Although second-generation everolimus-eluting stents (EESs) have demonstrated superiority over first-generation paclitaxel-eluting stents for a broad subset of patients and lesions, it is unclear whether the same applies to sirolimus-eluting stents (SESs). The present study compared the long-term clinical outcomes between EESs and SESs in patients with small coronary artery disease. A cohort of 643 patients treated with EESs (220 patients with 245 lesions) or SESs (423 patients with 523 lesions) in small vessel lesions (defined as those receiving stents ≤2.5 mm) were retrospectively analyzed. The end points included target lesion revascularization, target vessel revascularization, major adverse cardiovascular events (all-cause death, myocardial infarction, or target lesion revascularization), and definite stent thrombosis at 1 year of follow-up. The baseline characteristics were generally similar between the 2 groups, except that more systemic hypertension was seen in the EES group and more patients had a family history of coronary artery disease in the SES group. The 1-year target lesion revascularization (5.6% vs 4.8%, p = 0.68) and target vessel revascularization (5.6% vs 7.6%, p = 0.33) rates showed no significant differences between the EES and SES groups. Overall major adverse cardiovascular events occurred in 9.1% of the EES- and 8.6% of SES-treated patients (p = 0.83). This similar major adverse cardiovascular events rate remained after adjustment. The rate of stent thrombosis was 0% in the EES group and 1.2% in the SES group (p = 0.17). In conclusion, EESs demonstrated comparable clinical outcomes to those of SESs in small vessel interventions. The absence of stent thrombosis among patients treated with EESs suggests a good safety profile for this second-generation drug-eluting stent, which should be carefully studied in a larger series of patients with small vessel disease.
Although drug-eluting stents (DESs) have dramatically reduced the risk of restenosis and the need for repeat revascularization compared to bare metal stents, a small vessel size remains an independent predictor of angiographic restenosis and target lesion revascularization (TLR), even after the introduction of DESs. It has been reported that in small vessel disease, first-generation sirolimus-eluting stents (SESs) improved long-term clinical outcomes compared to paclitaxel-eluting stents, mainly owing to the reduction of TLR. Second-generation DESs, such as everolimus-eluting stents (EESs), have been developed to improve the safety and efficacy of first-generation DESs. EESs are among the most widely used newer generation DESs in contemporary clinical practice. The use of EESs versus paclitaxel-eluting stents has demonstrated better event-free survival rates in high-risk patients with small coronary artery disease requiring revascularization. It remains unclear, however, whether differences exist in the safety and efficacy between EESs and SESs in this lesion subset. The present study compared the long-term clinical outcomes between EESs and SESs in patients with small coronary artery disease.
Methods
Patients from our institution’s registry who had been treated from April 2003 to April 2011 with EESs (Xience V, Abbot Vascular, Santa Clara, California; or Promus, Boston Scientific, Natick, Massachusetts) or SESs (Cypher, Cordis, Miami Lakes, Florida) in small coronary artery lesions were retrospectively included in the present study. Small vessels were defined as those receiving stents ≤2.5 mm. Patients with a bare metal stent were excluded. Additional exclusion criteria were cardiogenic shock, a target lesion located in the left main trunk, and the use of stents >2.5 mm in diameter for a concomitant diseased vessel. The clinical and demographic data and clinical events during hospitalization were collected from the hospital charts, reviewed by qualified personnel who were unaware of the objectives of the study, and entered prospectively into the database. Every patient underwent 1-month, 6-month, and 1-year clinical follow-up by qualified personnel by telephone interview or office visit. Clinical events were adjudicated using source documentation by independent physicians not involved in the procedures. All patients provided written informed consent before cardiac catheterization. The study was conducted according to the principles of the Declaration of Helsinki.
The primary end point was major adverse cardiovascular events (MACE) at 1 year, defined as the composite of all-cause death, myocardial infarction, or TLR. The secondary end points included TLR, target vessel revascularization, and 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 cause (cardiac and noncardiac). Myocardial infarction was defined as a total creatinine kinase of ≥2 times the upper limit of normal and/or creatinine kinase-MB ≥20 ng/ml, together with symptoms and/or ischemic electrocardiographic changes. Q-wave myocardial infarction was defined as evidence of new pathologic Q waves (>0.4 seconds) in ≥2 contiguous leads on the electrocardiogram. TLR was defined as any clinically driven repeat percutaneous intervention or bypass grafting of the treated lesion, including in-stent and in-segments 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. Stent thrombosis was defined as definite stent thrombosis according to the Academic Research Consortium definition.
