Thrombin generation in patients undergoing carotid endarterectomy: Implications in acute vessel wall closure and antithrombotic therapy

Wells, J. K.; Nicosia, Sera; Wale, Catherine; Smith, Louisa; Buchanan, Michael R.

doi:10.1016/0049-3848(94)90257-7

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…A number of intra-operative factors could account for this transient form of 'aspirin resistance'. Firstly, platelet activation is well known to increase during surgery, including CEA (19), largely due to the release of known platelet agonists such as thrombin (20). Spontaneous aggregation, an ex vivo marker of platelet activation, increased by a small but significant amount at the end of surgery, but not to anywhere near the magnitude of the increase seen in the response to AA.…”

Section: Discussionmentioning

confidence: 99%

“…This gave only a small (12%) and non-significant increase in AAinduced aggregation, reinforcing the view that the increased platelet response to AA was not the result of release of epinephrine in vivo during surgery. Similarly, addition of unfractionated heparin in vitro, which is known to increase platelet response to agonists such as ADP (18)(19)(20), gave only a small (14.9%) and non-significant increase in AA response. Even with a combination of epinephrine and heparin the increase was only 23.5% (p >0.05 for all) (Fig.…”

Section: Effects Of Adrenergic Hormones and Heparinmentioning

confidence: 99%

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Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

Payne

Jones²,

Hayes³

et al. 2004

Thromb Haemost

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The majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for > or =2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 +/- 5.5% pre-surgery to 50.8 +/- 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8+/-7.2%; p = 0.0001), but fell to 45.9 +/- 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 micro g/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 micro M/l) to the samples taken at the end of surgery did not block the increased aggregation. The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 +/- 5.5% pre-angioplasty to 32.4 +/- 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 +/- 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment. This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Adrenergic Hormones and Heparinmentioning

confidence: 99%

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

Payne

Jones²,

Hayes³

et al. 2004

Thromb Haemost

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“…6 Thrombin, a potent platelet activator and procoagulant agent has been shown to be generated during CEA despite the use of unfractionated heparin. 7 This effect can persist perioperatively as thrombin is able to bind to the injured vessel wall. 8 All these factors may contribute to the development of cerebral microembolisation during carotid surgery.…”

Section: Introductionmentioning

confidence: 99%

Platelet Activation During Carotid Endarterectomy And the Antiplatelet effect of Dextran 40

et al. 2002

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“…Heparin is also used in intraoperative vascular surgery, generally before arterial cross-clamping is completed and often postoperatively to pre vent thrombosis of the bypass. However, in some settings, despite theoretically adequate levels of anticoagulation, UFH does not al ways prevent thrombin generation [1], raising the potential for thrombotic episodes. Bleed ing complications have also been reported [2], Low-molecular-weight heparins (LMWHs) are now widely used for the prevention and treatment of venous thromboembolism [2][3][4][5][6][7][8][9].…”

mentioning

confidence: 99%

Are Low-Molecular-Weight Heparins Useful for the Prophylaxis and Treatment of Arterial Thrombi?

Samama

Combe²,

Ill³

et al. 1996

Pathophysiol Haemos Thromb

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The pharmacologic specificity of low-molecular-weight heparins (LMWHs) has enabled multiple attractive developments in the prophylaxis and treatment of arterial thrombosis. Their high antithrombotic potency associated with a potentially lower induced bleeding risk, the lack of platelet interaction, the prevention of myointimal hyperplasia, and the lower incidence of heparin-induced thrombocytopenia, are major advantages. New studies in cardiology and vascular surgery demonstrate a high efficacy for LMWHs associated with a low risk.

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Thrombin generation in patients undergoing carotid endarterectomy: Implications in acute vessel wall closure and antithrombotic therapy

Cited by 7 publications

References 15 publications

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

Platelet Activation During Carotid Endarterectomy And the Antiplatelet effect of Dextran 40

Are Low-Molecular-Weight Heparins Useful for the Prophylaxis and Treatment of Arterial Thrombi?

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