(Circulation. 1995;91:1410-1418.)
© 1995 American Heart Association, Inc.
Articles |
Restenosis After Delayed Coronary Angioplasty of the Culprit Vessel in Patients With a Recent Myocardial Infarction Treated by Thrombolysis
From the Service de Cardiologie B et Hémodynamique, Hôpital Cardiologique, Lille Cedex, France.
Correspondence to M.E. Bertrand, MD, Service de Cardiologie B, Hôpital Cardiologique, Boulevard du Professeur J Leclercq, 59037 Lille Cedex, France.
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Abstract |
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Background Clinical follow-up after percutaneous transluminal coronary angioplasty (PTCA) of an infarct-related lesion has demonstrated a low incidence of recurrent symptoms and repeated revascularization. In the absence of systematic angiographic follow-up, this low rate of clinical restenosis may reflect either a truly lower incidence of anatomic restenosis or the lack of recurrent symptoms in patients with extensive infarction in the territory of the restenotic vessel.
Methods and Results We studied 300 consecutive patients who,
after a thrombolysis for myocardial infarction, underwent delayed
(10.5±6 days after the myocardial infarction) PTCA of the
infarct-related lesion. Procedural success was obtained in 253 patients
(84%), and angiographic follow-up was performed in 205 of this group
(81%) at a mean of 7.3±1.9 months. Restenosis (defined as the
recurrence of >50% stenosis) was present in 105 patients (51%).
Only 34 of the 105 patients (32%) with angiographic restenosis were
symptomatic; the other 68% had clinically silent restenosis. Of these
105 patients, 27 (13% of the total population undergoing follow-up
angiography) had reocclusion at the dilated site at follow-up. The
severity of the stenosis at follow-up and the late loss in minimal
lumen diameter followed a nearly Gaussian distribution if the lesions
that were totally occluded at follow-up were excluded. By multivariate
analysis, two independent predictors of reocclusion were
identified: a small reference diameter (P<.0005) and the
presence of collateral vessels before the procedure
(P<.01). Only one factor was associated with restenosis in
the 178 patients who did not have reocclusion at follow-up: a
Thrombolysis in Myocardial Infarction grade 
2 before the procedure
(P<.0001). At follow-up, there was a significantly
(P<.01) higher ejection fraction in patients without
restenosis (56.1±13.4%) and in patients with restenosis without total
occlusion (56.0±13.8%) than in patients with reocclusion
(46.4±13.0%).
Conclusions Despite a satisfactory clinical outcome, delayed PTCA of an infarct-related lesion is associated with a high rate of angiographic recurrence. Two distinct mechanisms account for recurrent stenosis: progressive luminal renarrowing as documented after angioplasty of stable lesions and reocclusion of the infarct-related lesion. Only reocclusion is associated with a deterioration in left ventricular function at follow-up.
Key Words: angioplasty • vessels • circulation
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Introduction |
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Percutaneous transluminal coronary angioplasty (PTCA) is a widely used technique for revascularization in patients after a thrombolysis for myocardial infarction.1 2 3 4 The experience of coronary angioplasty performed within the Thrombolysis in Myocardial Infarction (TIMI) II study has been recently described1 ; in the overall TIMI PTCA population, the cumulative incidence of repeated revascularization (20%)1 was lower than that reported for elective PTCA patients (32%).5 In the absence of systematic angiographic follow-up, this low rate of repeated revascularization may be related either to a truly lower incidence of anatomic restenosis or to the lack of recurrent symptoms in patients with extensive infarction in the territory of the restenotic vessel. The relatively low number of studies that addressed the problem of angiographic restenosis after PTCA performed for acute myocardial infarction have provided discordant results.6 7
No study has specifically examined with quantitative angiography the angiographic rate of restenosis when an angioplasty is performed in the infarct-related vessel after a thrombolysis for myocardial infarction. We studied the procedural outcome and the angiographic rate of restenosis, assessed by quantitative coronary angiography, in 300 consecutive patients who underwent such a procedure in our institution, where we recommend angiographic follow-up to all patients who undergo successful coronary angioplasty. We also examined whether changes in left ventricular function between PTCA and follow-up were influenced by the status of the dilated vessel at follow-up angiography.