Percutaneous coronary intervention was performed according to clinical guidelines current 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 the procedure. Dual antiplatelet therapy consisting of aspirin plus thienopyridines was continued for ≥1 year after stent implantation, followed by aspirin indefinitely. During coronary intervention, the patients received anticoagulation with bivalirudin (0.75 mg/kg bolus followed by a 1.75-mg/kg/hour infusion) or unfractionated heparin (40 U/kg bolus, with an additional dose to achieve an active clotting time of 250 to 300 seconds). Glycoprotein IIb/IIIa inhibitors (almost exclusively eptifibatide) were used at the operator’s discretion.
All statistical analyses were performed using SAS, version 9.1 (SAS Institute, Cary, North Carolina). Continuous variables are presented as the mean ± SD. Categorical variables are presented as numbers and percentages. Continuous variables were compared using an unpaired Student’s t test and categorical variables using the chi-square test or Fisher’s exact test, as appropriate. Multivariate Cox models were used to determine the predictors of MACE. The covariates were selected on the basis of overall clinical relevance, with particular attention given to the clinical and procedural factors that would make MACE more likely. The included variables were stent type used, systemic hypertension, type C lesion, stent diameter, and the use of intravascular ultrasound imaging. The covariates in the model are expressed as hazard ratios with 95% confidence intervals. MACE-free survival rates were calculated using the Kaplan-Meier method. The log-rank test was used to compare the survival curves between groups. Values of p <0.05 were considered statistically significant.
Results
A total of 643 patients were included in this registry: 220 patients with 245 lesions treated with EESs and 423 patients with 523 lesions treated with SESs. The baseline clinical characteristics are summarized in Table 1 . More patients in the EES group had systemic hypertension (90.5% vs 83.0%, p = 0.01) and fewer had a family history of coronary artery disease (48.9% vs 62.3%, p = 0.001). The number of diseased vessels per patient was similar between the 2 groups. However, a significant difference was seen in terms of the left ventricular ejection fraction between the 2 groups (0.52 ± 0.12% for EESs vs 0.48 ± 0.14% for SESs, p <0.001).
| Variable | EES (n = 220) | SES (n = 423) | p Value |
|---|---|---|---|
| Age (yrs) | 64.1 ± 10.9 | 63.9 ± 12.2 | 0.91 |
| Men | 120 (54.5%) | 248 (58.6%) | 0.32 |
| Systemic hypertension ∗ | 199 (90.5%) | 351 (83.0%) | 0.01 |
| Diabetes mellitus | 87 (40.1%) | 153 (36.7%) | 0.40 |
| Hypercholesterolemia † | 196 (89.1%) | 376 (89.1%) | 1.00 |
| Current smoker | 41 (18.6%) | 65 (15.4%) | 0.29 |
| Family history of coronary artery disease | 107 (48.9%) | 254 (62.3%) | 0.001 |
| Previous myocardial infarction | 63 (29.6%) | 101 (25.7%) | 0.31 |
| Previous coronary artery bypass grafting | 57 (25.9%) | 97 (23.2%) | 0.44 |
| Previous percutaneous coronary intervention | 81 (37.9%) | 128 (31.8%) | 0.13 |
| Chronic renal insufficiency ‡ | 22 (10.0%) | 53 (12.6%) | 0.33 |
| Peripheral vascular disease | 40 (18.2%) | 54 (13.0%) | 0.08 |
| Clinical presentation | |||
| Stable angina pectoris | 82 (37.3%) | 146 (34.5%) | 0.49 |
| Unstable angina pectoris | 115 (52.3%) | 188 (44.4%) | 0.06 |
| Acute myocardial infarction | 10 (4.5%) | 29 (6.9%) | 0.24 |
| Number of diseased vessels | 1.6 ± 0.8 | 1.7 ± 0.8 | 0.07 |
| Left ventricular ejection fraction (%) | 0.52 ± 0.12 | 0.48 ± 0.14 | <0.001 |
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