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J Am Coll Cardiol, 2006; 48:270-275, doi:10.1016/j.jacc.2006.03.039 (Published online 22 June 2006).
© 2006 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY

Effectiveness and Safety of Sirolimus Stent Implantation for Coronary In-Stent Restenosis

The TRUE (Tuscany Registry of Sirolimus for Unselected In-Stent Restenosis) Registry

Francesco Liistro, MD*,*, Massimo Fineschi, MD{dagger}, Paolo Angioli, MD*, Giuseppe Sinicropi, MD{dagger}, Giovanni Falsini, MD*, Tommaso Gori, MD{dagger}, Kenneth Ducci, MD*, Achille Bravi, MD{dagger} and Leonardo Bolognese, MD*

* Cardiovascular Departments of San Donato Hospital, Arezzo, Italy
{dagger} Le Scotte Hospital, Siena, Italy.

Manuscript received December 19, 2005; revised manuscript received March 13, 2006, accepted March 21, 2006.

* Reprint requests and correspondence: Dr. Francesco Liistro, Department of Cardiovascular Disease, San Donato Hospital, Via Pietro Nenni 22, Arezzo, 52100, Italy. (Email: francescoliistro{at}hotmail.com).


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: This study sought to evaluate the effectiveness and safety of the sirolimus-eluting stent in the treatment of in-stent restenosis (ISR) in consecutive unselected patients undergoing coronary intervention in a real-world scenario.

BACKGROUND: Restenosis after bare metal stenting is characterized by a high rate of re-restenosis once treated with repeated percutaneous coronary intervention.

METHODS: The study was designed as a prospective two-center registry. We enrolled 244 patients with ISR in a native coronary artery or saphenous vein graft who had clinical indication for repeat intervention.

RESULTS: Sirolimus stent implantation was successful in all lesions. At 9-month follow-up, death occurred in 4 (1.6%) patients, myocardial infarction in 4 (1.6%), and ischemia-driven target lesion revascularization (TLR) in 12 (4.9%), for a cumulative event-free survival of 227 (93%). Although 9-month follow-up angiography was planned in all patients, only 150 (62%) patients completed it, and restenosis was present in 13 (8.7%) patients. Diabetes and non–ST-segment elevation acute coronary syndrome at presentation were the only independent predictors of freedom from ischemia-driven TLR and major adverse cardiac events.

CONCLUSIONS: Sirolimus stent implantation for the treatment of ISR is effective and safe. In diabetic patients and in those with acute coronary syndrome, the higher rate of recurrence requires further evaluation.

Abbreviations and Acronyms
  BMS = bare-metal stent(s)
  CI = confidence interval
  DES = drug-eluting stent(s)
  ISR = in-stent restenosis
  MACE = major adverse cardiac event
  MI = myocardial infarction
  NSTEACS = non–ST-segment elevation acute coronary syndrome
  OR = odds ratio
  PCI = percutaneous coronary intervention
  SES = sirolimus-eluting stent(s)
  TIMI = Thrombolysis In Myocardial Infarction
  TLR = target lesion revascularization

In-stent restenosis (ISR) occurs at a rate of 15% to 50% after the implantation of a bare-metal stent (BMS), depending on patient subset, lesion characteristics, and type of stent (1). The recurrence after balloon angioplasty (percutaneous coronary intervention [PCI]) treatment of ISR is approximately 40%, and it depends on the angiographic pattern at presentation (2). Although the recent advent of drug-eluting stents (DES) significantly reduced the incidence of ISR in de novo coronary lesions even in high-risk patients (3–5), a policy of "DES them all" is difficult to apply in a real-world scenario because of the economic constraints we have to deal with. Consequently, BMS are still currently used and ISR remains a major challenge in daily practice. Several catheter-based techniques have undergone experimentation in the treatment of ISR, and among them only brachytherapy showed clinical benefit compared with standard balloon angioplasty (6–8). However, the significant risk of edge restenosis and late acute thrombosis (9,10), together with the need for a dedicated medical staff and equipment, contributed to the decline of this technique.

