Recurrent episodes of very late stent thrombosis in a patient with aspirin hypersensitivity, stent fracture and malapposition

Late stent thrombosis represents a life-threatening event, usually triggered by inadequate antiplatelet therapy and promoted by multiple risk factors, such as stenting of a chronic total occlusion, overlapping stenting, an abnormal vascular response to the eluted drug, stent malapposition and stent fracture. A 57-year-old man with aspirin hypersensitivity underwent successful percutaneous revascularization of a chronic total occlusion of the left anterior descending artery (LAD). He received two sirolimus-eluting stents overlapping for 2 mm and was discharged on clopidogrel and picotamide. Two years later, 15 days after clopidogrel discontinuation, he experienced an anterior ST-segment elevation myocardial infarction and underwent rescue percutaneous LAD thrombectomy after unsuccessful fibrinolysis. Coronary angiography showed fracture of the distal stent, with a 5 mm gap between the two portions, as well as severe late stent malapposition, confirmed by optical coherence tomography. Despite treatment with clopidogrel and picotamide, in the following days the patient experienced two new episodes of stent thrombosis, treated with thrombectomy and deployment of bioengineered stents. The patient underwent successful oral aspirin desensitization, with a complete in vitro inhibition of platelet function, and was discharged on aspirin, clopidogrel and warfarin, without experiencing other events at 6-month follow-up.     

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. (Int J Cardiovasc Intervent 2004; 6: 160-164)     

Lack of efficacy of clopidogrel pre-treatment in the prevention of myocardial damage after elective stent implantation

OBJECTIVES: The object of this study was to determine the effect of pre-treatment with clopidogrel in patients undergoing elective stent implantation. BACKGROUND: The treatment of patients with adenosine diphosphate receptor blockers after percutaneous coronary intervention (PCI) with stent implantation has been shown to decrease the incidence of subacute stent thrombosis. Furthermore, non-randomized studies on pre-treatment with clopidogrel among patients undergoing stent implantation have suggested a reduction in myocardial damage and clinical events. The effect of pre-treatment with clopidogrel has been studied in only a few randomized trials. METHODS: In a randomized trial, three days of pre-treatment with clopidogrel was compared with standard post-procedural treatment in 203 patients undergoing elective stent implantation. The primary end point was a rise in troponin I or creatine kinase-MB fraction (CK-MB) serum levels at 6 to 8 and 16 to 24 h after PCI. Secondary end points were death, stroke, myocardial infarction, coronary bypass grafting, repeated PCI, and subacute stent thrombosis at one and six months after PCI. RESULTS: No difference was found between non-pre-treated and pre-treated patients in the post-procedural elevation of troponin I (42 [43.3%] vs. 48 [51.1%], respectively, p = 0.31) or CK-MB (6 [6.3%] vs. 7 [7.4%], respectively, p = 0.78). Adjustment for possible confounding factors did not change these findings. Patient follow-up at one and six months showed no significant difference between the treatment groups in death, stroke, myocardial infarction, coronary artery bypass grafting, repeated PCI, or subacute stent thrombosis. CONCLUSIONS: In this randomized study, no beneficial effect of pre-treatment with clopidogrel on post-procedural elevation of troponin I and CK-MB or on clinical events after one and sixth months could be demonstrated. The study suggests that among patients with stable coronary syndromes in whom coronary stent implantation is planned, pre-treatment may not be beneficial in reducing early myocardial damage.     

A case of fatal stent thrombosis after Carbostent implantation: is clopidogrel alone antiplatelet therapy a safe alternative to aspirin alone antiplatelet therapy?

We describe a case of fatal stent thrombosis after Carbostent implantation and clopidogrel alone antiplatelet therapy in a patient affected by rectal cancer who does not tolerate aspirin. He had three-vessel disease, with occlusion of the right and left anterior descending coronary artery and a severe stenosis of the proximal left circumflex. High-risk circumflex percutaneous coronary intervention (PCI) was performed under left ventricular assistance by Impella device with an optimal final angiographic result. After 2 h, however, the patient developed chest pain with marked ST segment elevation in the infero-lateral leads, due to stent thrombosis, and hypotention which rapidly degenerated into cardiac arrest, electromechanical dissociation and death. At the present time the choice between PCI at high risk of stent thrombosis followed by low risk cancer resection and cancer resection at high risk of peri-operative myocardial infarction followed by low risk PCI remains difficult.     

