| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1995;91:1397-1402.)
© 1995 American Heart Association, Inc.
Articles |
Coronary Stenting Decreases Restenosis in Lesions With Early Loss in Luminal Diameter 24 Hours After Successful PTCA
From the Cardiac Unit, Anchorena Hospital, Buenos Aires, Argentina (A.E.R., O.S., M.L., M.F., R.S., N.P.B.); the Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston (J.B.N., I.F.P.); and the Cardiac Unit, University of Alabama, Birmingham (G.S.R.).
Correspondence to Igor F. Palacios, MD, Director of Interventional Cardiology, Cardiac Unit, Massachusetts General Hospital, Boston, MA 02114.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background Early loss of minimal luminal diameter (MLD) after successful percutaneous transluminal coronary angioplasty (PTCA) is associated with a higher incidence of late restenosis.
Methods and Results Sixty-six patients (66 lesions) with >0.3
mm
MLD loss at 24-hour on-line quantitative coronary angiography were
randomized into two groups: 1, Gianturco-Roubin stent (n=33) and 2,
Control, who received medical therapy only (n=33). All lesions were
suitable for stenting. Baseline demographic, clinical, and angiographic
characteristics were similar in the two groups. Restenosis (
50%
stenosis) for the overall group occurred in 32 of 66 patients (48.4%)
at 3.6±1-month follow-up angiography. Restenosis was significantly
greater in group 2 than in group 1 (75.7% versus 21.2%,
P<.001). Vascular complications (21.2% versus 0%) and
length of hospital stay (7.3±1 versus 2.4±0.5 days,
P<.01) were higher for the stent group. Although at
follow-up there were no differences in mortality or incidence of acute
myocardial infarction between the two groups, patients in the control
group had a higher incidence of repeat revascularization procedures
(73% versus 21%, P<.001).
Conclusions In patients with successful PTCA but reduced luminal diameter demonstrated by repeat angiography at 24 hours, the Gianturco-Roubin stent appears to reduce angiographic restenosis at follow-up.
Key Words: stents • stenosis • angioplasty
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Coronary restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) remains the main limitation of this technique. Its incidence of 30% to 50% has been unchanged by the use of different mechanical or pharmacological modalities.1 2 3 4 5 6 Although fibrointimal hyperplasia is important in restenosis,7 8 other factors such as early elastic arterial wall recoil may play a significant role. Elastic recoil has been shown to reduce the cross-sectional area of the dilated segment early after successful PTCA.9 10 11 12 13 14 We recently reported that a subgroup of patients at higher risk of developing restenosis after successful PTCA can be identified by angiography 24 hours after PTCA.11 Restenosis is significantly greater in lesions exhibiting >0.3-mm loss in minimal luminal diameter (MLD) and/or >10% increase in diameter stenosis at 24-hour angiography after successful PTCA. Coronary stenting has been demonstrated to alleviate the effects of elastic recoil after PTCA.9 10 11 Therefore, the present study was undertaken to determine whether coronary stenting would change the incidence of restenosis in this high-risk group with early loss in MLD after successful PTCA.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patient Population
From a total of 511 patients undergoing PTCA at the Anchorena Hospital (Buenos Aires) between November 1991 and April 1993, we identified 69 consecutive patients (of 191 patients who underwent repeat coronary arteriography 24 hours after PTCA) who met the criteria of "early loss" (>0.3-mm loss in MLD and/or >10% increase in diameter stenosis at angiography performed 24 hours after successful PTCA) and therefore were potential candidates for randomization in this study. Three of these later patients refused to be randomized. The other 66 patients composed the study group. No patients had symptoms of early angina preceding the 24-hour angiogram consistent with "pseudostenosis."
Randomization Protocol
After completion of angiography 24
hours after PTCA, these 66
patients were double-blind randomized into two groups: Group 1 patients
received a Gianturco-Roubin intracoronary stent (n=33), and group 2
received medical therapy (n=33).
Patients were eligible for the study and randomization if they fulfilled the following criteria: (1) successful PTCA of a de novo lesion; (2) evidence at 24-hour post-PTCA angiography of >0.3-mm loss in MLD and/or >10% increase in diameter stenosis (early loss); (3) lesions appropriate for coronary stenting (reference diameter >2.5 mm); (4) no contraindication for coronary stenting; and (5) signed written informed consent approved by the Human Study Committee of the Anchorena Hospital. The primary end point of the study was to compare the incidence of angiographic restenosis at follow-up angiography between patients treated with intracoronary stents (group 1) and those treated with medical therapy alone (group 2). Restenosis rate was determined by the binary restenosis classification (based on a 50% diameter stenosis criterion). In addition, a comparison of in-hospital major complications (death, acute myocardial infarction, and emergency coronary artery bypass graft surgery [CABG]), local vascular complications requiring blood transfusion or surgical repair, and incidence of major ischemic events at 6-month follow-up (death, acute myocardial infarction, and repeat revascularization procedure) was also undertaken. The study was monitored by a Safety and Data Monitoring Committee.
