Incidence Of Early Stent Thrombosis Research Articles

Clinical Benefit of Statins in Korean Patients with Acute Myocardial Infarction: Experience of the Korea Acute Myocardial Infarction Registry.

Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor) are among the most important medications for treating patients with acute myocardial infarction (AMI). Herein, we review the clinical benefit and future scope of statin therapy in Korean patients with AMI from the experience of the Korea AMI Registry. Statins are effective and safe in AMI patients, even in those with very low low-density lipoprotein cholesterol (LDL-C). Peri-procedural statin treatment could reduce the incidence of early stent thrombosis in patients with AMI after percutaneous coronary intervention. Reduction of high sensitivity C-reactive protein levels in patients with AMI plays an important role in the beneficial effect of statins on regression and compositional change of coronary plaques. Obtaining ≥50% reduction in LDL-C is associated with better clinical outcomes after AMI, whereas achieving <70 mg/dL LDL-C is not. Statin therapy has positive effects on clinical outcomes in patients with cardiogenic shock, ischemic heart failure, chronic kidney disease, and vasospasm. The combination of high-dose statin plus N-acetyl cysteine is associated with lower incidence of contrast-induced nephropathy in patients who underwent primary percutaneous coronary intervention. Moderate-intensity pitavastatin therapy is associated with a lower incidence of new-onset diabetes mellitus in patients with AMI and has similar clinical outcomes to moderate-intensity atorvastatin and rosuvastatin therapy. Future studies are required to assess the optimal intensity and LDL-C target concerning statin therapy, and the implementation of guidelines based cholesterol lowering practice in Korean patients with AMI.

Platelet function monitoring for stent thrombosis in critically III patients with an acute Coronary syndrome.

Patients after cardiac arrest or in cardiogenic shock due to acute coronary syndrome (ACS) are at high risk for stent thrombosis (ST) and recurrent cardiovascular events after primary percutaneous coronary intervention (PCI). High post-interventional platelet reactivity (HPR) might be an additional risk factor for ST in these critically ill patients. Between 2006 and 2016, 401 critically ill patients from a cardiologic intensive care unit underwent platelet function testing after primary PCI using whole blood impedance aggregometry. After exclusion of patients with an abnormal platelet count, 357 patients have been included into the final analysis of this retrospective observational study. The incidence of definite early ST was 19.2% in patients with HPR to P2Y12 antagonists and 1.2% in patients without HPR. Likewise, the incidence of early ST in patients with HPR to acetylsalicylic acid (ASA) was 21.4% versus 1.8% in patients without HPR. In contrast, the incidence of late ST or recurrent myocardial infarction in untreated lesions was not associated with HPR to ASA or P2Y12 antagonists. Platelet function testing in critically ill ACS patients identified patients at high risk for early ST and might be beneficial for risk stratification.

Incidence, predictors, and clinical outcomes of early stent thrombosis in acute myocardial infarction patients treated with primary percutaneous coronary angioplasty (insights from the University of Ottawa Heart Institute STEMI registry).

Early stent thrombosis (ST) remains an important complication of primary percutaneous intervention (PCI). To date, our information on angiographic and clinical predictors of early ST in ST-segment elevation myocardial infarction (STEMI) patients treated with primary PCI is limited. We tried to evaluate the incidence, predictors, and outcomes of early ST in real-world patients treated with primary PCI. We identified all the patients presenting with STEMI between June 2004 and January 2011 who underwent primary PCI as the primary mode of revascularization. Diagnosis of ST was made as per the standard definition proposed by the Academic Research Consortium. The incidence of early ST was 1% among 2,303 patients treated with primary PCI. Definite and probable early ST occurred in 22 and 2 patients, respectively. Patients with early ST had higher in-hospital (P = 0.03) and 30-day mortality (P = 0.048). The rate of cardiogenic shock (P = 0.0006) and cerebrovascular accident (P = 0.0004) was also greater in the early ST group. Smaller stent diameter and lower use of intracoronary glycoprotein IIb/IIIa inhibitor were associated with higher rate of early ST. There was a trend of higher bivalirudin use in ST group, which did not reach significance (P = 0.07) On IVUS imaging, stent malapposition and uncovered plaque area were noted in 6 out of 11 cases. The incidence of early ST in primary PCI cohort is low. However, it is still associated with higher mortality and morbidity. Small stent diameter and disuse of intracoronary glycoprotein IIb/IIIa inhibitor may be associated with early ST.