Prasugrel in Clopidogrel Nonresponders Undergoing Percutaneous Coronary Intervention: The RECLOSE-3 Study (REsponsiveness to CLOpidogrel and StEnt Thrombosis)

ObjectivesThis study sought to investigate the efficacy of prasugrel compared with clopidogrel in clopidogrel nonresponders.BackgroundClopidogrel nonresponsiveness is a strong marker of the risk of cardiac death and stent thrombosis after a percutaneous coronary intervention (PCI). It is unknown whether clopidogrel nonresponsiveness is a nonmodifiable risk factor or whether prasugrel with more potent and predictable platelet inhibition as measured by ex vivo techniques is associated with a positive effect on clinical outcome.MethodsThe RECLOSE-3 (REsponsiveness to CLOpidogrel and StEnt thrombosis) study screened clopidogrel nonresponders after a 600-mg loading dose of clopidogrel. Clopidogrel nonresponders switched to prasugrel (10 mg/day) the day of the PCI, and an adenosine diphosphate (ADP) test (10 μmol/l of ADP) was performed 6 days after the PCI. The primary endpoint was 2-year cardiac mortality. Patient outcome was compared with the RECLOSE-2–ACS study.ResultsWe screened 1,550 patients, of whom 302 were clopidogrel nonresponders. The result of the ADP test was 77.6 ± 6.2%. After switching to prasugrel, the ADP test result decreased to 47.1 ± 16.8%. The 2-year cardiac mortality rate was 4% in the RECLOSE-3 study and 9.7% in nonresponders of the RECLOSE-2–ACS study (p = 0.007). The definite and probable stent thrombosis rates were 0.7% and 4.4%, respectively (p = 0.004). On multivariable analysis, prasugrel treatment was related to the risk of 2-year cardiac death (hazard ratio: 0.32, p = 0.036).ConclusionsClopidogrel nonresponsiveness can be overcome by prasugrel (10 mg/day), and optimal platelet aggregation inhibition on prasugrel treatment is associated with a low rate of long-term cardiac mortality and stent thrombosis.     

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis following thrombocytopenia remission--a case report

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis. This article presents a case of a 62-years-old man with acute anterior myocardial infarction, treated with PCI and stent implantation, in whom profound acute thrombocytopenia was observed after abciximab administration. Nadir platelet count was 6 G/L (before treatment: 250 G/L). Pseudothrombocytopenia was excluded. The remaining antiplatelet drugs (heparin, ASA, clopidogrel) were discontinued. There were no symptoms of bleeding, but next morning (platelet count: 14 G/L) a gross hematoma at femoral puncture site was observed. The patient received 5 U transfusion of platelets. On the 4th day, when the platelet count reached 64 G/L, he was started again on ASA (150 mg) and clopidogrel (75 mg). On the 7th day (platelet count: 138 G/L) he developed anterior ischemia and stent reocclusion was diagnosed. After p.o. clopidogrel (300 mg), balloon PCI with i.c. heparin was performed and ischemia symptoms subsided. The platelet value before the patient's discharge, on subsequent therapy with ASA and clopidogrel, increased to 300 G/L. A review of current literature on this topic is provided.     

A case report of very late thrombosis of coronary bare-metal stent 10 years after stenting

Although late stent thrombosis is not uncommon with the use of drug-eluting stents, it is unusual with the use of bare-metal stents (BMS) because stent endothelialization is considered to be completed 4 weeks after the intervention.(1) A 64 year-old male had undergone percutaneous coronary intervention (PCI) for a proximal left anterior descending (LAD) artery lesion with a BMS and excellent angiographic results were obtained. Two hundred mg of ticlopidine was prescribed for one month and 100 mg of aspirin daily was continued. One year after stent implantation, coronary angiography (CAG) showed no restenosis. Ten years and 7 months after stent implantation, he suffered an acute myocardial infarction due to stent thrombosis. Intra-coronary aspiration thrombectomy was successful. To the best of our knowledge, the longest delayed case of BMS thrombosis is 5 years after stent implantation.(2) Our report demonstrated evidence of the latest reported case of stent thrombosis with the use of a BMS.     

