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CLINICAL STUDIES

Acute and nine-month clinical outcomes after "suboptimal" coronary stenting

Results from the STent anti-thrombotic regimen study (STARS) registry

Donald E. Cutlip, MD, FACC^*, Martin B. Leon, MD, FACC, Kalon K. L. Ho, MD, MSc, FACC, Paul C. Gordon, MD, FACC, Alessandro Giambartolomei, MD, FACC^||, Daniel J. Diver, MD, FACC^¶, David M. Lasorda, DO, FACC^#, David O. Williams, MD, FACC^**, Michelle M. Fitzpatrick, RN, April Desjardin, MS, Jeffrey J. Popma, MD, FACC, Richard E. Kuntz, MD, MSc, Donald S. Baim, MD, FACC for the STent Anti-thrombotic Regimen Study Investigators

^* University of Rochester Medical Center, Rochester, New York, USA
Washington Hospital Center, Washington, DC, USA
Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
Miriam Hospital, Providence, Rhode Island, USA
^|| St. Joseph’s Hospital, Syracuse, New York, USA
^¶ Georgetown Medical Center, Washington, DC, USA
^# Allegheny University Hospitals, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA
^** Rhode Island Hospital, Providence, Rhode Island, USA
Brigham and Women’s Hospital, Boston, Massachusetts, USA

Manuscript received December 29, 1998; revised manuscript received April 7, 1999, accepted May 16, 1999.

Reprint requests and correspondence: Dr. Donald S. Baim, Chief, Interventional Cardiology Section, Beth Israel-Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts
dbaim{at}bidmc.harvard.edu

	Abstract

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OBJECTIVES

This registry collected the 30-day and 9-month clinical outcomes of patients whose coronary stent implantation was suboptimal, and compared them with the cohort of patients with "optimal" stenting in the randomized portion of the STent Anti-thrombotic Regimen Study (STARS) trial.

BACKGROUND

Although "optimal" stenting combined with an aspirin and ticlopidine regimen carries a low (0.5%) incidence of subacute stent thrombosis, only limited data are available for patients in whom stents are deployed suboptimally.

METHODS

In the STARS, 312 (15.9%) of 1,965 patients enrolled were excluded from participation in the randomized trial based on a perceived "suboptimal" result of coronary stenting. Of these, 265 patients met prespecified criteria for suboptimal stenting, and were followed in a parallel registry, which was compared with the randomized STARS optimal stenting cohort. The primary end point was a 30-day composite of death, emergent target lesion revascularization, angiographic thrombosis of the target vessel without revascularization and nonfatal myocardial infarction (MI)unrelated to direct procedural complications.

RESULTS

Registry patients had a similar frequency of the primary end point compared with the overall randomized cohort (3.0% vs. 2.2%), with this end point correlating to use of multiple stents, smaller final lumen diameter and absence of ticlopidine from the poststent regimen. Overall 30-day mortality (1.1% vs. 0.06%, p = 0.009) and periprocedural non-Q wave MI (8.7% vs. 4.2%, p = 0.003) were more frequent in registry patients, and appeared to be related to acute procedural complications. Clinical restenosis was significantly higher for registry patients (26.8% vs. 16.0%, p = 0.001), relating to greater prevalence of independent predictors such as smaller final lumen diameter and multiple stent use.

CONCLUSIONS

In the STARS registry, the inability to perform optimal stenting correlated with smaller final lumen diameter and longer stent length. With ticlopidine-containing regimens, the acute clinical results of "suboptimal" stent deployment are clinically acceptable, although they are not quite as good as those of optimal stenting using similar drug therapy.

Abbreviations and Acronyms   MI = myocardial infarction   QMI = Q wave myocardial infarction   STARS = STent Anti-thrombotic Regimen Study   TIMI = thrombolysis in myocardial infarction   TLR = target lesion revascularization   TVF = target vessel failure   TVR = target vessel revascularization

More recently, registry data have shown that the use of "optimal" stent technique (including routine high-pressure balloon dilation after initial stent deployment) allows use of only antiplatelet agents (aspirin and ticlopidine) to yield similar or even lower stent thrombosis rates without excessive hemorrhagic complications (5–7). The superiority of aspirin and ticlopidine over aspirin and coumarin has been demonstrated in one single-center randomized trial of stent placement in high-risk patients (8), and in the randomized STent Anti-thrombotic Regimen Study (STARS). This large multicenter randomized trial demonstrated that stent thrombosis was significantly lower in patients assigned to aspirin plus ticlopidine (0.5%) compared with aspirin plus coumarin (2.7%) or the aspirin alone (3.6%) regimen (9).

