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At least 433 records · Page 24Linked to original sources
PubMed1996

Vasospasm-induced myocardial infarction with sumatriptan.

Sumatriptan, a 5-hydroxytryptamine1, (5-HT1) receptor agonist is an effective abortive agent for migraine headaches. A common side effect in 3% to 7.9% of patients is chest pain. Although most cases of chest pain are not thought to be of cardiac origin, its mechanism is not entirely understood. Rare examples of electrocardiogram changes consistent with transient ischemia have been reported. Isolated instances of angina, arrhythmia, myocardial infarction, and death have been temporally associated with sumatriptan administration. In most cases, it is unclear whether underlying cardiovascular disease existed or contributed to this adverse event. We report the history of a 56-year-old female patient with migraine who experienced a myocardial infarction shortly after using sumatriptan, despite having had a normal cardiovascular evaluation. As she had a normal cardiac catheterization after the event, we find it probable that sumatriptan induced coronary vasospasm and myocardial infarction.

Coronary Vasospasm↗
PubMedDate not supplied

Sumatriptan in the acute treatment of migraine without aura: efficacy of 50-mg dose.

We conducted an open study on the efficacy of 50 mg of sumatriptan as an acute treatment for migraine without aura. We recruited 200 consecutive patients, with an established history of migraine without aura, presenting at a headache center. The patients were instructed to take half a 100-mg sumatriptan tablet for their next migraine attack, and to record details of their headache in a diary. The primary outcome of the study was headache relief from one migraine attack. Attacks were moderately intense (46%), moderate to severe (7%), or severe (47%). Total or partial benefit at 2 hours from the 50-mg dose was reported by 140 of 200 patients (70%). Thirty-six patients received no benefit from half a tablet, and 24 did not take sumatriptan, preferring their habitual medication. Side effects were few, mild, and short lasting. We conclude that the 50-mg oral dose is generally effective for migraine without aura attacks of both moderate and severe intensity and recommend this dose for all such patients. If, however, sumatriptan is ineffective at that dose it can be increased to a maximum of 100 mg.

Acute Disease↗
PubMed2000

Alteration in nature of cluster headache during subcutaneous administration of sumatriptan.

OBJECTIVES: To document the relationship between the 5-HT receptor agonist sumatriptan and a change in the nature of cluster headache in four cases. To relate the findings to the literature on the use of sumatriptan in both cluster headache and migraine. BACKGROUND: Studies of the efficacy and adverse effects of long-term treatment with sumatriptan in cluster headache are limited and report conflicting findings. METHODS: Four cases are described. RESULTS: All four patients developed a marked increase in the frequency of attacks 3 to 4 weeks after initiating treatment with the drug for the first time. Three patients also developed a change in headache character, and 2 experienced prolongation of the cluster headache period. Withdrawal of the drug reduced the frequency of headaches and eliminated the newly developed type of headache. CONCLUSIONS: Determination of the effects of long-term use of sumatriptan will result in more precise guidelines for the frequency and duration of treatment with this otherwise extremely beneficial drug.

Adult↗
PubMed2000

Sumatriptan in patients with postdural puncture headache.

OBJECTIVE: To determine the efficacy of sumatriptan in the management of patients presenting for an epidural blood patch for the management of postdural puncture headache. BACKGROUND: Postdural puncture headache can be quite severe, requiring invasive therapy (ie, epidural blood patch). Sumatriptan has been used successfully in patients with postdural puncture headache, however, its use has not been investigated in a controlled fashion. METHODS: Ten patients with postdural puncture headache presenting for an epidural blood patch were given either saline or sumatriptan subcutaneously. The severity of the headache was evaluated at baseline and 1 hour following injection. If the headache remained severe, an epidural blood patch was performed. RESULTS: Only one patient in each group received relief from the injection. CONCLUSIONS: We do not recommend sumatriptan in patients who have exhausted conservative management of postdural puncture headache.

Adult↗
PubMed2001

Delivery outcome in women who used drugs for migraine during pregnancy with special reference to sumatriptan.

OBJECTIVE: To evaluate delivery outcome in women who used drugs for migraine during pregnancy with special reference to sumatriptan. BACKGROUND: The safety of the use of drugs for migraine during pregnancy is not established. DESIGN AND METHODS: Using the Swedish Medical Birth Registry which contains information on drug use reported by women at the first antenatal visit, 912 infants (born in 905 deliveries) whose mothers had used drugs for migraine were identified, the majority of whom (n = 658) had used sumatriptan. RESULTS: These women differed from the general population of women who had delivered by being older and more often of first parity, but they had similar smoking habits. Slightly more often, the infants were preterm, and they had a birth weight less than 2500 g; neither of these effects were statistically significant. There seemed to be no difference between infants exposed to sumatriptan and those exposed to other drugs used for migraine. No increase in the rate of congenital malformations was seen. CONCLUSIONS: The data indicate that use of sumatriptan in early pregnancy does not result in a large increase in teratogenic risk, but do not rule out the possibility of a moderate increase in risk for a specific birth defect.