雷帕霉素洗脱支架远期致冠状动脉局部血管瘤样扩张四例报告

目的分析雷帕霉素洗脱支架远期发生冠状动脉局部血管瘤样扩张的特点及原因。方法2004年4—7月接受介入治疗的冠心病患者4例,男3例,女1例,造影显示7支病变血管共置入9个支架,其中前降支置入Cypher select支架5个,回旋支置入Firebird支架2个,Pixel支架1个,右冠状动脉置入Cypher select支架1个。术后口服氯吡格雷75mg／d持续1年。结果4例均成功置入支架,病变血管达TIMI Ⅲ级血流灌注,心绞痛症状消失,无急性／亚急性血栓形成。平均随访（24．8±1．8）个月,无主要心脏不良事件发生。术后12个月冠状动脉造影随访,无支架内再狭窄及新病变出现。停用氯吡格雷,继续门诊随访,病情稳定。4例患者分别于术后16、18、22个月因心绞痛症状复发而再次入院,入院后给予氯吡格雷75mg／d,静脉注射硝酸甘油及皮下注射低分子肝素治疗。冠状动脉造影显示：3例于前降支近段,1例右冠状动脉中段置入Cypher支架的部位冠状动脉呈血管瘤样扩张,扩张处血管直径明显大于临接正常冠状动脉,其他置入支架的血管无病变。术后即刻给予替罗非班（0．1μg·kg^-1·min^-1）连续3天治疗,症状消失。继续随访3—6个月,全部存活,无心绞痛发生。结论雷帕霉素支架远期发生支架贴壁不良,导致血管重构是造成局部血管瘤样扩张的可能原因。     

Usefulness of the evaluation of stent fracture by 64-multi-detector row computed tomography

A 77-year-old man with unstable angina pectoris showed severe coronary stenosis with soft plaque in the left anterior descending coronary artery (LAD) as detected by 64-multi-detector row computed tomography (MDCT). Percutaneous coronary intervention (PCI) with a bare-metal stent to the LAD was performed, and stent fracture immediately after PCI was clearly detected by MDCT. MDCT may be useful for identifying a fractured stent and for management after stent implantation.     

In-stent restenosis and thrombosis 41 months after drug-eluting stent implantation

Evidence indicates that very late stent thrombosis (> 1 year) occurs more frequently in drug-eluting stents than in bare metal stents after discontinuation of clopidogrel. We present a case of an 83 year old man with an LAD in-stent thrombosis 41 months after stenting with a sirolimus-eluting stent in whom clopidogrel was discontinued after 6 months based on these days' guidelines. In-stent thrombus was aspirated and intracoronary ultrasound (ICUS) showed significant in-stent restenosis which had narrowed the minimal lumen diameter by 1 mm. The lesion was stented with a bare metal stent. The patient was discharged after recovery and had no recurrence of stent thrombosis in one month follow-up. We recommended indefinite dual antiplatelet therapy with aspirin and clopidogrel.     

Clopidogrel treatment surrounding percutaneous coronary intervention: When should it be started and stopped?

Clopidogrel pretreatment before percutaneous coronary intervention (PCI) has been shown to decrease major adverse cardiovascular events (MACE) at 1 month. This benefit has been demonstrated in patients spanning the entire spectrum of coronary artery disease. Subsequent dual antiplatelet therapy with aspirin and clopidogrel after stent placement is necessary for the prevention of stent thrombosis. The duration of clopidogrel therapy after stent placement is dependent upon the type of stent placed, and is recommended for a minimum of 4 weeks after bare-metal stent placement, 3 months after sirolimus-eluting stent placement, and 6 months after paclitaxel-eluting stent placement. A longer course of therapy with clopidogrel (12 months) has been recommended by the most recent American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Interventions guidelines for PCI based upon incremental reduction in cardiovascular complications (primarily myocardial infarction). This article reviews the data presently available regarding pretreatment with clopidogrel before PCI, and the strength of evidence supporting long-term dual antiplatelet therapy.     