After the evidence of restenosis reduction provided in de novo coronary lesions, DES have been tested in the treatment of ISR with positive results. Preliminary studies and recent registries of patients treated with sirolimus-eluting stents (SES) to treat ISR-documented angiographic recurrence in <10% of patients (11–13). The goal of our registry was to evaluate the long-term outcome of the results of systematic implantation of SES in a large series of consecutive patients with ISR treated in a real-world scenario and to assess clinical and angiographic predictors of late recurrence.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 References
 
The study was designed as a prospective single-arm 2-center registry to evaluate clinical outcome after the implantation of SES for the treatment of ISR. From July 2002 to March 2005, all patients presenting with ISR in a native vessel or in vein graft with objective evidence of ischemia and without clinical contraindication to prolonged double antiplatelet therapy were enrolled in two centers (San Donato Hospital, Arezzo, Italy, and Le Scotte Hospital, Siena, Italy). There were no exclusion criteria, neither related to clinical presentation or stable or unstable patients, nor to angiographic characteristics such as vessel diameter or lesion length.

None of the patients had been previously treated with vessel brachytherapy, and all patients enrolled in the registry were first-restenosis patients. All patients gave written informed consent. The trial was approved by the institutional ethics committees of the 2 participating centers.

Study protocol and data analysis.   All patients received a bolus of unfractionated heparin at a dose of 70 IU/kg before starting the procedure. Before SES implantation, balloon predilation was performed in all target lesions with a balloon of at least 2.5 mm in diameter. For the registry, SES lengths of 8, 18, 23, 28, and 33 mm and diameters of 2.5 to 3.5 mm were available. Stent length was chosen to fully cover the restenotic stent even when ISR was focal. In case of two-stent implantation, no gap between the stents was left. In case of dissection because of a SES implantation, another SES was always implanted to seal the dissected segment. The SES were always implanted at high pressure (>12 atm). Stent postdilation with a larger balloon was performed only in case of suboptimal results judged by visual estimation.

Combined antiplatelet therapy with aspirin (at least 100 mg daily) and ticlopidine 500 mg daily (or clopidogrel 75 mg daily) was started at least 48 h before the procedure and continued for at least 6 months. Glycoprotein IIb/IIIa inhibitors were left to the operator’s discretion. Plasma concentrations of creatine kinase and its MB isoenzyme were systematically determined for 48 h after the intervention. All patients were asked to return for a repeat coronary angiography at 9 months after the index coronary intervention, and at specified intervals to the outpatient clinic for follow-up. Relevant data were collected and entered into a computer database.

Angiographic analysis.   All angiograms were analyzed in a random sequence by two experienced observers who were blinded to the clinical characteristics of the patients. Coronary angiograms were analyzed by a semiautomated edge contour detection computer analysis system (QCA CMS version 4, Medis Medical Imaging Systems, Inc., Leiden, the Netherlands). Manual editing of stenosis contours was considered necessary by operators in a few cases with subocclusive complex coronary ISR. The ISR was classified according to the angiographic patterns reported by Mehran et al. (2). Reference diameter (RD), minimal lumen diameter (MLD), percentage diameter stenosis (DS), and lesion length were measured before and at the end of the procedure as well as at follow-up in those patients who underwent 9-month angiography. Acute gain, late loss, and loss index were calculated using standard morphologic criteria.

Follow-up.   After hospital discharge, patients were referred to their private physicians, who regulated therapy. No attempt was made to standardize therapy, apart from the antithrombotic regimen. All patients were asked to return to the outpatient clinic for evaluation by one of the investigators 6 and 9 months after discharge. For those patients who did not return to the clinic at the designated time, follow-up information was collected by telephone interview. All patients reporting symptoms of chest pain were requested to come to the outpatient clinic for clinical, electrocardiographic, laboratory, and eventually, angiographic assessment.

Definitions and outcome measures.   Procedural success was defined by the absence of a significant residual stenosis postprocedure, judged by operator visual estimation, with Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 in the target vessel. Post-SES binary restenosis at follow-up was defined as ≥50% diameter stenosis occurring in the segment inside the SES or within a 5-mm segment proximal or distal to the stent.

