ISR published

World Journal of Cardiovascular Diseases, 2014, 4, **-**
Published Online December 2014 in SciRes. http://www.scirp.org/journal/wjcd
doi
How to cite this paper: Author 1, Author 2 and Author 3 (2014) Paper Title. World Journal of Cardiovascular Diseases, 4,
**-**. http://dx.doi.org/10.4236/***.2014.*****
Incidence, Predictors, Treatment, and
Long-Term Prognosis of Patients with
Restenosis after Long Drug-Eluting Stent
Implantation for Coronary Arteries
Aram J Mirza
Department of Cardiology, Sulaimany Cardiac Hospital, Sulaimany, Region of Kurdistan, Iraq
Email: arammerza@ymail.com
Received **** 2014
Copyright © 2014 by authors and Scientific Research Publishing Inc.
This work is licensed under the Creative Commons Attribution International License (CC BY).
http://creativecommons.org/licenses/by/4.0/
Abstract
Background: Few data on the clinical course and management of patients experiencing restenosis
after implantation of long drug-eluting stents treatment for coronary arteries was available. Ob-
jectives: The aim of this study was to evaluate the incidence, predictors, and long-term outcomes
of patients with in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) with long
(33 mm & 38 mm) drug-eluting stents (DES) for long lesions in coronary arteries including left
anterior descending artery (LAD), Lt circumflex artery (Lt Cx), Right coronary artery (RCA), obtuse
marginal artery (OM) & Posterior descending artery (PDA). Methods: Between July 2009 and Oc-
tober 2010, 421 long DES had being implanted in 421 consecutive patients with significant coro-
nary artery stenosis, with 371 patients (88%) undergoing routine follow up, clinical follow up
done by exercise stress test at 6 & 12 months after stenting for 126 patients (34%), in 124 patients
(33.5%) follow up was done by Computed Tomography angiography & 121 patients (32.5%) with
clinically driven angiographic follow-up. A major adverse cardiac event was defined as the compo-
site of death, myocardial infarction (MI), or target-lesion revascularization (TLR) within 15 months.
Results: All patients who underwent clinical follow up were asymptomatic. The overall incidence
of angiographic (CT or conventional) ISR with long (33 mm & 38 mm) DES was 4% (15 out of 371
stents) with 8 (53.3%) focal-type and 7 (46.7%) with diffuse-type ISR. Six patients (40%) under-
went repeated PCI, seven (46.7%) underwent bypass surgery, and 2 (13.3%) were treated medi-
cally. During long-term follow-up (ranging from 12 - 26 months), there were no deaths, 3 (0.8%)
MI, and 13 (3.5%) repeated target-lesion revascularization (PCI or CABG) cases. The incidence of
major adverse cardiac event was 5.3% in the medical group, 10.1% in the repeated PCI group, and
21.4% in the bypass surgery group. Multivariate analysis showed that the occurrence of DES-ISR

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did not affect the risk of death or MI. Conclusions: The incidence of ISR was 4% after long DES
stenting for coronary arteries. The long-term clinical prognosis of patients with long DES-ISR as-
sociated with coronary artery stenting might be benign, if the patient has optimal treatment.
Keywords
Coronary Arteries, Restenosis, Long Stent
1. Introduction
Percutaneous coronary intervention (PCI) was introduced as an alternative means of coronary revascularization
to CABG surgery in 1979 [1]. Restenosis or reduction in lumen diameter after angioplasty and stent implantation
has been historically considered the most significant problem in coronary interventional treatment [2]. The me-
chanism of restenosis after stent implantation is the result of arterial damage with subsequent neointimal tissue
proliferation (hyperplasia), as stents resist arterial remodeling [3]-[6]. Binary angiographic restenosis is defined
as ≥50% luminal narrowing at follow-up angiography.
Four types of ISR have been defined: 1) Focal (≤10 mm in length); 2) Diffuse (ISR ˃10 mm within the stent);
3) Proliferative (ISR ˃ 10 mm extending outside the stent); and 4) Occlusive ISR. Type I has been further sub-
divided into types IA to ID based on the site of focal ISR in relation to the stent [7]. An additional type of ISR
has been proposed, that of “aggressive ISR”, defined as ISR that is longer and/or more severe than the original
lesion [8], this type is noteworthy in that the clinical course is not benign, with patients more likely to have more
severe symptoms and higher rates of myocardial infarction [8].
