, 0 to 47 days). The 4 patients who had revascularization surgery were placed on the waiting list for the procedure at the time of angiography. The median delay of 127 days (range, 74 to 289 days) before surgery is common in our public hospital system.
The intraobserver study demonstrated that the accuracy for both minimum
luminal diameter and reference diameter was 0.01 mm. The precision
for both was 0.17 mm. For percent diameter stenosis,
accuracy was -0.53% and precision was 7.28%. Twice the SD of
repeated measurements in the intraobserver study was 0.34 mm. Of
the 115 lesions that had early and late angiography, 47 lesions showed
regression of 0.34 mm, and 11 lesions had progression of
0.34 mm. No lesion of <50% diameter stenosis at early
follow-up became >50% narrowed at late follow-up. In other words, no
lesion developed late restenosis by the 50% diameter loss
definition. One lesion of 57% diameter loss at early angiography
progressed to complete occlusion at late angiography.
The change in stenosis severity between early and late
angiography correlated with the stenosis severity at early
angiography (r=-.58, P<.001). Lesions were
divided into five groups according to stenosis severity at
early angiography (Fig 2). In the patient subset with
lesions of 0% to 19% severity at early angiography, there was a
nonsignificant increase in stenosis severity by late follow-up.
In those with 20% to 29% and 30% to 39% stenosis early,
some lesions increased and some decreased in severity, but overall
there was no significant change in stenosis severity. The
remaining two groups (stenosis severity of 40% to 49% and
50% at early angiography) showed a significant reduction in
stenosis severity by late angiography, with the more severe
lesions showing the greatest regression (Fig 2).
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The subset of 107 nondilated lesions in 39 patients from the study
population of 84 patients was compared with the 115 dilated lesions of
the 84 study patients (Table 5). Between early and late
angiography, the nondilated lesions progressed from stenosis
severity of 35.5±11.3% to 39.1±15.9%, whereas the dilated lesions
regressed from 36.3±14.2% to 29.6±13.5%. The calculated regression
to the mean of 4.5% from the nondilated lesion data was only a third
of the observed regression of 12.5% in the study population in those
patients with early stenosis severity of 40%. For dilated
lesions of stenosis severity of <30% at early angiography,
there was an observed small decrease in stenosis severity of
0.6%, whereas from the regression to the mean calculations, a 4.8%
increase in late severity was estimated.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates that lesion regression at the dilated site is a frequent occurrence between early and late after coronary angioplasty. This contrasts with the overall slow progression observed in nondilated lesions. The likelihood of lesion regression was influenced by early lesion severity. All but one of the lesions of
50% diameter loss showed regression, and most of those of 40% to
49% severity also regressed. This is the only study to follow a large
cohort of consecutive patients with a full range of lesion severity.
Other strengths of the study include the use of a well-validated
quantitative angiography system, the high rate of angiographic
follow-up (86%), and the long interval between angiographic
studies.
Time Course of Luminal Enlargement
Late lesion regression in our study occurred between a mean of 7
months and 4.5 years after angioplasty. Smaller studies that did not
use quantitative angiography have shown lesion regression between 6
months and 3 years7 and between 1 and 2
years.16 Changes during the first 12 months after
angioplasty have been rigorously evaluated in a definitive
study5 with serial quantitative angiography at 1, 3, 6,
and 12 months. That study showed that most of the reduction in vessel
lumen (restenosis) occurred between 1 and 3 months after
angioplasty and that there was no change in mean minimum luminal
diameter from 6 to 12 months.
The time course of changes after stent implantation appears similar. In
a serial quantitative angiographic study22 of patients 6
months, 1 year, and 3 years after Palmaz-Schatz stent implantation,
significant luminal narrowing occurred at the stented site between the
procedure and the 6-month angiogram. There was no change in mean
minimum luminal diameter between 6 months and 1 year, and late luminal
enlargement occurred between 1 and 3 years after stent deployment. Late
lesion regression has also been demonstrated between 6 and 27 months
after Gianturco-Roubin stent implantation.23
When these data are taken together, there appears to be a continuum of changes occurring after both coronary angioplasty and coronary stent deployment with three distinct phases. Phase 1, which occurs in the first 6 months, is characterized by a reduction in vessel minimum luminal diameter (restenosis). Phase 2, from 6 to 12 months, is characterized by little change in minimum luminal diameter (although individual lesions may show some progression or regression). Phase 3, beyond 12 months, is characterized by enlargement of vessel minimum luminal diameter (lesion regression).
Mechanisms of Restenosis and Late Regression
Late lesion regression may be a reversal of the restenotic
process that occurs early after angioplasty. The mechanism of
restenosis, which occurs in 30% to 40% of lesions to
50% diameter loss after angioplasty,5 24 25 26 27 is complex
and multifactorial. Some elastic recoil occurs early after the
procedure.28 Neointimal thickening is a major
contributor to restenosis.29 30 31 32 33 34 Balloon injury
into the atherosclerotic plaque or arterial media initiates
a healing process that results in the appearance of smooth muscle cells
in the intima, neointimal proliferation of these smooth
muscle cells, and production of extracellular
matrix.29 30 31 32 33 34 Contributing to vessel renarrowing is also a
less-understood process called remodeling or vessel
shrinkage.35 36 37 38 39 40 41 Experimental, pathological, and
intracoronary ultrasound studies show that this constriction or
shrinkage of the arterial wall plays a greater role in
restenosis than has previously been
appreciated.35 36 37 38 39 40 41
In animals, the myointimal thickening in response to balloon injury
reaches a maximum before 6 months and then regresses.1 2 3 4
After intracoronary metallic stent implantation in dogs, the
neointima reaches a maximum thickness at 8 weeks and
then becomes progressively thinner over a period of 6 to 9
months.42 Pathological studies in humans dying at various
time intervals after angioplasty found that
histological evidence of neointimal
proliferation decreases with time and was difficult to find in those
dying more than 2 years after angioplasty.33
The observation of late lesion regression in Palmaz-Schatz and Gianturco-Roubin stents in humans21 22 and in Palmaz-Schatz stents in dogs42 provides some insight into possible mechanisms of regression after angioplasty. Stents prevent elastic recoil and vessel remodeling but are a more potent stimulus for intimal hyperplasia than angioplasty. Lesion regression in stents must be due to regression of this hyperplasia. This mechanism is likely to account for at least part of the late regression that occurs after angioplasty. Whether further remodeling plays a role in late lesion regression is unknown, but if it is a major contributor to restenosis, it is likely to contribute to late regression.
