Published online before print January 26, 2009, doi: 10.1161/CIRCULATIONAHA.108.804203
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(Circulation. 2009;119:687-698.)
© 2009 American Heart Association, Inc.
Interventional Cardiology |
Early Stent Thrombosis in Patients With Acute Coronary Syndromes Treated With Drug-Eluting and Bare Metal Stents
The Acute Catheterization and Urgent Intervention Triage Strategy Trial
From Columbia University Medical Center and the Cardiovascular Research Foundation, New York, NY (J.A., A.J.L., R.M., J.M., H.P., M.B.L., G.W.S.); Hôpital Cardiologique, Lille, France (M.E.B.); AnMed Health, Anderson, SC (B.T.M.); Mid Carolina Cardiology, Charlotte, NC (D.A.C.); Cleveland Clinic, Cleveland, Ohio (A.M.L.); Duke University Medical Center, Durham, NC (E.M.O.); and Auckland City Hospital, Auckland, New Zealand (H.D.W.).
Correspondence to Gregg W. Stone, MD, 161 Ft Washington Ave, 5th Floor, New York, NY 10032. E-mail gs2184{at}columbia.edu
Received July 3, 2008; accepted November 12, 2008.
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Abstract |
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Background— The clinical and angiographic predictors of early (<30 days) stent thrombosis (ST) have not been reported in high-risk patients with acute coronary syndromes.
Methods and Results— Qualitative and quantitative coronary angiographic analyses were performed in 3405 patients with moderate- and high-risk acute coronary syndromes in whom stents were implanted in the prospective randomized Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial, including 3043 patients (89.4%) in whom drug-eluting stents were implanted. Within 30 days, definite or probable ST occurred in 48 patients (1.4%). ST rates were not significantly different in patients treated with bare metal stents compared with drug-eluting stents (1.4% versus 1.4%; P=1.00) or with heparin plus glycoprotein IIb/IIIa inhibitors (1.1%) compared with bivalirudin with or without IIb/IIIa inhibitors (1.6% and 1.5%, respectively; P=0.26 and P=0.37, respectively). Compared with patients without ST, patients with ST more frequently had insulin-requiring diabetes mellitus and baseline renal insufficiency, a greater overall burden of coronary atherosclerosis, and suboptimal final angiographic results. ST also was more common in patients without preprocedural thienopyridine administration and with inconsistent antiplatelet drug use within 30 days. By multivariable analysis, the strongest independent predictors of definite ST were a smaller final stent minimal lumen diameter, a lack of preprocedural thienopyridine administration, the extent of coronary artery disease, and higher baseline hemoglobin level.
Conclusions— Occurring in nearly 1 in 70 patients, early ST is relatively common in acute coronary syndromes, occurs with similar frequency after anticoagulation with either heparin plus glycoprotein IIb/IIIa inhibitors or bivalirudin with or without IIb/IIIa inhibitors, and is predicted by diffuse atherosclerosis, suboptimal angiographic results, and inadequate pharmacotherapy.
Key Words: acute coronary syndrome • stent • thrombosis
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Introduction |
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Recent guidelines from the American College of Cardiology/American Heart Association and the European Society of Cardiology recommend an early invasive approach in high-risk patients with non–ST-segment elevation acute coronary syndromes (ACS).1,2 Notwithstanding concerns of an increased risk of stent thrombosis (ST) in patients with ACS because of heightened systemic and intracoronary thrombogenicity and inflammation, as well as delayed endothelialization, drug-eluting stents (DES) are widely used in such patients in daily practice.3–7 In the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) quality initiative registry, 66.2% of 8852 patients with high-risk non–ST-segment elevation ACS were treated with DES.4 Moreover, although DES have to date proven safe and effective for patients with ST-segment elevation myocardial infarction (MI) (such as shown in randomized trials such as the Trial to Assess the Use of the Cypher Stent in Acute Myocardial Infarction Treated With Balloon Angioplasty [TYPHOON] and the Randomized Comparison of Paclitaxel Eluting Stent Versus Conventional Stent in STEMI [PASSION] trial),8,9 the incidence and predictors of ST with bare metal stents (BMS) and DES, including clinical and angiographic characteristics and procedural outcomes, and the impact of antiplatelet therapy adherence have not been investigated in patients with non–ST- segment elevation ACS.
