Secondary Stroke Preventiion | Treatment

References:
Albers et al. Chest 1998;114: 683-698.
Barnett et al. N Engl J Med 1998; 339: 1415-1425.

Antiplatelet agents are recommended for non-cardioembolic strokes, which constitute the majority of ischemic strokes, as well as for long-term prevention after carotid endarterectomy.
Anticoagulation, usually with warfarin, is the recommended therapy after cardioembolic stroke.
Anticoagulants are indicated after most types of cardioembolic stroke and for prevention of first stroke in patients with atrial fibrillation.Antiplatelet agents are recommended for recurrent stroke prevention in all other situations, including after carotid endarterectomy.

	Mode of Action of Antiplatelets

Comparison between antiplatelet agents

Further information

	Aspirin and Dipyridamole

		Prevention of Vascular Events in Stroke/TIA Patients Aspirin vs. Placebo: Efficacy by Dose

		ESPS 2: Effects on Stroke - Relative Risk Reduction (Pairwise Comparisons)

		ESPS 2: Effects on Stroke - Events Prevented (Pairwise Comparisons)

		ESPS 2: Effects on Stroke - Survival Curves ("Non-event" Probability)

		ESPS 2 Secondary Endpoint: TIA (Pairwise Comparison)

		ESPS 2 Conclusions ASA/ER-DP is about twice as effective as aspirin alone in stroke prevention


	Clopidogrel in the Secondary Prevention

		Clopidogrel in the Secondary Prevention of Stroke Clopidogrel vs. Aspirin in Patients at Risk of Ischaemic Events (CAPRIE)

		CAPRIE Results by Subgroup Analysis in the Combined Endpoint Relative Risk Reduction (%)

		Stroke Prevention Therapy An Indirect Comparison of Stroke Enrolles in CAPRIE and ESPS 2

		Clopidogrel in Unstable Angina to Prevent Recurrent Ischaemic Events (CURE) 12,562 patients enrolled with acute coronary syndromes

		CURE: Net Event Rate Combined Endpoints vs. Major Bleed

Mode of Action of Antiplatelets

Platelets have multiple surface receptors for pro-aggregator stimuli, including collagen, adenosine diphosphate (ADP), and thrombin. Ligand-binding to these receptors triggers a cascade of intracellular signals, finally leading to the conversion of the platelet surface glycoprotein IIb/IIIa complex (GP IIb/IIIa) to a binding site for fibrinogen, von Willebrand factor and other adhesion molecules, which anchor adjacent platelets into aggregates. Antithrombotic agents target different steps in this cascade of prothrombotic signals.

Acetylsalicylic acid (ASA) irreversibly inhibits the cyclooxygenase and thus prevents the conversion of arachidonic acid to thromboxane A2 (TxA2). This effect translates into the inhibition of thromboxane A2-dependent platelet aggregation and vasoconstriction.

Ticlopidine and clopidogrel interfere with the signal transduction triggered by binding of ADP to its platelet receptor.

ADP released from activated platelets is rapidly metabolized to adenosine monophosphate (AMP) and adenosine. Adenosine is a potent inhibitor of platelet aggregation similar to prostacyclin (PgI2).

Dipyridamole effectively inhibits the uptake of adenosine into cells (red blood cells, platelets, endothelial cells). Thus dipyridamole increases the local concentration of adenosine, which accumulates in the microenvironment of a growing thrombus.

GP IIb/IIIa antagonists block the binding of fibrinogen and other ligands to the platelet GP IIb/IIIa receptor. They inhibit platelet aggregation independently of the nature of the proaggregatory stimuli.

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