The most widely accepted definition of clinical restenosis, assessed as a requirement for ischemia-driven re-
peat revascularization, was proposed by the Academic Research Consortium. This definition requires both an
assessment of luminal narrowing and the patient’s clinical context [9]. Neointimal hyperplasia is strongly inhi-
bited by Drug-eluting stents DESs [10], thus dramatically diminished but not eradicated in-stent restenosis (ISR).
Despite the significant advances in the technology to reduce DES restenosis, conservative estimates still suggest
that the incidence of in-stent restenosis (ISR) requiring target vessel revascularization (TVR), so-called DES
failure, to be 5% - 10%, with one estimate suggesting >200000 repeat revascularizations in the United States
alone [11]. Several randomized trials have shown that diabetes, small vessel size, and long lesions may increase
the risk of restenosis after DES implantation [12]-[14]. Emerging evidence now suggests that between 30% -
60% of ISR cases present with an acute coronary syndrome with unstable angina being the most common pres-
entation and up to 5% of patients even reported to present with ST-elevation myocardial infarction (STEMI) [15]
[16].
Yet there is a lack of solid evidence pertaining to the safety and effectiveness of long DES stents for treating
long lesions and there is a great need to demonstrate this; therefore, we evaluated the clinical and angiographic
outcomes of long lesion coverage using long (33mm & 38mm) Everolimus-eluting stents (XIENCE PRIME) in
the real world clinical practice.
2. Patients
Between July 2009 and October 2010, at Sulaimany Cardiac Hospital more than 1250 PCIs were performed in a
year, 421 long (33 mm, 38 mm) (XIENCE PRIME LL, Abbott Vascular, USA) had being implanted in 421
consecutive patients with significant coronary artery stenosis. All the patients had both the clinical indications for
PCI and an angiographic diameter stenosis ≥ 50% - 60% with 371 patient (88%) undergoing routine follow-up,
the inclusion criterion was the presence of de novo coronary lesions that were implanted with either (33 mm or 38
mm) XIENCE PRIME LL stent. Patients with previous in-stent restenosis, lesions in saphenous vein grafts, end
stage renal disease on hemodialysis, severe allergic reaction to contrast & patients with severe concomitant dis-
ease had being excluded from angiographic follow-up.
Written informed consent was obtained from all patients, the design of the study & use of the data had being
proved by Ethics Committee of the hospital.

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3
3. Methods
3.1. Stenting Procedure
Drug eluting stent (XIENCE PRIME LL, Abbott Vascular, USA) (33 mm & 38 mm) was used in all patients; the
operator selected the stent and the implantation done according to the standard techniques. Complete lesion
coverage was recommended, any segment with stenosis ≥ 20% were completely covered with stents, as well as
angiographic optimization, with <10% - 20% residual stenosis by visual estimate. The length and number of the
required stents were decided upon by the operating doctor according to visual estimation. All the procedures were
performed without intravascular ultrasound guidance.
For the scheduled procedures, all the patients were on Aspirin 100mg/day at least 10 days before the procedure
& received 300 mg loading dose of Clopidogrel 8 - 12 hours prior to the procedure, the emergency patient re-
ceived 300 mg loading dose of Aspirin, 600 mg Clopidogrel & some of them received either abciximab or tiro-
fiban. During the procedure, patients received a bolus of 7.500 unit of un-fractionated heparin, with a repeat bolus
of 2000 unit to maintain activated clotting time ≥ 300 seconds. After the procedure, the patients received 300 mg
aspirin for 30 days and then 100 mg daily indefinitely with clopidogrel 75 mg for one year.
3.2. End Points and Definitions
The primary end point was the incidence of major adverse cardiac events, defined as the composite of death, acute
myocardial infarction (MI), or target lesion revascularization (TLR) (repeat angioplasty or coronary artery bypass
surgery) after stent implantation. All events were based on clinical diagnosis and re-judged by a couple of inde-
pendent clinicians. Death was defined as death from any cause. Myocardial infarction was based on the devel-
opment of electrocardiographic changes in form of ST segment elevation or new Q waves in at least two conti-
guous leads with an elevated creatine kinase myocardial band fraction or elevated serum creatinine kinase-MB
level of more than three times than the upper limit measured 24 hours after the procedure. A target lesion revas-
cularization (TLR) was defined as percutaneous or surgical revascularization for stenosis either within the stent or
within 5 mm of the stent. Stent thrombosis was assessed according to the Academic Research Consortium defi-
nitions, with pre-specified key end point being definite or probable [17], and the timing of the presentation, stent
thrombosis was classified as acute occurred within 24 hour, sub-acute (2 - 30) days, late ≤1 year and very late ˃1
year. Restenosis was defined by by a diameter stenosis of ≥50% occurring in the segment inside the stent or 5 mm
segment proximal or distal to the stent at the follow-up angiography.) Restenotic lesions were classified as focal
(type I, ˂10 mm), diffuse (type II), proliferative (type III), or total occlusion (type IV) [7].