Editorial p 657
Clinical Perspective p 698
In the multicenter, prospective, randomized Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial, coronary stents were implanted in 7162 patients with moderate- and high-risk ACS, and core laboratory qualitative and quantitative coronary angiographic (QCA) analyses were performed in 3405 patients as part of a formal substudy, representing the largest stent QCA database to date.10 ACUITY thus provides a unique opportunity to investigate the prognostic utility of clinical and angiographic data in patients with ACS. We therefore sought to evaluate the frequency and predictors of ST occurring within the first 30 days after stent implantation in patients with ACS in the ACUITY trial.
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Methods |
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Patient Population and Study Protocol
The ACUITY trial design has been described elsewhere.10,11 In brief, 13 819 patients with moderate- and high-risk ACS in whom an early, invasive strategy was intended were randomly assigned to a heparin (unfractionated or enoxaparin) plus glycoprotein IIb/IIIa inhibitors (GPI), bivalirudin plus GPI, or bivalirudin monotherapy before angiography. Patients assigned to heparin plus GPI or bivalirudin plus GPI underwent a second randomization to routine upfront treatment with GPI immediately after the first randomization or to deferred selective treatment with GPI in those undergoing percutaneous coronary intervention (PCI) starting in the cardiac catheterization laboratory. Angiography was performed in all patients within 72 hours of randomization. Patients were then triaged to PCI, coronary artery bypass graft surgery, or medical management at the discretion of the physician, depending on the coronary anatomy and the suitability of lesions for revascularization. In patients who were triaged to PCI, selection of stent type (BMS or DES) was left to the operator’s discretion. The present analysis is restricted to patients in whom
1 stents were implanted in the index procedure.
All interventions were performed using standard techniques. Aspirin (300 to 325 mg orally or 250 to 500 mg IV) was administered daily during the index hospitalization, and 75 to 325 mg/d was recommended to be prescribed indefinitely after discharge. The initial dosing and timing of clopidogrel were left to the investigator’s discretion, with a 300-mg initial loading dose required in all cases no later than 2 hours after PCI. Clopidogrel (75 mg/d) was strongly recommended for 1 year after discharge. Compliance with aspirin and thienopyridine administration on >50% of days after hospital discharge was recorded at the 1-month follow-up visit. The study protocol was approved by the institutional review board or ethics committee at each center, and written informed consent was obtained in all patients.
Clinical End Points and Definitions
ST and major adverse clinical events, including death resulting from any cause, MI, unplanned revascularization for ischemia, and major bleeding, were adjudicated by an independent clinical events committee blinded to treatment assignment with review of original source documents. The primary end-point definitions have previously been detailed.11 ST was classified as either definite or probable. Definite ST was defined as angiographic thrombus or subacute closure within the stented vessel at the time of clinically driven angiography for ischemia. Probable ST was defined as any death not attributed to a noncardiac cause or any Q-wave MI in the absence of documented angiographic stent patency.