Coronary Angioplasty
All patients received aspirin,
dipyridamole, and a calcium
channel blocker starting at least 24 hours before PTCA. After arterial
access, systemic anticoagulation was achieved by administration of a
bolus dose of 10 000 IU heparin IV. In addition, patients received a
continuous infusion of intravenous nitroglycerin and heparin during
PTCA. Coronary angioplasty was performed by standard
techniques.15 The ratio of dilating balloon to reference
diameter used during PTCA was not greater than 1.1. Final angiographic
outcome after PTCA was obtained by single-view angiographic projection
of the dilated vessel recorded immediately after the last balloon
inflation. The immediate post-PTCA measurements were made within the
first 5 minutes after PTCA. Specifically, after the last balloon
inflation, the balloon and guide wire were removed, intracoronary
nitroglycerin was administered, and the final angiogram to assess the
results of the PTCA was performed (no later than 5 minutes after the
last balloon inflation). A successful outcome from PTCA was defined as
a >20% decrease in diameter stenosis and a residual diameter stenosis
<50% of the vessel lumen after PTCA, with no major complications
occurring during hospitalization. Medications after PTCA (up to the
24-hour repeat angiogram) consisted of a continuous infusion of
intravenous heparin to maintain a partial thromboplastin time between
60 and 80 seconds, intravenous nitroglycerin, aspirin, and a calcium
channel blocker.
Coronary Angiography and Measurement of Coronary Stenosis
Patients were examined angiographically before PTCA, immediately
and 24 hours after PTCA, immediately after stent placement (group 1),
and at 3.6±1-month follow-up after PTCA. Similar single-view
projections were used at each procedure. The percent degree of coronary
stenosis, reference diameter, and MLD were determined by on-line
digital quantitative coronary analysis (QCA) after the
intracoronary administration of 100 µg nitroglycerin using a
computerized program.11 On-line QCA was used because it
allowed immediate measurement of the artery without the need to develop
the film. This program uses operator-traced scan lines across the area
of maximal narrowing and in the reference area proximal to the stenosis
for automated edge detection. Arterial border outlines and lesion
contours are plotted automatically. Vessel diameter at the area
proximal to the stenosis and at the area of maximal obstruction was
determined by direct measurement of the distance in pixels from edge to
edge of each area of the vessel. Absolute reference diameter and MLD in
millimeters were determined with the guiding catheter filled with
contrast for calibration. For each lesion, the single view showing the
most severe degree of stenosis was used for analysis. When the
segment of the artery proximal to the stenosis was abnormal, the
segment of the vessel distal to the obstruction was used as reference
luminal diameter. Absolute dimensions were measured with an accuracy of
0.08 mm and a highly reproducible intraobserver variability
(r=.90). To minimize the foreshortening effect, the view
most perpendicular to the artery was used. Only
end-diastolic frames were analyzed. The distance between
the patient and the radiography system was the same in the initial and
each of the following studies. The lesion was considered to have
restenosed when the diameter stenosis at follow-up was 50%.
Stent Placement
At angiography 24 hours after PTCA, the 33
patients randomized
to group 1 received a flexible Gianturco-Roubin intracoronary
stent.16 17 Immediately after randomization, patients
in
group 1 were placed on an infusion of dextran 40 at 100 mL/h started 1
hour before stenting. A bolus of 10 000 IU heparin IV was administered
before stent placement. If needed, additional heparin was administered
to maintain an activated clotting time >300 seconds. A continuous
infusion of intravenous nitroglycerin was started. Both groups of
patients continued to receive aspirin, dipyridamole, and calcium
channel blockers indefinitely. A coronary stent slightly larger than
the reference diameter of the vessel to be stented (ratio of 1.1:1,
stent to reference diameter) was used. Stents were deployed at the
lower pressure that completely expanded the stent (not greater than 6
atm). Arterial and venous sheaths were removed, with the patient on
dextran 40 infusion, the day after the procedure when the activated
clotting time was 
180 seconds. Intravenous heparin was restarted 2
hours after sheath removal and maintained until a therapeutic
prothrombin time of 16 to 18 seconds was achieved by administration of
oral warfarin. Patients in group 1 received warfarin for 6 weeks.
Patients in the stent group were discharged after a therapeutic
prothrombin time was achieved. Patients in group 2 were discharged the
day after sheath removal.
Follow-up
Repeat coronary arteriography was performed in all
patients: at
3.6±1.3 months in the stent group and at 2.1±2 months in the
control
group. Patients were followed up clinically for 6 months after PTCA.
End points of follow-up were major ischemic events (death, myocardial
infarction, and repeat revascularization procedures). At 1-month
follow-up, all patients underwent an exercise radionuclide or
ergometric test. Clinical evaluation was performed by direct or
telephone interview of the patient by trained medical personnel.
Statistical Analysis
Assuming an incidence of restenosis of
70% for lesions with
early loss after successful PTCA11 and a decrease in the
incidence of restenosis to 30% for the stent group,9 the
power of the study to detect a difference between the two groups of
patients with P<.05 was 80% when the conservative
continuity-corrected method was used. The power was 92% without the
use of the continuity correction.
