Prospective evaluation of hemostatic predictors of subacute stent thrombosis after coronary palmaz-schatz stenting

Neumann, Franz‐Josef; Gawaz, Meinrad; Ott, Ilka; May, Andreas E.; Mössmer, Georg; Schömig, Albert

doi:10.1016/0735-1097(95)00433-5

Cited by 96 publications

(41 citation statements)

References 35 publications

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“…61 Tschoepe and colleagues 41 found that an increased fraction of platelets surface expressing P-selectin or thrombospondin is predictive for occurrence of ischemic events after PTCA. We 43,62 showed that GP IIb/IIIa levels before stenting were an independent risk factor for stent thrombosis (Figure 12). …”

Section: Platelet Analysis and Risk Stratificationmentioning

confidence: 99%

Evaluation of Platelet Membrane Glycoproteins in Coronary Artery Disease

1999

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Platelets play a fundamental role in atherogenesis and development of ischemic complications. [1][2][3] Under physiological conditions, platelets do not interact with the vessel wall. Injury of vascular intima disrupts the antithrombotic properties of endothelium and exposes the blood to adhesive molecules of the subendothelium. Platelet adhesion to the damaged vessel wall is the first step in hemostasis and thrombosis. 4 Platelet adhesion is followed by spreading and activation, resulting in release of granule components and aggregate formation. 5,6 On initial contact, platelet glycoprotein (GP) Ib/V/IX complex binds to von Willebrand factor associated with collagen on the subendothelial surface (Figure 1) 4,5 and thus arrests the platelet on the vessel surface. The collagen receptor ␣ 2 ␤ 1 is an important secondary receptor for platelet adhesion. ␣ 2 ␤ 1 -Collagen interaction leads to platelet activation and is critical for the spreading process involving the fibrinogen receptor GP IIb/IIIa to ensure close contact of the spread platelet with the surface. 5 Other adhesion receptors, including the fibronectin receptor ␣ 5 ␤ 1 and the laminin receptor ␣ 6 ␤ 1 , support and strengthen secondary adhesion ( Figure 1). The fibrinogen receptor GP IIb/IIIa is particularly important in platelet-platelet coadhesion, termed aggregation. This requires conformational changes in GP IIb/IIIa that allow binding of soluble fibrinogen to the platelet membrane ( Figure 2). Thus, fibrinogen bridging allows formation of platelet aggregates (Figure 2). 6 -9 Platelet adhesion and aggregation induce intracellular signaling, which mediates several responses, such as formation and secretion of thromboxane A2 (TXA 2 ), serotonin, and ADP 6 (Figure 1). These substances reinforce platelet activation, vasoconstriction, and slowing of blood flow and therefore increase platelet-platelet and platelet-vessel wall interaction. 3,6 Platelet Membrane ReceptorsThe most abundant platelet membrane glycoprotein is the ␤ 3 -integrin GP IIb/IIIa (60 000 to 100 000 per platelet and 1% to 2% of the total platelet protein), the inducible platelet fibrinogen receptor. 7 Eighty percent of GP IIb/IIIa is randomly distributed and expressed on the platelet surface in its resting state, and the remaining 20% is located within the surface connecting system (SCS) and in ␣-granule membranes 5,10 (Figure 3). GP IIb/IIIa stored in this internal pool becomes surface expressed as functional receptor on platelet activation. 11 Congenital deficiencies of GP IIb/IIIa in Glanzmann thrombasthenia lead to defective platelet aggregation and enhanced bleeding. 5 As is the case with other integrins, GP IIb/IIIa is a heterodimer consisting of an ␣-subunit (GP IIb) and a ␤-subunit (GP IIIa) 9 (Figure 4). Although the expression of GP IIb/IIIa (␣ IIb ␤ 3 ) is limited to megakaryocytes and platelets, the other ␤ 3 -integrin present on platelets, the vitronectin receptor ␣ v ␤ 3 , is more widely distributed and is also found on endothelial and smooth muscle cells. 12 ␣ v ␤ 3 shar...

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Section: Platelet Analysis and Risk Stratificationmentioning

confidence: 99%

Evaluation of Platelet Membrane Glycoproteins in Coronary Artery Disease

1999

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“…Neuman et al 3 have shown that the level of platelet glycoprotein (GP) IIb/IIIa expression was an independent predictor of stent thrombosis. According to the European Society of Cardiology guidelines, 4 the use of GP IIb/IIIa inhibitors (GPIs) is reasonable as bailout therapy in the event of angiographic evidence of large thrombus, slow or no reflow, and other thrombotic complications.…”

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confidence: 99%

Efficacy and safety of tirofiban-supported primary percutaneous coronary intervention in patients pretreated with 600 mg clopidogrel: results of propensity analysis using the Clinical Center of Serbia STEMI Register

Mrdović

Savić

Lasica

et al. 2013

European Heart Journal: Acute Cardiovascular Care

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Background: Studies with platelet glycoprotein IIb/IIIa receptor inhibitors (GPIs) showed conflicting results in primary percutaneous coronary intervention (PPCI) patients who were pretreated with 600 mg clopidogrel. We sought to investigate the short-and long-term efficacy and safety of the periprocedural administration of tirofiban in a largest Serbian PPCI centre. Methods: We analysed 2995 consecutive PPCI patients enrolled in the Clinical Center of Serbia STEMI Register, between February 2007 and March 2012. All patients were pretreated with 600 mg clopidogrel and 300 mg aspirin. Major adverse cardiovascular events, comprising all-cause death, nonfatal infarction, nonfatal stroke, and ischaemia-driven target vessel revascularization, was the primary efficacy end point. TIMI major bleeding was the key safety end point. Results: Analyses drawn from the propensity-matched sample showed improved primary efficacy end point in the tirofiban group at 30-day (OR 0.72, 95% CI 0.53-0.97) and at 1-year (OR 0.74, 95% CI 0.57-0.96) follow up. Moreover, tirofiban group had a significantly lower 30-day all-cause mortality (secondary end point; OR 0.63, 95% CI 0.40-0.90), compared with patients who were not administered tirofiban. At 1 year, a trend towards a lower all-cause mortality was observed in the tirofiban group (OR 0.74, 95% CI 0.53-1.04). No differences were found with respect to the TIMI major bleeding during the follow-up period. Conclusions: Tirofiban administered with PPCI, following 600 mg clopidogrel pretreatment, improved primary efficacy outcome at 30 days and at 1 year follow up without an increase in major bleeding.

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“…Another strategy to limit reperfusion injury uses monoclonal antibodies to adhesion receptors such as p selectin (present on endothelial cells and PLTs), CD11/CD18 (present on leukocytes), and the vitronectin receptor (present on endothelial cells). Abciximab not only blocks GP IIb-IIIa on PLTs, but also the vitronectin receptor on endothelial cells explaining its favorable effect on myocardial perfusion, microcirculation, and recovery of left ventricular function [14][15][16][17].…”

Section: Plt-mediated Inflammationmentioning

confidence: 99%