3.3. Follow-up
Patients were divided in to three groups for the follow up, the first group (n = 126, 34%) were completely
asymptomatic during the follow-up period underwent exercise stress test at 6 & 12 months with meticulous
clinical follow-up after stenting, the occurrence of inducible ischemia on stress test (with or without ischemic
chest pain) or the recurrence of ischemic chest pain subjected the patients for angiographic follow-up. As long as
Multi Detector Computed Tomography Angiography (MDCTA) has a good negative predictive value for ruling
out coronary artery stenosis [18]-[20]; a group of asymptomatic patients (n = 124, 33.5%) were followed-up using
MDCTA, if there was evidence of in-stent restenosis by MDCTA the patient was subjected for conventional co-
ronary angiography. The third group of patients (n = 121, 32.5%) with clinical suspicion of restenosis and the
majority of patients with small size stent (2.5 mm & 2.75 mm) have underwent coronary angiography for fol-
low-up which done after (10 - 16 months) for recommended patients. If any clinical evidence of myocardial
ischemia developed at during follow-up time, then coronary angiography was recommended. Angiographic binary
restenosis was defined as a narrowing of ≥50% of the vessel diameter inside the previously implanted stent.
3.4. Angiographic Analysis
Quantitative coronary angiographic analysis was performed according to two observers. At least two orthogonal
projections were selected for analysis; these were obtained after 100 - 200 mgs of intra-coronary nitroglycerin, the
minimal lumen diameter, the lesion length and the percentage diameter stenosis were analyzed for a group of
patients.

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4
3.5. Statistical Analysis
The data was analyzed by SPSS (Statistical Package for the Social Sciences-verstion 16.0) package software
program for statistical analysis. Descriptive statistics (numbers and percentages) were calculated for variables,
as well as analytical statistics was done to find the relations between variables. Association between variables
was detected by using the appropriate statistical tests such as Chi-square and, t-test. A p-value ≤ 0.05 was con-
sidered as significant.
4. Results
4.1. Incidence, Pattern, and Clinical Presentation of Long Drug-Eluting In-Stent Restenosis
During long-term follow-up period of 15 months ranging from (12 - 26 months), angiographic (conventional &
MDCTCA) ISR was 6.1% (15 out of 245), but the overall incidence of ISR in all patients,
groups who underwent
clinical & angiographic follow-up was 4% (15 out of 371) patients. The restenosis pattern was focal in (n = 8,
53.3%) & diffuses in (n = 7, 46.7%). Eight patients (53.3%) presented with stable angina, four patients (26.7%)
presented with silent ischemia, two (13.4%) presented as unstable angina and one patient (6.6%) presented as
non fatal ST elevation myocardial infarction. During the follow-up period, the cumulative incidence of definite
or probable stent thrombosis was (0.8%), three patients; 1 definite and 2 probable. The different characteristics
of patients are shown in Table 1.
4.2. Predictors of Long DES ISR
This study showed that diabetes mellitus, ejection fraction, ostial lesions and small stent diameter had an impact
on occurrence of long DES ISR (Figures 1-4) whereas hypertension, hyperlipidemia, smoking, family history of
coronary artery disease and which coronary artery being stented failed to show significant effects (Figures 5-9).
4.3. Treatment and Long-Term Prognosis of Long DES ISR
Among 15 patients with long DES ISR, 2 (13.3%) treated medically, 6 (40%) patients treated by repeat PCI (2
with only balloon angioplasty and 4 with additional DES implantation), and 7 (46.7%) underwent CABG sur-
gery. All patients who underwent clinical follow up were asymptomatic. The overall incidence of angiographic
(CT or conventional) ISR with long (33 mm & 38 mm) DES was 4% (15 out of 371 stents) with 8 (53.3%) foc-
Table 1. Baseline clinical, angiographic, and procedural characteristics of overall patients who underwent follow-up.
