Serotonin antagonism improves platelet inhibition in clopidogrel low-responders after coronary stent placement: an in vitro pilot study

Increased residual platelet reactivity remains a burden for coronary artery disease (CAD) patients who received a coronary stent and do not respond sufficiently to treatment with acetylsalicylic acid and clopidogrel. We hypothesized that serotonin antagonism reduces high on-treatment platelet reactivity. Whole blood impedance aggregometry was performed with arachidonic acid (AA, 0.5 mM) and adenosine diphosphate (ADP, 6.5 μM) in addition to different concentrations of serotonin (1-100 μM) in whole blood from 42 CAD patients after coronary stent placement and 10 healthy subjects. Serotonin increased aggregation dose-dependently in CAD patients who responded to clopidogrel treatment: After activation with ADP, aggregation increased from 33.7 ± 1.3% to 40.9 ± 2.0% in the presence of 50 μM serotonin (p<0.05) and to 48.2 ± 2.0% with 100 μM serotonin (p<0.001). The platelet serotonin receptor antagonist ketanserin decreased ADP-induced aggregation significantly in clopidogrel low-responders (from 59.9 ± 3.1% to 37.4 ± 3.5, p<0.01), but not in clopidogrel responders. These results were confirmed with light transmission aggregometry in platelet-rich plasma in a subset of patients. Serotonin hence increased residual platelet reactivity in patients who respond to clopidogrel after coronary stent placement. In clopidogrel low-responders, serotonin receptor antagonism improved platelet inhibition, almost reaching responder levels. This may justify further investigation of triple antiplatelet therapy with anti-serotonergic agents.     

Early double stent thrombosis associated with clopidogrel hyporesponsivenesss

A 57-year-old male patient without cardiovascular history suffered an acute myocardial infarction and underwent drug-eluting stent implantation in the left anterior descending artery. A few days later, the right coronary artery was also stented (drug-eluting stent). Three days later, he was re-admitted to our hospital in cardiogenic shock. Emergent coronary angiography showed total occlusion of both stents. Platelet function analysis (PFA) showed attenuated platelet inhibition in response to clopidogrel treatment. The patient was the carrier of a loss-of-function polymorphism in the CYP2C19 gene, which has been associated with increased incidence of adverse thrombotic events. Antiplatelet therapy was switched to prasugrel and PFA revealed an adequate antiplatelet effect.     

血栓弹力图指导支架内血栓后不稳定心绞痛治疗1 例及文献复习

目的:探讨在血栓弹力图监测血小板抑制率的情况下,调整氯吡格雷及阿司匹林用量,治疗冠心病、PCI术后支架内再发血栓患者的临床意义。方法:报告中国人民解放军总医院1例支架内亚急性血栓患者的临床资料并复习相关文献,对其临床表现、诊断、在血栓弹力图指导下的治疗进行分析。结果:1例支架内亚急性血栓患者经治疗病情好转出院,出院后继续调整氯吡格雷及阿司匹林用量,达到满意血小板抑制率,患者症状消失。结论:冠状动脉介入治疗后发生支架内血栓的患者,应用血栓弹力图指导氯吡格雷及阿司匹林用量,可达到令人满意的血小板抑制率,并防止出血情况发生。     

Stent thrombosis in real-world patients: a comparison of drug-eluting with bare metal stents

BackgroundAlthough the introduction of drugeluting stents (DES) has been associated with an impressive reduction in target vessel revascularisation, there has been concern about the safety profile. The aim of this study was to determine the incidence of stent thrombosis in real-world patients and evaluate the contribution of drug-eluting stents. Methods A prospective observational cohort study was conducted at a high-volume centre in Utrecht, the Netherlands. All patients who underwent a percutaneous coronary intervention (PCI) between 1 January and 31 December 2005 were evaluated. The patients were pretreated with aspirin and clopidogrel, which was continued for six months in bare metal stents (BMS) and 12 months in DES. ResultsIn 2005, 1309 patients underwent a percutaneous coronary intervention procedure with stent implantation. After a median follow-up of nine months, 1.8% (n=23) of the patients had suffered from stent thrombosis. Two cases could be attributed to incorrect use of antiplatelet agents. In 8/23 cases, a technical reason was found such as an unrecognised dissection or stent underexpansion. The timing of stent thrombosis was acute in 1/23 patients, subacute in 20/23 patients and late in 2/23 patients. In both cases of late stent thrombosis, a BMS had been used. There were no differences in stent thrombosis rates between DES and BMS (1.4 vs. 1.9%, ns.). This is remarkable since DES were used in more complex and longer lesions. ConclusionThe use of DES in routine daily practice does not appear to be associated with a higher rate of stent thrombosis than BMS. (Neth Heart J 2007;15:382-6).     

