Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Knight, Charles; Panesar, M; Wilson, Darren; Patrineli, A.; Chronos, Nicolas; Wright, Christine; Clarke, Debbie; Patel, Deven; Fox, Kim; Goodall, Alison H.

doi:10.1053/euhj.1998.1047

Cited by 47 publications

(22 citation statements)

References 37 publications

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“…Furthermore, heparin is known to have a dual role in blood coagulation. 14,[25][26][27][28][29] Immobilized heparin may act in initiating the intrinsic pathway of coagulation, but this activity may be effectively counterbalanced by the antithrombin activity of the anticoagulant species of heparin. 26 Clinically, heparin-coated stents may improve early results of stenting through their anticoagulant activity, but they may have no inhibitory effect on neointimal proliferation, 30 for which purpose other antiproliferative agents, suitable for a local stent-delivery system, have been sought.…”

Section: Discussionmentioning

confidence: 99%

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Hietala

Maasilta

Välimaa

et al. 2003

J Biomedical Materials Res

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Despite modern stent technology and effective antiplatelet therapy, metallic stents carry the risk of (sub)acute thrombosis. Our aim was to examine short-term differences in platelet deposition and coagulation activation between biodegradable polylactide (PLA), heparin-polycaprolactone-L-lactide-coated polylactide (hepa-P(CL95/L-LA5)-PLA), and stainless steel (SS) stent struts. Gel-filtered platelets (GFP) and platelet-rich plasma (PRP) were labeled with 10 nM (3)H-serotonin. Platelet deposition was measured after incubation of the stent struts in human serum albumin-coated wells at 37 degrees C in either GFP or PRP. Platelet morphology was studied by scanning electron microscopy (SEM). For coagulation activation, the stent struts were incubated in either PRP or platelet-poor plasma (PPP), anticoagulated with D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK), followed by measurement of fibrinogen, thrombin time (TT), prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT). SS showed adherence of larger amounts of GFPs than did PLA at a platelet density of 300 x 10(6)/mL (p < 0.05). Furthermore, representative SEM studies showed more platelet spreading on SS than on PLA stent struts. Between PLA and SS, coagulation activity did not differ at any assessment. Based on prolonged TT values in plasma, the heparin coating strongly inhibited coagulation (p < 0.05). The values of soluble TAT and F1+2 for PLA were similar to those of controls, i.e., to incubated suspensions without a stent strut. In conclusion, when compared with stainless steel, both PLA and hepa-P(CL95/L-LA5)-PLA appear hemocompatible as intravascular stent materials.

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Section: Discussionmentioning

confidence: 99%

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Hietala

Maasilta

Välimaa

et al. 2003

J Biomedical Materials Res

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“…The activating potential of heparin on platelets is well known, and its ability to potentiate the expression of activation-dependent markers has recently been reported. 34 Whereas there is a standard dose of drug, there is no such thing as a standard patient. Thus, increased biological testing to assess whether platelet function is adequately inhibited might improve the success rate with all anti-GPIIbIIIa drugs.…”

Section: Interindividual Variability In the Response To Treatmentmentioning

confidence: 99%

Platelet Glycoprotein IIb/IIIa Inhibitors

Nurden

Poujol

Durrieu-Jaïs

et al. 1999

ATVB

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“…[2][3][4][5] There are not many studies on the effects and safety of LMWH during PCI, although it is known that LMWH are superior to UFH. [8][9][10][11] However, as mentioned above, because accurate measurement of anticoagulation is required and the anticoagulation state can be simply reflected by activated clotting time (ACT) measurement, LMWH use is still limited in many coronary laboratories, and furthermore, guidelines currently do not exist.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5][6][7] Although there have been few studies on the therapeutic efficacy and safety of LMWH during percutaneous coronary intervention (PCI), it is known that the effect of LMWH is superior to that of UFH due to no intrinsic platelet activation and aggregation, and the favorable clinical results obtained. [8][9][10][11] Also, it is known that LMWH has a more effective and stable anticoagulation effect than UFH. The major reason is the superior bioavailability, and the minor causes are the decrease in nonspecific protein binding, and decreases in the responsiveness for neutralization by platelet factor 4 and easy control of release of von Willebrand factor.…”

mentioning

confidence: 99%

Comparison of Abciximab Combined With Dalteparin or Unfractionated Heparin in High-Risk Percutaneous Coronary Intervention in Acute Myocardial Infarction Patients

et al. 2006

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SUMMARYThe purpose of this study was to determine the clinical outcomes of abciximab combined with the low molecular weight heparin (LMWH), dalteparin, in high-risk percutaneous coronary intervention (PCI) patients with acute myocardial infarction (AMI). A total of 140 high-risk PCI patients with AMI were divided into 2 groups: unfractionated heparin (UFH) with abciximab (group I: 70 patients, 58.7 ± 10.5 years), and dalteparin with abciximab (group II: 70 patients, 59.6 ± 9.8 years). Major adverse cardiac events (MACE) during hospitalization and at 4 years after PCI were examined. Baseline clinical characteristics, laboratory findings, echocardiography parameters, and baseline angiographic characteristics were not different between the 2 groups. The incidence of thrombotic total occlusion lesions was 62.9% in both groups. Procedural success was achieved in 91.4% in group I and 90.0% in group II. Bleeding and hemorrhagic events were not different between the 2 groups. No significant intracranial bleeding was observed in either group. The incidence of in-hospital MACE was 7 (10.0%) in group I and 4 (5.7%) in group II. Four-year clinical follow-up was performed in 97% of the patients. Four years after PCI, death occurred in 6 (8.6%) patients in group I and in 7 (10.0%) in group II. MI occurred in 4 (5.7%) and 4 (5.7%), target vessel revascularization (TVR) in 23 (32.9%) and 16 (22.9%), and bypass surgery in 3 (4.3%) and 1 (1.4%), respectively. Overall, a MACE occurred in 33 (47.1%) patients in group I and in 26 (35.1%) patients in group II (P = 0.23). The long-term clinical outcome with dalteparin combined with abciximab may be comparable to that of UFH plus abciximab in high risk PCI patients with AMI. (Int Heart J 2006; 47: 821-831)

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Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Cited by 47 publications

References 37 publications

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Platelet Glycoprotein IIb/IIIa Inhibitors

Comparison of Abciximab Combined With Dalteparin or Unfractionated Heparin in High-Risk Percutaneous Coronary Intervention in Acute Myocardial Infarction Patients

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