Clinical
follow-up
Angiographic follow-up
(CT or conventional)
Demographic characteristics Overall (n = 371) (n = 126) (n = 245) P value
Age (yrs) 52.5 ± 11.0 53 ± 10.9 52.9 ± 10.4 0.89
Male 196 71 125 0.324
Female 175 55 120
Cardiac or existing conditions
Diabetes mellitus 149 (40.16) 26 (20.6) 123 (50.20) 0.131
Hypertension 182 (49.0) 40 (31.7) 142 (57.9) 0.0001
Current smoking 155 (41.7) 46 (36.5) 109 (44.4) 0.012
Renal failure 2 (0.53) 0 (0) 2 (8.1) 0.001
Family history of CAD 145 (39.0) 31 (24.6) 114 (46.5) 0.0003
Previous revascularization (CABG OR PCI) 1 5 (3.9) 29 (11.83) 0.012
Ejection fraction ˃ 55% 198 (80.8) 101 (80.1) 198 (80.8) 0.81
Ejection fraction ˂ 45% 15.90 17 (13.49) 42 (17.1) 0.316
Clinical indication
STEMI 66 7 (5.55) 14 (5.71) (0.251)
Unstable angina 59 (42.85) 47 (37.30) 112 (45.71)
Chronic stable angina 91 (51.48) 72 (57.14) 119 (48.57)

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Figure 1. Shows that diabetes mellitus is a strong predictor of ISR after long
DES Implantation.
Figure 2. Shows the relation between EF & ISR, that the lower the ejection
fraction the higher the incidence of ISR after long DES implantation.
al-type and 7 (46.7%) with diffuse-type ISR. Six patients (40%) underwent repeated PCI, seven (46.7%) under-
went bypass surgery, and 2 (13.3%) were treated medically. During long-term follow-up (ranging from 12 - 26
months), there were no deaths, 3 (0.8%) MI, and 13 (3.5%) repeated target-lesion revascularization (PCI or CABG)
cases. The incidence of major adverse cardiac event was 5.3% in the medical group, 10.1% in the repeated PCI
group, and 21.4% in the bypass surgery group. Multivariate analysis showed that the occurrence of DES-ISR did
not affect the risk of death or MI. Tables 2-4.

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Figure 3. Shows that the incidence of ISR after long DES implantation was higher with ostial
lesion compared to other arterial locations.
Figure 4. Shows that the smaller the stent diameter the higher the incidence of ISR after long
DES implantation.
Figure 5. Shows that hypertension did not have an impact on ISR after long DES implantation.

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Figure 6. Shows that hyperlipidemia had no effect on ISR after long DES
implantation.
Figure 7. Shows that there was no relation between smoking & long DES ISR.
Table 2. Follow-up results of patients with angiographic ISR.
Follow-up in days 450 (365 - 775)
Event-free (death, MI, TLR)
Death 0
MI 3 (0.8)
TLR 13 (3.5)

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Figure 8. Shows that family history of CAD did not have an
effect on ISR after long DES implantation.
Figure 9. Shows no significant difference in the incidence of ISR after long
DES implantation between different coronary arteries.
5. Discussion
We have demonstrated that the rate of in-stent restenosis after long ( 33 mm & 38 mm) everolimus DES im-
plantation in routine clinical practice is nearly similar to the restenosis rate for shorter (≤28 mm) DES size re-
ported in clinical trials.
Lesion length and stent length correlated weakly with restenosis, the stent length is not an independent pre-
dictor of restenosis. These results indicate that, for DESs stent length has less influence on restenosis than it
does with bare metal stents, supporting the current strategy of complete lesion coverage.
Our results have also showed that the major determinant of long DES ISR were post intervention final lumen
size, diabetes mellitus, location of the stent; the ostial stent has higher incidence of ISR compared to proximal,
mid and distal part, stent diameter; the smaller stent diameter the higher incidence of ISR, the decrease in ejec-
tion fraction < 45% has higher incidence of ISR, and deployment pressure also is an important predictor of ISR;
the higher deployment pressure the lower ISR rate.
In the era of bare metal stent, restenosis was a major limiting factor for angioplasty when many studies shows

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Table 3. Clinical, lesion, and procedural characteristics in patients with or without ISR among those receiving angiographic
follow-up.