Major adverse cardiac events (MACEs) were defined as death from any cause, nonfatal repeat acute myocardial infarction, and target lesion revascularization (TLR). Myocardial infarction was defined as the presence of new Q waves in 2 or more contiguous electrocardiography leads or an elevation of creatine kinase or its MB isoenzyme to ≥3 times the upper limit of normal in two samples during hospitalization or to 2 times the upper limit of normal after discharge. The TLR was defined as any repeat PCI or aortocoronary bypass surgery because of restenosis (DS ≥50%) within the stent or in the 5 mm distal or proximal segments associated with symptoms or objective signs of ischemia (ischemia-driven TLR). We defined stent thrombosis as the occurrence of any of the following events: angiographic documentation of partial or total stent occlusion detected within 30 days of the procedure (an acute clinical ischemic event in addition to angiographic documentation had to be present when the event occurred after 30 days), or sudden cardiac death or myocardial infarction (MI) after successful stent implantation not clearly attributable to another coronary lesion. Primary end points of the study were 9-month freedom from MACE and ischemia-driven TLR.

Statistical analysis.   Values are reported as numbers with relative percentage or standard deviation. Nominal variables were compared using the Fisher exact test, continuous variables were compared with the t test. Logistic regression was used to identify predictors of MACE, ischemia-driven TLR, and restenosis. The analysis included all baseline variables shown in Tables 1 and 2,Go considering the entire population for the assessment of the independent predictors of MACE and ischemia-driven TLR, and patients who completed follow-up angiography for the assessment of independent predictors of restenosis. Odds ratio (OR) and 95% confidence intervals (CIs) were reported with two-tailed probability value: a value of p < 0.05 was considered statistically significant. Survival analysis was performed with the Kaplan-Meier method in diabetic patients and those presenting with non–ST-segment elevation acute coronary syndrome (NSTEACS). All statistical computations were performed using StatView (SAS Institute Inc., Cary, North Carolina) version 6 procedures.


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  		Table 1. Baseline Clinical Characteristics
 

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  		Table 2. Procedural and Angiographic Characteristics
 

   Results
Top
 Abstract
 Methods
 Results
Discussion
 References
 
Baseline clinical and lesion characteristics.   From July 2002 to March 2005, 244 consecutive patients were enrolled in the registry. The SES was successfully implanted in all restenotic lesions. Follow-up angiography was performed in 150 patients (62%) at a mean time of 8.6 ± 2.3 months. Reasons for missing angiography were death or patient refusal. All patients completed the clinical follow-up.

Baseline clinical characteristics of the entire population are reported in Table 1. Seventy-three (30%) patients presented with NSTEACS, and 61 (25%) patients had diabetes. Angiographic and procedural characteristics of the entire population are reported in Table 2. Fifty-four (22%) patients underwent multivessel intervention, and 15 (6%) of them had ISR in two different sites. Twenty-four patients (10%) needed more than one SES to entirely cover the restenotic segment. All patients were discharge from the hospital with aspirin and thienopyridine to be continued for at least 6 months.

Clinical outcome.   Clinical follow-up was obtained in all patients at 9 months (Table 3). No MACE occurred during hospitalization. Death occurred in four patients (mean age 77.7 ± 11.3 years) and it was cardiac-related in three of them: one patient experienced a sudden death 3 months after SES implantation in an unprotected left main restenosis, one patient died for MI not related to the culprit lesion, and the last patient with severe left ventricle systolic dysfunction died of heart failure. The remaining patient died of lung cancer. Nonfatal MI occurred in four patients, and it was related to SES thrombosis in one of them, plaque thrombosis in the target vessel far from the SES implanted in two patients, and thrombosis of a nonculprit vessel in one patient. Ischemia-driven TLR was performed in 12 (4.9%) patients (PCI in 11 patients and coronary artery bypass graft in 1 patient). A total of 227 (93%) patients did not experience any event on long-term follow-up. An SES thrombosis occurred in two patients: the patient who died suddenly 3 months after the procedure and the patient who experienced a nonfatal MI because of stent thrombosis documented by coronary angiography. Logistic regression analysis showed that the presence of diabetes (OR 0.19, 95% CI 0.052 to 0.68 for freedom from TLR, p = 0.01, and OR 0.17, 95% CI 0.05 to 0.68 for freedom from MACE, p = 0.002) and acute coronary syndrome at presentation (OR 0.18, 95% CI 0.047 to 0.70 for freedom from TLR, p = 0.01 and OR 0.26, 95% CI 0.08 to 0.87 for freedom from MACE, p = 0.01) significantly reduced freedom from ischemia-driven TLR and MACE.