Randomization in STARS, however, was predicated on having achieved "optimal" stent results (9). Patients who failed to achieve these results were not so randomized, but rather, entered into a parallel nonrandomized registry where the antithrombotic regimen was selected by the operator. Clinical follow-up, however, was identical to that in the randomized cohort. The purpose of this analysis is to compare the 30-day clinical outcomes and late clinical restenosis outcomes for patients in the suboptimal stenting STARS registry with "optimal" stenting patients in the main randomized STARS trial.

	Methods

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Study design and patient selection.   The details of the STARS design and analysis plan have been previously reported (9). In summary, all patients undergoing elective coronary stent procedures at the 50 participating investigational sites in the U.S. were screened for enrollment. Patients were deemed eligible if they had one or two target lesions with >60% diameter stenosis in a 3- to 4-mm reference diameter native coronary artery, which did not involve the left main coronary or a major bifurcation. Other exclusion criteria were additional stenoses within the target vessels, myocardial infarction (MI) within seven days, known contraindications to study drugs (aspirin, ticlopidine or coumarin) and a history of bleeding diathesis. "Optimal" results were defined as: 1) achieving <10% residual diameter stenosis within the stented segment (by visual estimate); 2) no evidence of poststent thrombus; 3) no evidence of severe dissection (NHLBI grade D) or abrupt closure anytime during the procedure or significant poststent dissection (NHLBI grade >B); 4) thrombolysis in myocardial infarction (TIMI) 3 flow; and 5) no more than two Palmaz-Schatz stents used to treat one long (25-mm-length) lesion or two focal (12-mm-length) lesions in one or two native coronary arteries. To facilitate optimal results, stent implantation was routinely followed by high-pressure dilation. Patients with "optimal" results were eligible to be randomly assigned to one of the three antithrombotic drug regimens. Patients who did not meet all of the optimal angiographic criteria were entered into a parallel registry, in which anti-thrombotic regimens were left to the discretion of the investigator. The results of this registry are reported in this communication.

Of 1,965 patients enrolled in STARS, 1,653 patients met angiographic criteria for "optimal" stent placement and were randomized; the remaining 312 (15.9%) patients were entered in the registry. Of these 312 registry patients, 47 patients were eliminated from further analysis: 27 met all angiographic criteria for randomization but were assigned to the registry at the investigator’s discretion. In addition, 8 patients never received a stent due to delivery failure, 11 patients were transferred directly from the cardiac catheterization laboratory for emergency bypass surgery, and 1 patient died during the stenting procedure. The remaining 265 patients with suboptimal stenting procedures thus comprise the primary population for this analysis.

Data collection and end point analysis.   Detailed case report forms were completed by the clinical coordinator at each site, monitored by independent study monitors and submitted to the data coordinating center (Cardiovascular Data Analysis Center [CDAC], Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts). All electrocardiograms were interpreted by the Electrocardiographic Core Laboratory blinded to clinical events and cardiac enzyme data (ECG Core Laboratory, CDAC, Boston, Massachusetts). Procedural angiograms were submitted to the Angiographic Core Laboratory (Washington Hospital Center, Washington, DC), where they were analyzed using the CMS system (Medis, Leiden, The Netherlands). Clinical follow up for adverse events (death, recurrent ischemia and MI, repeat revascularization, bleeding and vascular complications) was obtained at hospital discharge, 30 days, 6 months and 9 months.

