Risk Factor For Stent Thrombosis Research Articles

Percutaneous Coronary Intervention Outcomes in a Low-Volume Center

American College of Cardiology (ACC) guidelines state that percutaneous coronary interventions (PCI) be performed at centers and by operators with high-volume (>400 yearly/center) whose historical and current risk-adjusted outcomes statistics are comparable to those reported in large registries. Tripler Army Medical Center is a low-volume treatment facility but has a geographic need and special mission requirement for providing this service. We computed 30-day incidence of stent thrombosis, need for repeat revascularization, and all-cause mortality for all PCIs performed at Tripler from January 2002 through June 2008. The New York State Registry regression model was selected among 3 risk-adjustment models that we assessed in our patients. This model was used to compute expected mortality rate based on patient risk factors. The 30-day incidence of stent thrombosis and repeat revascularization was also determined, and the long-term incidence of these events was estimated with the Kaplan-Meier method as was survival. For all 546 PCI procedures, 30-day mortality was 1.47%, the incidence of stent thrombosis 2.1%, the incidence of any repeat revascularization 5.1%, and the combined event rate 5.9%. Based on risk factors used in the New York State Registry, our expected mortality was 1.93% and not significantly different from the observed rate. Although survival at 1 and 3 years appeared comparable with benchmarks at 94.6% and 89.3%, as did repeat revascularization rates at 13.0% and 21.4%, the incidence of stent thrombosis was regarded as high whether the definition included possible cases (3.2% and 3.9%) or only those regarded as definite or probable (2.7% and 3.1%). We did not identify any remediable risk factors for stent thrombosis, nor were we able to identify significant differences by year or by operator. However, visual inspection of a plot of deciles of New York State risk of death demonstrated 2 outlier cases among the 8 who died, who could have been considered candidates for thorough peer review. We recommend other low-volume interventional programs enter all patients undergoing PCI into a database, their own local registry even if not a national one such as the American College of Cardiology National Cardiovascular Data Registry, obtain information about survival and cardiac events during follow-up, compute and risk-adjust in-hospital or 30-day mortality, and use the objective assessment of risk in individual patients to identify outliers when outcome is adverse, and possibly as a means of triaging patients to appropriate therapy before choosing PCI.

Stent thrombosis: who's guilty?

Stent thrombosis is a devastating complication of percutaneous coronary intervention (PCI) which remains unsolved as it is poorly predicted and prevented. Its frequency appears to be low (0.8–2%) but most evaluations come from registries that are likely to underestimate the real prevalence. The mortality associated with stent thrombosis is high, within a range of 25–40%, comparable with that of many cancers. Because of its low incidence, stent thrombosis has been neglected for too long by the interventional community. Recent understanding of the underlying mechanisms has reactivated our consciousness and opened up new avenues for dedicated preventive approaches. Some of the explanations for stent thrombosis will be found in relation to the patient. A number of simple clinical traits have been identified as risk factors for stent thrombosis including diabetes, active smoking, prior or ongoing myocardial infarction, heart failure, recent cancer, or renal insufficiency.1 Angiographic characteristics have also been associated with stent thrombosis including small arteries, long lesions, bifurcations, thrombotic or ulcerated lesions, or low TIMI flow. Among biological factors, the markers of necrosis, inflammation, and high platelet reactivity on double antiplatelet therapy, have frequently been associated with stent thrombosis. However, evidence has accumulated to suggest that the strongest factor associated with stent thrombosis is the discontinuation of clopidogrel treatment. This is again highlighted in the study of Schulz and colleagues who report the powerful preventive effect of clopidogrel within the first 6 months of drug-eluting stent (DES) implantation.2 The causal relationship between clopidogrel discontinuation and stent thrombosis during this period cannot be demonstrated but is suggested by the average 9-day delay between interruption and stent thrombosis, an estimated time frame for platelet functional recovery. The average time to stent thrombosis of 104 days if discontinuation occurs >6 months after DES placement and the much lower frequency of stent … *Corresponding author. Tel: +33 1 42 16 30 06, Fax: +33 1 42 16 29 31, Email: gilles.montalescot{at}psl.aphp.fr

Clopidogrel Adherence following Percutaneous Coronary Intervention with a Drug-Eluting Stent in a VA Medical Center

