Mechanism Of Stent Thrombosis Research Articles

TCT-46 OCT-based management of late stent thrombosis: results from the SAFE registry

Late stent thrombosis is an infrequent complication of PCI, but is associated with high risk of recurrent ischemic events. OCT can help determine the mechanism of stent thrombosis and thus optimize management. We hypothesize that the use of OCT in stent thrombosis will substantially change how PCI

Stent-related defects in patients presenting with stent thrombosis: differences at optical coherence tomography between subacute and late/very late thrombosis in the Mechanism Of Stent Thrombosis (MOST) study

Subacute, late, and very late stent thrombosis (ST) may occur after stent implantation, but they are characterised by different underlying pathophysiological mechanisms. We sought to appraise differences between subacute and late/very late ST at the thrombus site by optical coherence tomography (OCT). The Mechanism Of Stent Thrombosis (MOST) study was a prospective multicentre non-randomised registry which enrolled six subacute ST and six controls (subacute ST study), and 17 late/very late ST and 17 controls (late/very late ST study). Patients with subacute ST had a minimum stent area at the thrombus site of 2.1 mm² (1st-3rd quartile 1.3-4.5) vs. 2.9 mm² (2.4-5.0) in the matched control (p=0.05). Uncovered struts were 26.2% (16.5-35.9) vs. 13.9% (8.9-18.9), p=0.001. Malapposed struts were 18.8% (13.1-24.5) vs. 15.2% (12.8-17.6), p=0.001. In patients with late/very late ST, uncovered struts were 23.6% (13.9-33.3) vs. 5.2% (0.5-10.2), p=0.001. Malapposed struts were 12.1% (6.4-17.8) vs. 2.8% (0.4-5.2), p=0.001, and maximum malapposition distance was 0.45 mm (0.32-0.62) vs. 0.12 mm (0-0.25), p=0.01. Notably, all patients with ST had previously discontinued dual antiplatelet therapy (n=14) or showed high residual platelet reactivity on clopidogrel therapy. Subacute ST had a significant stent underexpansion while late/very late ST had a greater stent strut malapposition distance at the thrombus site. These findings explain how procedure-related complications and vessel remodelling have a specific impact on the segment characterised by thrombus. High platelet reactivity also seems a necessary cofactor for both subacute and late/very late ST. http://www.clinicaltrials.gov unique identifier NCT01410539.

Management of late/very late stent thrombosis: Utility of ıntravenous ultrasonography (IVUS) in clinical practise

To the editor We read with great interest the article by Aksu et al. [1] on the management of very late bare metal stent thrombosis. They performed intracoronary thrombus aspiration and inflated balloon in-stent for restenosis. During percutaneous coronary interventions, interventionalists have often to deal with thrombus-laden lesions in coronary vessels. Plaque characteristics and distribution, severity and extent of calcification, arterial remodeling and the presence of dissection or thrombi can affect the decision to use a particular treatment before and after PCI. Clear identification of the characteristics of culprit vessels can help to improve clinical outcomes after interventions [2]. While the mechanism of stent thrombosis is yet to be completely understood, stent fracture and/or late acquired stent apposition could set the stage for late stent thrombosis (LST). Some types of late-acquired stent malapposition are caused by positive vessel remodeling due to biological reactions to the stent, which may allow motion and/or kinking of the stent, leading to stent fracture. Alternatively, stent fracture can lead to local mechanical irritation of the vessel, which may lead to stent malapposition. Exposure of a free metal strut after fracture into the vessel lumen could trigger platelet activation, stent thrombosis and subsequent myocardial infarction. Intravascular ultrasound (IVUS) is a useful diagnostic tool for the assessment of lesion severity leading to revascularization, selection of the revascularization strategy and assessment of lesion composition leading to a change in interventional strategy and can contribute to reaching an optimal decision for intervention [3, 4]. In this case, if had considered, an IVUS study may have revealed late-acquired stent malapposition was highly prevalent in patients with LST. In addition, in real world, most very late stent thrombosis cases are associated with discontinuation of anti-platelet agents due to dental procedure or non-cardiac surgery and it appears more closely related to discontinuation of aspirin. In stent thrombosis cases, despite ongoing anti-platelet agent, resistance must be considered and evaluated to avoid future complications.

Repeated intra-stent thrombus formation in a patient with acute coronary syndrome due to poor responsiveness to clopidogrel may be associated with cytochrome P-450 2C19*2 polymorphism

A drug-eluting stent was implanted at the culprit lesion in a 65-year-old man with acute coronary syndrome. Nine days after the procedure, he suffered stent thrombosis, and a bare-metal stent was subsequently implanted. Twelve days after this second procedure, a follow-up angiogram showed a newly emerged thrombus at the site of stent implantation. Although the patient had continued dual anti-platelet therapy with aspirin and clopidogrel since the first procedure, platelet optical aggregation test showed no inhibition of aggregation. Further, genetic analysis revealed him to be homozygous for the CYP2C19*2 polymorphism. This case suggests that the mechanism of stent thrombosis, while multi-factorial, is affected greatly by crossover of poor responsiveness to clopidogrel due to the CYP2C19*2 polymorphism.

Stent thrombosis with drug‐eluting stents: A re‐examination of the evidence

The excitement of drug-eluting stents and their promise for reduced restenosis rates have been tempered by recent reports of stent thrombosis. The mechanism of stent thrombosis is multifactorial but appears to be related to delayed endothelialization and healing, late stent malapposition, and antiplatelet resistance. The most important risk factor appears to be the discontinuation of dual antiplatelet therapy. The data from clinical trials suggest that drug-eluting stents are associated with increased incidence of death or myocardial infarction compared with bare metal stents at long-term follow-up, suggesting that the window of thrombotic risk with drug-eluting stents may extend far beyond that for bare metal stents. Measures to possibly decrease the incidence of stent thrombosis include improvements in antiplatelet regimens and newer generation of drug-eluting stents which have biodegradable polymers or are polymer-free. In addition, percutaneous coronary intervention with bare metal stents in patients may be helpful in those known to be intolerant or noncompliant to antiplatelet therapy, have planned procedures or surgeries, or have overwhelming risks which may require discontinuation of dual antiplatelet therapy.

Two distinct mechanisms are involved in stent thrombosis under flow conditions

The mechanism of stent thrombosis was evaluated by a flow chamber model. A Palmaz-Schatz stent was placed on glass surfaces coated with type I collagen in a parallel-plate flow chamber. Platelets were rendered fluorescent with mepacrine and whole blood was perfused through the chamber. Platelet thrombi formed around the implanted stents were continuously recorded by epi-fluorescent video-microscopy. Platelet thrombi appeared on the collagen surface within a few minutes in the absence of function blocking monoclonal antibodies. Antibody blocking vWF interaction with GP Ib f completely inhibited the platelet thrombi around the stent, but had no effect on platelet thrombus formation in the space between the stents and collagen, while both were inhibited by anti-GP IIb/IIIa. Our results suggest that two distinct mechanisms, one mediated by vWF interaction with GP Ib f occurring at high shear rates, and the other mediated exclusively by GP IIb/IIIa occurring at low shear rates, are involved in the process of platelet thrombus formation in the presence of stents.