Study end points.   The primary end point of the study was a patient-based 30-day hierarchical composite of: 1) death, 2) emergent target lesion revascularization, 3) angiographic thrombosis of the target vessel without revascularization or 4) nonfatal MI unrelated to direct procedural complications. Secondary end points included acute procedure success, procedure-related MI, hematologic dyscrasia, major bleeding, vascular complications, target lesion revascularization (TLR), target vessel revascularization (TVR) and target vessel failure (TVF), defined as death, MI or TVR. All deaths within 30 days were considered procedure related. Acute procedure success was defined as achievement of <50% residual diameter stenosis and freedom from death, or emergent bypass surgery. Myocardial infarction was defined as new pathologic Q waves in two or more contiguous leads as determined by the ECG Core Laboratory or a creatine kinase more than twice the upper limit of normal in the presence of elevated creatine kinase-MB isoform (CK-MB). To ensure complete ascertainment of procedural CK elevations, serial CK and MB fractionation were obtained immediately and every 6 to 8 h after the procedure, for at least 24 h or the time of hospital discharge. Myocardial infarctions that were attributed entirely to acute procedure related complications were not considered as part of the composite end point. Major bleeding complications were defined as any bleeding episode requiring transfusion. Vascular complications were defined as any vascular access complication requiring surgical repair or ultrasound compression. All clinical events were adjudicated by an independent Clinical Events Committee.

Statistical analysis.   The analysis of the STARS registry was designed to compare 30-day and 9-month clinical outcomes of patients after suboptimal stent implantation to the pooled randomized patients with optimal stent results. All statistical analyses were performed using the SAS for Windows versions 6.08-6.12 (SAS Institute, Cary, North Carolina). Continuous variables are expressed as mean ± standard deviation and were compared using t tests or Wilcoxon nonparametric tests. Discrete variables are expressed as counts and percentages and were compared using chi-square or Fisher exact tests. Stepwise multivariable logistic regression models of the 30-day primary end point and nine-month target vessel failure in the entire STARS cohort were used to simultaneously evaluate effect of baseline predictors, antithrombotic treatment, procedural results and registry enrollment (10). Survival estimates were computed using Kaplan-Meier methods and compared using log-rank tests.

	Results

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Patient characteristics and indication for registry enrollment.   Patients enrolled in the registry were more likely to have multivessel coronary artery disease than randomized patients (42% vs. 32%, p < 0.01), but had otherwise similar baseline clinical features to STARS-randomized patients (Table 1).

Acute lesion success (<50% diameter stenosis after final treatment) was extremely high in both groups (97.7% for registry and 99.4% for randomized lesions). Final diameter stenosis was slightly but significantly higher for registry lesions (10.3 ± 12.8% vs. 8.5 ± 11.4%, p = 0.013; Fig. 1).

View larger version (17K): [in this window] [in a new window]   Figure 1 Cumulative distribution frequency of percent diameter stenosis at baseline (pre) and after final stent postdilation (post). At baseline, there is no difference in stenosis severity for registry compared with randomized patients. The final diameter stenosis is slightly, but significantly, worse for registry patients.

Nine-month clinical follow up
At 9 months (Table 6), clinical follow up was complete in 99% of patients, showing major adverse cardiac events (death, MI, TLR) that were significantly higher for registry patients. This difference was driven by the increase in procedure-related non-QMI as well as increased TLR (15.4% vs. 10.3%, p = 0.013).

Survival free from TVF (death, MI or TVR) was thus significantly lower in registry compared with randomized patients (72.9 vs. 83.6%, p = 0.0001) (Fig. 2).

View larger version (12K): [in this window] [in a new window]   Figure 2 Estimated freedom from TVF for registry compared with randomized patients. There is a significant increase in TVF events early for registry patients with further separation of the survival curves during the first year, consistent with increased frequency of periprocedural MI as well as later target vessel revascularization.

Stepwise multivariable models of TVF at nine months showed that predictors included final minimal lumen diameter (OR 0.36/mm, p = 0.0001), larger number of stents (OR ratio 1.40/stent, p = 0.0007) and a history of diabetes (OR 1.42, p = 0.049). After adjustment for these variables, enrollment in the registry was no longer an independent predictor of nine-month TVF.