A two-factor MANOVA was performed on the percent stenosis and MLD data with the BMDP program P4V.18 The two factors were stent group (a between-group factor) and time (a within-group factor). In the face of a highly significant stent-times-time interaction, which could not be removed by the transformation of the data, the MANOVA was broken down into two separate repeat-measures MANOVAs, one for the stent group and one for the no-stent group. Since the stent main effect was highly significant in the first MANOVA (P<.00005), we used the concept of protected tests19 to carry out comparisons between stent and no-stent groups at each time point with the use of T2 tests. Comparisons between different times within each group were carried out with the contrasts provided in P4V.
Comparison of demographics between both groups of patients was performed by nonparametric tests.
The results are expressed as mean±SD. A value of P<.05 was considered significant.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patient Population
The patient population included 66 patients, 12 women and 54 men, with a mean age of 56±10 years (range, 39 to 74 years). All patients presented with unstable angina. Forty-seven had recent onset of angina, 14 had worsening angina, and 5 had post–myocardial infarction angina. There were no significant differences in demographic and baseline clinical and angiographic characteristics between the two groups of patients (Tables 1
and 2).
|
|
Immediate Results After Stent
The Gianturco-Roubin stent was
deployed in all patients without
immediate complications. Three 2.5-mm, twenty-two 3.0-mm, six 3.5-mm,
and two 4.0-mm Gianturco-Roubin stents were used in the 33 patients
of group 1. Five stents were deployed in the circumflex system (1 in
the proximal and 4 in the marginal segments of the circumflex), 7 in
the right coronary artery (3 in the proximal segment, 2 in the middle
segment, and 2 in the distal segments), and 21 in the left anterior
descending coronary artery (2 in ostial lesions, 12 in the proximal
segment of the left anterior descending proximal to the first septal
perforator, 6 between the first septal perforator and the second
diagonal branch, and 1 distal to the second diagonal branch).
In-hospital complications and length of hospital stay for both groups
of patients are shown in Table 3. There were no deaths,
emergency CABG, or abrupt closure in either group. One patient in the
stent group suffered a Q-wave myocardial infarction. Subacute occlusion
occurred in 3 patients (9%) at 4 and 5 days after stent placement.
These 3 patients were successfully treated with intravenous
streptokinase. Although 1 patient sustained a Q-wave myocardial
infarction, repeat coronary arteriography before hospital discharge
demonstrated a patent vessel in each of these 3 patients. Vascular
complications occurred in 7 of 33 patients (21.2%) of the stent group.
They included 4 pseudoaneurysms (12.1%), 2 arteriovenous fistulas
(6%), and 1 retroperitoneal bleeding episode (3%). Length of hospital
stay was 7.3±1 days for the stent group and 2.4±0.5 days for the
control group (P<.01).
|
Angiographic Restenosis
The incidence of late angiographic
restenosis for the overall
group was 48.4% (32/66). As shown in Table 4 and the
Figure, restenosis was significantly greater in group 2
than in group 1 (75.7% [25/33] versus 21.2% [7/33],
P<.001). Asymptomatic patients had repeat coronary
angiography of the target artery 3 to 4 months after intervention. The
time of follow-up angiography was determined by the recurrence of
symptoms. Seventeen patients in the control group had recurrence of
angina or had a positive stress test between 1 and 2 months after PTCA.
These patients were studied earlier than 3 months after PTCA, and
restenosis was documented in all of them. Although it is possible that
the incidence of restenosis could be higher at 6-month follow-up
angiography, the end point of the study was to compare the incidence of
angiographic restenosis 3 months after PTCA.
|
|
MLD and Diameter
Stenoses
The results of reference diameter, MLD, and diameter stenoses
are
shown in Table 2
and the Figure. There were no
significant differences
in reference diameter between patients in groups 1 and 2 (3.22±0.25
versus 3.14±0.25 mm, respectively, P=NS). Similarly,
there
were no significant differences in MLD before (0.85±0.35 versus
0.75±0.47 mm), immediately after (2.57±0.37 versus
2.54±0.24 mm),
and 24 hours after (1.83±0.44 versus 1.76±0.32 mm) PTCA between
patients in groups 1 and 2, respectively. There was an increase in MLD
to 3.16±0.28 mm in group 1 after stent placement. At follow-up
angiography, there was a significant difference in MLD between groups 1
and 2 (2.46±0.82 versus 1.15±0.66 mm, respectively,
P<.001). There were no significant differences in diameter
stenoses before PTCA between patients in groups 1 and 2 (73.6±10.7%
versus 75.9±15.3%, respectively, P=NS). Similarly,
there
were no significant differences in diameter stenoses immediately after
and at 24 hours after PTCA between the two groups of patients and in
the incidence of lesions exhibiting 50% diameter stenosis at 24-hour
post-PTCA angiography (24% versus 27% for the stent and the control
group, respectively). There was a decrease in diameter stenoses to
1.8±6.9% in group 1 after stent placement. At follow-up angiography,
there was a significant difference in diameter stenoses between groups
1 and 2 (23.4±25.4% versus 63.5±20.7%, respectively,
P<.001).
