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| Scanning electron micrograph of human red blood cells, monocyte (orange), T lymphocyte (green), and activated platelets (blue). |
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Antiplatelet Therapy
Antithrombotic therapy is critical in modifying the ischemic disease process and its progression to MI, recurrent MI or death. The combination of aspirin, intravenous unfractionated heparin and a platelet GP IIb/IIIa receptor antagonist is considered the most effective therapy for patients with continuing ischemia or with other high-risk features and in patients oriented to an early invasive strategy. The intensity of treatment should be tailored to the individual patient’s level of risk.1
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Aspirin (also known as acetylsalicylic acid or ASA) irreversibly inhibits cyclooxygenase-1 within platelets to prevent the formation of thromboxane A2, thereby diminishing platelet aggregation by this pathway, leaving other pathways unaffected. Because these effects are observed at low doses, this platelet inhibition is the suggested mechanism for clinical benefits. The anti-inflammatory effect of aspirin may also help, but at the low doses often prescribed, it is deemed to be unlikely.1
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The prompt action of ASA and its ability to reduce mortality rates in patients suspected of AMI led to the recommendation that ASA be administered immediately in the ED once the diagnosis of ACS is made or suspected. The protective effect of ASA in unstable angina has been sustained for at least 1 to 2 years while on aspirin therapy; however, it is considered prudent to continue ASA indefinitely, unless a contraindication develops.1
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Adenosine Diphosphate Receptor Antagonists have irreversible platelet effects, but take several days to maximize their effectiveness. Because the two thienopyridines (ticlopidine and clopidogrel) have similar activity to that of aspirin, they are used in patients with unstable angina, non-ST-segment elevation MIs and those who are unable to tolerate aspirin.1
Ticlopidine has been successfully used for the secondary prevention of MI and stroke, and for the prevention of graft occlusion and stent closure. However, the adverse effects of this drug limit its usefulness. It has been associated with gastrointestinal problems, neutropenia and thrombocytopenia purpura. Many prefer clopidogrel to ticlopidine because of the more rapid antiplatelet effect and its favorable safety profile.1
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