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  		Table 3. Cumulative In-Hospital and 9-Month Clinical Outcomes
 
Angiographic outcome.   Follow-up angiography was performed in 150 (62%) patients with 158 lesions at a mean time of 8.6 ± 2.3 months (Table 2). Late loss was 0.32 ± 0.54 mm. Cumulative distribution curve of angiographic late loss (Fig. 1) shows that the vast majority of the lesions (80%) had a late loss between –0.20 and 0.35 mm. Overall, post-SES restenosis was observed in 13 (8.7%) patients. The restenotic pattern was focal in 9 lesions, proliferative in 2 lesions, and totally occluded in 2 lesions. Of the patients with an occluded target vessel at follow-up angiography, subacute occlusive thrombosis with nonfatal MI developed in one and the other had an angiographic documentation of vessel occlusion not preceded by an acute coronary syndrome. Logistic regression analysis performed in the 150 patients with angiographic follow-up documented lesion length as the only angiographic independent predictor of 9-month restenosis (OR 1.16, 95% CI 1.09 to 1.31, p = 0.03) and diabetes (OR 3.21, 95% CI 1.01 to 6.4, p = 0.01), and NSTEACS at presentation (OR 2.89, 95% CI 1.16 to 5.6, p = 0.01) as clinical independent predictors of restenosis.


Figure 1
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  		Figure 1 Cumulative distribution of late loss at angiographic follow-up. Restenosis and ischemia-driven target lesion revascularization (TLR) is reported corresponding to the respective late loss value for each lesion.

 
Subgroup analysis.   We performed subgroup analysis to estimate the treatment effect within diabetic patients and patients with ISR and NSTEACS.

Sixty-one (25%) patients were diabetic, mean age 68 ± 10 years. These patients experienced a higher rate of clinical events compared with nondiabetic patients: ischemia-driven TLR 7 (11.6%) versus 5 (2.7%) (p = 0.01), MACE 10 (16.6%) versus 7 (3.8%) (p = 0.001), respectively. Figure 2 shows Kaplan-Meier survival analysis for freedom from MACE (Fig. 2A) and ischemia-driven TLR (Fig. 2B). Follow-up angiographic restenosis was present in 7 of 40 (17.5%) diabetic patients versus 6 of 110 (5.4%) in nondiabetic patients (p = 0.04) and lesion late loss was 0.70 ± 1.0 versus 0.26 ± 0.6, p = 0.01, respectively.


Figure 2
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  		Figure 2 (A) Kaplan-Meier analysis for 9-month major adverse cardiac event (MACE)-free survivals in diabetic and nondiabetic patients. (B) Kaplan-Meier analysis for survivals free from 9-month ischemia-driven target lesion revascularization (TLR) in diabetic and nondiabetic patients.

 
In this registry, 73 (30%) patients (mean age 69.4 ± 11 years) presented with NSTEACS as an indication to SES implantation for ISR lesions. Diabetes was equally distributed among these patients (25%) and patients with stable angina (24.5%) (p > 0.9). The NSTEACS patients experienced a higher rate of clinical events during follow-up compared with patients who presented with stable angina: ischemia-driven TLR 8 (11.1%) versus 4 (2.3%) (p = 0.007), MACE 10 (13.8%) versus 7 (4%) (p = 0.01), respectively. Figure 3 shows Kaplan-Meier survival analysis for freedom from MACE (Fig. 3A) and ischemia-driven TLR (Fig. 3B). Follow-up angiographic restenosis was present in 9 of 43 (20.9%) NSTEACS patients versus 4 of 107 (3.7%) in stable angina patients (p = 0.001), and lesion late-loss was 0.79 ± 1.1 versus 0.19 ± 0.5, p = 0.01, respectively.


Figure 3
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  		Figure 3 (A) Kaplan-Meier analysis for 9-month major adverse cardiac event (MACE)-free survivals in patients with non–ST-segment elevation acute coronary syndrome (NSTEACS) and in those with stable angina. (B) Kaplan-Meier analysis for survivals free from 9-month ischemia-driven target lesion revascularization (TLR) in NSTEACS patients and in those with stable angina.