Clinical Follow-up
At follow-up, there were no deaths. One
patient from the control
group had an acute myocardial infarction, but there were no myocardial
infarctions in the stent group. Of the 7 patients who developed
restenosis after coronary stenting, 5 underwent repeat PTCA and 2 had
CABG. Of the 25 patients who developed restenosis in the control group,
4 underwent CABG and 20 had repeat PTCA. Thus, at 6-month follow-up,
the need for a repeat revascularization procedure (CABG or PTCA) was
significantly greater in group 2 than in group 1 (72.7% versus 21.2%,
P<.001).
Ongoing clinical follow-up of these patients since the time that this article was submitted showed that 3 additional patients in the stent group developed angina by follow-up at 21±3 months (range, 15 to 27 months). However, coronary angiography demonstrated restenosis at the stent site in only 1 patient; the other 2 had lesions in other vessels and no evidence of restenosis at the stent site. Thus, when this additional patient with restenosis is included, there is an overall incidence of restenosis of 24.2% at >1-year follow-up in the stent group.
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
The present study demonstrates that the Gianturco-Roubin intracoronary stent reduces late restenoses in lesions with early loss in MLD after successful PTCA detected at 24-hour angiography. Although there were no differences in mortality and in the incidence of nonfatal myocardial infarction at follow-up, patients in the control group more frequently received new revascularization procedures (CABG or PTCA) than those in the stent group (73% versus 21%, respectively).
The long-term outcome after successful PTCA is significantly diminished by the recurrence of restenosis in 30% to 50% of the patients.1 2 3 4 5 6 7 8 9 10 11 20 A decrease in restenosis has not been achieved despite extensive studies of the pathology and time course of this phenomenon. Smooth muscle cell proliferation resulting in intimal hyperplasia and elastic wall recoil are the more important mechanisms determining restenosis after PTCA.9 11 21 22 There are some clinical and angiographic predictors of restenosis. A high predictive value for late restenosis has been reported for positive thallium exercise test and exercise gated blood pool scan performed early after PTCA.23 24 25 26 27 28 Since the introduction of PTCA by Andreas Gruentzig in 1977, changes in MLD have been shown to occur early after PTCA.8 11 20 29 In our study, 69 of the 191 patients (36%) who had 24-hour post-PTCA angiography had >0.3 mm in MLD loss. However, only 17 of the 191 patients (8.9%) had a stenosis >50% at 24 hours. These results are in agreement with those of Nobuyoshi et al,20 who reported 14% of lesions with a diameter stenosis >50% at 24 hours after PTCA.
Recently, lesions exhibiting early loss after successful PTCA, defined
as 10% increase in diameter stenosis or 0.3-mm loss in MLD at
24-hour post-PTCA angiography, have been shown to have a greater
incidence of restenosis at 6-month follow-up
angiography.11 It is also well known that smooth muscle
cell proliferation resulting in intimal hyperplasia is not present
this early after PTCA. Smooth muscle cell migration into the intima and
its phenotype modulation to the synthetic state occur at 4 and 7 days
after PTCA, respectively.21 22 Although the mechanism
of
this early loss in MLD is unknown, it is possible that several
processes, such as early elastic wall recoil, dissection, vasospasm,
and thrombus formation alone or in combination may be responsible for
this loss. Recent intravascular coronary ultrasonic, angioscopic, and
angiographic studies have suggested that elastic wall recoil may play a
dominant role in the mechanism of restenosis, particularly in type B
and C lesions.13 14 In the present study, 98% of the
treated lesions were type B and C.
Stents have been shown to be useful in decreasing the incidence of
restenosis in a selected group of patients with de novo
lesions.9 16 29 30 31 32 33
However, the cost and the incidence of
post-stenting complications and hospital stay are greater than those
for PTCA alone. Thus, it is of prime importance to identify patients
with lesions more likely to develop restenosis after PTCA. We
demonstrated previously that patients with lesions exhibiting a loss
10% in diameter stenosis or 0.3 mm in MLD at 24-hour post-PTCA
angiography ("early loss") have a greater incidence of restenosis
at 6-month follow-up angiography.11 The present study
demonstrates that the Gianturco-Roubin intracoronary stent decreases
the incidence of restenosis in this high-risk subgroup of patients. The
decrease in the rate of restenosis produced by coronary stenting seems
to be due to a larger luminal diameter achieved with this intervention
without a reduction in neointimal proliferation. Our study
shows that the loss in MLD at follow-up was slightly greater in the
stent than in the control group (from 3.16±0.28 to 2.46±0.82 mm
and
from 1.76±0.32 to 1.15±0.66 mm for the stent and control groups,
respectively), and this phenomenon probably represents
neointimal hyperplasia secondary to smooth muscle cell
proliferation. Although the late loss was slightly greater in the stent
group, restenosis was significantly lower in this group of patients
because they started from a larger postintervention MLD than the
control group (3.16±0.28 versus 1.76±0.32 mm,
P<.001).