Excluded registry patients.   Of the 312 patients originally assigned to the registry, 47 were excluded from this analysis because they did not meet the criteria for suboptimal stent results. Twenty-seven patients actually met all angiographic criteria for randomization but were assigned to the registry by the operator. Most of these cases involved failure to meet other inclusion criteria, which was not recognized before enrollment. None of these patients experienced the 30-day combined end point, died or had an MI during the follow-up period. There were six patients (22.2%) who required TVR. Eleven other patients who sustained serious angiographic complications during the stenting procedure and who were sent directly from the cardiac catheterization laboratory to emergency bypass surgery were also excluded. One of these patients suffered a QMI, and four patients had a non-QMI. There were no deaths or late target vessel events among these patients. In addition, eight patients who never received a study stent due to delivery failure were excluded. Two of these patients were referred for urgent bypass surgery, and six were treated with successful balloon angioplasty. There were no acute deaths or MI in this group and no patient required repeat revascularization. One patient was readmitted three months later for non-QMI. Finally, one patient who died during the stent procedure from spontaneous pulmonary hemorrhage was also excluded from this analysis.

	Discussion

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Although the primary component of STARS was a randomized trial comparing three antithrombotic regimens after "optimal" stenting, 312 (15.9%) of 1,965 patients who consented to participate in the randomized trial were enrolled instead into a parallel registry of suboptimal stenting. For 265 of these patients, this decision was based on failure to obtain "optimal" stent results, defined as no more than two 15-mm Palmaz-Schatz stents, a <10% final residual stenosis, no final dissection > NHLBI grade B, no interim thrombus, abrupt closure or dissection > NHLBI grade D at any time during the procedure and normal (TIMI grade 3) flow. Patients in the registry were more likely to have multivessel coronary artery disease (42% vs. 32%, p = 0.01) and complex lesion morphology (ACC/AHA class C, 15% vs. 8%, p < 0.01), which explains their increased frequency of dissections and the need for multiple stents. Indeed, the requirement for multiple stents was the most common reason for failure to meet randomization criteria that led to enrollment in the registry. By using similar poststent dilation pressures and balloon/artery ratios as for the randomized cohort, however, investigators were able to achieve final lesion success (<50% diameter stenosis with TIMI 3 flow) in the registry that nearly matched the excellent results seen in the randomized patients (97.7% vs. 99.4%, p > 0.20).

Acute clinical outcomes.   The combined 30-day end point of death, emergent TLR, angiographic reocclusion without revascularization and acute MI (other than simple low-level periprocedural CK elevation) was selected as a surrogate for stent thrombosis. This combined end point was not different for registry compared with randomized patients overall (3.0% vs. 2.2%, p > 0.20). Registry patients who received ticlopidine therapy had an even lower rate of the combined end point (ASA and ticlopidine only, 0%; any ticlopidine-containing combination, 1.9%), similar to results seen with ticlopidine in the randomized optimal stenting patients (9). Patients who received ASA plus continued anticoagulation with heparin and coumarin in the absence of ticlopidine had significantly higher rates of the 30-day end point (8.8%) than seen in the corresponding arm of the randomized trial (2.9%). Patients who received the combination of aspirin, coumarin and ticlopidine, however, had an event rate of 2.2%. This suggests that the high thrombosis rate on ASA and coumarin reflects lack of ticlopidine protection, rather than a toxic effect of coumarin.

Using a more conservative definition for stent thrombosis (one requiring angiographic documentation of stent reocclusion) registry patients again compared favorably with the randomized cohort (2.3% vs. 2.0%). Smaller final lumen dimension, multiple stent use and absence of ticlopidine independently predicted stent thrombosis.

Registry patients did, however, have a significantly higher incidence of 30-day mortality (1.1% vs. 0.06%, p < 0.009) and periprocedural non-QMI (8.7% vs. 4.2%, p = 0.003) than seen in the randomized cohort. Two of the three early deaths in the registry were clearly due to complications of the procedure, including one that resulted in subacute stent thrombosis, and the third may have been related to a more aggressive anticoagulation regimen that was selected because of the suboptimal results. Although only one of these deaths occurred in patients receiving ticlopidine, it is unclear if the choice of antithrombotic treatment had any effect on the outcome. We have previously reported that the independent predictors of MI after stenting in the STARS study were lesion length, major angiographic complications and failure to achieve a large final minimal lumen diameter. Both lesion length and angiographic complications were more common in registry patients, so a higher incidence of non-QMI is not surprising. It is important to note, however, that these periprocedural non-QMIs after an otherwise successful STARS procedure were not associated with an increase in any adverse outcome, including late mortality or recurrent MI, during one-year follow up (11).

