Wiping Out CGRP: Potential Cardiovascular Risks. (September 2016)

• Record Type: Journal Article
• Authors: MaassenVanDenBrink, Antoinette; Meijer, Joris; Villalón, Carlos M.; Ferrari, Michel D.
• Is Part Of: Trends in pharmacological sciences. Volume 37:Number 9(2016)
• Page Start: 779
• Page End: 788
• Publication Date: 2016-09
• Subjects: CGRP -- migraine -- antibody -- cardiac ischemia -- cerebral ischemia; Pharmacology -- Periodicals; Pharmacology -- trends -- Periodicals; Pharmacologie -- Périodiques; Pharmacology; Electronic journals; Periodicals; 615.1
• DOI: 10.1016/j.tips.2016.06.002
• Languages: English
• ISSNs: 0165-6147

Abstract

Abstract : Migraine is a common episodic neurovascular brain disorder associated with increased risk of cardio- and cerebrovascular ischemia. Migraine headache is likely caused by activation of the trigeminovascular system and release of calcitonin gene-related peptide (CGRP). Monoclonal antibodies against CGRP or its receptor are currently being evaluated for the prevention of migraine attacks. Preliminary efficacy data are promising. However, because CGRP may act as a vasodilatory safeguard during cerebral and cardiac ischemia, CGRP blockade could transform transient mild ischemic events into full-blown infarcts. Here, we review the cerebro- and cardiovascular risks that might be associated with CGRP blockade and which clinical and preclinical studies should be conducted to better assess the potential safety issues of this new promising class of drug. Trends: Migraine headache is probably caused by trigeminovascular system activation with associated release of CGRP. Three antibodies directed against the peptide CGRP and one antibody directed against the CGRP receptor are currently being clinically evaluated for their prophylactic antimigraine efficacy. Besides its role in the pathophysiology of migraine, CGRP may act as a vasodilator safeguard during cerebral and cardiac ischemia. Thus, the concern arises that, after CGRP blockade, mild and usually transient ischemic events might be transformed into full-blown infarcts.