These findings led the authors of these studies to recommend that surgery be delayed if possible to allow patients to withdraw from anti-platelet therapy. Several clinical studies have linked the use of platelet activation inhibitors to increased bleeding during surgery resulting in excess blood loss, increased transfusion rates, and reoperation. Clopidogrel and aspirin can be used individually or in combination for dual anti-platelet therapy. This prevents the conversion of arachidonic acid to thromboxane A 2 and subsequent thromboxane stimulated platelet aggregation. Aspirin irreversibly inhibits cyclooxygenase enzymes, COX1 and COX2. ADP mediated activation of the GPIIb/IIIa complex is therefore abated. Clopidogrel acts as an inhibitor of adenosine diphosphate (ADP) induced platelet aggregation by covalently binding to its receptor, P2Y 12. Platelet aggregation is disrupted by these inhibitors via two distinct pathways.
Both drugs reduce mortality in patients with chronic atherosclerotic disease and are also effective drugs for the acute treatment of infarcts.
Clopidogrel and aspirin (acetylsalicylic acid) are commonly used platelet inhibitors. Following myocardial infarction or stroke, the American Heart Association and American College of Cardiology guidelines recommend that patients take platelet inhibitors to reduce the risk of further atherothrombotic events. They also contribute to atherosclerotic disease by stimulating and stabilizing thrombi. Platelets contribute to physiological hemostasis by aggregating at the site of a lesion, providing surfaces for hemostatic reactions, and supplying regulatory hemostatic factors. These results suggest that platelet inhibitors do not negatively impact clot kinetics, strength, and structure when clotting is initiated with thrombin based gelatin matrices and fibrin sealants. FESEM images supported TEG findings in that similar morphologies were observed in ex vivo formed clots from both donor groups when thrombin based gelatin matrices and fibrin sealants were used. TEG results indicated similar clot kinetics and strength between clopidogrel and control donor groups for blood alone and when clotting was induced using thrombin based gelatin matrices and fibrin sealants. Heparinization of donor blood resulted in similarly elevated ACTs for both donor groups. However, blood from both donor groups had an elevated thrombin induced aggregation response. Aggregometry indicated that aggregation response to adenosine diphosphate (ADP) for clopidogrel donors was 12% of that for the controls (p = 0.0021), an expected result of clopidogrel induced platelet inhibition. Resultsīlood component profiles were similar for both donor groups. Field Emission Scanning Electron Microscopy (FESEM) was used to analyze clot structure. Clot kinetics and strength were analyzed using thrombelastography (TEG). Blood component analysis, whole blood platelet aggregometry, and activated clotting time (ACT) were used to monitor compliance to therapy and identify any differences between donor groups. Methodsīlood was collected and heparinized from donors on clopidogrel (and aspirin) and age matched control donors. The aim of this study was to determine the impact of platelet inhibitors, specifically clopidogrel and aspirin, on clot kinetics, strength, and/or structure during the use of thrombin based gelatin matrices and fibrin sealants. Platelet inhibitors are commonly used to reduce the risk of atherothrombotic events.