There was a trend for registry patients to have more vascular complications requiring surgery or transfusion than randomized patients (5.3% vs. 3.0%, p = 0.10). This may have been due to the more common continuation of intravenous heparin in registry compared with randomized patients. Similar to results in randomized patients, antiplatelet therapy with ASA and ticlopidine was not associated with a significant reduction in rates of bleeding requiring transfusion compared with anticoagulant-containing regimens. This suggests that much of the observed reduction in hemorrhagic complications since early stent trials relates to better timing and technique for sheath removal, rather than a significantly lower bleeding propensity on newer antiplatelet drug regimens.

Clinical restenosis.   Clinically evident restenosis at nine months, defined as repeat TLR (15.5% vs. 10.2%, p = 0.015), or, more broadly, as TVF (26.8% vs. 16.0%, p < 0.001), was significantly higher for registry than randomized patients. This appears to have been based on the greater prevalence of smaller lumens and multiple stent use in the registry, rather than a prorestenotic effect of being in the registry itself. Because routine angiographic follow up was not performed, it is not possible to relate this increase in clinical restenosis to angiographic binary restenosis (>50% diameter stenosis) and other parameters of angiographic restenosis (e.g., loss index). Lack of angiographic follow up in both the STARS registry and randomized trial, however, allows for accurate assessment of clinical restenosis without the bias introduced by routine angiographic follow up to significantly increase the observed rates of TLR (12,13).

Comparison with previous studies.   Acute clinical outcomes for patients enrolled in the STARS registry after suboptimal stenting compare favorably with other reports in the modern era of routine high-pressure postdilation and antiplatelet therapy. Moussa et al. (7) noted a 1.9% subacute stent thrombosis rate in 1,042 patients treated with only antiplatelet therapy after intravascular ultrasound-guided stent placement. Multiple stent use, residual dissections and slow flow were the independent predictors of subacute thrombosis in this group. This thrombosis rate is identical to that observed in ticlopidine-treated patients in the STARS registry. In the STARS registry, however, final dissection and slow flow were not predictors of stent thrombosis, perhaps as the result of a strategy that allowed for use of multiple stents so that comparatively few lesions were left with significant residual dissection ( NHLBI grade C) or reduced flow.

Schomig et al. (8) reported on 517 patients randomized to aspirin and ticlopidine or aspirin and coumarin after successful stenting for nonelective indications. The 1.6% primary cardiac end point in the ticlopidine group was almost identical to the ticlopidine-treated patients in the STARS registry (1.9%). These authors, however, attributed significantly higher (6.2%) rate of thrombosis in the anticoagulant (coumarin) group to a toxic platelet activation effect in patients who received continued anticoagulant therapy with heparin and coumarin. In contrast, the STARS randomized trial showed that coumarin therapy was not associated with an increased risk of stent thrombosis compared with aspirin alone. The incidence of stent thrombosis in the registry patients receiving coumarin (any coumarin 5.5%, aspirin plus coumarin combination 8.8%) is substantially higher than in the corresponding STARS randomized arm (aspirin plus coumarin = 2.9%). Although Schomig et al. (8) believed that this was due to a toxic effect of anticoagulant therapy (predisposition to stent thrombosis, perhaps through platelet activation) (14), both the STARS randomized trial and the suboptimal registry suggest that a more plausible explanation for the high thrombosis rates with ASA plus coumarin is the lack of protective effect of ticlopidine. This is apparent in the 2.2% incidence of stent thrombosis in patients receiving aspirin, coumarin and ticlopidine, which was significantly less than other coumarin combinations (5% to 8%) and not significantly different from the results with aspirin plus ticlopidine.