Variables With angiographic follow-up ISR No ISR P value
(n = 245) (n = 15) (n = 230)
Demographic characteristics P value
Age (yrs) 52.9 ± 10.4 53.7 ± 10.1 52.7 ± 10.7 (0.59
Male 125 (51.01) 71 (473.33) 196 (85.2) 0.49
Female 120 (48.9) 55 (366.6) 175 (76.08) 0.51
Cardiac or coexisting conditions
Diabetes mellitus 123 (50.2) 14 (93.3) 109 (47.39) 0.001
Hypertension 142 (57.9) 9 (60) 133 (57.82) 0.852
Hyperlipidemia 109 (44.48) 8 (53.3) 101 (43.91) 0.461
Smoking (current) 99 (40.4) 6 (40) 93 (40.43) 0.921
Renal failure 2 (0.8) 0 (0) 2 (0.86) 0.717
Family history of CAD 114 (46.5) 7 (46.66) 107 (46.52) 0.899
Previous PCI or CABG 29 (11.83) 3 (20) 26 (11.30) 0.312
Ejection fraction ˃ 55 % 198 (80.8) 6 (40) 192 (83.47) 0.001
Ejection fraction < 45 42 (17.14) 5 (33.33) 37 (16.08) 0.083
STEMI 14 (5.7) 1 (6.66) 13 (5.65) 0.962
Unstable Angina 112 (45.7) 7 (46.66) 105 (45.06) 0.59
Chronic stable angina 48.57 7 (46.66) 112 (48.69) 0.53
Table 4. Clinical and angiographic characteristics of patient with ISR, according to treatment strategy.
Variable
Medical
therapy
(n = 2, 13.3%)
Repeated PCI
(n = 6, 40%)
CABG (n =
7, 46.7%)
P
value
Variable
Medical
therapy (n = 2,
13.3%)
Repeated PCI
(n = 6, 40%)
CABG
(n = 7,
46.7%)
P value
Clinical
indication
0.036
location
involved
STEMI 0 1 0 0.251 Ostium 0 0 4
Unstable angina 0 5 2 Proximal 0 3 1
Chronic stable
angina
2 0 5 Mid part 0 2 2
Lesion
characteristic
of ISR
Distal 2 1 0
LAD 0 3 3
Focal pattern
(n = 8)
1 5 2
L Cx 0 1 1
Diffuse
pattern (n = 7)
1 1 5
RCA 0 2 2 MACE % 5.3 10.1 21.4
OM 1 0 1 Death 0 0 0
PDA 1 0 0
that post intervention final lumen diameter is the most powerful predictor of restenosis after bare metal implan-
tation [21]-[23] and our study shows the same effect.
Coronary artery disease is more aggressive in diabetic than in non-diabetic patients and coronary revasculari-
zation procedures are associated with less favorable outcomes in diabetic patients. Many randomized trials, de-
monstrates durable clinical and angiographic benefits for diabetic patients after DES implantation, but it was
unclear whether diabetes increased the risk of restenosis after DES implantation [12]-[14]. Our results have

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10
demonstrated that diabetes is a predictor of restenosis after long DES implantation.
In-stent restenosis, which is secondary to neointimal hyperplasia, presents in different patterns. Focal in-stent
restenosis was the most favorable pattern with respect to late outcome after repeat intervention [7]. Our study
has shown that, similar to previous results with shorter DESs, [2] [3] in-stent restenosis occurred mostly (about
53.3%) as a focal pattern. In addition our results suggest that long DES implantation is highly effective in rou-
tine clinical practice, providing a rationale for its use.
There are several potential limitations in our study, first, only one kind of everolimus eluting stent had being
used which may lead to possible bias, second, our study was limited by incomplete angiographic follow-up, thus
possibly leading to potential error for the restenosis rate.
6. Conclusion
The incidence of ISR 15 months after successful long DES implantation in consecutive real-world patient with
significant coronary artery lesion was approximately 4%. Diabetes mellitus, ostial location, low ejection frac-
tion > 45%, stent diameter & pressure of employment were identified as major predictors of long DES-ISR. The
clinical consequences of long DES ISR, seem to be benign. Different modalities for long DES ISR don’t have
significant impact on the incidence of major adverse cardiac events given that these patients treated optimally by
their clinicians.