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Methods |
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Patients
From the records of our catheterization laboratory, we identified 300 consecutive patients, 264 men and 36 women with a mean (±SD) age of 57 (±10) years, who, between January 1989 and December 1991, underwent delayed PTCA at the infarct-related lesion after a thrombolysis for myocardial infarction (Table 1
). The
infarct-related
artery was determined from the entry ECG, ventriculographic contraction
abnormalities, and coronary angiographic findings. During the time
period of this study, the strategy for patients undergoing coronary
angiography after a thrombolysis for myocardial infarction in our
institution was to perform immediate angioplasty of the infarct-related
vessel, provided that the diameter stenosis was >50% and that the
overall anatomy of the coronary vessels did not preclude angioplasty,
eg, left main disease and lesions judged nonamenable for angioplasty at
the discretion of the operator. Patients having PTCA within 3 days of
the myocardial infarction or having multilesion PTCA were excluded.
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Angioplasty Procedure
Angioplasty was performed according to
the standard technique in
our laboratory as previously described.8 All patients
received aspirin (300 mg/d); a bolus dose of heparin (10 000 IU) was
administered just before PTCA. The procedure was considered successful
when the residual luminal narrowing in the dilated segment immediately
after angioplasty was <50% and when no major complication (ECG or
enzymatic evidence of myocardial infarction, the need for bypass
surgery during hospitalization, or in-hospital death) occurred.
Angiography was performed in at least two projections, after the
intracoronary injection of isosorbide dinitrate (2 mg) and just before
and immediately after angioplasty. These projections were recorded in
our database, and the follow-up angiogram was performed after the
intracoronary injection of isosorbide dinitrate in the same
projections.
Six-Month Follow-up
We routinely attempt to obtain a
follow-up angiogram 6 months
after successful angioplasty, regardless of symptomatic status;
angiography is performed earlier if there is a clinical indication.
Restenosis was defined by quantitative coronary angiography as the
recurrence of 
50% luminal narrowing in a segment that had previously
been dilated to <50%. Clinical data were recorded for all patients at
the time of hospitalization for angiographic follow-up; the clinical
status of the patients who did not undergo the scheduled
hospitalization was obtained by contact with the referring
cardiologist.
Qualitative Angiographic Analyses
Two experienced
interventional cardiologists performed the
qualitative analyses independently. Disagreements were resolved by a
further joint reading. Lesions were classified as concentric (symmetric
narrowing with an identical or almost identical appearance in
orthogonal projections) or eccentric (asymmetric narrowing with the
stenotic lumen appearing to lie within the outer half of the
"normal" lumen of the vessel in at least one projection). The
presence of calcification or thrombus (a discrete intraluminal filling
defect) was also noted. The anterograde blood flow before angioplasty
was graded with the TIMI Study Group classification.9 The
collateral circulation was graded with the classification proposed by
Sabia et al.10
Quantitative Coronary Angiography
Quantitative
computer-assisted angiographic measurements of the
dilated lesion were performed on angiograms obtained just before
angioplasty, immediately after angioplasty, and at a 6-month follow-up.
Measurements were performed on end-diastolic frames with
the CAESAR (Computer Assisted Evaluation of Stenosis And
Restenosis) System. A detailed description of this system and the
inter- and intraobserver variations of measurements obtained under
routine clinical conditions were reported
previously.11
Quantitative Evaluation of Global Left Ventricular Function
Ventricular function was evaluated on single-plane left
ventricular angiograms obtained before angioplasty and at follow-up.