Incidence and Clinical Features of Early Stent Thrombosis in the Era of New P2y12 Inhibitors (PLATIS-2).

Early stent thrombosis (EST) (≤ 30 days after stent implantation) is a relatively rare but deleterious complication of percutaneous coronary intervention (PCI). Administration of newer P2Y12 inhibitors (prasugrel and ticagrelor) combined with aspirin has been shown to reduce the incidence of sub-acute and late stent thrombosis, compared with clopidogrel. We investigated the “real life” incidence of EST in patients from a large acute coronary syndrome (ACS) national registry, where newer P2Y12 inhibitors are widely used. Patients were derived from the ACS Israeli Survey (ACSIS), conducted during 2006, 2008, 2010 and 2013. Major adverse cardiac events (MACE) at 30days were defined as all-cause death, recurrent ACS, EST and stroke.Of the 4717 ACS patients who underwent PCI and stenting, 83% received clopidogrel and 17% newer P2Y12 inhibitors. The rate of EST was similar in both groups (1.7% in the newer P2Y12 inhibitor group vs. 1.4% in the clopidogrel-treated patients, p = 0.42). Results were consistent after multivariate analysis (adjusted HR = 1.06 [p = 0.89]). MACE occurred in 6.4% in the newer P2Y12 inhibitor group compared with 9.2% in the clopidogrel group (P<0.01). However, multivariate logistic regression modeling showed that treatment with newer P2Y12 inhibitors was not significantly associated with the secondary endpoint of MACE when compared with clopidogrel therapy [OR = 1.26 95%CI (0.93–1.73), P = 0.136]. The incidence of "real life" EST at 1month is relatively low, and appears to be similar in patients who receive newer P2Y12 inhibitors as well as in those who receive clopidogrel.

Low real-world early stent thrombosis rates in ST-elevation myocardial infarction patients and the use of bivalirudin, heparin alone or glycoprotein IIb/IIIa inhibitor treatment: A nationwide Swedish registry report

In recent studies of primary percutaneous coronary intervention (PCI), bivalirudin compared with heparin has been associated with increased risk of stent thrombosis (ST). Our aim was to describe incidence and outcome of definite, early ST in a large contemporary primary PCI population divided in antithrombotic therapy subgroups. A prospective, observational cohort study of all 31,258 ST-elevation myocardial infarction patients who received a stent in Sweden from January 2007 to July 2014 in the SWEDEHEART registry was conducted. Patients were divided into 3 groups: bivalirudin, heparin alone, or glycoprotein IIb/IIIa inhibitor treated. Primary outcome measure was incidence of definite early ST (within 30 days of PCI). Secondary outcomes included all-cause mortality. Incidence of early ST was low, regardless of bivalirudin, heparin alone, or glycoprotein IIb/IIIa inhibitor treatment (0.84%, 0.94%, and 0.83%, respectively). All-cause mortality at 1 year was 20.7% for all ST patients (n = 265), compared with 9.1% in those without ST (n = 31,286; P < .001). Patients with ST days 2-30 had numerically higher all-cause mortality at 1 year compared with patients with ST days 0-1 (23% vs 16%, P = .20). In this real-world observational study of 31,258 ST-elevation myocardial infarction patients, the incidence of early ST was low, regardless of antithrombotic treatment strategy. Early ST was associated with increased mortality. Numerically higher all-cause mortality at 1 year was noted with ST days 2-30 compared with ST days 0-1 post-PCI.

