Methods

From April 2003 to December 2011, patients in whom native coronary arteries were treated with overlapping EES (Xience V, Abbott Vascular, Santa Clara, California or Promus, Boston Scientific, Natick, Massachusetts) or sirolimus-eluting stents (SES; Cypher, Cordis, Miami Lakes, Florida) or paclitaxel-eluting stents (PES; Taxus, Boston Scientific Corporation) were retrospectively included in this study from our institution’s registry. The choice of stent type was at the discretion of the operator. Stent overlap was defined as the presence of ≥2 stents within a single treated lesion and an overlapping stent zone of ≥1 mm, as determined by angiography. Total stent length per lesion was reported based on the cumulative length of the adjacent stents. We excluded patients who received a BMS. Patients who received heterogenous overlapping stents (e.g., SES-PES) were also excluded. Clinical and demographic data as well as clinical events during hospitalization were collected from hospital charts, reviewed by qualified personnel blinded to the objectives of the study, and entered prospectively into the database. Every patient underwent 30-day, 6-month, and 1-year clinical follow-up by qualified personnel through telephonic interview or office visit. Clinical events were adjudicated by source documentation by independent physicians not involved in the procedures. Written, informed consent was obtained from all patients before the cardiac catheterization. The study complied with the principles of the Declaration of Helsinki regarding investigations in humans.

Percutaneous coronary intervention was performed by the standard manner according to clinical guidelines at the time of procedure. All patients received aspirin 325 mg before the procedure and a clopidogrel loading dose of 300 to 600 mg or prasugrel 60 mg during or immediately after stent implantation. Dual antiplatelet therapy consisting of aspirin (≥75 mg/day) and thienopyridines (75 mg/day clopidogrel or 10 mg/day prasugrel) was continued for ≥12 months after stent implantation, followed by aspirin indefinitely. During the procedure, patients were anticoagulated with bivalirudin (0.75 mg/kg bolus followed by a 1.75 mg/kg/h infusion) or unfractionated heparin (40 U/kg bolus with an additional dose to achieve an active clotting time of ≥250 seconds). The use of glycoprotein IIb/IIIa inhibitors (almost exclusively eptifibatide) was left to the discretion of the operator.

The primary end point of the present study was major adverse cardiovascular events (MACE) at 12 months, defined as the composite of all-cause death, myocardial infarction (MI), or target lesion revascularization. Secondary end points included target lesion revascularization, target vessel revascularization, and definite stent thrombosis at 1 year. Angiographic success was defined as postprocedural stenosis of <30% with Thrombolysis In Myocardial Infarction flow grade 3. All-cause death was defined as death from any cardiac or noncardiac cause. MI was defined as a total creatine kinase of ≥2× the upper limit of normal and/or creatine kinase-MB ≥20 ng/ml, together with symptoms and/or ischemic electrocardiographic changes. Q-wave MI was defined as evidence of new pathologic Q waves (>0.4 second) in ≥2 contiguous leads on electrocardiogram. Target lesion revascularization was defined as any clinically driven repeat percutaneous intervention or bypass grafting of the treated lesion including in-stent and in-segment 5-mm proximal or distal to the initial stent edges. Target vessel revascularization was defined as any clinically driven percutaneous intervention or bypass grafting of the target vessel. Major bleeding was defined as the composite of gastrointestinal bleeding, a ≥15% absolute decrease in the hematocrit, or hematoma of >4 cm in diameter. Stent thrombosis was defined as definite stent thrombosis according to the Academic Research Consortium definition.

All statistical analyses were performed using SAS, version 9.1 (SAS Institute, Cary, North Carolina). Data are presented as mean ± SD or number (%). Analyses of the differences among the 3 groups were performed using analysis of variance for continuous variables and the chi-square test or Fisher’s exact test for categorical variables. Cox proportional hazard analysis was performed to determine predictors of 1-year MACE. Variables were selected on the basis of overall clinical relevance, with particular attention paid to clinical and procedural factors that would make MACE more likely. Variables included in the model were male gender, systemic hypertension, stent type used, left anterior descending artery, type C lesion, total stent length per lesion, and number of implanted stents. After univariate analysis, all variables with a p value of <0.1 were incorporated into the multivariate analysis. The results are presented as adjusted hazard ratios with their 95% confidence intervals and p values. MACE-free survival rates and stent thrombosis rates were calculated using the Kaplan-Meier method. The log-rank test was used to compare the differences in curves among groups. Values of p <0.05 were considered to be statistically significant.