References
[1] Gruntzig, A.R., Senning, A. and Siegenthaler, W.E. (1979) Nonoperative Dilatation of Coronary Artery Stenosis: Per-
cutaneous Transluminal Coronary Angioplasty. The New England Journal of Medicine, 301, 61-68.
http://dx.doi.org/10.1056/NEJM197907123010201
[2] Dangas, G. and Fuster, V. (1996) Management of Restenosis after Coronary Intervention. American Heart Journal,
132, 428-436. http://dx.doi.org/10.1016/S0002-8703(96)90442-1
[3] Schatz, R.A., Palmaz, J.C., Tio, F., Garcia, F., Garcia, O. and Reuter, S.R. (1987) Balloon Expandable Intracoronary
Stents in the Adult Dog. Circulation, 76, 450-457. http://dx.doi.org/10.1161/01.CIR.76.2.450
[4] Hoffman, R., Mintz, G.S., Dussaillant, G.R., et al. (1996) Patterns and Mechanisms of Instent Restenosis: A Serial
Intravascular Ultrasound Study. Circulation, 94, 1247-1254. http://dx.doi.org/10.1161/01.CIR.94.6.1247
[5] Dussaillant, G.R., Mintz, G.S., Pichard, A., et al. (1995) Small Stent Size and Intimal Hyperplasia Contribute to Res-
tenosis: A Volumetric Intravascular Ultrasound Analysis. Journal of the American College of Cardiology, 26, 720-724.
http://dx.doi.org/10.1016/0735-1097(95)00249-4
[6] Gordon, P.C., Gibson, M., Cohen, D.J., Carroza, J.P., Kuntz, R.E. and Baim, D.S. (1993) Mechanisms of Restenosis
and Redilation within Coronary Stents—Quantitative Angiographic Assessment. Journal of the American College of
Cardiology, 21, 1166-1174. http://dx.doi.org/10.1016/0735-1097(93)90241-R
[7] Mehran, R., Dangas, G., Abizaid, A., et al. (1999) Angiographic Patterns of In-Stent Restenosis: Classification and
Implications for Long-Term Outcome. Circulation, 100, 1872-1878. http://dx.doi.org/10.1161/01.CIR.100.18.1872
[8] Goldberg, S.L., Loussararian, A., De Gregorio, J., Di Mario, C., Albiero, R. and Colombo, A. (2001) Predictors of
Diffuse and Aggressive Intrastent Restenosis. Journal of the American College of Cardiology, 37, 1019-1025.
http://dx.doi.org/10.1016/S0735-1097(01)01107-X
[9] Cutlip, D.E., Windecker, S., Mehran, R., et al. (2007) Clinical End Points in Coronary Stent Trials: A Case for Stan-
dardized Definitions. Circulation, 115, 2344-2351. http://dx.doi.org/10.1161/CIRCULATIONAHA.106.685313
[10] Costa, M.A. and Simon, D.I. (2005) Molecular Basis of Restenosis and Drug-Eluting Stents. Circulation, 111, 2257-
2273. http://dx.doi.org/10.1161/01.CIR.0000163587.36485.A7
[11] Garg, S. and Serruys, P.W. (2010) Coronary Stents: Current Status. Journal of the American College of Cardiology, 56,
S1-S42. http://dx.doi.org/10.1016/j.jacc.2010.06.007
[12] Moses, J.W., Leon, M.B., Popma, J.J., Fitzgerald, P.J., Holmes, D.R., O’Shaughnessy, C., Caputo, R.P., Kereiakes,
D.J., Williams, D.O., Teirstein, P.S., Jaeger, J.L. and Kuntz, R.E. (2003) Sirolimus-Eluting Stents versus Standard
Stents in Patients with Stenosis in a Native Coronary Artery. New England Journal of Medicine, 349, 1315-1323.
http://dx.doi.org/10.1056/NEJMoa035071
[13] Colombo, A., Drzewiecki, J., Banning, A., Grube, E., Hauptmann, K., Silber, S., Dudek, D., Fort, S., Schiele, F.,
Zmudka, K., Guagliumi, G. and Russell, M.E. (2003) Randomized Study to Assess the Effectiveness of Slow- and
Moderate-Release Polymer-Based Paclitaxel-Eluting Stents for Coronary Artery Lesions. Circulation, 108, 788-794.
