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Coronary angioplasty enhances platelet reactivity through von Willebrand factor release
  1. D A Gorog,
  2. H Douglas,
  3. N Ahmed,
  4. D C Lefroy,
  5. G J Davies
  1. Division of Cardiology, Hammersmith Hospital & Imperial College School of Medicine, London, UK
  1. Correspondence to:
    Dr Diana Gorog, Department of Cardiology, Kings College London, The Rayne Institute, St Thomas' Hospital, London SE1 7EH, UK;
    diana.gorog{at}kcl.ac.uk

https://doi.org/10.1136/heart.89.3.329

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    Shear induced platelet activation is responsible for arterial thrombosis. The role of fibrinogen is established at low shear stress, but at high shear stress von Willebrand factor (vWF), not fibrinogen, is essential for platelet adhesion and aggregation.1 Patients with vWF deficiency exhibit resistance to thrombosis,2 and raised vWF is a risk factor for acute coronary syndromes. Interpretation of vWF concentrations is, however, complicated since vWF may be an acute phase reactant. The effect of vWF on thrombosis in the normal (non-vWF deficient) population remains unknown. The aim of this study was to determine the effect of coronary occlusion on plasma vWF level in vivo and the effect of raised vWF on thrombosis/haemostasis in vitro.

    METHODS

    Effect of coronary angioplasty

    Eleven patients with single vessel coronary disease and stable angina, undergoing elective angioplasty to the left anterior descending or circumflex artery, were enrolled and 10 000 U of heparin were administered. Balloon inflations (2.5 (0.5) per patient) were followed by stent implantation in eight patients. Blood was drawn from a coronary sinus (CS) catheter immediately before the first balloon inflation and at 1, 5, 10, 15, 20, and 30 minutes, and from the femoral vein before and 30 minutes after the …

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