Two hour bivalirudin infusion after PCI for ST elevation myocardial infarction

The standard of care for STEMI PCI for the past decade has been aspirin, clopidogrel, heparin, and a glycoprotein IIbIIIa receptor inhibitor (GPI). A bivalirudin strategy was shown to be superior to a GPI strategy in the HORIZONS AMI trial for net adverse clinical events (combined MACE and bleeding). An increased risk of acute stent thrombosis in the bivalirudin arm may have prevented broader adoption of bivalirudin for this indication. We hypothesized that acute stent thrombosis risk could be ameliorated by a 2 h infusion of bivalirudin following STEMI PCI. We implemented a multicenter, prospective registry for all STEMI patients in Vermont treated at a single PCI center. Each patient was routinely pre-loaded with dual antiplatelet therapy and 75% received an unfractionated heparin bolus prior to PCI. The utilization of bivalirudin bolus and continued 2 h infusion after PCI was routine with GPI bailout optional. 128 consecutive STEMI patients underwent primary PCI from October 1, 2008 to September 30, 2009. 92% of primary PCI patients received bivalrudin during and after the procedure with a 9% rate of bail out GPI. There was one case of probable or definite acute stent thrombosis (0.7%), and this single case occurred despite use of bailout GPI. Despite the prolonged infusion of bivalirudin, major bleeding occurred in only 1.7% of STEMI patients. In conclusion, prolonging bivalirudin for 2 h after STEMI PCI may be a promising method to alleviate acute stent thrombosis risk without losing the bleeding complication benefit of the bivalirudin strategy.     

Optimal management of platelet function after coronary stenting

Opinion statement Coronary stenting elicits vessel wall damage, and subsequent activation of platelets is implicated as a major component of complications such as acute, subacute, and late stent thrombosis. As such, dual antiplatelet therapy using aspirin and clopidogrel has become a routine adjunct to coronary stenting. Use of aspirin and clopidogrel with or without glycoprotein IIb/IIIa inhibitors after coronary stenting reduces the complication rate and improves long-term outcomes. Dual antiplatelet therapy using aspirin and clopidogrel is recommended for at least 4 weeks with bare metal stents, and for 3 to 6 months with drug-eluting stents for prevention of major adverse cardiac events. After coronary stenting, 1 year of dual antiplatelet therapy is recommended for prevention of future cardiac events. However, despite the use of antiplatelet agents, stent thrombosis occurs in approximately 1% of patients, with an increased likelihood of occurrence in high-risk patients or a lesion subset of patients. Although the incidence of stent thrombosis is low, stent thrombosis usually presents as acute coronary syndrome and the mortality rate is up to 45%. Thus, considering the widespread use of stents, a considerable number of people are inadequately protected from thrombotic events despite current standard antiplatelet therapy using aspirin and clopidogrel. A concern with clopidogrel is the loading time and loading dose required to achieve and maintain optimal inhibition of platelet aggregation. The current recommendation for ensuring maximum antiplatelet activity is administration of a 300-mg loading dose of clopidogrel initiated at least 6 hours prior to percutaneous coronary intervention (PCI), and ideally the day before. If this is not possible, a loading dose of 600 mg of clopidogrel should be administered at least 2 hours before PCI. Recently, new combinations of antiplatelet agents (ie, triple therapy using aspirin, clopidogrel, and cilostazol) and new drugs with potent antiplatelet effects (ie, Prasugrel [currently being developed by Sankyo Pharmaceuticals and Ube Pharmaceuticals in Japan and by Eli Lilly and Co. (Indianapolis, IN) in the United States], Cangrelor [currently being developed by AstraZeneca Pharmaceuticals, Wilmington, DE], and AZD6140) have been evaluated in clinical trials; such treatments may help reduce the number of cardiac events after coronary stenting.     