The ventriculogram was performed in a 30° right anterior oblique
projection. The left ventricular contours on end-systolic and
end-diastolic frames were traced manually by a single
observer who was unaware of the design of the study protocol. The
tracings were then digitized with a writing tablet and light pen into a
PC 486/25 SX microcomputer. The left ventricular
end-diastolic volume index (LVEDVI, mL/m2) and
the ejection fraction (EF, %) were calculated according to the
area-length method.12
Statistical Analysis
Data are presented as mean±SD.
Comparisons between groups
for continuous data were made with an unpaired Student's t
test or ANOVA followed by the Student-Newman-Keuls test. Differences
between proportions were assessed by 
2
analysis. Linear regression was used to analyze the relation
between continuous variables. Multivariate correlates of reocclusion
and restenosis were determined by stepwise logistic regression
(SAS Software). A value of P<.05 was
considered to indicate statistical significance.
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Results |
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Baseline Characteristics
Table 1
lists the
baseline characteristics of the
study population. Most of the patients were men with a mean age (±SD)
of 57±10 years. The majority had single-vessel disease with a mean
left ventricular EF of 52.6±12.3%. The dilated lesion was located
with almost equal frequency in the left anterior descending artery
(42%) and the right coronary artery (43%) and less often in the left
circumflex artery (14%). Twenty-two percent of the lesions had TIMI
grade 2 flow before angioplasty; angiographically visible collateral
vessels were observed in 21% of cases.
Immediate Outcome
Procedural success was obtained in 253
patients (Table 2). There were 11 major in-hospital
complications: 5
patients had recurrent myocardial infarction, 3 had emergent coronary
bypass surgery, and 3 died during hospitalization. Uncomplicated
failure (residual stenosis 50% by quantitative coronary angiography)
occurred in 36 patients. More detailed analysis of these 36
patients with uncomplicated failure revealed that 12 (33%) had total
occlusion before angioplasty and that 16 (44%) had a residual stenosis
after angioplasty of <60% by quantitative coronary angiography.
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Six-Month Follow-up
All patients who had successful
procedures were asked to return
for angiographic follow-up at 6 months; 205 (81%) actually underwent
angiography at a mean of 7.3±1.9 months after angioplasty. Clinical
follow-up data were obtained for 47 of the 48 remaining patients; one
patient was lost to follow-up. Table 3 shows that except
for a significantly higher proportion of patients dilated at a right
coronary artery lesion in the 48 patients without angiographic
follow-up, there were no differences in major baseline characteristics
between the two groups of patients.
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Of the 252 patients, 7 (2.8%) died during the follow-up period, 3 (1.2%) had bypass surgery, and 3 (1.2%) had recurrent myocardial infarction. At 6 months, 188 (74.6%) were asymptomatic or had atypical chest pain, 51 (20.2%) had stable angina, and 6 (2.4%) had unstable angina.
Table 4 summarizes the quantitative angiographic
data of
the 205 patients with angiographic follow-up. The angioplasty procedure
was associated with an immediate increase in mean minimal lumen
diameter from 0.82±0.43 to 1.98±0.43 mm. Mean percent diameter
stenosis decreased from 72±13% to 32±10%. At follow-up
angiography,
the mean minimal lumen diameter had decreased to 1.34±0.77 mm, and
mean percent stenosis had increased to 55±25%. Restenosis, defined as
the presence of 50% stenosis in the dilated segment at follow-up,
was present in 105 (51%; 95% CI; range, 44% to 58%) of the 205
patients who underwent angiographic follow-up. Of these 105 patients,
27 (13% of the total population undergoing follow-up angiography; 95%
CI; range, 8% to 18%) had total occlusion at the dilated site at
follow-up.
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Fig 1 shows the distribution of the severity
of the
stenotic lesions at follow-up. If the lesions that were totally
occluded at follow-up are excluded, both minimal lumen diameter and
percent stenosis follow a nearly Gaussian distribution. When the
distribution of the late loss in minimal lumen diameter from
immediately after angioplasty to follow-up was analyzed (Fig
2), a similar pattern was observed.