These findings are in agreement with the concept of "acute gain"
and "late loss" and support the hypothesis that coronary stenting
decreases restenosis because the greater acute gain obtained with this
device offsets the loss associated with neointimal
proliferation.34 Our results are in agreement with those
recently reported by Kimura et al30 using the
Palmaz-Schatz stent. They showed that compared with a cohort of
patients treated with conventional PTCA alone, patients receiving the
intracoronary Palmaz-Schatz stent had both no significant loss in
diameter gain at 24-hour follow-up angiography and a lower incidence of
restenosis at 6-month follow-up angiography. Although our
postintervention diameters seem to be in the high size range, they are
in agreement with those of Kimura et al, who reported post-PTCA MLDs of
2.1±0.5 mm for a group of 179 lesions with a mean reference diameter
of 3.0±0.6 mm and a poststent MLD of 2.9±0.4 mm in 96 lesions
with a
reference diameter of 3.4 mm. Similar poststent MLD has also been
reported by other investigators.35 36 37
Our population
included lesions in large coronary arteries suitable for stent
placement with reference diameters of 3.22 and 3.14 mm for the stent
and PTCA groups, respectively. We believe that, in addition to patient
selection, on-line QCA may also account in part for our large
postintervention MLD. Software analyses and their validation for
on-line and off-line QCA are quite variable.38 In the
present study, however, the same QCA system was used for the
measurements in both groups of patients and should not account for our
findings that stent placement decreases the incidence of restenosis in
this group of patients with early loss after successful PTCA who are at
high risk for restenosis. Thus, our findings may suggest a more
rational use of intracoronary stenting to decrease restenosis after
PTCA.
Study Limitations
1. Sample size may be regarded as a
limitation of this study.
Although our patient population is small, it was sufficient to detect a
difference between the two groups of patients at P<.05 with
a power of 80% because of our selected patient population (lesions
with early loss after successful PTCA).
2. While patients in the stent group received aspirin, dipyridamole, dextran, prolonged intravenous heparin, long-term aspirin, and anticoagulation with warfarin, control patients received only 24 hours of intravenous heparin and long-term aspirin. It is possible that the lack of similar regimens of anticoagulation in the stent and the control groups might account in part for the difference in restenosis rates between the two groups of patients. In fact, the same factors need to be considered in analyzing the results of other published and ongoing stent versus PTCA restenosis trials. Further studies are necessary to determine whether the intensive anticoagulation regimen used in patients receiving intracoronary stents may play a role in the decrease in restenosis rate observed with the use of this device.
|
Acknowledgments |
|---|
We are grateful to Dr Jose Luis Palazzo and to the Anchorena Foundation for their support of this study.
Received June 22, 1994; revision received September 26, 1994; accepted October 9, 1994.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Thornton MA, Gruentzig AR, Hollman J, King SB III, Douglas JS. Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study. Circulation. 1984;69:721-727.
2. Corcos T, David PR, Bal PG, Renkin J, Dangoissac V, Rapold HG, Bourass MG. Failure of diltiazem to prevent restenosis after percutaneous transluminal coronary angioplasty. Am Heart J. 1985; 109:926-931.
3. Reis GJ, Sipperly ME, Boucher TM. Randomized trial of fish oil for prevention of restenosis after coronary angioplasty. Lancet. 1989;2:177-181. [Medline] [Order article via Infotrieve]
4. Buchwald A, Werner G, Unterber C, Wieand V. Malignant restenosis after primary successful excimer laser coronary angioplasty. Clin Cardiol. 1990;13:397-400. [Medline] [Order article via Infotrieve]
5. Gant KN, Holmes DR, Bell MR, Garratt KN, Holmes DR Jr, Bell MR, Bresnahan JF, Kaufman UR, Ulictstra R, Edwards WD. Restenosis after directional coronary atherectomy: difference between primary atheromatous and restenosis lesions and influence of subintimal tissue resection. J Am Coll Cardiol. 1990;16: 1665-1671.
6.
Topol EJ, Leya F, Pinkerton CA, Whitlow PL, Hofling B,
Simonton CA, Masden RR, Serruys PW, Leon MB, Williams DO, King SB III,
Mark DB, Isner JM, Holmes DR, Ellis SG, Lee KL, Keeler GP, Berdan LG,
Hinohara T, Califf RM. A comparison of directional atherectomy with
coronary angioplasty in patients with coronary artery disease. N
Engl J Med. 1993;329:221-227.
7.
Essed CE, Van den Brand M, Becker AE. Transluminal coronary
angioplasty and early restenosis: fibrocellular occlusion after wall
laceration. Br Heart J. 1983;49:393-396.
8. Serruys PW, Luijten HE, Beutt KJ, Geuskens R, de Feyter PJ, Van den Brand M, Reiber JHC, Ten Katen HJ, Van Es GA, Hugenholtz PG. Incidence of restenosis after successful coronary angioplasty: a time related phenomenon: a quantitative angiographic study in 342 consecutive patients at 1, 2, 3 and 4 months. Circulation. 1988;77: 361-371.
