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Harnessing the platelet
1Department of Medicine, University of Miami School of Medicine, Fla, USA.
Insights
Aspirin significantly reduces cardiovascular events by inhibiting platelet aggregation. New drugs targeting the platelet fibrinogen receptor GP IIb/IIIa offer improved specificity and safety for treating arterial thrombosis.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Platelets play a critical role in cardiovascular disease, particularly in arterial thrombosis.
- Aspirin's antiplatelet effect demonstrated a 25% reduction in myocardial infarction, stroke, and vascular death.
Observation:
- Platelet aggregation is primarily mediated by the platelet fibrinogen receptor, GP IIb/IIIa.
- GP IIb/IIIa receptor binding to fibrinogen is the final common pathway for thrombus formation.
Findings:
- Abciximab, an early GP IIb/IIIa inhibitor, effectively reduced thrombotic complications in acute coronary events.
- Newer synthetic peptide GP IIb/IIIa inhibitors exhibit enhanced specificity, are nonimmunogenic, and cause less bleeding.
Implications:
- Targeting platelet action is crucial in managing acute coronary events and arterial thrombosis.
- Oral GP IIb/IIIa inhibitors are anticipated to become standard therapy for unstable angina.
Abstract:
Appreciation of the critical role of platelets in cardiovascular disease came when it was shown that aspirin, by virtue of its ability to block platelet aggregation, reduced the combined incidence of MI, stroke, and vascular death by 25%. Understanding the key role played by platelets in acute thrombotic vascular events prompted the development of a new class of drugs to control platelet action. Platelet aggregation is mediated exclusively by the platelet fibrinogen receptor GP IIb/IIIa. The binding of the receptor with fibrinogen is the final common pathway leading to platelet aggregation and thrombus formation. Abciximab, the first GP IIb/IIIa platelet receptor inhibitor, effectively reduces the thrombotic complications in acute coronary vascular events. The newer GP IIb/IIIa inhibitors, the synthetic peptide antagonists, have been shown to be more specific, to be nonimmunogenic, and to cause less bleeding. It is predictable that an oral GP IIb/IIIa inhibitor will become part of the standard repertoire in patients with unstable angina. The platelet has taken center stage in the battle against arterial thrombosis. The direction of our medical attack on acute coronary events is clear: harness the platelet.