CYP2C19 Phenotype,Stent Thrombosis,Myocardial Infarction,and Mortality in Patients with Coronary Stent Placement in a Chinese Population

Background

Several studies have indicated that CYP2C19 loss-of-function polymorphisms have a higher risk of stent thrombosis (ST) after percutaneous coronary interventions (PCIs). However, this association has not been investigated thoroughly in a Chinese population. In this study, we aimed to determine the effect of CYP2C19*2 and CYP2C19*3 loss-of-function polymorphisms on the occurrence of ST and other adverse clinical events in a Chinese population.

Methods

We designed a cohort study among 1068 consecutive patients undergoing intracoronary stent implantation after preloading with 600 mg of clopidogrel. CYP2C19*2 and CYP2C19*3 were genotyped by using polymerase chain reaction-restriction fragment length polymorphism analysis. The adverse clinical events recorded were ST, death, myocardial infarction (MI), and bleeding events. The primary end point of the study was the incidence of cumulative ST within 1 year after PCI. The secondary end point was other adverse clinical outcomes 1 year after the procedure.

Results

The cumulative 1-year incidence of ST was 0.88% in patients with extensive metabolizers (EMs) (CYP2C19*1/*1 genotype), 4.67% in patients with intermediate metabolizers (IMs) (CYP2C19*1/*2 or *1/*3 genotype), and 10.0% in patients with poor metabolizers (PMs) (CYP2C19*2/*2, *2/*3, or *3/*3 genotype) (P<0.001). The one-year event-free survival was 97.8% in patients with EMs, 96.5% in patients with IMs, and 92.0% in patients with PMs (P = 0.014). Multivariate analysis confirmed the independent association of CYP2C19 loss-of-function allele carriage with ST (P = 0.009) and total mortality (P<0.05).

Conclusion

PM patients had an increased risk of ST, death, and MI after coronary stent placement in a Chinese population.     

Cangrelor increases the magnitude of platelet inhibition and reduces interindividual variability in clopidogrel-pretreated subjects

BackgroundInadequate platelet inhibition despite aspirin and clopidogrel therapy during and after a percutaneous coronary intervention is associated with an impaired clinical outcome. Cangrelor, a direct and reversible P2Y₁₂ inhibitor that is currently in development, has the potential to achieve higher levels of inhibition of ADP-induced platelet aggregation than clopidogrel. The aim of the present study was to compare the magnitude of platelet inhibition in clopidogrel-pretreated patients before and after the in vitro addition of a subtherapeutic dose of cangrelor. MethodsBlood samples were drawn from patients pretreated with clopidogrel and aspirin who were undergoing elective percutaneous coronary intervention (n=39). Platelet function analysis with ‘classical’ light transmittance aggregometry (both peak and late aggregation [at 6 min]) was performed before and after the in vitro addition of cangrelor (0.25 μmol/l) to platelet-rich plasma (PRP). After an incubation period of five minutes, platelet aggregation was induced by 5 and 20 μmol/l ADP. ResultsThe in vitro addition of 0.25μmol/l cangrelor to the PRP from clopidogrel-treated subjects resulted in an additional reduction in ADP-induced platelet aggregation. For ADP concentrations of 5 and 20 μmol/l, peak aggregation showed a decrease of 75 and 85%, respectively (p<0.001 for both), while late aggregation was almost completely diminished (p=0.003 and p<0.001, respectively). Furthermore, the interindividual variation in inhibition of ADP-induced platelet aggregation by clopidogrel was greatly reduced after the addition of cangrelor. ConclusionWe demonstrate that the in vitro addition of even a subtherapeutic dose of cangrelor to the PRP of clopidogrel-pretreated patients results in an additional reduction of ADP-induced platelet aggregation. Moreover, cangrelor was able to diminish the interindividual variation observed in clopidogrel-inhibited platelet aggregation. (Neth Heart J 2009;17:195–8.)     

Reduced number of cardiovascular events and increased cost-effectiveness by genotype-guided antiplatelet therapy in patients undergoing percutaneous coronary interventions in the Netherlands

Aim

This study explores clinical outcome in cytochrome P450 2C19 (CYP2C19)-related poor metaboliser patients treated with either clopidogrel or prasugrel after percutaneous coronary intervention (PCI) and investigates whether this could be cost-effective.