9. Serruys PW, Strauss BH, Van Beusekom HM, Van Der Giessen WJ. Stenting of coronary arteries: has a modern Pandora's box been opened? J Am Coll Cardiol. 1991;17(suppl B):143B-154B.
10. Rensing BJ, Hermans WRM, Beatt KJ, Laarman GJ, Suryapranata H, van den Brand M, de Feyter PJ, Serruys PW. Quantitative angiographic assessment of elastic recoil after percutaneous transluminal coronary angioplasty. Am J Cardiol. 1990;66:1039-1044. [Medline] [Order article via Infotrieve]
11. Rodriguez A, Santaera O, Larribau M, Sosa MI, Palacios IF. Early decreases in minimal luminal diameter predicts late restenosis after successful coronary angioplasty. Am J Cardiol. 1993;71:1391-1395. [Medline] [Order article via Infotrieve]
12. Post M, Van Even L, Veloma E, Bentala M, Borst C. Which part of the angiographic diameter reduction after balloon dilation is due to intimal hyperplasia? J Am Coll Cardiol. 1993;21:36A. Abstract.
13. Kovach J, Mintz G, Kent K, Pichard AD, Satler LF, Popma JJ, Leon MB. Serial intravascular ultrasound studies indicate that chronic recoil is an important mechanism of restenosis following transcatheter therapy. J Am Coll Cardiol. 1993;21:484A. Abstract.
14. De Franco A, Tuzcu EM, Abdelmegnid A, Lincoff AM, Brown D, Bernardi M, Ellis SG, Whitlow PL, Sutton JM, Casale PN, Raymond RE, Topol EJ, Nissen SE. Intravascular ultrasound assessment of PTCA results: insights into the mechanism of balloon angioplasty. J Am Coll Cardiol. 1993;21:484A. Abstract.
15. Myler RK, Topol EJ, Shaw RE, Stertzer SH, Clark DA, Fishman J, Murphy MC. Multiple vessel coronary angioplasty: classification, results and patterns of restenosis in 494 consecutive patients. Cathet Cardiovasc Diagn. 1987;13:1-15. [Medline] [Order article via Infotrieve]
16. Cannon A, Roubin GS. Gianturco Roubin stent to treat vessel closure complicating angioplasty. In: Roubin GS, Califf RM, O'Neal WW, Phillips HR, Stack RS, eds. Interventional Cardiovascular Medicine: Principles and Practice. New York, NY: Churchill Livingstone; 1993:865-891.
17.
Roubin GS, Cannon AD, Agrawal SK, Macander PJ, Dean LS,
Baxley WA, Breland J. Intracoronary stenting for acute and threatened
closure complicating percutaneous transluminal coronary angioplasty.
Circulation. 1992;85:916-927.
18. Dixon WJ, ed. BMDP Statistical Software Release 7, 1992. Berkeley/Los Angeles: University of California Press; 1992;2:1259-1310.
19. Bock RD. Multivariate Statistical Methods in Behavioral Research. New York, NY: McGraw-Hill; 1975:423.
20. Nobuyoshi M, Kimura T, Nosaka H, Mioka S, Veno K, Yokoi H, Hamasaki N, Horiuchi H, Ohishi H. Restenosis after successful percutaneous transluminal coronary angioplasty: serial angiographic follow-up of 229 patients. J Am Coll Cardiol. 1988;12: 616-623.
21. Ip JH, Fuster V, Badimon L, Badimon J, Taubman MB, Chesebro JH. Syndromes of accelerated atherosclerosis: role of vascular injury and smooth cell proliferation. J Am Coll Cardiol. 1990;15: 1667-1687.
22.
Liu MW, Roubin GS, King SB III. Restenosis after coronary
angioplasty: potential biologic determinants and role of intimal
hyperplasia. Circulation. 1989;79:1374-1387.
23. Hardoff R, Shefer A, Gips S, Merdler A, Flugelman MY, Halon DA, Lewis BS. Predicting late restenosis after coronary angioplasty by very early (12 to 24 hs) thallium 201 scintigraphy: implications with regard to mechanisms of late coronary restenosis. J Am Coll Cardiol. 1990;15:1486-1492. [Abstract]
24. Jain A, Mahumarian JJ, Borges NS, Johnston DL, Cashion WR, Lewis JM, Raizner AE, Verani MS. Clinical significance of perfusion defects by thallium 201 single photon emission tomography following oral dipyridamole early after coronary angioplasty. J Am Coll Cardiol. 1988;11:970-976. [Abstract]
25. El Taimini H, Davies GJ, Hackett D, Fragasso G, Maseri A. Very early prediction of restenosis after successful coronary angioplasty: anatomic and functional assessment. J Am Coll Cardiol. 1990;15: 259-264.