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We also analyzed the
relation between clinical status at 6 months and
the occurrence of restenosis in the 205 patients who underwent
angiographic follow-up (Table 5). The majority of
patients undergoing follow-up angiography were asymptomatic (148,
72%); 57 (28%) were symptomatic (48 had stable angina, 6 had unstable
angina, and 3 had suffered recurrent myocardial infarction before the
follow-up angiogram). The percentage of patients with 50% diameter
stenosis at follow-up was 48% in asymptomatic patients and 60% in
symptomatic patients (P=NS). The percentage of patients with
total occlusion at follow-up was also similar in asymptomatic and
symptomatic patients. Only 34 (32%) of the 105 patients with
angiographic restenosis were symptomatic; the other 68% had clinically
silent restenosis.
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Predictors of Reocclusion and Restenosis
We analyzed
predictors of reocclusion and of restenosis in the 205
patients with angiographic follow-up.
Table 6 shows the
univariate predictors of reocclusion.
The severity of the stenosis before PTCA (percent stenosis and minimal
lumen diameter), the minimal lumen diameter after PTCA, the presence of
angiographically visible collateral vessels before PTCA, a TIMI grade
of 2 before angioplasty, and a smaller reference diameter were all
associated with a greater risk of reocclusion by univariate
analysis. By multivariate analysis, two independent predictors
of reocclusion were identified: a small reference diameter
(P<.005) and the presence of collateral vessels before the
procedure (P<.01).
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Table 7 lists the
univariate predictors of restenosis in
the 178 patients without reocclusion at follow-up. Percent stenosis
before PTCA, the presence of collateral vessels before PTCA, and a TIMI
grade of 2 before PTCA were associated with a greater risk of
restenosis by univariate analysis. By multivariate analysis,
only one factor was associated with restenosis in patients without
total occlusion at follow-up: a TIMI grade of 2
(P<.0001).
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Table 8 shows the occurrence of
restenosis and
reocclusion as a function of the TIMI grade before PTCA. Lesions that
had TIMI grade 2 flow before angioplasty had a higher risk of
reocclusion and restenosis compared with lesions that had TIMI grade 3
flow before angioplasty. Although the number of patients in the groups
with TIMI grades of 0 and 1 was too small to draw definite conclusions,
restenosis and reocclusion rates were similar among the groups with
TIMI grades of 0, 1, and 2.
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Changes in Left Ventricular Function
Among the 205 patients
with angiographic follow-up, 197 (96%) had
paired ventriculograms (before PTCA and at follow-up) that were
suitable for determination of left ventricular function (Table
9). In the group as a whole, there was a small but
statistically significant (P<.01) increase in EF from
52.7±12.1% before PTCA to 54.7±13.8% at follow-up. The LVEDVI at
follow-up (86.2±22.3 mL/m2) was similar to the LVEDVI
before PTCA (86.6±21.9 mL/m2, P=NS). If
patients were classified into subgroups based on the angiographic
findings at the dilated site at follow-up (no restenosis,
restenosis without reocclusion, reocclusion), there were no
significant differences in EF or LVEDVI among subgroups before PTCA.
During the follow-up period, however, there was an increase in EF in
both the subgroup that had not developed restenosis (+2.5±10.4
absolute percent) and the subgroup with a restenosed but nonoccluded
vessel (+3.4±10.3 absolute percent). In contrast, in the subgroup
that
had reocclusion of the dilated vessel at follow-up, there was a
decrease in EF (-3.3±10.4 absolute percent). These changes
resulted
in a significantly (P<.01) higher EF in both the
no-restenosis group (56.1± 13.4%) and the
restenosis-without-reocclusion group (56.0±13.8%) compared with the
reocclusion group (46.4±13.0%). The LVEDVI at follow-up was similar
in all groups.
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We further assessed a possible relation between the
severity of the
stenosis at follow-up and the changes in EF from angioplasty to
follow-up in the 170 patients who had a nonoccluded vessel at follow-up
regardless of whether restenosis had occurred (Fig 3).