Methods and results

This single-centre, observational study included 3260 patients scheduled for elective PCI between October 2010 and June 2013 and followed for adverse cardiovascular events until October 2014. Post PCI, CYP2C19 poor metaboliser patients were treated with clopidogrel or prasugrel, in addition to aspirin. In total, 32 poor metabolisers were treated with clopidogrel and 41 with prasugrel. The number of adverse cardiovascular events, defined as death from cardiovascular cause, myocardial infarction, stent thrombosis, every second visit to the catheterisation room for re-PCI in the same artery, or stroke, within 1.5 years of PCI, was significantly higher in the CYP2C19 poor metaboliser group treated with clopidogrel (n = 10, 31?%) compared with the poor metaboliser group treated with prasugrel (n = 2, 5?%) (p = 0.003). Costs per gained quality-adjusted life years (QALY) were estimated, showing that genotype-guided post-PCI treatment with prasugrel could be cost-effective with less than € 10,000 per gained QALY.

Conclusion

This study provides evidence that for CYP2C19-related poor metabolisers prasugrel may be more effective than clopidogrel to prevent major adverse cardiovascular events after PCI and this approach could be cost-effective.

     

Stent thrombosis in patients treated with thienopyridines: clinical description of 10 cases

Subacute stent thrombosis (SAST) is a major thrombotic complication of coronary stenting. Its occurrence has been substantially reduced by thienopyridine treatment. However, information on clinical profile of patients with SAST in clopidogrel era is limited. In order to define the incidence and factors predisposing to stent thrombosis, we analyzed the computerized angiographic database of three interventional cardiology centers. Out of a total number of 5903 percutaneous coronary interventions (PCIs) with stent implantation, we found 10 patients with SAST (0.17%). The indication for PCI was usually an early invasive approach (90%) during an acute coronary syndrome. All patients were treated with an apparently optimal antithrombotic regimen (90% received heparin or LMWH and 70% received IIb/IIIa receptor inhibitors and all given aspirin). In each of the patients, we could identify high-risk angiographic findings. SAST presentation was always clinically significant with definite myocardial infarction in 100% of cases. 80% of cases occurred during the first six days post PCI. Two patients had a recurrent event. Finally, despite earlier reports of atorvastatin-mediated inhibition of clopidogrel activation we did not find any patient with SAST taking both drugs. Thus, patients with stent thrombosis during thienopyridine treatment usually exhibit high-risk angiographic features. Prospective studies should be performed to elucidate drug interactions that may reduce clopidogrel efficacy and contribute to stent thrombosis.     

Results of the Ticlid or Plavix Post-Stents (TOPPS) trial: do they justify the switch from ticlopidine to clopidogrel after coronary stent placement?

In the Ticlid or Plavix Post-Stents (TOPPS) trial, 1016 patients undergoing successful coronary stent placement were randomized to receive aspirin and either ticlopidine or clopidogrel. In this trial, the dosages and regimens of ticlopidine and clopidogrel resembled more closely those used in most catheterization laboratories than did the two previous randomized trials comparing ticlopidine and clopidogrel. The results of the TOPPS trial support the current practice of substituting ticlopidine for clopidogrel in stent patients.     

Coronary aspirate TNFα reflects saphenous vein bypass graft restenosis risk in diabetic patients

Background

Patients with diabetes mellitus (DM) have an increased risk for periprocedural complications and adverse cardiac events after percutaneous coronary intervention. We addressed the potential for coronary microvascular obstruction and restenosis in patients with and without DM undergoing stenting for saphenous vein bypass graft (SVG) stenosis under protection with a distal occlusion/aspiration device.

Methods

SVG plaque volume and composition were analyzed using intravascular ultrasound before stent implantation. Percent diameter stenosis was determined from quantitative coronary angiography before, immediately after and 6?months after stent implantation. Coronary aspirate was retrieved during stent implantation and divided into particulate debris and plasma. Total calcium, several vasoconstrictors, and tumor necrosis factor (TNF)α in particulate debris and coronary aspirate plasma were determined.