Background: Antiplatelet therapy with aspirin and a thienopyridine is the standard of care for prevention of thrombosis following coronary stent implantation. Recent evidence suggests a prolonged risk of stent thrombosis; therefore, clopidogrel therapy for at least 1 year is recommended following implantation of a drug-eluting stent. Premature discontinuation of clopidogrel is a well-recognized risk factor for stent thrombosis. Objective: To identify the rate of adherence to clopidogrel therapy among patients who have undergone percutaneous coronary intervention (PCI). Methods: We queried the central Veteran Affairs (VA) pharmacy database for each patient who underwent PCI with a drug-eluting stent between September 2004 and August 2005 at a single VA medical center. Based on pharmacy refill records, patients were considered adherent to clopidogrel if they filled more than 80% of the clopidogrel prescriptions. Results: We observed that 20.3% of patients were nonadherent to clopidogrel therapy for the course that they were assigned. Shorter duration of therapy was the only factor that predicted increased adherence. Race, polypharmacy, marital status, prior clopidogrel use, and age did not have a significant impact on adherence. Multivariable analysis did not demonstrate any other significant relationships. Conclusions: In this high-risk cohort of patients who have undergone PCI, we observed a 20% incidence of nonadherence to clopidogrel therapy. Shorter duration of therapy had a significant impact on improving rates of adherence in our analysis. This observation is of particular concern given the recent recommendations to prolong antiplatelet therapy to at least 1 year following PCI with a drug-eluting stent.

Aspirin noncompliance is the major cause of “aspirin resistance” in patients undergoing coronary stenting

We investigated the hypothesis that biological aspirin "resistance" may often be related to noncompliance in patients undergoing coronary stenting. Premature discontinuation of antiplatelet therapy has been identified as a major risk factor for stent thrombosis and prior aspirin withdrawal has been associated with poor prognosis after acute coronary syndrome. We prospectively investigated the occurrence of aspirin noncompliance in 136 consecutive patients undergoing coronary stenting receiving aspirin 75 mg daily. We analyzed posttreatment maximal intensity of arachidonic acid-induced platelet aggregation (AA-Ag) during hospitalization after controlled intake of aspirin and 1 month after hospital discharge. After 1 month, all "nonresponders" received controlled aspirin 75 mg and assessment of response was repeated. Aspirin nonresponse was defined by AA-Ag >30%. During inhospital period, the range of AA-Ag varied from 0% to 34% with a mean value of 7.5% +/- 10%, and 4 patients (3%) were classified as nonresponders. One month after discharge, AA-Ag of the population was significantly higher than during the hospital phase (15.3 +/- 23 vs 7.5 +/- 10%, P = .0004), and 19 patients (14%) were identified as nonresponders. After controlled administration of aspirin, all but one of these nonresponders became responders and were identified as patients with noncompliance rather than biological resistance. Aspirin resistance is rare in compliant patients using methods that directly indicate the degree of platelet cyclooxygenase inhibition. More than 10% of patients receiving aspirin for coronary stenting are noncompliant for aspirin therapy during the first month after stenting. These results suggest a need for improved education of these patients.

Chronic kidney disease and dipstick proteinuria are risk factors for stent thrombosis in patients with myocardial infarction

Kidney failure (stage 5 chronic kidney disease [CKD]) is an independent risk factor for stent thrombosis (ST). Moderate (stage 3-4) CKD and proteinuria are both associated with adverse cardiovascular events, including worse outcomes after myocardial infarction (MI). Whether moderate CKD and proteinuria increase the risk of ST after MI is not known. This study evaluated the risk of ST associated with moderate CKD and dipstick proteinuria. We retrospectively analyzed clinical and laboratory data from 956 non-stage 5 CKD patients who were admitted with MI and received intracoronary stenting. Clinical follow-up was collected at 1 year for definite or probable ST, as well as for all-cause mortality, nonfatal MI or death, and target vessel revascularization or coronary artery bypass graft surgery. After adjustment for multiple clinical and biochemical covariates, patients with both estimated glomerular filtration rate (GFR) of 15 to 59 mL min(-1) 1.73 m(-2) and > or =30 mg/dL dipstick proteinuria had increased cumulative incidence of ST (hazard rate [HR] 3.69, 95% CI 1.54-8.89), all-cause mortality (HR 2.68, 95% CI 1.34-5.37), and nonfatal MI or death (HR 3.20, 95% CI 1.77-5.81) at 1 year. In addition, estimated GFR of 15 to 59 mL min(-1) 1.73 m(-2) was a significant independent predictor of ST (HR 2.61, 95% CI 1.33-5.10). Dipstick proteinuria > or =30 mg/dL was associated with a trend toward increased risk for all outcomes. In an acute MI population, moderate CKD was identified as a novel prognostic marker for ST. In addition, patients with both decreased GFR and proteinuria had higher incidences of all-cause mortality and nonfatal MI or death than patients with either condition alone.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Noncardiac Surgery for Patients with Coronary Artery Stents