There was no relation between percent stenosis severity or absolute
minimal lumen diameter at follow-up assessed by quantitative
angiography and the change in EF between angioplasty and
follow-up.
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Discussion |
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Procedural Outcome
The overall results of the PTCA procedure were favorable, with 84% procedural success (ie, residual stenosis <50% by quantitative coronary angiography without in-hospital complication). With a different definition (normal or improved TIMI flow grade with both improvement of the residual stenosis by >20% and a residual stenosis <60%), the angiographic success for the 1414 patients of the TIMI II study who underwent PTCA of the infarct-related vessel within 42 days of a thrombolysis for myocardial infarction was 80.5%.1 The 1% rate of emergent bypass surgery, the 1.7% rate of myocardial infarction, and the 1% mortality rate in the present study are also concordant with those in prior studies.1 This may be explained in part by the timing of the procedure (10.5±6 days after the myocardial infarction) because it has been demonstrated that patients undergoing delayed PTCA in the TIMI II study had a higher rate of procedural success and a lower risk of acute complication than patients undergoing immediate PTCA.1
Reocclusion and Restenosis Rates
Although a large number of
reports have analyzed restenosis rates
after elective coronary angioplasty, only a few studies have
specifically examined restenosis after PTCA for acute myocardial
infarction, and those provided discordant results. Honan et
al7 reported the angiographic follow-up of 144 patients
from a total population of 289 who had successful PTCA within 24 hours
of acute myocardial infarction. With restenosis determined visually by
use of a grading scale, 40% of patients had 75% stenosis at
follow-up. Conversely, Simonton et al6 reported on the
angiographic follow-up of 79 patients from a total population of 91 who
had successful PTCA after acute myocardial infarction. Only 19% of
these patients had restenosis defined visually by the recurrence of a
>50% stenosis at follow-up. Differences in patient selection, rates
of angiographic follow-up, and techniques used to assess the follow-up
angiogram may account for this disparity between studies. In our
institution, we recommend angiographic follow-up to all patients who
have successfully undergone PTCA. The rate of follow-up angiography
(81%) in the consecutive patient population reported here is similar
to our overall angiographic follow-up for elective
PTCA.8 13 Independent observers analyzed the
follow-up
angiograms with quantitative coronary angiography. Thus, the results
reflect, with reasonable accuracy, the angiographic probability of
restenosis in our patient population.
We observed a rate of restenosis
(defined as the recurrence of a 50%
stenosis at follow-up) of 51%. This rate is relatively high compared
with the 39% to 43% of restenosis encountered during the same time
period in our institution after elective
PTCA.8 13 14 This
rate is also higher than the 28% to 40% of restenosis in recent large
clinical trials that examined the effect of various treatments on
restenosis15 16 and higher than the rate of
restenosis
after balloon angioplasty in another recent study that compared
restenosis rates after balloon angioplasty with those after atherectomy
using the same angiographic definition of restenosis as the present
study.17 This rate, however, is similar to that observed
after balloon angioplasty in the CAVEAT study18 ; this may
be explained by the high prevalence of patients with unstable angina in
the CAVEAT population. The overall loss in minimal lumen diameter from
after angioplasty to follow-up (late loss) in the present study was
0.64 mm; this value is higher than the 0.27 to 0.50 mm reported in
different studies in which most of the patients underwent elective
PTCA.15 17 19
Overall, these
results suggest that infarct-related lesions have a
greater tendency to recur after successful PTCA. However, more detailed
analysis of our results suggests that two distinct mechanisms
contribute to lesion recurrence after successful PTCA of
infarct-related lesions. As Table 4 and Fig 1
show, a relatively high
proportion of the patients with restenosis had total occlusion of the
dilated vessel at follow-up. Rensing et al19 suggested
that in a population undergoing elective coronary angioplasty, although
the overall restenotic process followed a nearly Gaussian distribution,
the progression toward total occlusion at follow-up may be, at least in
part, due to a mechanism other than progressive luminal renarrowing,
which appears to be responsible for restenosis without total occlusion.