Results

Patients with and without DM had similar plaque volume, but larger necrotic core and greater particulate debris release in patients with than without DM (20.3±2.7 vs. 12.7±2.6% and 143.9±19.3 vs. 75.1±10.4?mg, P<0.05). The TNFα concentration in particulate debris and coronary aspirate plasma was higher in patients with than without DM (15.9±6.6 vs. 5.1±2.4 pmol/mg and 2.2±0.7 vs. 1.1±0.2 pmol/L, P<0.05), whereas total calcium and vasoconstrictors were not different. Patients with DM had a greater percent diameter stenosis 6?months after stent implantation than those without DM (22.17±5.22 vs. 6.34±1.11%, P<0.05). The increase in TNFα immediately after stent implantation correlated with restenosis 6?months later (r=0.69, P<0.05).

Conclusion

In diabetics, particulate debris and coronary aspirate plasma contained more TNFα, which might reflect the activity of the underlying atherosclerotic process.

Trial registration

URL: http://www.clinicaltrials.gov/ct2/results?term=NCT01430884; unique identifier: NCT01430884     

Stent Thrombosis is the Primary Cause of ST-Segment Elevation Myocardial Infarction following Coronary Stent Implantation: A Five Year Follow-Up of the SORT OUT II Study

Background

The widespread use of coronary stents has exposed a growing population to the risk of stent thrombosis, but the importance in terms of risk of ST-segment elevation myocardial infarctions (STEMIs) remains unclear.

Methods

We studied five years follow-up data for 2,098 all-comer patients treated with coronary stents in the randomized SORT OUT II trial (mean age 63.6 yrs. 74.8% men). Patients who following stent implantation were readmitted with STEMI were included and each patient was categorized ranging from definite- to ruled-out stent thrombosis according to the Academic Research Consortium definitions. Multivariate logistic regression was performed on selected covariates to assess odds ratios (ORs) for definite stent thrombosis.

Results

85 patients (4.1%), mean age 62.7 years, 77.1% men, were admitted with a total of 96 STEMIs, of whom 60 (62.5%) had definite stent thrombosis. Notably, definite stent thrombosis was more frequent in female than male STEMI patients (81.8% vs. 56.8%, p = 0.09), and in very late STEMIs (p = 0.06). Female sex (OR 3.53 [1.01–12.59]) and clopidogrel (OR 4.43 [1.03–19.01]) was associated with increased for definite stent thrombosis, whereas age, time since stent implantation, use of statins, initial PCI urgency (STEMI [primary PCI], NSTEMI/unstable angina [subacute PCI] or stable angina [elective PCI]), and glucose-lowering agents did not seem to influence risk of stent thrombosis.

Conclusion

In a contemporary cohort of coronary stented patients, stent thrombosis was evident in more than 60% of subsequent STEMIs.     

Impact of Coronary Artery Curvature on the Longitudinal Stent Foreshortening: Real-World Observations

Longitudinal stent foreshortening is a known phenomenon, however, the impact of coronary artery curvature on longitudinal stent foreshortening remains unclear. The aim of this study is to determine the impact of coronary artery curvature on the longitudinal stent foreshortening in the real-world scenarios. A total of 86 consecutive patients underwent coronary stent implantation were included in the present study. The degree of coronary artery curvature was defined as the length of the coronary artery curvature divided by the straight length. Longitudinal stent foreshortening was defined as the stent length after implantation divided by the stent length before implantation. The mean longitudinal foreshortening rate of coronary stents was about 94% in curved coronary arteries. Longitudinal stent foreshortening rate was positively correlated with the degree of coronary artery curvature (r = –0.86, P < 0.01). Coronary artery curvature is associated with significant longitudinal foreshortening of coronary stents, thus longitudinal foreshortening should be considered on deciding the stent length in curved coronary artery and a longer stent is usually needed in curved coronary artery.     

Paraoxonase-1 is a major determinant of clopidogrel efficacy

Clinical efficacy of the antiplatelet drug clopidogrel is hampered by its variable biotransformation into the active metabolite. The variability in the clinical response to clopidogrel treatment has been attributed to genetic factors, but the specific genes and mechanisms underlying clopidogrel bioactivation remain unclear. Using in vitro metabolomic profiling techniques, we identified paraoxonase-1 (PON1) as the crucial enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite formation. We tested the clinical relevance of the PON1 Q192R genotype in a population of individuals with coronary artery disease who underwent stent implantation and received clopidogrel therapy. PON1 QQ192 homozygous individuals showed a considerably higher risk than RR192 homozygous individuals of stent thrombosis, lower PON1 plasma activity, lower plasma concentrations of active metabolite and lower platelet inhibition. Thus, we identified PON1 as a key factor for the bioactivation and clinical activity of clopidogrel. These findings have therapeutic implications and may be exploited to prospectively assess the clinical efficacy of clopidogrel.     