Clinical, angiographic, and intravascular ultrasound predictors of early stent thrombosis in patients with acute myocardial infarction

Risk factors reported for early stent thrombosis (EST) included acute coronary syndrome, suboptimal antiplatelet therapy, procedural factors such as residual dissection and underexpansion of stents, and smaller final lumen area and inflow/outflow disease (residual stenosis or dissection) by intravascular ultrasound (IVUS) [1–4]. However, the predictors of EST including all variables such as baseline characteristics, laboratory data, angiographic and IVUS findings in patients with acute myocardial infarction (AMI) are still not well known. From January 2007 to December 2009, we identified 418 consecutive patients with a first AMI who underwent pre-percutaneous coronary intervention (PCI) IVUS within 24 h from symptom onset, were stented successfully, and had post-PCI IVUS imaging. EST included acute (b24 h) and subacute ST (1 to 30 days) after stent implantation. Cardiac-specific troponin I (cTnI) levels were measured by a paramagnetic particle, chemiluminescent immunoenzymatic assay (Beckman, Coulter Inc., Fullerton, California). No-reflow was defined as postPCI TIMI grade 0, 1, or 2 flow. Tissue prolapse was defined as tissue extrusion through the stent strut at post-PCI. The baseline characteristics, angiographic and IVUS findings are summarized in Table 1. EST occurred in 16 patients (3.8%). Glycoprotein IIb/IIIa inhibitor was used more frequently in patients with EST compared with those without EST. Pre-PCI peak creatine kinase-MB and cTnI were significantly higher in patients with EST compared with those without EST. Pre-PCI TIMI flow grade was significantly lower in patients with EST compared with those without EST. More stents were deployed in patients with EST compared with those without EST. Noreflow during or after PCI was developed more frequently in EST group than in non-EST group (87.5% vs. 12.2%, p b 0.001). Plaque burden at the minimum lumen site was significantly greater in patients with EST compared with those without EST. Pre-PCI plaque rupture and IVUSdetected thrombuswere observedmore frequently in patients with EST compared with those without EST. Post-stenting tissue prolapse was observed more frequently in patients with EST compared with those without EST (68.8% vs. 32.6%, p= 0.003). Independent predictors of EST are summarized in Table 2. Multivariate analysis showed that noreflow, pre-PCI peak cTnI, and tissue prolapse were the independent predictors of EST. No-reflow can occur easily in lesions with various kinds of vulnerable plaque including plaque rupture and thrombus and this no-reflow is associated with microvascular damage which is likely to slow the epicardial coronary blood flow and to stagnate blood flow which may accelerate local thrombus formation [5]. The mechanism underlying the association between pre-PCI peak cTnI level and EST is not clear, although cTnI is associated with high thrombus grade with promoted thrombus formation in patients with AMI, who already have heightened systemic and intracoronary platelet reactivity, thrombin generation, and inflammation. Tissue prolapse may represent a source for thrombus accumulation in an environment that already has a high potential for thrombogenesis. Impaired arterial healing and ST have been associated with the prolapse of the necrotic core between stent struts. This is especially relevant in the setting of AMI, because such patients already have an increased risk for this devastating event [6]. In conclusion, the incidence of EST after stenting of infarct-related arteries was 3.8%. No-reflow, pre-PCI peak cTnI and tissue prolapse were associated with the development of EST after stent implantation in patients with AMI.

