Composition of thrombi in late drug-eluting stent thrombosis versus de novo acute myocardial infarction
Department of Cardiology, Miyazaki Medical Association Hospital, and Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan. Thrombosis Research
(Impact Factor: 2.45).
11/2009; 126(3):254-7. DOI: 10.1016/j.thromres.2009.11.010
To determine the compositions of thrombi in DES thrombosis and de novo AMI, we histologically examined 9 patients with late/very late DES thrombosis and 29 with AMI who had undergone thrombus removal via an aspiration catheter. All DES thrombi were composed of aggregated platelets and fibrin, along with erythrocytes and white blood cells. Immunohistochemical staining revealed constitutive presence of GPIIb/IIIa, fibrin, glycophorin A, P2Y12 receptor, VWF, and CD16 positive cells in all thrombi, findings that were similar to those of de novo AMI. P2Y12 receptor colocalized with GPIIb/IIIa. CD34-positive cells were occasionally found in small clusters, and covered organizing thrombi. Eosinophils were evident in 5 patients with DES thrombosis, as a minor component. The immunopositive areas (%) or cell numbers did not differ between late/very late DES thrombi and de novo coronary thrombi. The similar composition of late DES and de novo coronary thrombi suggests the importance of intensive platelet inhibition and the similar mechanisms of symptomatic thrombus formation in patients with DES implantation and de novo AMI.
Available from: Tatsuya Nakama
- "However, to recruit a large number of patients is complicated by the very low rates of ST. The incidence of definite LST and VLST after DES implantation is only 0.5% at our institutions, which is similar to that of several studies   . Further investigations are required to confirm our observations. "
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ABSTRACT: Although drug-eluting stents (DES) have considerably reduced the incidence of in-stent restenosis, late and very late stent thrombosis (ST) after DES implantation have emerged as major safety concerns. We morphologically investigated the age of DES thrombi aspirated during percutaneous coronary intervention (PCI) from patients with either late or very late ST that resulted in acute myocardial infarction (AMI).
We obtained DES thrombi during PCI from 16 consecutive patients with ST (late and very late ST, n=4 and n=12, respectively), who presented with AMI within 24 h of the onset of anginal symptoms. Thrombi were morphologically classified as fresh, lytic, and organized. Fresh thrombus was identified in 5 (31%) of the 16 patients and lytic thrombus was found in 3 (19%). Organized thrombus was notably found in 8 (50%) patients, of whom 5 (31%) had only the organized type and 3 (19%) had both fresh and organized thrombi. The frequency of fresh thrombus tended to be higher in patients with stent failure such as stent malapposition and fracture, but the difference did not reach significance (p=0.06).
Although the study group is small, about two-thirds of DES thrombi in late and very late ST were days or weeks old. These findings suggest an important discrepancy between the time of onset of the intra-stent thrombotic process and the occurrence of acute clinical symptoms, and provide further information about another potential mechanism of DES thrombosis.
Available from: PubMed Central
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ABSTRACT: Thrombus formation on a disrupted atherosclerotic plaque is a key event that leads to atherothrombosis. Because thrombus is induced by chemical or physical injury of normal arteries in most animal models of thrombosis, the mechanisms of thrombogenesis and thrombus growth in atherosclerotic vessels should be investigated in diseased arteries of appropriate models. Pathological findings of human atherothrombosis suggest that tissue factor, an initiator of the coagulation cascade, significantly affects enhanced platelet aggregation and fibrin formation after plaque disruption. We established a rabbit model of atherothrombosis based on human pathology in which differences in thrombus formation between normal and atherosclerotic arteries, factors contributing to thrombus growth, and mechanisms of plaque erosion can be investigated. Emerging transgenic and stem cell technologies should also provide an invaluable rabbit experimental model in the near future.
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