Physicians are increasingly being confronted with questions regarding the appropriate management of patients with recently implanted coronary stents who are in need of noncardiac surgery. Specifically, what is the optimal timing of elective procedures and how should antiplatelet therapy be managed in these patients, especially in those in need of emergent procedures? Continued antiplatelet therapy through the perioperative period might increase the risk of surgical bleeding while interruption of antiplatelet therapy predisposes to stent thrombosis, particularly in the setting of systemic hypercoagulation that frequently occurs after some surgeries.1 In this issue of Anesthesiology, two papers from the Mayo Clinic in Rochester, Minnesota provide further insight into these perplexing issues.2,3

Revealing the Silver and Red Lining in Drug-Eluting Stents With Angioscopy

Drug-eluting stents (DES) are widely used in percutaneous coronary intervention and have resulted in significant reductions in target-vessel revascularization as compared with bare-metal stents (BMS) in randomized, controlled trials and in unrestricted patient and lesion subsets.1,2 Comprehensive analyses have proven the safety of sirolimus-eluting stents (SES) and paclitaxel-eluting stents (PES) compared with BMS, with similar rates of death and myocardial infarction after as much as 4 years of follow-up2,3; however, a valid safety concern remains, given that DES increase the risk of late (>30 days) and very late (>1 year) stent thrombosis compared with BMS. Our understanding of the risk factors for stent thrombosis has been derived from experimental models, pathological findings, and clinical trials. The mechanisms underlying the increased thrombogenicity of DES are multifactorial and include patient, lesion, and procedural factors, as well as compliance with and response to antiplatelet therapy.4–6 However, all currently available DES may be susceptible to late and very late stent thrombosis because of the delayed arterial healing and impaired endothelialization that accompany the drugs used to inhibit neointimal hyperplasia. We can postulate that the rate of healing varies from patient to patient, and even from lesion to lesion within the same patient, but we do not have a method to assess or measure healing after stenting. Therefore, we have empirically recommended that dual-antiplatelet therapy be extended for at least 12 months after DES implantation in an effort to reduce events during the period when the stent is prone to thrombus formation.7 Articles see pp 20 and 28 In terms of assessing the mechanisms of stent failure, including restenosis and stent thrombosis, intravascular ultrasound (IVUS) has been helpful. Subacute stent thrombosis (<30 days) in BMS and DES alike often has a cause that is identifiable by IVUS, such as severe …

Very Late Stent Thrombosis After Dual Antiplatelet Therapy Discontinuation in a Patient with a History of Acute Stent Thrombosis

To describe a case of very late stent thrombosis after dual antiplatelet discontinuation in a patient with a previous history of stent thrombosis. A 62-year-old man with a history of coronary artery disease, multiple acute coronary syndromes requiring percutaneous coronary interventions with multiple stent placements, and acute stent thrombosis resulting in ST segment elevation myocardial infarction presented to the hospital with chest pain. The chest pain was not relieved by 4 sublingual nitroglycerin tablets. Five days prior to his presentation, the patient had been instructed to discontinue both aspirin and clopidogrel in preparation for a left ankle fusion procedure. He was taken to the cardiac catheterization laboratory where he was found to have thrombosis in a sirolimus-eluting stent placed more than 3 years ago. Thrombectomy and balloon angioplasty were performed, and the patient completed his hospital course without complications. Stent thrombosis associated with drug-eluting stents is a complicated pathophysiologic phenomenon with multiple patient-, procedure-, and device-related factors. Application of these risk factors to quantify the risk of stent thrombosis as they apply to a single patient is unknown. Discontinuation of recommended dual antiplatelet therapy with aspirin plus a thienopyridine has been identified as a major risk factor for stent thrombosis, but the optimal duration of dual antiplatelet therapy remains unknown. Current recommendations suggest extending dual antiplatelet therapy beyond one year in patients with low bleeding risk. Given the overall data at this time and the severity of stent thrombosis, it seems prudent to continue dual antiplatelet therapy with aspirin indefinitely plus a thienopyridine for at least one year, with continuation beyond one year on a case-by-case basis depending on the risks of in-stent thrombosis and bleeding. In patients with a low risk of bleeding, indefinite continuation of dual antiplatelet therapy may be reasonable.