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
To our knowledge this registry is the largest series of patients treated with SES for ISR lesions in a real-world scenario with no exclusion criteria concerning patients’ clinical status as well as angiographic criteria. The SES implantation was successful in all patients, and an optimal angiographic result was possible in all of the target lesions. The results at 9-month follow-up confirm the efficacy of SES in the prevention of recurrences with an ischemia-driven TLR rate of 4.9% significantly lower than those reported in similar settings with balloon angioplasty (TLR rate 20% to 40%) (14–16) and coronary brachytherapy (TLR rate 15%–20%) (6,9,17–19). Our data also compare favorably with a previous study focusing the results of SES implantation in ISR lesions: 8% TLR in the sirolimus arm (100 patients) of the ISAR-DESIRE (Intracoronary Stenting and Angiographic Results Drug-Eluting Stents for In-Stent Restenosis) study (20), 7.4% TLR reported in the TROPICAL (Multicenter, Nonrandomized Sirolimus-Eluting Stent in the Treatment of Patients with an In-Stent Restenotic Native Coronary Artery Lesion) registry (150 patients) (12), 11.6% TLR in the RESEARCH (Rapamycin-Eluting Stent Evaluated at Rotterdam Cardiology Hospital) registry (11), and 8% TLR in the study (136 patients) by Migliorini et al. (13). These differences might be explained by the percentage of angiographic follow-up reported in our registry (62%) compared with that reported in most of those studies (>90%). The TLR rate of these trials might have been artificially inflated by reinterventions because of ultrasound or angiographic findings not always clinically driven or justified by predefined angiographic criteria.

In our registry, the presence of diabetes and NSTEACS as an indication to PCI were independent predictors of 9-month ischemia-driven TLR as well as 9-month MACE. There was also a significantly higher restenosis and late loss in these subgroups compared with patients who did not have these clinical variables. The higher rate of restenosis and clinical recurrence in patients with diabetes is reported in several studies with DES for de novo coronary lesions (21,22), and it has been related to an exaggerated intimal proliferative response to stent-related trauma proper of diabetic patients. The higher ischemia-driven TLR rate observed in unstable patients is also reported in previous trials concerning the use of SES for ISR (13,23). It is possible that the inflammatory status of the target lesion in patients with unstable angina may produce an intensive intimal response to SES implantation resulting in a higher rate of recurrence. Thus, these data suggest that patients with diabetes and unstable angina undergoing SES implantation for ISR lesions should be scheduled for 9-month coronary angiography because of the high rate of recurrence.

No clear differences in the rates of repeat restenosis were noted among higher-risk categories (that is, Mehran classes II, III, and IV), in which the rates of repeat restenosis are high with conventional treatment. Thus, it is possible that SES implantation reduces the prognostic value of the ISR pattern for nonfocal ISR, although the limited number of our observations does not allow a definitive conclusion. Conversely, our data suggest that lesion length may still have an impact on recurrent restenosis.

In our registry, SES for ISR lesions showed an acceptable safety profile, and stent thrombosis was observed in two (0.8%) patients, sensibly lower than that reported with coronary brachytherapy (24).

Study limitations.   The rate of angiographic follow-up (62% of patients), although similar to that of other registries that enrolled patients with recurrent ISR (RESEARCH registry), is insufficient to allow for determination of the true binary restenosis rate for the entire cohort. Actually, the low angiographic follow-up rate does not affect the clinical relevance of the data because all patients without angiographic follow-up were free from symptoms and inducible ischemia. On the other hand, a higher angiographic follow-up rate would have allowed for more reliable information on restenosis rate, but not on the incidence of ischemia-driven TLR, one of the major end points of the registry.

Because of the unavailability in our hospitals of coronary brachytherapy equipment, we could not compare in any fashion, randomized or nonrandomized, our results with those achievable with this technique. However, our data suggest a greater efficacy and safety profile with SES compared with historical data (6,9,18,19) concerning the use of brachytherapy in the treatment of ISR lesions.

Conclusions.   Systematic use of SES to treat ISR seemed safe und effective in unselected series of consecutive patients treated in a real-world scenario providing a very low 9-month ischemia-driven TLR and MACE rate. In patients with diabetes and in those presenting with unstable angina, SES seemed to be less efficacious. Further analysis with larger series and more prolonged follow-up, as well as a direct comparison with brachytherapy in a randomized fashion, will provide further scientific information regarding SES effectiveness in these settings.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

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D. O. Williams, J. D. Abbott, K. E. Kip, and for the DEScover Investigators
Outcomes of 6906 Patients Undergoing Percutaneous Coronary Intervention in the Era of Drug-Eluting Stents: Report of the DEScover Registry
Circulation, November 14, 2006; 114(20): 2154 - 2162.
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j.jacc.2006.03.039v1
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