Quantitative Coronary Angiography
Core laboratory coronary QCA was planned in at least the first 6300 US patients enrolled in the ACUITY trial as a formal substudy. All angiograms were reviewed at an independent angiographic laboratory (the Cardiovascular Research Foundation, New York, NY) for determination of baseline and post-PCI epicardial blood flow rates, myocardial perfusion, and procedural complications.11 In total, QCA was performed in 6921 patients enrolled in ACUITY (88% of all 7851 US patients), including 3664 patients in whom PCI was performed (86% of all 4254 US patients who underwent PCI) and 3405 patients in whom 1 stents were implanted. QCA was performed on the baseline and post-PCI angiograms by a technician blinded to randomization assignment and clinical outcomes using validated quantitative methods.12 Measures included reference vessel diameter, minimal lumen diameter (MLD), and percentage diameter stenosis (DS). DS was reported separately within the stented segment and the lesion segment, which includes the stented segment and 5 mm proximal and distal to the stented segment. Acute gain was calculated as final MLD minus baseline MLD. Furthermore, the total burden of atherosclerosis in the coronary tree was estimated in each patient by measuring the number of stenotic segments with DS >30% per patient, the extent of disease burden per patient (defined as the sum of the lengths of the lesions with >30% DS), and the Duke jeopardy score.13 In addition, adverse procedural angiographic complications, including new thrombus formation, spasm, abrupt closure, no reflow, perforation, distal embolism, and dissection, were reported. Lesion morphology, Thrombolysis in Myocardial Infarction (TIMI) flow grades, uncorrected and corrected TIMI frame counts, and myocardial blush score were determined according to previously defined criteria.12,14,15
Statistical Analysis
The study population consisted of the 3405 patients in whom 1 stents were implanted and in whom QCA was performed within the formal substudy. Continuous variables are expressed as mean±SD and were compared by use of the Student t test. Categorical variables were compared by use of the 
2 test or Fisher exact test. Univariate and multivariable analyses by logistic regression were performed to identify the predictors of ST. After univariate selection, the multivariable model was built by stepwise variable selection with entry and exit criteria set at the P=0.1 and P=0.2 levels, respectively. The following patient-level candidate predictors were evaluated: all variables in Tables 1 through 3
(except antiplatelet drug compliance after discharge, which, if included, would necessitate excluding patients who died before hospital discharge)16 and all procedure-related factors in Table 4. The exact lesion in which ST occurred could not be assigned in patients without angiographic or autopsy follow-up who received multiple stents. Therefore, lesion-level data were not entered into the predictive model of definite or probable ST (but were for the model of definite ST). Thus, 6 variables (insulin-requiring diabetes mellitus, renal insufficiency, 3-vessel disease, number of lesions per patient, Duke jeopardy score, and preprocedural thienopyridine administration) were entered into the multivariable model for definite or probable ST, and 11 variables (insulin-requiring diabetes mellitus, baseline hemoglobin, extent of coronary artery disease per patient, Duke jeopardy score, any thrombus, any abrupt closure, any no reflow, composite adverse angiographic events, final stent MLD, final stent percent DS, and preprocedural thienopyridine administration) were entered into the multivariable model for definite ST. Because strong colinearity was found between final stent and lesion MLD and between final stent and lesion percentage DS, only final stent MLD and final stent percent DS were included in the model. All statistical tests were 2 tailed. Statistical significance was set at a level of 0.05.
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The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Frequency, Timing, and Outcomes of ST
Among the 3405 study patients (in whom a total of 4636 lesions were treated),
1 DES (with or without BMS) were implanted in 3043 patients (89.4%), whereas 362 patients received only BMS (Figure 1). ST within 30 days occurred in 48 patients (1.4%), including 32 definite and 16 probable ST. ST occurred in 43 of 3043 patients (1.4%, including 29 definite and 14 probable ST) in whom DES were implanted and in 5 of 362 patients (1.4%, including 3 definite and 2 probable ST) in whom only BMS were implanted (relative risk, 1.00; 95% confidence interval [CI], 0.91 to 1.10; P=1.00). ST occurred at a median time of 5 days after implantation (interquartile range, 1.5 to 8 days; range 0 to 28 days) (Figure 2). As shown in Table 1, compared with patients without ST, those with definite ST had significantly higher 30-day rates of MI and unplanned revascularization for ischemia, whereas patients with definite or probable ST had significantly higher rates of death, MI, unplanned revascularization, and major bleeding.