Abciximab‐Induced Thrombocytopenia: Management of Bleeding in the Setting of Recent Coronary Stents

This case report and subsequent literature review describes the management difficulties in a patient who developed abciximab-induced thrombocytopenia and gastrointestinal bleeding. Abciximab was used to treat the no-reflow phenomenon, which occurred during insertion of three sequential Taxus coronary artery stents. Resuscitation of this bleeding patient with fluids, blood, and platelet transfusion, and the cessation of antiplatelet agents, was complicated by acute stent thrombosis. We discuss the risk factors for stent thrombosis and discuss abciximab-induced thrombocytopenia, looking at its incidence, pathophysiology, differential diagnosis, investigation, course, management, preventative strategies, and prognostic implications.

Risk Factors for Stent Thrombosis After Implantation of Sirolimus-Eluting Stents in Diabetic and Nondiabetic Patients: The EVASTENT Matched-Cohort Registry

We sought to assess the frequency and causes of stent thrombosis in diabetic and nondiabetic patients after implantation of sirolimus-eluting stents. Safety concerns about late stent thrombosis have been raised, particularly when drug-eluting stents are used in less highly selected patients than in randomized trials. The EVASTENT study is a matched multicenter cohort registry of 1,731 patients undergoing revascularization exclusively with sirolimus stents; for each diabetic patient included (stratified as single- or multiple-vessel disease), a nondiabetic patient was subsequently included. Patients were treated with aspirin + clopidogrel for at least 3 months and were followed for 465 (range 0 to 1,062) days (1-year follow-up in 98.5%). The primary end point was a composite of stent thrombosis (according to Academic Research Consortium definitions), cardiovascular death, and nonfatal myocardial infarction (major adverse cardiac events [MACE]). During follow-up, MACE occurred in 78 patients (4.5%), cardiac death in 35 (2.1%), and stent thrombosis in 45 (2.6%): 30 definite, 23 subacute, and 22 late, including 9 at >6 months. In univariate analysis, the 1-year stent thrombosis rate was 1.8 times higher in diabetic than in nondiabetic patients (3.2% vs. 1.7%; log rank p = 0.03), with diabetic patients with multiple-vessel disease experiencing the highest rate and nondiabetic single-vessel disease patients the lowest (4.3% vs. 0.8%; p < 0.001). In multivariate analysis, in addition to the interruption of antithrombotic treatment, independent stent thrombosis predictors were previous stroke, renal failure, lower ejection fraction, calcified lesion, length stented, and insulin-requiring diabetes. The risk of sirolimus stent thrombosis is higher for multiple-vessel disease diabetic patients.

Hidden drugs, hidden risks—Is cocaine use a new risk factor for stent thrombosis?

Hidden drugs, hidden risks—Is cocaine use a new risk factor for stent thrombosis?

A look at drug eluting stents with optical coherence tomography

In the last year, following several publications in peer reviewed journals and presentations during the 2006 European Society of Cardiology congress,1 concerns have been raised about a possible increase in the incidence of death and myocardial infarction in patients treated with drug eluting stents (DESs) due to the occurrence of stent thrombosis. The incidence of stent thrombosis in the bare metal stent (BMS) era has become low after the introduction of dual antiplatelet therapy.2 Stent thrombosis in this setting is associated with persistent dissection, stent length, and final diameter.3 With paclitaxel and sirolimus-eluting stents, premature discontinuation of thienopyridine therapy has become the most important risk factor for stent thrombosis.4 In event-free patients 6 months after stent implantation, there was still an increase in death and/or myocardial infarction at 24 months follow-up in patients treated with DES without long-term thienopyridine therapy compared with DES with thienopyridine therapy.5 This impact on outcome of clopidogrel was not … *Corresponding author. Tel: +31 50 3611347; fax: +31 50 3611347. E-mail address : b.j.g.l.de.smet{at}thorax.umcg.nl

Drug-eluting stents and stent thrombosis: a cause for concern?