It is interesting that increasing lesion severity is a stimulus for both early lumen loss (restenosis) and late lumen gain. This raises the possibility that the response to the associated increased shear may be quite different in the presence or absence of recent vascular injury. Although increased shear early after percutaneous transluminal coronary angioplasty augments platelet-thrombus deposition and the release of mitogens such as platelet-derived growth factor,43 once re-endothelialization has occurred and smooth muscle and other cells are quiescent, increased shear may promote compensatory enlargement of the more normal segments of the vessel wall.36 37 Whether such changes represent a later phase of vessel remodeling is unclear. Long-term studies using intravascular ultrasound are needed to further elucidate the mechanisms involved.
The late luminal enlargement in this study is unlikely to be due to differences in vasomotor tone, because nitroglycerin was administered before angiography at both early and late follow-up. It is also unlikely that lowering of serum cholesterol was responsible for late regression. The 5% reduction in mean total serum cholesterol between baseline and late follow-up was small and the 14% increase in luminal diameter between early and late follow-up was large compared with lipid-lowering trials. For instance, in a study of patients with coronary disease treated with colestipol and niacin,44 there was a 32% reduction in LDL and a 43% increase in HDL cholesterol but an increase in the mean minimal diameter of nine proximal segments of only 0.035 mm, or 1.8% between baseline and 2 1/2-year follow-up.
Study Limitations
A limitation of this study is that 14 of the 98 study-eligible
patients did not have late angiography, leading to a potential bias. A
concern might be that these patients may be more prone to clinical
events or lesion progression and therefore lost to follow-up. However,
clinical characteristics at baseline and angiographic findings at
baseline and early follow-up in these 14 patients did not differ
significantly from those of the 84 study patients (Table 2). All 8 of
the 14 patients with clinical follow-up were free of angina. It is
unlikely that disease progression would be greater in these patients,
because patients with progression would be more likely to present
with recurrent symptoms.
Another possible source of bias is exclusion of patients who had repeated angioplasty or revascularization surgery after the early angiogram. However, this patient group had severe restenosis at the time of early angiography, and a decision regarding revascularization was made at the time of early angiography.
While this would not influence the overall finding of lesion
regression, the greater regression observed in the more severe lesions
might be a manifestation of regression to the mean. To determine the
likely magnitude of this effect, a cohort of nondilated lesions was
compared at early and late angiography. Because some change in these
lesions would be expected (and was observed), determination of the
expected regression to the mean from this data set would be an
overestimation of the true effect. Despite this limitation, the
estimated regression to the mean accounted for only one third of the
observed lesion regression in those lesions of 40% at early
angiography.
For an occasional patient, the technician analyzing cinefilms may not have been completely blinded to the order of early and late cinefilms because of possible deterioration of film quality with time.
Clinical Significance
These findings may aid management of the patient with lesions of
borderline hemodynamic significance 6 months after
angioplasty. Late regression of these lesions is frequent, and late
progression to >50% diameter loss did not occur in this study. This
is consistent with the favorable clinical outcome observed in
such patients, in whom cardiac events are uncommon.45 A
conservative management approach might be appropriate in those who are
asymptomatic or have mild angina. However, it remains
unknown whether lesion regression and symptom improvement would occur
in patients with more severe symptoms, because these patients were
excluded from the present study.
This study questions the appropriateness of angiography 6 months after intervention as an end point in trials of restenosis. Because of late lesion regression, a later time for angiography might be more appropriate, although less practical. Because restenosis rarely presents as myocardial infarction or death and because of late lesion regression, 6-month angiography should be for symptomatic patients and not carried out routinely in all patients.
Conclusions
Lesion regression at the angioplasty site occurs frequently late
after intervention. It is more likely to occur and be of greater
magnitude in more severe lesions. Lesion progression to >50% diameter
stenosis did not occur in this study. Regression probably
starts beyond 12 months after angioplasty and may be viewed as one
phase in a continuum of changes that occur at the dilated site.
Although the mechanism of regression is uncertain, the finding of
similar changes after stent deployment indicates that regression of
myointimal proliferation and extracellular matrix deposition are likely
to be at least part of the process. A conservative management approach
should be considered in patients with lesions of moderate severity 6
months after angioplasty.
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Acknowledgments |
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The authors are grateful to Peter Ruygrok for manuscript review.
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Footnotes |
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Dr Roche died September 11, 1993.
Presented in part at the 43rd Annual Scientific Meeting of the Cardiac Society of Australia and New Zealand, Canberra, Australia, August 6-9, 1995, and at the 45th Scientific Sessions of the American College of Cardiology, Orlando, Fla, March 24-28, 1996.
Received November 18, 1997; revision received February 3, 1997; accepted February 10, 1997.
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