26. Brienblatt W, Weiland F, Sapaccavento L. Stress thallium-201 imaging after coronary angioplasty predicts restenosis and recurrent symptoms. J Am Coll Cardiol. 1988;12:1199-1204. [Abstract]
27. Stukey T, Burwell L, Nygaard TH, Gibson R, Wetson D, Beller G. Quantitative exercise thallium-201 scintigraphy for predicting angina recurrence after PTCA. Am J Cardiol. 1989;63:517-521. [Medline] [Order article via Infotrieve]
28. Wijns W, Serruys PW, Reiber JHC, De Feyter P, Van den Brand M, Smoons M, Hugenholtz P. Early detection of restenosis after successful percutaneous transluminal coronary angioplasty by exercise-redistribution thallium scintigraphy. Am J Cardiol. 1985;55:357-361. [Medline] [Order article via Infotrieve]
29. Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L. Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med. 1987;316:701-706. [Abstract]
30. Kimura T, Nosaka H, Yokol H, Iwabuchi M, Nobuyoshi M. Serial angiographic follow-up after Palmaz-Schatz stent implantation: comparison with conventional balloon angioplasty. J Am Coll Cardiol. 1993;21:1557-1563. [Abstract]
31. Carroza J, Kuntz R, Levine M, Romerantz RM, Fisherman RF, Mansour M, Gibson CM, Senerchia CC, Diver DJ, Safian RD, Baim DS. Angiographic and clinical outcome of intracoronary stenting: immediate and long term results from a large single-center experience. J Am Coll Cardiol. 1992;20:328-337. [Abstract]
32. DeJaegere PP, Hermans W, Rensing BJ, Strauss BH, DeFeyter PJ, Serruys PW. Matching based on quantitative coronary angiography as a surrogate for randomized studies: comparison between stent implantation and balloon angioplasty of native coronary artery lesions. Am Heart J. 1993;125-310.
33. Ellis SG, Savage M, Baim D, Hirshfeld J, Cleman M, Teirstein P, Topol EJ. Intracoronary stenting to prevent restenosis: preliminary results of a multicenter study using the Palmaz-Schatz stent suggest benefit in selected high risk patients. J Am Coll Cardiol. 1990;15:118A. Abstract.
34. Sutton JM, Kuntz RE, Safian RD, Levine MJ, Reis GJ, Diver DJ, Baim D. Novel approach to the analysis of restenosis after the use of the new coronary devices. J Am Coll Cardiol. 1992;19:1493-1499. [Abstract]
35. Strauss BH, Serruys PW, Bertrand ME, Puel J, Meier B, Goy JJ, Kappenberger L, Rickards AF, Sigwart U. Quantitative angiographic follow-up of the coronary Wallstent in native vessels and bypass grafts. Am J Cardiol. 1992;69:475-481. [Medline] [Order article via Infotrieve]
36.
Haude M, Erbel R, Straub U, Dietz U, Meyer J. Short and long
term results after intracoronary stenting in human coronary arteries:
monocenter experience with the balloon-expandable Palmaz-Schatz.
Br Heart J. 1991;66:337-345.
37. Carrozza JP, Kuntz RK, Schatz R, Leon M, Goldberg S, Savage M, Fishman D, Senerchia C, Diver DJ, Baim DS. Interseries differences in the restenosis rate of Palmaz Schatz coronary stent placement: differences in demographics and post-procedure lumen diameter. Cathet Cardiovasc Diagn. 1994;31:173-178. [Medline] [Order article via Infotrieve]
38. Reiber JHC. An overview of coronary quantification techniques. In: Reiber JHC, Serruys PW, eds. New Developments in Quantitative Coronary Arteriography. Dordrecht, Netherlands: Kluwer Academic Publishers; 1988;4:80.
This article has been cited by other articles:
 |
|
 |
|
  A. E. Rodriguez, J. F. Granada, M. Rodriguez-Alemparte, C. F. Vigo, J. Delgado, C. Fernandez-Pereira, A. Pocovi, A. M. Rodriguez-Granillo, D. Schulz, A. E. Raizner, et al. Oral Rapamycin After Coronary Bare-Metal Stent Implantation to Prevent Restenosis: The Prospective, Randomized Oral Rapamycin in Argentina (ORAR II) Study J. Am. Coll. Cardiol., April 18, 2006; 47(8): 1522 - 1529. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A E Rodriguez, M Rodriguez Alemparte, C F Vigo, C Fernandez Pereira, C Llaurado, D Vetcher, A Pocovi, and J Ambrose Role of oral rapamycin to prevent restenosis in patients with de novo lesions undergoing coronary stenting: results of the Argentina single centre study (ORAR trial) Heart, November 1, 2005; 91(11): 1433 - 1437. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. Rodriguez, J. Baldi, C. F. Pereira, J. Navia, M. R. Alemparte, A. Delacasa, F. Vigo, D. Vogel, W. O'Neill, I. F. Palacios, et al. Five-Year Follow-Up of the Argentine Randomized Trial of Coronary Angioplasty With Stenting Versus Coronary Bypass Surgery in Patients With Multiple Vessel Disease (ERACI II) J. Am. Coll. Cardiol., August 16, 2005; 46(4): 582 - 588. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Karavidas, A. D. Vrachatis, M. A. Alpert, D. J. Nikas, D. J. Achtypis, M. G. Foukarakis, E. P. Matsakus, C. S. Thedocharis, and A. A. Zacharoulis Primary Stenting Produces Earlier and More Efficient Myocardial Reperfusion than Primary PTCA Alone in Patients with Acute ST Segment Elevation MI Angiology, March 1, 2003; 54(2): 195 - 203. [Abstract] [PDF]