Drug-eluting stents, most commonly sirolimus-eluting stents and polymer-based paclitaxel-eluting stents, are now widely used during percutaneous coronary interventions, and have largely replaced bare-metal stents to treat a variety of native coronary artery and saphenous vein graft lesions. Stent thrombosis, a complication of both bare-metal and drug-eluting stents, is associated with significant morbidity and mortality including high rates of myocardial infarction and death. Recently, several studies in the literature have raised concern about increased rates of overall stent thrombosis and late stent thrombosis in drug-eluting stents in the so-called 'real world' where off-label uses of drug-eluting stents are common. Hypersensitivity reactions to the polymers used in drug-eluting stents, delayed endothelialization of the stents, and discontinuation of dual antiplatelet therapy have all been implicated in the pathophysiology of drug-eluting stents stent thrombosis. The incidence of total stent thrombosis as well as late stent thrombosis, however, does not seem to be significantly higher in drug-eluting stents than in bare-metal stents. An important risk factor for stent thrombosis in both types of stents appears to be the premature discontinuation of dual antiplatelet therapy, and physicians should educate their patients about the importance of adhering to dual antiplatelet therapy, given the dire clinical consequences of stent thrombosis.

Frequency of and Risk Factors for Stent Thrombosis After Drug-Eluting Stent Implantation During Long-Term Follow-Up

Despite concerns regarding the long-term safety of drug-eluting stent (DES) implantation because of late-onset stent thrombosis, the actual incidence of stent thrombosis after 1 year is unknown. We investigated the incidence, risk factors, and association of antiplatelet therapy interruption for the development of stent thrombosis after DES implantation during long-term follow-up. A total of 1,911 consecutive patients with DES implantation were enrolled (sirolimus-eluting stents in 1,545 patients, 2,045 lesions; paclitaxel-eluting stents in 366 patients, 563 lesions). During long-term follow-up (median 19.4 months, interquartile range 15.3 to 24.3), 15 patients (0.8%, 95% confidence interval 0.5% to 1.3%) developed stent thrombosis within 6 hours to 20.4 months. Eleven patients (0.6%, 95% confidence interval 0.3% to 1.0%) had late thrombosis (median 6.1 months). The incidence of stent thrombosis was 3.3% (4 of 121 patients) in patients with complete interruption of antiplatelet therapy (vs 0.6% in those without, p = 0.004) and 7.8% (5 of 64 patients) with premature interruption of aspirin or clopidogrel, or both (vs 0.5% in those without, p < 0.001). Independent predictors of stent thrombosis were premature antiplatelet therapy interruption, primary stenting in acute myocardial infarction, and total stent length. Stent thrombosis also developed while patients were on dual antiplatelet therapy (all patients with acute/subacute stent thrombosis and 36% of those with late stent thrombosis; 47% of total with stent thrombosis). In conclusion, stent thrombosis occurred in 0.8% after DES implantation during long-term follow-up. The incidence of late stent thrombosis was 0.6%, similar to that for bare metal stents. The predictors of stent thrombosis were premature antiplatelet therapy interruption, primary stenting in acute myocardial infarction, and total stent length.

Dual Antiplatelet Therapy for Coronary Stenting

It was an important and indeed remarkable observation when several trials reported the consistent finding that dual antiplatelet therapy with aspirin and a thienopyridine was superior to aspirin and oral anticoagulation for prevention of major adverse cardiac events after deployment of a stent in a coronary artery.1 A major benefit of dual antiplatelet therapy was a lower rate of stent thrombosis. The incidence of coronary stent thrombosis in the modern era is reported to be approximately 1%, with an increased likelihood of occurrence in high-risk patient or lesion subsets. Although this rate may seem relatively low, stent thrombosis is associated with major myocardial infarction (MI) in 60% to 70% of cases, resulting in an early mortality rate of 20% to 25%. With increased use of percutaneous coronary intervention (PCI) as a revascularization strategy and implantation of stents in coronary arteries with a small diameter, it is anticipated that the number of patients at risk for stent thrombosis may increase. It therefore continues to be important to construct pharmacological regimens that minimize its occurrence. Several risk factors for stent thrombosis have been identified, including patient- and/or lesion-specific characteristics, procedure-related factors, and inherent stent thrombogenicity.2 These risk factors, in turn, contribute to a state of enhanced platelet reactivity and thrombus formation, which promotes abrupt vessel closure. See p 1153 Although initial studies highlighting the benefits of dual antiplatelet therapy used aspirin and ticlopidine, clopidogrel is the thienopyridine of choice today because it is associated with a lower rate of intolerable side effects. It is noteworthy that clopidogrel as part of the dual antiplatelet regimen to support PCI has not undergone the type of extensive evaluation demanded of ACE inhibitors, angiotensin receptor blockers, or such devices as implantable cardioverter-defibrillators before they were recommended in practice guidelines for management of patients with …