52例冠状动脉支架内血栓形成患者的临床特点及介入治疗

目的探讨冠状动脉支架置入术后支架内血栓形成的临床特点及治疗措施。方法回顾性分析近6年我院心内科住院冠心病患者中52例发生冠状动脉支架术后支架内急性和亚急性血栓患者的临床及冠状动脉造影特点,并评价其治疗方法的疗效。结果2000年1月至2006年5月,我院共52例患者于冠心病的介入治疗术后发生支架内急性或亚急性血栓形成(发生率0.75%)。术后发生支架内血栓形成的时间为30min～20d,平均(3.6±4.2)d。多因素回归分析表明急性心肌梗死(AMI)、术前存在心功能不全、病变血管支数、前降支病变及B2/C型病变是支架内血栓发生的独立危险因子。支架内血栓形成后多数患者出现典型的临床表现及心电图改变。行急诊冠状动脉造影复查证实原支架内完全血栓性闭塞48例,原支架内新出现70%～95%狭窄伴血栓影像4例。经急诊经皮冠状动脉介入治疗,47例患者治愈存活出院。5例患者抢救无效死亡(院内病死率9.6%)。结论支架内血栓形成多发生于AMI、术前存在心功能不全、多支血管病变、前降支病变及B2/C型复杂病变的患者。其发病时间主要在支架置入术后1周之内。急诊再次介入治疗是治疗支架内血栓形成的首选治疗方案,尽早实施急诊经皮冠状动脉介入治疗可增加抢救成功率。     

Novel antiplatelet agent ticagrelor in the management of acute coronary syndrome

Current clinical guidelines recommend dual antiplatelet agents namely aspirin and clopidogrel for the treatment of patients suffering from acute coronary syndrome (ACS). But the efficacy of clopidogrel is variable as it is a pro-drug, which has to be metabolized to become an active drug thus exhibiting variable platelet inhibition, increases risk of bleeding, stent thrombosis, and ischemia. To overcome this limitation, prasugrel was developed with increased antiplatelet activity thereby reducing the risk of myocardial ischemia and stent thrombosis. This action of prasugrel was associated with an increased risk of major bleeding. Finally, a novel reversible and direct-acting oral adenosine diphosphate (ADP) receptor antagonist, ticagrelor was developed that showed consistent and increased P2Y12 inhibition with similar incidence of bleeding but greater reduction in cardiac events compared to clopidogrel. The focus of this article is to review ticagrelor as a new class of P2Y12 inhibitor.     

他汀类药对氯吡格雷抗血小板作用的影响

目的 前瞻性评价普伐他汀、氟伐他汀、阿托伐他汀对氯吡格雷抗血小板作用的影响.方法 人选连续1015例急性冠状动脉综合征或稳定性心绞痛行冠状动脉造影和(或)支架术患者,分为普伐他汀组(228例)、氟伐他汀组(179例)、阿托伐他汀组(481例)和对照组(127例).比较各组术后支架内血栓发生率、不同浓度(2、5、10、20 μmol)二磷酸腺苷(ADP)诱导的1 min(ADP-1)、5 min(ADP-5)和最大血小板聚集力(ADP-M)及其影响因素.结果 4组患者基础临床情况(除年龄、高血压及冠状动脉造影复查率外)和冠状动脉病变和(或)支架术情况相似,术后支架内血栓发生率(普伐他汀组0.9%、氟伐他汀组1.1%、阿托伐他汀组1.0%、对照组0.8%,P>0.05)和ADP-1、ADP-5、ADP-M与对照组相比差异均无统计学意义(P均>0.05).多因素回归分析显示,年龄(B=0.21,P=0.001)、氯吡格雷总量(B=7.30,P=0.002)及低分子肝素的使用(OR=6.71,P=0.01)是影响氯吡格雷抗血小板作用的独立决定因素.结论 普伐他汀、氟伐他汀和阿托伐他汀对氯吡格雷的抗血小板作用无明显影响,而年龄、氯吡格雷总量及低分子肝素使用是决定氯吡格雷抗血小板作用的独立因素.     