|
|
|
|
|
|
A Rodriguez, M Rodriguez Alemparte, J Baldi, J Navia, A Delacasa, D Vogel, R Oliveri, C Fernandez Pereira, V Bernardi, W O'Neill, et al. Coronary stenting versus coronary bypass surgery in patients with multiple vessel disease and significant proximal LAD stenosis: results from the ERACI II study Heart, February 1, 2003; 89(2): 184 - 188. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.Y Salame, S Verheye, I.R Crocker, N.A.F Chronos, K.A Robinson, and S.B King III Intracoronary radiation therapy Eur. Heart J., April 2, 2001; 22(8): 629 - 647. [PDF]
|
|
|
|
|
|
A. Rodriguez, V. Bernardi, J. Navia, J. Baldi, L. Grinfeld, J. Martinez, D. Vogel, R. Grinfeld, A. Delacasa, M. Garrido, et al. Argentine randomized study: coronary angioplasty with stenting versus coronary bypass surgery in patients with multiple-vessel disease (ERACI II): 30-day and one-year follow-up results J. Am. Coll. Cardiol., January 1, 2001; 37(1): 51 - 58. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.J. Knight, N.P. Curzen, P.H. Groves, D.J. Patel, A.H. Goodall, C. Wright, D. Clarke, P.J. Oldershaw, and K.M. Fox Stent implantation reduces restenosis in patients with suboptimal results following coronary angioplasty Eur. Heart J., December 2, 1999; 20(24): 1783 - 1790. [Abstract] [PDF]
|
|
|
|
|
|
T. Akiyama, I. Moussa, B. Reimers, M. Ferraro, Y. Kobayashi, S. Blengino, L. Di Francesco, L. Finci, C. Di Mario, and A. Colombo Angiographic and clinical outcome following coronary stenting of small vessels: A comparison with coronary stenting of large vessels J. Am. Coll. Cardiol., November 15, 1998; 32(6): 1610 - 1618. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Rodriguez, F. Ayala, V. Bernardi, O. Santaera, E. Marchand, C. Pardinas, C. Mauvecin, D. Vogel, L. C. Harrell, I. F. Palacios, et al. Optimal coronary balloon angioplasty with provisional stenting versus primary stent (OCBAS): Immediate and long-term follow-up results J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1351 - 1357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. Holmes Jr., J. Hirshfeld Jr., D. Faxon, R. Vlietstra, A. Jacobs, S. B. King III, T. M. Bashore, N. D. Bridges, C. B. Higgins, L. F. Hiratzka, et al. ACC expert consensus document on coronary artery stents: Document of the American College of Cardiology J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1471 - 1482. [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Ormiston, F. M. Stewart, A. H. G. Roche, B. J. Webber, R. M. L. Whitlock, and M. W. I. Webster Late Regression of the Dilated Site After Coronary Angioplasty : A 5-Year Quantitative Angiographic Study Circulation, July 15, 1997; 96(2): 468 - 474. [Abstract] [Full Text]
|
|
|
|
|
|
T. Kimura, S. Kaburagi, T. Tamura, H. Yokoi, Y. Nakagawa, H. Yokoi, N. Hamasaki, H. Nosaka, M. Nobuyoshi, G. S. Mintz, et al. Remodeling of Human Coronary Arteries Undergoing Coronary Angioplasty or Atherectomy Circulation, July 15, 1997; 96(2): 475 - 483. [Abstract] [Full Text]
|
|
|
|
|
|
P. R. Moreno, V. H. Bernardi, J. Lopez-Cuellar, J. B. Newell, C. McMellon, H. K. Gold, I. F. Palacios, V. Fuster, and J. T. Fallon Macrophage Infiltration Predicts Restenosis After Coronary Intervention in Patients With Unstable Angina Circulation, December 15, 1996; 94(12): 3098 - 3102. [Abstract] [Full Text]
|
|
|
|
|
|
Y. Ozaki, D. Keane, P. Ruygrok, W. J. van der Giessen, P. de Feyter, and P. W. Serruys Six-Month Clinical and Angiographic Outcome of the New, Less Shortening Wallstent in Native Coronary Arteries Circulation, June 15, 1996; 93(12): 2114 - 2120. [Abstract] [Full Text]
|
|
|
|
|
|
C. M. Goods, K. F. Al-Shaibi, S. S. Yadav, M. W. Liu, B. H. Negus, S. S. Iyer, L. S. Dean, S. P. Jain, W. A. Baxley, J. M. Parks, et al. Utilization of the Coronary Balloon-Expandable Coil Stent Without Anticoagulation or Intravascular Ultrasound Circulation, May 15, 1996; 93(10): 1803 - 1808. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||