Risk factors for acute and subacute stent thrombosis after high-pressure stent implantation: A study by intracoronary ultrasound

Background In the era of coronary stenting with high-pressure expansion, stent thrombosis remains a major life-threatening risk. Because of its superior imaging mode, intracoronary ultrasound could provide insight into potential risk factors for stent thrombosis. Patients and Methods In 215 patients with stent implantations controlled by intracoronary ultrasound, four occurrences of subacute stent thrombosis, two complete acute thrombotic occlusions, and four occurrences of incomplete acute thrombosis were observed. All stents were expanded with inflation pressures of at least 14 atm (17 ± 3 atm). The clinical data and the qualitative and quantitative ultrasound information were compared between stents with thrombosis and stents without thrombosis. The luminal area and the plaque border of the reference segments, and of the smallest and largest site of the stented segment after the initial and final expansion, were measured. Results Stents in the left anterior descending artery were more often involved in stent thrombosis than other vessels, but the vessel dimensions in this target vessel were smaller than in the right coronary artery. The plaque burden was considerably larger after stent implantation with subsequent thrombosis compared with no thrombosis (74.1 ± 8.8% vs 63.6 ± 8.0%; p < 0.001), and the stent area was smaller (4.80% ± 1.33 mm 2 vs 6.86 ± 2.08 mm 2; p < 0.01). In stents with thrombosis the plaque burden of the stent site with the smallest and largest lumen differed by 15.2%, whereas the difference in plaque burden in stents without thrombosis was 2.7%. Intracoronary ultrasound showed that the best risk predictor of thrombosis was the residual plaque burden of the stented segment (odds ratio 15.7 [confidence interval 2.4 to 104.7]), and a small stent area after implantation (odds ratio 6.8 [confidence interval 1.9 to 24.3]). Conclusion In a multivariate risk analysis plaque burden was the strongest independent risk factor for stent thrombosis. The amount of residual plaque mass around the stent might be a potential trigger for thrombus formation. (Am Heart J 1998;135:300-9.)

Role of activation-dependent platelet membrane glycoproteins in development of subacute occlusive coronary stent thrombosis

Platelets have an important role in coronary thrombosis. We studied 151 consecutive patients undergoing implantation of Palmaz-Schatz stents because of suboptimal results after coronary balloon angioplasty treated by intense anticoagulation. Surface exposure of the constitutively expressed glycoprotein complex IIb-IIIa (CD41), P-selectin (CD62P) and of the GPIIb-IIIa complex activated exposure (of ligand-induced binding site-1) were determined, in addition to platelet count and plasma fibrinogen, before and daily for 12 days after stenting in peripheral venous blood samples. Six of 151 patients (3.9%) developed subacute stent thrombosis within the first week after stenting. The relative risk of stent thrombosis was 18.5-fold for patients with enhanced GPIIb-IIIa surface expression (P < 0.003; 95% confidence interval 2.1 to 163.1) before stent placement. In the period after stenting, platelet activation occurred, with an increase in fibrinogen receptor activity and P-selectin degranulation above pre-stent values (P < 0.01). In logistic regression analysis, GPIIb-IIIa before stenting emerged as a risk factor for stent thrombosis, independent of the activational status of platelets, platelet count or fibrinogen levels (P < 0.02). However, after stenting, P-selectin surface expression acquired prognostic importance for stent thrombosis (P < 0.05). We conclude that changes in platelet membrane glycoproteins are of prognostic value in predicting subacute stent thrombosis.