Acute Stent Thrombosis: Rare but Still There

curring in the first 24 hours), subacute (occurring in the first 30 days after the procedure), and late (occurring more than 30 days after the procedure), with stent thromboses occurring in the first month sometimes called ‘early’ and those occurring after more that one year sometimes called ‘very late.’ In the early days of stenting, the incidence of early stent thrombosis was very high, as patients were predominantly treated with anticoagulants. The use of dual antiplatelet therapy and high pressure stent balloon inflation have markedly decreased the occurrence of stent thrombosis. 2 The incidence of acute stent thrombosis ranges from 0.5–1.4% in bare metal stent studies 2–4 and is similar in more recent drug-eluting stent studies. 5 Although the incidence is low, the consequences are oftentimes dire with a majority of patients presenting with large myocardial infarctions, but also with sudden death. It is important to identify patients at risk and to have a high index of suspicion when evaluating patients who have undergone percutaneous coronary revascularization presenting with acute coronary syndromes. Despite its low incidence, acute stent thrombosis is a serious concern given the overall high number of patients undergoing percutaneous revascularization. The patients with acute stent thrombosis often present with myocardial infarction with high thrombus burden, as well as electrical and hemodynamic instability. Despite restoration of flow, these patients will often have refractory angina, need repeat percutaneous or surgical revascularization, and up to 20% will die in the hospital. 3 Several patient factors can lead to an increased predisposition for stent thrombosis. These include presentation with acute myocardial infarction, older age, diabetes mellitus, renal insufficiency, and low left ventricular systolic function. Bifurcation lesions, residual vessel dissection, residual thrombus, and inadequate stent apposition are procedural factors associated with acute/early stent thrombosis. 3

The incidence and clinical predictors of early stent thrombosis in patients with acute coronary syndrome

Acute coronary syndrome (ACS) is associated with activation of platelets and the coagulation system which could influence the incidence of early stent thrombosis (EST). We aimed to determine the incidence and predictors of EST in patients undergoing coronary stenting during ACS. The study comprised 1202 consecutive patients, drawn from a nationwide ACS survey, who underwent coronary stenting during ACS and were followed up for 30 days. Early stent thrombosis was based on the Academic Research Consortium definition. Thirty patients (2.5%) sustained EST. The occurrence of EST in patients with unstable angina/non-ST-elevation myocardial infarction and ST-elevation myocardial infarction (STEMI) was 0.9% and 3.9%, respectively (P < .05), and was even higher (5.2%) in STEMI patients who underwent primary percutaneous coronary intervention. On multivariate analysis, STEMI (OR 6.3, 95% CI 2.1-18, P = .0008), multivessel disease (OR 5.9, 95% CI 1.9-21, P = .003) and Killip class >/=2 (OR 2.9, 95% CI 1.3-6.6, P = .008) were independent correlates of EST. The use of bare versus drug-eluting stents was not associated with any significant difference in EST. Patients presenting with STEMI who are hemodynamically unstable and have multivessel coronary disease undergoing coronary stenting during ACS, are at increased risk of EST.

Abstract 6022: The Effect of Pre-Hospital Tirofiban on Early Stent Thrombosis in STEMI Patients Undergoing Primary PCI

Objective The aim of this analysis was to assess the effect of pre-hospital initiation of high-dose (HD) tirofiban on the incidence of early stent thrombosis (ST) in patients undergoing primary PCI for acute myocardial infarction. Methods Patients were randomized to HD tirofiban or no tirofiban in the ambulance on top of 600 mg clopidogrel, 500 mg aspirin and 5000 IU unfractionated heparin. ST was defined according to the Academic Research Consortium definitions of “definite” and “probable” stent thrombosis. Results A total of 1073 out of 1398 patients (76.8%) underwent primary PCI with stent implantation. Overall, “definite” or “probable” ST occurred in 39 patients (3.6%) at 30 days. The incidence in the no tirofiban or placebo group was 5.2% (28/537; 27 definite and 1 probable) versus 2.1% (11/536; 10 definite and 1 probable) in the HD tirofiban group (p=0.006). In univariate analysis, predictors of ST were no pre-hospital initiation of HD tirofiban (p=0.006), previous myocardial infarction (p=0.016), TIMI risk score &gt;3 (p=0.027) and TIMI major bleeding (p=0.002). By multivariate analysis, no pre-hospital initiation of HD tirofiban (Odds ratio [OR] 2.54, 95% confidence interval [CI] 1.21–5.32; p=0.013), previous myocardial infarction (OR 3.32, 95%-CI 1.35– 8.18; p&lt;0.01), and TIMI major bleeding (OR 8.40, 95%-CI 2.24 –31.46; p=0.002) were independent predictors of early ST. Thirty day mortality was significantly higher in those with ST (10.3% versus 1.7%, p&lt;0.001). Conclusion Pre-hospital initiation of high dose tirofiban reduces the 30-day incidence of stent thrombosis in STEMI patients treated with primary PCI. Early stent thrombosis was associated with poor outcome.