Despite excellent results in terms of the 30-day combined end point, late clinical restenosis in the STARS registry was significantly more common than in the randomized patients (TVF, 26.8% vs. 16.0%, p < 0.001). This finding is consistent with a study by Mathew et al. (15), which followed 45 patients treated with three or more stents for indications of threatened or abrupt closure. Lesion success was over 97%, but by six months, 23.3% of patients experienced death, MI or repeat target vessel revascularization. Kastrati et al. (16) examined predictors of clinical and angiographic restenosis in over 1,000 consecutive stent patients. The strongest predictors of clinical restenosis were the same as those identified in our study, namely, smaller final lumen diameter, use of multiple stents and diabetes mellitus.

Conclusions.   About 15% of patients undergoing stenting of favorable lesions have suboptimal stenting, most commonly because of residual dissections or the need for multiple (three or more) stents. With the use of aggressive high-pressure postdilation, such patients still can have excellent acute results that do not differ significantly from those in the randomized cohort of "optimal" stenting in terms of lesion success (97.8% vs. 99.4%), 30-day adverse clinical events (3.0% vs. 2.1%) and documented stent thrombosis (2.3% vs. 2.0%). Similar to the findings in the randomized STARS cohort, the rates of stent thrombosis were significantly less for patients treated with a ticlopidine-containing regimen. Thus, there is no information in the STARS trial or elsewhere suggesting that more aggressive antithrombotic regimens beyond aspirin and ticlopidine further reduce subacute thrombosis, even in suboptimally treated patients. The observed higher 30-day mortality rate and increased frequency of non-QMI appears to be directly related to acute procedural complications. Further studies will be required to determine if pretreatment with ticlopidine, use of alternative antiplatelet agents such as clopidogrel or addition of IIb/IIIa inhibitors will modify these acute outcomes or further reduce subacute stent thrombosis events after similar suboptimal results. Late clinical restenosis (TLR, 15.5% vs. 10.2%, p = 0.015; TVF, 26.8% vs. 16.0%, p < 0.001) was also significantly more common in registry patients, reflecting their smaller final minimum lumen diameter and multiple stent use. With these caveats, the clinical results of "suboptimal" stent deployment with ticlopidine-containing regimens are clinically acceptable and compare well with those of optimal stenting with similar drug therapy.

Limitations.   This registry analysis has several limitations. The first limitation is the small population size and the exclusive use of the Palmaz-Schatz stent. A study of a larger number of patients with suboptimal stent results or similar patients treated with other available stents may have found significant differences for the combined 30-day end point compared with patients with optimal results. Nevertheless, this study represents the largest reported series of patients with suboptimal stent results in the modern era of routine high-pressure poststent dilation and antiplatelet therapy, and there is little evidence from current stent-versus-stent trials that suggest major difference in the thrombotic behavior of other devices. The second limitation is that conclusions regarding antithrombotic regimens are limited, because these regimens were assigned by operator preference rather than in a randomized fashion. Although we could not demonstrate it by objective criteria, had operators chosen one regimen (e.g., coumarin) for worse stent results, the negative outcomes of that therapy may have been partially the result of this selection bias rather than a shortcoming of the drug regimen itself. Our findings of the protective effect of ticlopidine, however, are supported by the results of two large randomized trials of optimal stent results. The third limitation is that the absence of angiographic follow up prevents the determination of restenosis parameters, such as late loss and loss index. Clinical restenosis, however, has been shown to correlate closely with angiographic restenosis, and by not subjecting patients to routine angiographic followup, a potential bias toward increased repeat target lesion revascularization may be avoided. The fourth limitation is that the registry did not adequately assess the role of IIb/IIIa inhibitor therapy, due to infrequent use of this class of drugs (9% of registry patients). Reports from the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) trial (17) suggest that routine use of such agents may have decreased the incidence of CK elevations after suboptimal stenting, although the long-term benefits of such treatment are still uncertain. Finally, the results from the STARS registry may not be generalizable to settings of more complex lesion morphology, or abrupt closure/threatened closure in which more severe dissection may be combined with reduced flow that is not improved with use of additional stents. In these situations, there may be benefit to supplementing aspirin and ticlopidine with additional antithrombotic therapy, including IIb/IIIa inhibitors.

	Footnotes

 
This work was supported by a grant from Cordis, a Johnson and Johnson Company, Warren, New Jersey.

	References

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