Restenosis begets restenosis: implications for stent selection

Background. Identifying the risk for restenosis is of critical importance in the stent selection process of patients undergoing percutaneous coronary intervention (PCI). Therefore, we sought to determine if a history of clinical recurrence (CR) after PCI increases the risk of CR after treatment of a de novo lesion in another coronary artery. Methods. We retrospectively analysed all 12,763 patients who underwent PCI between 1993 and 2004 and selected patients with two or more interventions in two different native vessels. These patients were divided into two groups: patients without CR, and patients with CR after the first PCI. Clinical recurrence was defined as revascular-isation of the target vessel by either PCI or CABG within one year. Results. A total of 1010 patients with two or more interventions in two different native vessels were identified: 727 patients without and 283 patients with CR after the first PCI. Baseline patient characteristics and conventional risk factors were comparable between the two groups. Patients with a history of CR had a higher risk of CR after a second intervention in a second vessel (OR=3.4, 95% CI=2.3 to 4.9). A total of 112 patients also had a third intervention in a third native vessel: 12 patients with two CR, 30 patients with one CR and 70 patients with no CR after the first two interventions. CR rates in these patients were 50, 17 and 3%, respectively (p<;0.001). Conclusion. Patients with a history of CR have a markedly increased risk of developing CR after a second or third PCI in a different coronary artery. Therefore, in the decision-making process on whether to use a bare metal stent or drug-eluting stent, the history of CR is a simple and powerful aid. (Neth Heart J 2008;16:376-81.)     

Stent thrombosis associated with first-generation drug-eluting stents: issues with antiplatelet therapy

Notice of the rare but catastrophic occurrence of stent thrombosis in association with deployment of drug-eluting stents has focused attention on the adequacy of the current dual antiplatelet regimen of aspirin and clopidogrel. Some patients will not respond to clopidogrel and a glycoprotein (GP) IIb/IIIa inhibitor may be strongly considered during stenting procedures, especially in high-risk patients or those not receiving pretreatment with clopidogrel. Insisting upon and confirming adherence to antiplatelet therapy are complicated tasks, especially because the reasons for premature discontinuation are myriad, from cost to bleeding complications to the need for minor surgery. Nevertheless, the concern about adherence to antiplatelet therapy represents a new and significant clinical reality in our stenting era, one previously less appreciated with the deployment of bare metal stents. (Neth Heart J 2007;15:148-50.)     

Comparative study of ticagrelor and clopidogrel in therapeutic effect of acute myocardial infarction patients undergoing percutaneous coronary intervention

ObjectivesComparison of Ticagrelor vs clopidogrel in antiplatelet therapeutic effect of acute myocardial infarction patients undergoing percutaneous coronary intervention.MethodsThe study focused on 2000 acute myocardial infarction patients undergoing percutaneous coronary intervention (PCI) in our hospital from January 2013 to December 2015. To reduce the formation of acute stent thrombosis caused by clopidogrel resistance, we had two options, one was to double the dosage of clopidogrel, and the other was to substitute ticagrelor for clopidogrel. Based on random number table method, the 2000 patients were divided into experimental group and control group, each containing 1,000 patients. The patients in experimental group took 180 mg ticagrelor before PCI and 90 mg ticagrelor twice a day after PCI (Gu, 2016). In contrast, the patients control group took 600 mg clopidogrel before PCI and 150 mg clopidogrel once a day after PCI. Both groups were drawn 2.7 ml of fasting venous blood for platelet aggregation rate test before PCI and 2 h, 24 h, 7 days after PCI respectively. Turbidimetric method was used to measure the ADP-induced platelet aggregation rate and observe change of platelet aggregation rate and success rate. Incidence of liver and kidney malfunction and adverse actions were monitored. All patients accepted a 6-month of follow-up examination to record and compare incidences of major adverse cardiac and cerebrovascular events. The statistical results of both groups are analyzed and compared.ResultsThe platelet aggregation rate of experimental group before PCI and 2 h, 24 h, 7 days after PCI was 59.71% ± 7.24%, 59.20% ± 7.70%, 48.66% ± 7.80% and 43.39% ± 8.28%; The control group was 58.04% ± 5.61%, 56.25% ± 6.02%, 55.68% ± 3.14%, 53.94% ± 5.30%; Comparing the platelet aggregation rate of different time, P was less than 0.05. The success rate of platelet aggregation of experimental group and control group was 80.56% and 46.86% respectively. There were significant differences between the two groups and the P was less than .05. The postoperative serum creatinine level of experimental group was higher than that in the control group (P < .05). The incidence of adverse reactions in the experimental group was significantly lower than that of the control group. There were significant differences between the two groups and the difference was of statistical significance (P < .05). According to the 5-month follow-up examination: the incidence of major adverse cardiac and cerebrovascular events in experimental group was 2.60% (52/2000) ,while the control group was 13.00% (260/2000) . There were significant differences between the two groups and the difference was of statistical significance (P < .05).ConclusionsCompared with clopidogrel, ticagrelor can achieve better n antiplatelet effect for patients with acute myocardial infarction undergoing percutaneous coronary intervention (PCI). It can effectively reduce the incidence of postoperative adverse cardiac and cerebrovascular events and control the rate of adverse reactions within the acceptable range.     