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Baseline Predictors of ST
Compared with patients without ST, those with ST had a higher prevalence of insulin-requiring diabetes mellitus and renal insufficiency (Table 2). Other baseline demographic and laboratory features were comparable in patients with and without ST. Definite or probable ST within 30 days occurred in 1.1%, 1.6%, and 1.5% of patients assigned to heparin plus GPI, bivalirudin plus GPI, and bivalirudin monotherapy, respectively (P=0.26 for heparin plus GPI versus bivalirudin plus GPI; P=0.37 for heparin plus GPI versus bivalirudin monotherapy; P=0.81 for bivalirudin plus GPI versus bivalirudin monotherapy). In addition, the incidence of ST was not significantly different between bivalirudin (alone or plus GPI) and heparin plus GPI (P=0.28). Assignment to routine upstream versus deferred selective GPI use also was not a significant predictor of ST.
Quantitative Coronary Angiography
Baseline lesion and vessel parameters and QCA measures were comparable in patients with and without ST (Table 3). However, patients with ST were more significantly likely to have a higher number of stenotic lesions and greater Duke jeopardy score compared with patients without ST (Table 4). Patients subsequently developing ST also were more likely to experience intraprocedural angiographic complications such as new thrombus formation, no reflow, and abrupt closure, although no other significant differences were found in the incidence of adverse angiographic events, TIMI flow, or myocardial blush rates at the end of the procedure in patients with and without ST (Table 5). Patients in whom ST subsequently occurred had a higher postprocedural in-stent percentage DS and smaller MLD compared with those in whom ST did not develop. More severe stenoses and thrombus at baseline, the occurrence of adverse angiographic complications such as new thrombus formation, abrupt closure and no reflow during the procedure, and a higher postprocedural in-stent percentage DS and smaller MLD were associated with definite ST.
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Antiplatelet Medication Use
As shown in Table 6, patients with ST less frequently received preprocedural thienopyridines. ST also was more frequent in patients in whom aspirin and thienopyridines were used on <50% of days after hospital discharge.
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Multivariable Predictors of ST
By multivariable analysis using patient-level data, insulin-requiring diabetes mellitus, Duke jeopardy score, preprocedural thienopyridine administration, and renal insufficiency were independent predictors of definite or probable ST (Table 7). Predictors of definite ST by multivariable analysis on a lesion level included final stent MLD, preprocedural thienopyridine administration, extent of coronary artery disease per patient, and baseline hemoglobin level (Table 7).
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Generalizability of the Study Cohort
Because the QCA substudy was composed solely of patients enrolled in the United States, a comparison of patients undergoing PCI in ACUITY with and without QCA was performed. As shown in Table 8, compared with patients without QCA, those with QCA (eligible for the present study) were younger, were more often women, weighed more, and were more likely to have diabetes mellitus, hypertension, hyperlipidemia, prior MI, and renal insufficiency and to have undergone prior PCI and coronary artery bypass graft surgery, but they were less likely to have cardiac biomarker elevation or ST-segment deviation. Patients eligible for the present study also were more likely to be treated with DES rather than BMS and had a greater number of stents implanted. The incidence of definite or probable ST was 1.4% (52 of 3757) in patients without QCA, comparable to the 1.4% ST rate in patients with QCA. By logistic regression, significant independent predictors of definite or probable ST in all patients (including those with and without QCA) were insulin-requiring diabetes mellitus (odds ratio, 2.35; 95% CI, 1.36 to 4.07; P=0.002), previous MI (odds ratio, 1.91; 95% CI, 1.26 to 2.89; P=0.002), and ST-segment deviation (1 mm) (odds ratio, 1.90; 95% CI, 1.26 to 2.87; P=0.002).
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Discussion |
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The principal findings of this clinical and angiographic study examining the frequency, correlates, and implications of early ST after PCI in patients with moderate- and high-risk non–ST-segment elevation ACS are as follows. First, occurring in nearly 1 in 70 patients, ST within 30 days was relatively common in these high-risk patients, although the risk of ST was independent of randomization to heparin plus GPI or bivalirudin with or without GPI and of the timing of GPI. Second, as in other clinical syndromes, early definite or probable ST in patients with ACS was associated with a high rate of death, MI, and need for repeat revascularization within 30 days. Third, independent predictors of definite ST within 30 days in patients with ACS were final stent MLD, preprocedural thienopyridine administration, the extent of coronary artery disease, and baseline hemoglobin level. Finally, early ST also was associated with noncompliance with antiplatelet medications after hospital discharge.