Late Coronary Stent Thrombosis

Introduced >20 years ago,1 coronary artery stents have improved the safety and particularly the efficacy of percutaneous coronary interventions (PCIs).2 Abrupt vessel closure, complicating 6% to 8% of balloon angioplasty procedures, was associated with a 5% mortality, 40% rate of myocardial infarction (MI), and 40% rate of emergency coronary artery bypass grafting.3 Stents significantly reduced these adverse events (Figure 1).4,5 The reduction of restenosis afforded by bare metal stents (BMS) was modest (30% to 40%). Repeat revascularization still occurred in 15% to 20% of cases.6 Drug-eluting stents (DES) with antiproliferative drugs attached via polymers on the stent surface to minimize smooth muscle proliferation have reduced restenosis and rates of target lesion revascularization by 50% to 70% compared with BMS across nearly all lesion and patient subsets.7 Initially8 and again more recently,9–16 safety concerns were raised about DES, particularly about late stent thrombosis (ST). Figure 1. Outcome of 112 patients with abrupt vessel closure in the prestent balloon angioplasty experience of a registry (1985 to 1986; total, 1801 patients)3 and 339 patients with abrupt vessel closure during balloon angioplasty treated with BMS (Palmaz-Schatz) (total, 4596 patients).5 CABG indicates coronary artery bypass grafting. ST was a bane of stent implantation from the beginning. The initial experience with Wallstents in the late 1980s was overshadowed by ST rates approaching 24%.17 Subsequent series with Palmaz-Schatz and Gianturco-Roubin stents (still predominantly bailout stenting) observed ST in 6% to 12% of cases.4,18 The postprocedural antithrombotic regimen at the time consisted of aspirin, often in conjunction with oral anticoagulation. Dual antiplatelet therapy of aspirin and the thienopyridine ticlopidine in conjunction with a shift from bailout to elective stenting resulted in a significant reduction of ST to <2%.5,19 Earlier oral antiplatelet drug loading and …

Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: data from a large two-institutional cohort study

Stent thrombosis is a safety concern associated with use of drug-eluting stents. Little is known about occurrence of stent thrombosis more than 1 year after implantation of such stents. Between April, 2002, and Dec, 2005, 8146 patients underwent percutaneous coronary intervention with sirolimus-eluting stents (SES; n=3823) or paclitaxel-eluting stents (PES; n=4323) at two academic hospitals. We assessed data from this group to ascertain the incidence, time course, and correlates of stent thrombosis, and the differences between early (0-30 days) and late (>30 days) stent thrombosis and between SES and PES. Angiographically documented stent thrombosis occurred in 152 patients (incidence density 1.3 per 100 person-years; cumulative incidence at 3 years 2.9%). Early stent thrombosis was noted in 91 (60%) patients, and late stent thrombosis in 61 (40%) patients. Late stent thrombosis occurred steadily at a constant rate of 0.6% per year up to 3 years after stent implantation. Incidence of early stent thrombosis was similar for SES (1.1%) and PES (1.3%), but late stent thrombosis was more frequent with PES (1.8%) than with SES (1.4%; p=0.031). At the time of stent thrombosis, dual antiplatelet therapy was being taken by 87% (early) and 23% (late) of patients (p<0.0001). Independent predictors of overall stent thrombosis were acute coronary syndrome at presentation (hazard ratio 2.28, 95% CI 1.29-4.03) and diabetes (2.03, 1.07-3.83). Late stent thrombosis was encountered steadily with no evidence of diminution up to 3 years of follow-up. Early and late stent thrombosis were observed with SES and with PES. Acute coronary syndrome at presentation and diabetes were independent predictors of stent thrombosis.

