HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gnecchi–Ruscone, T. Articles by Camici, P. G. Search for Related Content PubMed PubMed Citation Articles by Gnecchi–Ruscone, T. Articles by Camici, P. G.

Effect of naratriptan on myocardial blood flow and coronary vasodilator reserve in migraineurs

From the MRC Cyclotron Unit and Department of Neurology (Drs. Gnecchi–Ruscone, Anderson, Legg, and Camici), Imperial College School of Medicine, Hammersmith Hospital, London, UK; Cyclotron Unit (Drs. Bernard, Pierre, and Melin), Université Catholique de Louvain, Belgium; and Glaxo Wellcome Neurology and Psychiatry Clinical Development (Drs. Bernard, Winter, Crisp, and H. Enahoro), Greenford, UK.

Address correspondence and reprint requests to Prof. Paolo G. Camici, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, Ducane Road, London W12 ONN, UK; e-mail: paolo.camici{at}csc.mrc.ac.uk

BACKGROUND: Migraine drugs can produce adverse cardiac effects. The authors have demonstrated previously that ergotamine can lead to a significant reduction of hyperemic myocardial blood flow, but little is known about the effect of the newer serotonin analogues. Coronary artery constriction caused by serotonin or its analogues is mediated mainly by 5HT₂ receptors. The selective 5HT_1B/1D agonist naratriptan has no significant activity at 5HT₂ receptors; however, like all 5HT_1B/1D agonists developed for the acute treatment of migraine, naratriptan could potentially constrict coronary arteries by activation of 5HT_1B receptors.

METHODS: The effects on myocardial blood flow of subcutaneous naratriptan 1.5 mg compared with placebo were assessed under resting and hyperemic conditions with PET using oxygen-15 labeled water during two separate visits. This study was a randomized, double-blind, placebo-controlled crossover trial in 34 migraine subjects with no evidence of ischemic heart disease, studied outside a migraine attack.

RESULTS: Naratriptan did not differ significantly from placebo in its effects on resting myocardial blood flow, but did evoke a small, significant fall in hyperemic myocardial blood flow (-13% versus placebo) and an increase in hyperemic coronary resistance (+19% versus placebo) without any signs or symptoms suggestive of myocardial ischemia. Naratriptan did not significantly affect the coronary vasodilator reserve (hyperemic/resting blood flow) compared with placebo.

CONCLUSIONS: These results show that at therapeutic doses, naratriptan exerts only a minor effect on myocardial blood flow, coronary vasodilator reserve, or coronary resistance among subjects with no evidence of ischemic heart disease. These results should not be extrapolated to patients with coronary artery disease, in whom all 5HT₁ agonists for migraine are contraindicated.

This article has been cited by other articles:

				E. M. Bednarczyk Functional Imaging for the Monitoring of Clinical Outcomes of Pharmacotherapy Journal of Pharmacy Practice, August 1, 2001; 14(4): 298 - 307. [Abstract] [PDF]