The low number of patients with total occlusion at follow-up in the
study of Rensing et al (70 of 1445, 4.8%) compared with the 13%
reported in the present study may reflect the different clinical
characteristics of the study population and suggests that
infarct-related lesions may have a greater propensity to occlusion
after angioplasty. In the present study, 27 of 105 patients (26%)
with 50% stenosis at follow-up had a total occlusion. As Figs
1 and 2 show, the severity of the stenosis at
follow-up and the late loss in
minimal lumen diameter follow a nearly Gaussian distribution only if
the lesions that had progressed toward total occlusion are excluded.
Our results therefore suggest that two different and important
mechanisms might be involved in lesion recurrence after PTCA of
infarct-related lesions: progressive luminal renarrowing, as documented
after angioplasty of stable lesions, and reocclusion. It is not clear
if reocclusion is related to thrombosis that occurs as a final step
after progressive renarrowing has produced a severe stenosis or if
silent thrombotic occlusion occurs early after successful angioplasty;
however, the high incidence of total occlusion in this series compared
with elective angioplasty supports the second hypothesis. Some insights
into the natural history of the infarct-related lesion during the
months after a thrombolysis for infarction have been provided by the
results of the APRICOT study20 ; in this study, 300
patients with a patent coronary artery within 48 hours of a
thrombolysis for infarction were randomized to either warfarin,
aspirin, or placebo and had angiographic follow-up 3 months after the
procedure. The 29% overall rate of reocclusion was not significantly
different among the three groups. This very high rate of spontaneous
reocclusion in the months after infarction is consistent with the
existence of another mechanism of restenosis (ie, thrombosis and
occlusion) after angioplasty of infarct-related lesions distinct from
the progressive renarrowing that follows coronary angioplasty of stable
lesions.
Predictors of Reocclusion and Restenosis
Because of the
suspicion that two distinct mechanisms accounted
for lumen renarrowing after PTCA of the infarct-related vessel, we
performed a two-step analysis to determine first the predictors of
reocclusion and second the predictors of restenosis in the patients who
had restenosis without occlusion. The severity of the pre-PTCA
stenosis, the presence of angiographically visible collateral vessels
before the procedure, a low TIMI grade before PTCA, and a small
reference diameter were associated with an increased risk of
reocclusion by univariate analysis. On multivariate analysis, a
small reference diameter and the presence of collateral vessels were
found to be independent predictors of reocclusion.
When analyzing the
determinants of restenosis in patients without total
occlusion at follow-up, we found that a TIMI grade flow of 2 before
angioplasty was the only independent predictor. It had already been
suggested that the rate of restenosis after angioplasty of total
occlusions was higher than that of nonoccluded vessels21 ;
our data extend this observation to the patient population undergoing
delayed angioplasty of an infarct-related vessel after a thrombolysis
for infarction and demonstrate that this high rate of restenosis is
related not only to an increase in the rate of reocclusion at follow-up
but also to an increase in the rate of restenosis without total
occlusion. Our data also demonstrate that the rate of reocclusion and
restenosis of TIMI grade 2 lesions is comparable to that of TIMI grade
0 and 1 lesions and clearly different from that of TIMI grade 3 lesions
(Table 8). Finally, the reference diameter of the vessel
appears
unrelated to the occurrence of restenosis when patients with
reocclusion are excluded. Because this factor was the strongest
predictor of reocclusion, this observation provides further evidence
for the existence of two different mechanisms to explain luminal
narrowing after PTCA of infarct-related vessels.
Changes in Left Ventricular Function
Several studies have
investigated whether delayed PTCA has a
beneficial impact on recovery in left ventricular function after a
myocardial infarction and have provided discordant
results.22 23 In the present study, we found a
statistically significant improvement in left ventricular EF as a whole
from 52.7% before PTCA to 54.7% at follow-up. The nonrandomized
nature of our study does not allow us to attribute this improvement to
the performance of PTCA; furthermore, the clinical significance of the
relatively small benefit observed cannot be determined.