Late Angiographic Stent Thrombosis (LAST) Events With Drug-Eluting Stents

We sought to describe the incidence of late angiographic stent thrombosis (LAST) events in an unselected drug-eluting stent (DES) population. Concerns have been raised that LAST may be a potential limitation of DES. We have previously reported the angiographic incidence of early stent thrombosis (1.0%) in this prospective cohort of 2,006 patients treated with either sirolimus-eluting stents (SES) (n = 1,017) or paclitaxel-eluting stents (PES) (n = 989). We continued long-term follow-up to determine the incidence of LAST events, defined as angiographically proven stent thrombosis associated with acute symptoms more than 30 days after DES implantation. All patients had at least 1 year of follow-up, mean duration 1.5 years. There were eight angiographically confirmed LAST events in seven patients: three with SES (at 2, 25, and 26 months) and five with PES (at 6, 7, 8, 11, and 14.5 months). Three cases were related to complete cessation of antiplatelet therapy, two cases occurred while patients were on aspirin therapy within one month of cessation of clopidogrel, and three cases occurred at a time when patients were apparently clinically stable on aspirin monotherapy. We observed no cases of LAST in patients who were on dual antiplatelet therapy. Two deaths occurred directly as a result of LAST. Angiographically proven late stent thrombosis occurs with an incidence of at least 0.35% (95% confidence limits 0.17% to 0.72%) in patients treated with DES. Importantly, it may also occur when patients are stable on antiplatelet monotherapy.

Single bailout stenting for threatened coronary closure complicating balloon angioplasty: acute and mid-term outcome.

Emergency stent implantation for the treatment of failed balloon angioplasty has been limited by a 3-33% incidence of early stent thrombosis and a paucity of information on restenosis. Accordingly, the objective of this study is to determine both the acute and midterm results following single bailout stenting for threatened closure after failed balloon angioplasty. Single stent placement with either a Gianturco-Roubin or Palmaz-Schatz stent for the treatment of threatened closure complicating conventional single-vessel balloon angioplasty of de novo native coronary lesions was carried out in 16 and 24 patients, respectively. Successful stent implantation was achieved in 39 patients (97.5%), reducing the diameter stenosis from 90 +/- 7% before 6 +/- 8% after the procedure. No early stent closure, myocardial infarction, or need for emergency coronary bypass surgery was observed. Furthermore, except for one death due to massive intracranial hemorrhage 1 1/2 weeks after a successful stent implantation, there was no mortality directly related to the procedure. Repeat angiographic study performed at a mean of 5 +/- 3 months after stenting in 30 (86 %) eligible patients revealed in-stent restenosis (> 50% diameter stenosis) in six patients (20%). Five had successful repeat balloon angioplasty. Restenosis rate was significantly higher in patients with diabetes mellitus (83 versus 21% in nondiabetics, P = 0.0047), who had small (< 3 mm diameter) stent (reflecting small vessel diameters) implanted (40 versus 10% for > or = 3 mm stents, P = 0.0528) and those who had received stents to rectify vessel recoil (60 versus 12% for dissection, P = 0.0264). During a follow-up period of 12 +/- 8 months, clinical benefits were maintained in most patients, with none requiring bypass surgery, and no myocardial infarction or death encountered. Our study suggests that single bailout stenting for threatened closure in selected patients is associated with a favorable short and mid-term outcome, with minimal risk of early stent closure and a low restenosis rate. Restenosis rate, however, remains high in diabetic patients, stent placement for vessel recoil indication and those receiving < 3 mm diameter stents.