Incidence and Implications of Early ST
ACS and thrombotic lesions are known risk factors for ST.17–20 In the present study, the rate of ST within 30 days was 1.4%, significantly higher than the 0.3% to 0.5% ST rates within the same period reported from the randomized controlled trials of DES in patients with mostly stable coronary artery disease and stent implantation in a single lesion21,22 but similar to the rates reported within 30 days after unrestricted use of stents.19,23,24 The incidence of early definite ST in the present study (0.9%) also was comparable to that in the network meta-analysis that included multiple high-risk patient and lesion cohorts (0.7%).25 No differences in the rates of early ST in the present study between BMS and DES were apparent, although in the previous randomized trials, such differences did not become apparent until after 1 year of follow-up.21,22 As such, longer-term follow-up from the present study is required to determine whether the incidence of ST varies between DES and BMS in thrombotic coronary syndromes.
In the present study, by 30 days, early definite or probable ST was associated with mortality in more than one quarter of patients, MI in nearly 80% of patients, and the need for repeat revascularization for management in two thirds of patients. Major bleeding also was increased in patients with early definite or probable ST, possibly as a result of repeat procedures in the setting of intense anticoagulation to treat the ST event, although the possibility that a major bleeding event resulted in discontinuation of antiplatelet agents with subsequent ST cannot be excluded from the present study. Of interest, when identification of ST was restricted to the "definite" definition (32 of the 48 total ST cases), the association with early mortality was not as great, reflecting the fact that the "probable" ST definition includes cardiac or unexplained death as a surrogate for ST, which in some cases is likely overly sensitive. Nonetheless, these data add to prior published reports emphasizing the dire nature of ST, mandating optimized procedural technique, optimal adjunct pharmacology, and safer stents to prevent this rare but devastating complication of PCI. As described below, several of the variables most strongly associated with ST may in part be under physician and patient control.
Predictors of Early ST
Predictors of early ST with both DES and BMS have previously been investigated, although predominantly in patients with stable coronary artery disease. In the BMS era, early ST was associated with procedure-related factors such as total stent length, multiple stents, stent overlap, lower maximal inflation pressure, smaller balloon size, final MLD within the stent, persistent slow flow, and persistent dissection, as well as comorbidities such as congestive heart failure and metastatic cancer.17,26–31 Intravascular ultrasound studies also have suggested that early ST may be related to smaller poststent luminal dimensions, lack of stent expansion, residual dissection, plaque burden, incomplete stent apposition, and in-stent thrombus and tissue prolapse but not to preintervention baseline features, although these studies were small and thus less than definitive.27,29,32–34 No study has clearly demonstrated that procedural anticoagulation affects the rate of early ST in patients with ACS, although in the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial, the addition of abciximab to unfractionated heparin was associated with a reduced rate of ST at 30 days in patients with ST-segment elevation acute MI.35 In addition to procedure-related factors, premature antiplatelet medication discontinuation and baseline characteristics denoting increased thrombogenic risk such as ACS, renal failure, diabetes mellitus, multivessel disease, and low ejection fraction have previously been identified as important predictors of ST with DES,23,36–41 in part because of delayed endothelial healing.6,7,42
In the present large-scale investigation of patients with moderate- and high-risk ACS in which DES were used in 
90% of stented patients, several patient-related variables were independently associated with early definite or probable ST, including insulin-requiring diabetes mellitus and baseline renal insufficiency. A unique design aspect of ACUITY was a large independent angiographic core laboratory study blinded to randomization and adjudicated clinical events, which identified the extent of coronary atherosclerosis and a high poststent residual stenosis as correlates of early ST. Several variables related to suboptimal antiplatelet medication administration either before or after the procedure also were associated with early ST. By multivariable analysis, however, baseline clinical variables such as insulin-requiring diabetes mellitus and renal insufficiency were not predictive of definite ST; the 4 independent determinates of definite ST within 30 days were a higher postintervention residual stenosis, nonadministration of a thienopyridine agent before the procedure, the extent of coronary artery disease, and a higher baseline hemoglobin level. The presence of diffuse vessel disease may reflect underlying endothelial dysfunction, which has been associated with more advanced coronary artery disease,40,43 or the hemodynamic effects of inflow or outflow disease, which is difficult to measure directly. Diabetes mellitus and chronic kidney disease are known to be associated with more diffuse atherosclerosis, a variable infrequently considered in prior risk models of ST. This may explain why the extent of coronary artery disease remained a significant predictor for ST, whereas diabetes mellitus and chronic renal insufficiency did not. The mechanism underlying the association between baseline hemoglobin level and ST is not clear, although theoretically high viscosity may promote thrombus formation in patients with ACS, who already have heightened systemic and intracoronary platelet reactivity, thrombin generation, and inflammation. Overfitting of the multivariable regression model also cannot be excluded as contributing to selection of this variable. Of note, the rates of ST were similar with heparin plus GPI, bivalirudin plus GPI, and bivalirudin monotherapy, consistent with the similar rates of ischemia demonstrated with these 3 anticoagulation regimens at 30 days.10