Results

A total of 350 patients treated with overlapping stents were included: EES: 169 patients, 237 lesions; SES: 102 patients, 252 lesions; and PES: 79 patients, 182 lesions. As listed in Table 1 , baseline clinical characteristics were generally comparable among the 3 groups, save for male gender, systemic hypertension, and a history of MI. Angiographic and procedural characteristics are listed in Table 2 . SES and PES were more frequently implanted in the left anterior descending coronary artery, whereas EES were more frequently implanted in the left circumflex artery. There were some differences among groups with respect to the lesion location. The EES group had more complex lesions as indicated by a roughly threefold higher rate of type C lesions compared with those of the SES and PES groups (64.1% vs 22.3% vs 24.7%, respectively, p <0.001). Although the average number of stents implanted per patient was higher in EES-treated patients, the total stent length per lesion was similar among the 3 groups. Angiographic success was lesser in the SES group. Abrupt closure after the procedure was observed in 1.8% of the SES group but did not occur in the EES and PES groups.

Table 3 lists adverse clinical events. There were no significant differences with respect to in-hospital adverse events between the EES and first-generation DES groups. At 30 days, clinical event rates were similar among groups, except that lower incidences of target lesion revascularization, target vessel revascularization, and stent thrombosis were observed in the EES group. During 1-year follow-up, overall MACE occurred in 11 EES-treated patients (6.5%), 17 SES-treated patients (16.8%), and 8 PES-treated patients (10.1%; p = 0.026 for all groups, p = 0.014 for EES vs SES, and p = 0.458 for EES vs PES, respectively; Figure 1 ) All-cause mortality was similar among the 3 groups (EES 3.6% vs SES 9.0% vs PES 5.1%, p = 0.162). The rate of MI was the lowest in the EES group: EES 0 versus SES 1.0% versus PES 2.5% (p = 0.080). At 1 year, EESs were associated with a numerically lower rate of target lesion revascularization compared with that of SES and PES, respectively (3.1% vs 8.2% vs 6.5%, p = 0.181) but reached statistical significance only when compared with SES (p = 0.033). There was a trend toward lower 1-year target vessel revascularization rates with EES compared with those of SES and PES, respectively (3.7% vs 9.1% vs 11.7%, p = 0.051).

Table 3

Clinical outcomes in-hospital, at 30-day, and at 1-year follow-up

Variable	EES (n = 169)	SES (n = 102)	PES (n = 79)	p
In-hospital
Emergent intra-aortic balloon pump	7 (4.2)	5 (5.0)	1 (1.3)	0.468
All-cause death	2 (1.2)	4 (3.9)	2 (2.5)	0.331
Cardiac death	2 (1.2)	3 (2.9)	1 (1.3)	0.567
Q-wave MI	0	1 (1.0)	1 (1.3)	0.264
Coronary artery bypass graft	0	0	0	—
Acute renal failure	4 (2.4)	5 (4.9)	3 (3.8)	0.479
Cerebrovascular accident	1 (0.6)	0	0	1.000
Major bleeding	3 (1.8)	2 (2.0)	1 (1.3)	1.000
30-day follow-up
MACE	3 (1.8)	5 (4.9)	4 (5.1)	0.199
All-cause death	3 (1.8)	4 (3.9)	2 (2.5)	0.508
Cardiac death	2 (1.2)	3 (2.9)	1 (1.3)	0.567
Any MI	0	1 (1.0)	1 (1.3)	0.265
Q-wave MI	0	0	1 (1.3)	0.226
Non–Q-wave MI	0	1 (1.0)	0 (1.3)	0.516
Target lesion revascularization	0	1 (1.0)	3 (3.8)	0.022
Target vessel revascularization	1 (0.6)	1 (1.0)	4 (5.1)	0.045
Stent thrombosis	0	4 (3.9)	2 (2.5)	0.014
1-yr follow-up
MACE	11 (6.5)	17 (16.8)	8 (10.1)	0.026
All-cause death	6 (3.6)	9 (9.0)	4 (5.1)	0.162
Cardiac death	3 (1.8)	4 (3.9)	3 (3.7)	0.501
Any MI	0	1 (1.0)	2 (2.5)	0.080
Q-wave MI	0	0	1 (1.3)	0.228
Non–Q-wave MI	0	1 (1.0)	1 (1.3)	0.266
Target lesion revascularization	5 (3.1)	8 (8.2)	5 (6.5)	0.181
Target vessel revascularization	6 (3.7)	9 (9.1)	9 (11.7)	0.051
Stent thrombosis	0	4 (3.9)	2 (2.5)	0.014

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