Recent advances in the pharmacogenetics of clopidogrel

Clopidogrel has been used to prevent recurrent ischemic events after acute coronary syndrome and/or coronary stent implantation. An impaired platelet response to this drug (residual high platelet reactivity) has been identified as a risk factor for recurrent ischemic events. The platelet response to clopidogrel is highly heritable (73%) suggesting a substantial genetic component. Two sequential cytochrome P450-dependent oxidative steps are required to convert clopidogrel to its active metabolite. The first step leads to the formation of 2-oxo-clopidogrel, which is then metabolized to the active metabolite. Cytochrome P450s are large highly polymorphic family of mono-oxygenases. Many alleles have been reported, and some of these are able to modify the activity of proteins, reducing or increasing the concentration of active metabolites and the drug effect. Loss-of-function variants in the hepatic cytochrome 2C19 (mainly *2 allele) system have been found to be the predominant genetic mediators of clopidogrel response. Variant carriers have higher treatment platelet reactivity and higher risk of adverse cardiac events including stent thrombosis, myocardial infarction, and death. Although value of CYP2C19 genotyping has been demonstrated in ACS population treated with PCI, there is still a wide interindividual variability within each genotype to systematically advocate this genetic testing in clinical practice. The CYP2C19*2 variant only explained 12% of the platelet response to clopidogrel. In the near future, it is highly probable that additional gene variants or epigenetic phenomenon will emerge as significant contributors to clopidogrel response that will allow recommending genetic testing for routine use. The purpose of this review is to discuss the contribution of individual genetic differences responsible for variations of action and clopidogrel efficacy.     

One-year clinical follow-up of a registry evaluating a percutaneous revascularisation strategy combining a pre-specified simple selection process with the use of a new thin-strut bare cobalt-chromium stent

Objectives. To evaluate clinical events in a specifically selected cohort of patients with obstructive coronary artery disease (CAD), using a new generation thin-strut bare cobalt-chromium coronary stent. Methods. Patients with single- or multi-vessel, stable or unstable CAD eligible for percutaneous implantation of at least one bare cobalt-chromium stent were evaluated in a single-centre registry. Prospective pre-specified criteria for bare cobalt-chromium stent implantation in our centre were: any acute ST-elevation myocardial infarction (MI), otherwise 1) de novo coronary lesion, and 2) lesion length <20 mm, and 3) reference vessel diameter >2.6 mm, and 4) no diabetes, unless reference vessel diameter >3.5 mm. Endpoints, retrospectively collected, were death, MI and clinically driven target-lesion revascularisation (TLR) and target-vessel revascularisation (TVR) after 12 months. Results. Between September 2005 and June 2007, 712 patients (48.7% one-vessel, 29.9% two-vessel, 20% three-vessel and 1.4% left main disease; 7.9% diabetics) were treated with 800 bare cobalt-chromium stents, for stable angina (40.9%), unstable angina (20.9%) or acute ST-elevation MI (38.2%). The procedural success rate was 99.3%. Peri-procedural MI rate was 2.2% in the semi-elective group. At 12 months there were 17 deaths (2.4%), of which nine non-cardiac, 20 (2.8%) MI, 19 (2.7%) TLR and 29 (4.1%) TVR. Early and late definite stent thrombosis occurred in four (0.6%) and three (0.4%) patients, respectively. Conclusion. A strategy aimed at minimising drug-eluting stent use and combining a pre-specified simple selection process with the use of a new thin-strut bare cobalt-chromium stent is safe and effective at one-year clinical follow-up. (Neth Heart J 2010;18:486-92.)