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

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...

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Bibliographic Details
Published in:	Neurology Vol. 55; no. 1; pp. 95 - 99
Main Authors:	GNECCHI-RUSCONE, T, BERNARD, X, PIERRE, P, ANDERSON, D, LEGG, N, ENAHORO, H, WINTER, P. D. O, CRISP, A, MELIN, J. A, CAMICI, P. G
Format:	Journal Article
Language:	English
Published:	Hagerstown, MD Lippincott Williams & Wilkins 12-07-2000
Subjects:	Adult Biological and medical sciences Cardiovascular system Coronary Circulation - drug effects Coronary Circulation - physiology Female Heart - diagnostic imaging Heart - drug effects Heart - physiology Humans Indoles - administration & dosage Indoles - adverse effects Male Medical sciences Middle Aged Migraine Disorders - drug therapy Myocardium - metabolism Pharmacology. Drug treatments Piperidines - administration & dosage Piperidines - adverse effects Serotonin Receptor Agonists - administration & dosage Serotonin Receptor Agonists - adverse effects Tomography, Emission-Computed Tryptamines Vascular Resistance - drug effects Vascular Resistance - physiology Vasodilation - drug effects Vasodilation - physiology Vasodilator agents. Cerebral vasodilators Heart Radionuclide study Agonist Cardiovascular disease 5-HT1 Serotonine receptor Serotonin agonist Vascular disease Randomization Pain Adult Cerebrovascular disease Human Regional blood flow Nervous system diseases Antimigrainous agent Migraine Crossover study Biological activity Cerebral disorder Chemotherapy Treatment Central nervous system disease Double blind study Myocardium Circulatory system Hemodynamics Naratriptan Positron Emission tomography
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Summary:	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 5HT1B/1D agonist naratriptan has no significant activity at 5HT2 receptors; however, like all 5HT1B/1D agonists developed for the acute treatment of migraine, naratriptan could potentially constrict coronary arteries by activation of 5HT1B receptors. 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. 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. 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.
ISSN:	0028-3878 1526-632X
DOI:	10.1212/WNL.55.1.95