Early changes in local hemostasis activation following percutaneous coronary intervention in stable angina patients: a comparison between drug-eluting and bare metal stents

Mahemuti, Ailiman; Meneveau, Nicolas; Seronde, Marie‐France; Schiele, François; Descotes-Genon, Vincent; Ecarnot, Fiona; Blonde, Marie-Cécile; Mercier, Mariette; Racadot, E; Bassand, Jean‐Pierre

doi:10.1007/s11239-008-0266-2

Cited by 11 publications

(4 citation statements)

References 41 publications

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“…In particular, the more aggressive the procedures (i.e. with RA), the more pronounced this biomarker reduction, suggesting that endothelial dysfunction potentially occurs post‐PCI, in line with previous studies [8,10–12,23]. In the context of coronary atherosclerosis, a close relationship between platelets and the endothelium has been described: intact endothelium normally prevents platelet adhesion, whereas, in the presence of endothelial damage and activation, selectins mediate the first loose contact between circulating platelets and the vascular endothelium [24–26].…”

Section: Discussionsupporting

confidence: 74%

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Periprocedural variations of platelet reactivity during elective percutaneous coronary intervention

Mangiacapra

Bartúnek

Bijnens

et al. 2012

Journal of Thrombosis and Haemostasis

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) and clopidogrel (600 mg, 12 h before PCI): 15 with coronary angiography (CA group), 40 with PCI (PCI group), and 10 with rotational atherectomy plus PCI (RA group). PR was assessed by ADP, high-sensitivity ADP and thrombin receptor activator peptide 6 tests prior to, immediately after and 24 h after the procedure. E-selectin and ICAM-1 were assessed prior to and immediately after the procedure. In vitro, PR was measured during pulsatile blood flow at baseline, after balloon inflation and after stent implantation in six porcine carotid arteries and five plastic tubes. PR declined in the CA group, but significantly increased in the PCI and RA groups immediately postprocedure, and decreased to baseline at 24 h. DPR increased across the three groups (P < 0.0001). In the PCI group, DPR was directly related to total inflation time (r = 0.435, P = 0.005) and total stent length (r = 0.586, P < 0.001). The change in Eselectin significantly and inversely correlated with DPR (P < 0.001). No correlation was found with sICAM-1. PR increased significantly more in patients with PMI than in patients without PMI (P = 0.013). In vitro, platelet activation was observed in the presence of carotid arteries but not in the presence of plastic tubes. Conclusions: Despite dual antiplatelet therapy, PCI affected platelet function proportionally to procedural complexity and the extent of vascular damage.

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Section: Discussionsupporting

confidence: 74%

“…A coronary interventional procedure by itself is another important determinant of PR [7–13], which may significantly vary in the periprocedural setting. In particular, significant platelet activation has been associated with aggressive coronary interventions, such as rotational atherectomy (RA) [14].…”

Section: Introductionmentioning

confidence: 99%

Periprocedural variations of platelet reactivity during elective percutaneous coronary intervention

Mangiacapra

Bartúnek

Bijnens

et al. 2012

Journal of Thrombosis and Haemostasis

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“…In both RCA and SVG-RCA, neither TF-bearing MPs nor plasma TF were increased after stent implantation. This is in line with previous studies demonstrating no increase of intracoronary plasma TF level immediately after stent implantation in stable CAD [ 1 , 3 , 4 , 26 , 51 , 52 ] and in acute myocardial infarction [ 22 ]. However, there is a delayed increase of TF in coronary sinus blood 24 h after stent implantation [ 53 ], possibly secondary to immunological or inflammatory processes.…”

Section: Discussionsupporting

confidence: 93%

Release of Intracoronary Microparticles during Stent Implantation into Stable Atherosclerotic Lesions under Protection with an Aspiration Device

et al. 2015

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ObjectiveStent implantation into atherosclerotic coronary vessels impacts on downstream microvascular function and induces the release of particulate debris and soluble substances, which differs qualitatively and quantitatively between native right coronary arteries (RCAs) and saphenous vein grafts on right coronary arteries (SVG-RCAs). We have now quantified the release of microparticles (MPs) during stent implantation into stable atherosclerotic lesions and compared the release between RCAs and SVG-RCAs.MethodsIn symptomatic, male patients with stable angina and a stenosis in their RCA or SVG-RCA, respectively (n = 14/14), plaque volume and composition were analyzed using intravascular ultrasound before stent implantation. Coronary aspirate was retrieved during stent implantation with a distal occlusion/aspiration device and divided into particulate debris and plasma. Particulate debris was weighed. Platelet-derived MPs (PMPs) were distinguished by flow cytometry as CD41+, endothelium-derived MPs (EMPs) as CD144+, CD62E+ and CD31+/CD41-, leukocyte-derived MPs as CD45+, and erythrocyte-derived MPs as CD235+.ResultsIn patients with comparable plaque volume and composition in RCAs and SVG-RCAs, intracoronary PMPs and EMPs were increased after stent implantation into their RCAs and SVG-RCAs (CD41+: 2729.6±645.6 vs. 4208.7±679.4 and 2355.9±503.9 vs. 3285.8±733.2 nr/µL; CD144+: 451.5±87.9 vs. 861.7±147.0 and 444.6±74.8 vs. 726.5±136.4 nr/µL; CD62E+: 1404.1±247.7 vs. 1844.3±378.6 and 1084.6±211.0 vs. 1783.8±384.3 nr/µL, P<0.05), but not different between RCAs and SVG-RCAs.ConclusionStenting in stable atherosclerotic lesions is associated with a substantial release not only of PMPs, but also of EMPs in RCAs and SVG-RCAs. Their release does not differ between RCAs and SVG-RCAs.Trial RegistrationClinicalTrials.gov NCT01430884

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“…Previous studies have shown that arterial wall injury caused by PCI triggers transient hemostatic activation, leading to localized thrombosis and distal embolism. Strong and early activation of the hemostatic system occurs, which is possibly related to endothelial and atheromatous plaque disruption in response to balloon-induced arterial wall trauma [17,18]. Vascular endothelial damage during PCI leads to activation of platelet aggregation and subsequent distal embolism of microthrombi, and we considered that these distal embolisms are a major factor in the pathogenesis of PMI along with other lesion-related or procedural factors.…”

Section: Discussionmentioning

confidence: 99%

Association between changes in platelet reactivity during elective percutaneous coronary intervention and periprocedural myocardial infarction: A pilot study

Kawai

Miyoshi

Nakamura

et al. 2019

Journal of Cardiology

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Early changes in local hemostasis activation following percutaneous coronary intervention in stable angina patients: a comparison between drug-eluting and bare metal stents

Abstract: Early changes in local hemostasis activation following PCI, were related to balloon predilation. Neither DES nor BMS increased markers of platelet activation, coagulation, or fibrinolysis, under dual antiplatelet and anticoagulant pretreatment.

Cited by 11 publications

References 41 publications

Periprocedural variations of platelet reactivity during elective percutaneous coronary intervention

Periprocedural variations of platelet reactivity during elective percutaneous coronary intervention

Release of Intracoronary Microparticles during Stent Implantation into Stable Atherosclerotic Lesions under Protection with an Aspiration Device

Association between changes in platelet reactivity during elective percutaneous coronary intervention and periprocedural myocardial infarction: A pilot study

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