Platelet activity and selective beta-blockade in migraine prophylaxis.

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Abstract
Migraine is associated with increased platelet activity and an incidence of cerebrovascular ischemic events. Because cerebrovascular events might result from platelet aggregation, enhancing platelet activity further in the treatment of migraine is not desirable. .beta.-Adrenoceptor blockers effective in migraine prophylaxis include propranolol (nonselective) and metoprolol (.beta.1-selective), but it is uncertain how .beta.-receptor subtype selectivity might influence platelet behavior in migraine. In 29 patients, comparable clinical responses were obtained with therapeutic doses during 1 month of treatment with propranolol, metoprolol, and the .beta.2-selective Li 32-468. Propranolol increased and metoprolol decreased platelet aggregation and ATP release, and the effect of Li 32-468 could be related to that of propranolol. These actions can be largely explained in terms of what is known of platelet .beta.-receptors and therefore can be generalized to other effective .beta.-blockers. Since altered platelet activity does not account for the efficacy of these agents in migraine, the actions of .beta.-blockers on platelet should be considered as side effects. Those .beta.-blockers inhibiting platelet activity should be preferred in migraine treatment, assuming equal efficacy, which implies the use of .beta.1-selective blockers.

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