http://dx.doi.org/10.1161/01.CIR.0000086926.62288.A6

A. J Mirza
11
[14] Finn, A.V., Palacios, I.F., Kastrati, A. and Gold, H.K. (2005) Drug-Eluting Stents for Diabetes Mellitus: A Rush to
Judgment? Journal of the American College of Cardiology, 45, 479-483. http://dx.doi.org/10.1016/j.jacc.2004.10.060
[15] Rathore, S., Kinoshita, Y., Terashima, M., Katoh, O., Matsuo, H., Tanaka, N., Kimura, M., Tsuchikane, E., Nasu, K.,
Ehara, M., Asakura, K., Asakura, Y. and Suzuki, T. (2010) A Comparison of Clinical Presentations, Angiographic Pat-
terns and Outcomes of In-Stent Restenosis between Bare Metal Stents and Drug Eluting Stents. EuroIntervention, 5,
841-846. http://dx.doi.org/10.4244/EIJV5I7A141
[16] Steinberg, D.H., Pinto Slottow, T.L., Buch, A.N., Javaid, A., Roy, P.K., Garg, S., Okabe, T., Torguson, R., Smith, K.A.,
Xue, Z., Suddath, W.O., Kent, K.M., Satler, L.F., Pichard, A.D., Lindsay, J. and Waksman, R. (2007) Impact of
In-Stent Restenosis on Death and Myocardial Infarction. American Journal of Cardiology, 100, 1109-1113.
http://dx.doi.org/10.1016/j.amjcard.2007.05.033
[17] Laskey, W., Yancy, C. and Maisel, W. (2007) Thrombosis in Coronary Drug-Eluting Stents: Report from the Meeting
of the Circulatory System Medical Devices Advisory Panel of the Food and Drug Administration Center for Devices
and Radiologic Health, December 7-8, 2006. Circulation, 115, 2352-2357.
http://dx.doi.org/10.1161/CIRCULATIONAHA.107.688416
[18] Abdulla, J., Abildstrom, S.Z., Gotzsche, O., Christensen, E., Kober, L. and Torp-Pedersen, C. (2007) 64-Multislice
Detector Computed Tomography Coronary Angiography as Potential Alternative to Conventional Coronary Angio-
graphy: A Systematic Review and Meta-Analysis. European Heart Journal, 28, 3042-3050.
http://dx.doi.org/10.1093/eurheartj/ehm466
[19] Garcia, M.J., Lessick, J. and Hoffmann, M.H. (2006) Accuracy of 16-Row Multidetector Computed Tomography for
the Assessment of Coronary Artery Stenosis. JAMA, 296, 403-411. http://dx.doi.org/10.1001/jama.296.4.403
[20] Budoff, M.J., Dowe, D., Jollis, J.G., Gitter, M., Sutherland, J., Halamert, E., et al. (2008) Diagnostic Performance of
64 Multidetector Row Coronary Computed Tomographic Angiography for Evaluation of Coronary Artery Stenosis in
Individuals without Known Coronary Artery Disease: Results from the Prospective Multicenter ACCURACY (As-
sessment by Coronary Computed Tomographic Angiography of Individuals Undergoing Invasive Coronary Angiogra-
phy) Trial. Journal of the American College of Cardiology, 52, 1724-1732.
http://dx.doi.org/10.1016/j.jacc.2008.07.031
[21] Hoffmann, R., Mintz, G.S., Mehran, R., Pichard, A.D., Kent, K.M., Satler, L.F., Popma, J.J., Wu, H.S. and Leon, M.B.
(1998) Intravascular Ultrasound Predictors of Angiographic Restenosis in Lesions Treated with Palmaz-Schatz Stents.
Journal of the American College of Cardiology, 31, 43-49. http://dx.doi.org/10.1016/S0735-1097(97)00438-5
[22] Kastrati, A., Schomig, A., Elezi, S., Schühlen, H., Dirschinger, J., Hadamitzky, M., Wehinger, A., Hausleiter, J., Wal-
ter, H. and Neumann, F.J. (1997) Predictive Factors of Restenosis after Coronary Stent Placement. Journal of the
American College of Cardiology, 30, 1428-1436. http://dx.doi.org/10.1016/S0735-1097(97)00334-3
[23] Hoffmann, R., Mintz, G.S., Pichard, A.D., Kent, K.M., Satler, L.F. and Leon, M.B. (1998) Intimal Hyperplasia Thick-
ness at Follow-Up Is Independent of Stent Size: A Serial Intravascular Ultrasound Study. American Journal of Cardi-
ology, 82, 1168-1172. http://dx.doi.org/10.1016/S0002-9149(98)00603-1

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