We observed an improvement in EF in patients with or without angiographic restenosis, providing that the dilated vessel was still patent at follow-up; in contrast, in the subgroup of patients with a total occlusion of the dilated vessel at follow-up, there was a decrease in EF. These results are in agreement with the APRICOT study,20 which showed that in patients with a patent coronary artery 48 hours after a thrombolysis for myocardial infarction and randomized to different antithrombotic regimens, there was a significant increase in EF in patients with persistent patency at 3 months but no recovery in patients with reocclusion. These results emphasize the importance of a patent infarct-related vessel 3 to 6 months after the infarction regardless of the chosen therapeutic option.
In a series of 67 patients treated by emergency primary
angioplasty for
acute myocardial infarction, Rothbaum et al24 reported
that restenosis in the absence of reocclusion did not have an adverse
effect on the recovery of global left ventricular function. Conversely,
Linderer et al25 studied 145 consecutive patients who had
successful PTCA of the infarct-related vessel 5±6 months after
infarction and found that only patients without restenosis had an
improvement in left ventricular function at angiographic follow-up.
Differences in patient selection and in time from infarction to PTCA
may account for these discrepancies. In the current study, the subgroup
of 170 patients who had a patent vessel at follow-up had a significant
improvement in EF that was independent of the degree of stenosis at the
PTCA site at follow-up (Fig 3).
We found no relation between vessel patency and LVEDVI at follow-up. In a recent study,26 the patency of the infarct-related vessel after a thrombolysis for myocardial infarction was shown to influence left ventricular remodeling; patients with a total occlusion of the infarct-related vessel had a significantly higher LVEDVI at follow-up than patients with a patent vessel. Among the multiple factors that may explain the lack of left ventricular dilation in the 27 patients with reocclusion in the current study are the late timing of reocclusion (between 10 days and 6 months after the infarction), the well-preserved EF at baseline (50%), and the relatively low number of patients (n=14) with an anterior myocardial infarction.
Study Limitations
This was a retrospective single-center
study; thus, the technique
of PTCA and medical management at our institution might have influenced
the results. However, the patients were a consecutive group that
underwent the angioplasty procedure in an institution where the
probability that a patient undergoes follow-up angiography is less
dependent on the symptomatic status after angioplasty. The high rate of
angiographic follow-up, coupled with the use of quantitative coronary
angiography to assess the angiographic outcome, allowed an objective
assessment of the angiographic probability of restenosis. In addition,
our study included only patients who underwent delayed angioplasty of
an infarct-related lesion (3 days); it has been reported that
emergency coronary angioplasty may represent an interesting
alternative to intravenous thrombolysis in patients with acute
infarction27 ; reocclusion and restenosis rates after PTCA
in this acute setting and without thrombolysis may not necessarily be
similar to those observed after a delayed procedure. However, a recent
report of the Primary Angioplasty Registry28 demonstrates
that there is also a high incidence of reocclusion and restenosis when
emergency PTCA is performed without prior thrombolytic therapy.
Clinical Implications
This study demonstrates that despite a
satisfactory clinical
outcome, coronary angioplasty of infarct-related lesions is associated
with a high incidence of angiographic recurrence that is often silent.
Of the patients with a successful angioplasty in this study, 13% had
total occlusion of the dilated lesion at follow-up; this rate, which
appears extremely high compared with the angiographic outcome of
patients undergoing angioplasty of stable lesions, does compare
favorably with the very high spontaneous rate of reocclusion of the
infarct-related lesion observed in the months after
infarction.20 However, the negative impact of reocclusion
on left ventricular function at follow-up emphasizes the need for new
strategies designed to prevent reocclusion in this setting; whether
these strategies should be pharmacological (antithrombotic agents) or
mechanical (coronary stenting) remains to be determined.
Received June 2, 1994; revision received September 14, 1994; accepted October 2, 1994.
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TopAbstractIntroductionMethods Results Discussion References |
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