Optimizing antiplatelet therapy in acute coronary syndrome and percutaneous coronary intervention

Dual antiplatelet therapy with aspirin and clopidogrel is the standard of care for patients with acute coronary syndrome (ACS) and those undergoing percutaneous coronary intervention (PCI). It is well established that inhibition of platelet aggregation reduces the risk of recurrent thrombotic events and stent thrombosis. However, some patients show a reduced antiplatelet response to standard clopidogrel loading (300 mg) and maintenance (75 mg day^?1) doses, which has been associated with poorer patient outcomes. Pharmacodynamic and pharmacokinetic studies show that higher‐than‐standard clopidogrel dosing strategies facilitate more rapid platelet inhibition of a greater intensity as a result of greater plasma concentrations of the clopidogrel active metabolite. Recently completed studies suggest that in patients with ACS undergoing PCI, higher‐than‐standard clopidogrel dosing regimens provide greater inhibition of platelet function and improved clinical outcomes with a small but significant increase in major bleeding. Newer, more potent antiplatelet agents such as prasugrel and ticagrelor are other alternative strategies that result in more rapid, greater inhibition of platelet function and better outcomes than standard‐dose clopidogrel. Whether platelet reactivity‐guided therapy or genotyping for cytochrome P450 polymorphisms is useful in managing patients needs to be further defined. Most importantly, early and effective antiplatelet therapy results in the best short‐ and long‐term outcomes for patients with ACS or those undergoing PCI. © 2011 Wiley‐Liss, Inc.     

Treatment of rotablation‐induced ostial left circumflex perforation by papyrus covered stent and its fenestration to recover the left anterior descending artery during CHIP procedure

Coronary artery perforation is a rare complication of percutaneous coronary intervention (PCI). Covered stents have been successfully used in these situations. We report a case of ostial left circumflex (LCx) artery perforation during rotablation PCI of left main coronary artery (LMCA) and LCx artery. After failed attempts to balloon tamponade the perforation, a PK Papyrus covered stent was deployed from proximal LCx into LMCA. This resulted in acute exclusion of the left anterior descending (LAD) artery from coronary circulation. Using a dual lumen catheter, a stiff wire was advanced through the side port toward the occluded LAD to fenestrate the membrane of the covered stent. A series of balloons were used to dilate the fenestration in the covered stent to restore a normal flow into the LAD.     

Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on thrombotic events after drug-eluting stent implantation.

AIMS: The aim of this study was to determine whether platelet reactivity on clopidogrel therapy, as measured by a point-of-care platelet function assay, is associated with thrombotic events after percutaneous coronary intervention (PCI) with drug-eluting stents (DESs). METHODS AND RESULTS: Platelet reactivity on clopidogrel (post-treatment reactivity) was measured with the VerifyNow P2Y12 assay (Accumetrics Inc., San Diego, CA, USA) in 380 patients undergoing PCI with sirolimus-eluting stents. Receiver-operating characteristic curve analysis was used to derive the optimal cut-off value for post-treatment reactivity in predicting 6 month out-of-hospital cardiovascular (CV) death, non-fatal MI, or stent thrombosis. The mean post-treatment reactivity was 184 +/- 85 PRU (P2Y12 reaction units). The optimal cut-off for the combined endpoint was a post-treatment reactivity > or =235 PRU [area under the curve 0.711 (95% confidence interval 0.529-0.893), P = 0.03], which was similar to the threshold of the upper tertile (231 PRU). Patients with post-treatment reactivity greater than the cut-off value had significantly higher rates of CV death (2.8 vs. 0%, P = 0.04), stent thrombosis (4.6 vs. 0%, P = 0.004), and the combined endpoint (6.5 vs. 1.0%, P = 0.008). CONCLUSION: High post-treatment platelet reactivity measured with a point-of-care platelet function assay is associated with post-discharge events after PCI with DES, including stent thrombosis. Investigation of alternative clopidogrel dosing regimens to reduce ischaemic events in high-risk patients identified by this assay is warranted.