Importantly, several of the risk factors for ST identified in the present report may to some extent be under the control of the patient or the physician. Ensuring thienopyridine administration before the procedure in patients with ACS and emphasizing the importance of antiplatelet agent compliance after stenting (or not performing PCI in the patient likely to be noncompliant or requiring discontinuation of antiplatelet agents for planned surgery, etc) may reduce the incidence of ST within 30 days. The fact that smaller postprocedure lumen dimensions as assessed by angiography predicted ST provides important confirmatory and complementary evidence to the earlier small intravascular ultrasound studies suggesting the role of optimum technique in potentially improving patient outcomes.27,29,32–34 Thus, the routine use of techniques known to increase stent dimensions such as high-pressure stent implantation or postdilatation at high pressure with noncompliant balloons, adequate lesion preparation in calcified plaques, or intravascular ultrasound–guided stenting may optimize stent expansion and reduce early ST, even if angiography is a relatively insensitive imaging tool to detect small changes in luminal dimensions.
Study Limitations
Although the largest such investigation to date of ST in patients with ACS, the present study has several limitations that should be acknowledged. As a post hoc analysis, the results should be considered exploratory and hypothesis generating, especially in that corrections for multiple comparisons were not made to adjust for the multiple correlates of ST examined. The angiographic core laboratory substudy, although the largest such analysis ever performed, was undertaken in only approximately half of the patients, specifically those enrolled in the United States. Not surprisingly, therefore, the baseline demographic and procedural characteristics differed between patients with and without QCA. The results of the present study thus apply most strongly to those patients enrolled in the United States or those with representative clinical and angiographic features as in the study cohort. A high prevalence of DES use in the United States during the period in which ACUITY enrolled patients hinders comparison of ST rates between DES and BMS. Antiplatelet medication data at 30 days consisted only of whether aspirin, clopidogrel, or ticlopidine was taken on 50% of days since hospital discharge based on patient reports; detailed data as to the reasons for medication noncompliance and exact use at the time of ST after hospital discharge were not available. Thus, the prognostic role of antiplatelet agent discontinuation, as previously demonstrated,37,44,45 may have been incompletely characterized in our model. The exact timing and loading dose of clopidogrel was not assessed in patients who received this agent before randomization. However, as per accepted practice, clopidogrel was administered no later than 2 hours after PCI; thus, subacute ST most commonly occurred after a time when maximal inhibition of the P2Y12 platelet receptor would have been expected. Further studies should assess the potential impact of the timing and dose of thienopyridine loading on the incidence of acute and subacute ST. Stented lesion length, maximal dilatation pressure, and the performance of postdilatation, factors that were predictors of early ST in some earlier reports, were not available in the present analysis.17,28 Left ventricular ejection fraction also was not available in all patients, and the majority of patients had a normal global ejection fraction. Thus, the impact of reduced systolic function on subsequent ST might be underestimated. Intravascular ultrasound was not routinely performed or analyzed in a core laboratory in the present study; the extent to which intravascular ultrasound parameters of stent expansion or residual disease may have complemented or supplanted the angiographic predictors of ST is unknown. The number of ST events might be insufficient to have identified all independent covariates in the multivariable model, and potential overfitting of the multivariable regression model cannot be completely eliminated. Thus, the present results should be considered hypothesis generating and validated in future studies. Similarly, given the relatively infrequent occurrence of ST, the varying predictors of acute versus subacute ST and ST after DES versus BMS (or paclitaxel-eluting versus sirolimus-eluting stent) could not be studied reliably in the present analysis. Even larger studies are required to determine whether differences in the characteristics between patients with and without ST among subgroups exist and to create more stable multivariable models. Finally, the results of the present study apply to ST occurring within 30 days; the correlates of late ST may vary and will be elucidated with longer-term follow-up of the patients enrolled in the ACUITY trial in a separate analysis.
Conclusions and Clinical Implications
Early ST in patients with ACS occurs in 1 in 70 patients, a rate higher than previously described in patients with more stable ischemic heart disease but with equally devastating consequences. Attention to the prognostic variables predictive of early ST as identified in the present study (eg, maximizing the poststent MLD by use of high-pressure, appropriately sized balloons for postdilatation, or both in combination and using strategies to reduce antiplatelet noncompliance) may lessen the frequency of ST, thereby improving event-free survival in these high-risk patients.
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Acknowledgments |
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Sources of Funding
The ACUITY trial was sponsored and funded by The Medicines Co (Parsippany, NJ) and Nycomed (Roskilde, Denmark).
Disclosures
Dr Lansky reports receiving research grants from The Medicines Co, Cordis, Boston Scientific, Medtronic, and Abbott. Dr Mehran is on the speakers’ bureau for The Medicines Co, Cordis, and Boston Scientific and has received honoraria from The Medicines Co. Dr Moses reports receiving consulting fees from Cordis and is on the speakers’ bureau for AstraZeneca. Dr Bertrand reports receiving consulting fees from Servier Laboratories, Sanofi Aventis, and Nycomed and lecture fees from Servier Laboratories and Sanofi Aventis. Dr Cox reports receiving consulting fees from Boston Scientific, Guidant, St Jude, Cordis, and The Medicines Co and lecture fees from The Medicines Co, Boston Scientific, Guidant, St Jude, and Cordis. Dr Lincoff reports receiving lecture fees from The Medicines Co and grant support from The Medicines Co and Centocor. Dr Ohman has received consulting fees from The Medicines Co, Liposcience, Inovise Medical, Response Biomedical, Datascope, and Abiomed; equity interests in Medtronic and Savacor; lecture fees from Schering-Plough, Bristol-Myers Squibb, and Datascope; and grant support from The Medicines Co, Schering-Plough, Bristol-Myers Squibb, Sanofi-Aventis, Millennium Pharmaceuticals, Eli Lilly, and Daiichi Sankyo. Dr Ohman is on the speakers’ bureau for CV Therapeutics and The Medicines Co. Dr White has received grant support from The Medicines Co, Sanofi-Aventis, Schering-Plough, Eli Lilly Co, Merck Sharpe and Dohme, National Institutes of Health, Pfizer, Roche, Johnson & Johnson, and AstraZeneca. Dr Leon is the member of the scientific advisory board for Abbott, Boston Scientific, and Medtronic. Dr Stone reports receiving research support from The Medicines Co, Boston Scientific, and Abbott Vascular and honoraria from Eli Lilly. The other authors report no conflicts.
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Footnotes |
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Clinical trial registration information—URL: http://clinicaltrials.gov. Unique identifier: NCT00093158.
Guest Editor for this article was Antonio Colombo, MD.
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Circulation 2009 119: 649-651.
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