Adult↗
PubMed2002

Sumatriptan scavenges superoxide, hydroxyl, and nitric oxide radicals: in vitro electron spin resonance study.

BACKGROUND: The molecular mechanisms of migraine have not yet been clarified. Oxygen free radicals have been implicated in the genesis of many pathological processes, including migraine. Sumatriptan succinate is known to be a very effective drug for acute relief of migraine attack. OBJECTIVE: To investigate the direct scavenging activities of sumatriptan for superoxide, hydroxyl, and nitric oxide (NO) radicals using electron spin resonance (ESR) spectroscopy. METHODS: Measurement of superoxide and hydroxyl radical scavenging activities was performed by ESR using 5,5-dimethyl-1-pyrroline-N-oxide as a spin trap. NO was generated from 1-hydroxy-2-oxo-3-(N-3-methyl-3-aminopropyl)-3-methyl-1-triazene and analyzed by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl produced from the reaction between 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide and NO. RESULTS: The ESR study demonstrated that sumatriptan scavenged superoxide, hydroxyl, and NO in a dose-dependent manner. CONCLUSIONS: Sumatriptan has direct scavenging activity on free radicals and NO. Acute migraine drugs with antioxidant properties may provide heretofore unheralded benefits via this mechanism.

Electron Spin Resonance Spectroscopy↗
PubMed2003

Activation of pain by sumatriptan.

OBJECTIVE: To demonstrate that sumatriptan may induce activation or aggravation of pain at sites of inflammation caused by trauma or disease. METHODS: Case reports from the national pharmaco vigilancecenters of 2 countries, The Netherlands and New Zealand, are presented. These reports come from programs that use 2 methodologies to monitor drugs for adverse reactions: spontaneous reporting and a prospective observational cohort study. The potential mechanisms for pain production by sumatriptan are discussed in detail. RESULTS: Thirteen case reports of activation of pain by sumatriptan following injury and 8 associated with inflammatory diseases are presented. Most patients had one or more positive rechallenges. This type of reaction occurred at a higher rate with the subcutaneous formulation than with the oral preparation. Pain mostly was severe but short-lasting; pain was prolonged in some patients with inflammatory disease. CONCLUSIONS: A strong association has been demonstrated between the use of sumatriptan and the production of pain at sites of inflammation, and there is a plausible pharmacological mechanism for this reaction. Pain activation may be a class effect of the selective serotonergic agonists used in the treatment of migraine.

Adult↗
PubMed1996

Sumatriptan can inhibit trigeminal afferents by an exclusively neural mechanism.

Mechanical distortion of the human cranial venous sinuses is painful as is cranial venous sinus distension during migraine. Sumatriptan, the serotonin (5HT)IB/D-like receptor agonist, is highly effective in relieving migraine headache and part of its action may be due to constriction of cranial dural blood vessels. Using immunohistochemical detection of the immediate early gene Fos, we have mapped the spatial pattern of neural activation in the caudal medulla and the upper cervical spinal cord (C1, C2 and C3) in cats following either electrical or mechanical stimulation of the superior sagittal sinus. Fourteen cats were anaesthetized with alpha-chloralose and prepared for physiological monitoring of blood pressure, heart rate, rectal temperature and expired CO2. Electrical stimulation evoked significant increases in the (median) numbers of Fos-positive cells in laminae I and IIo of the superficial dorsal horn of C1, C2 and C3 cervical spinal cord (88, 92 and 18 cells, respectively) and of the trigeminal nucleus caudalis (TNC) (81 cells). Mechanical stimulation revealed a similar pattern of neural activation but with reduced intensity in laminae I and IIo of the TNC (38 cells) and of C1 and C2 (32 and 31 cells, respectively). The temporalis muscle was stimulated mechanically in the control group and the numbers and distribution of Fos-positive cells were no different from those in non-stimulated controls. Treatment with sumatriptan reduced the numbers of Fos-positive cells found in laminae I and IIo of the TNC and C2 (6, 13 cells and 9 cells, respectively) after mechanical stimulation. These data suggest that the neural effect of sumatriptan alone is sufficient for significant attenuation of transmission in the trigeminal system. The fact that sumatriptan can inhibit trigeminal activation without its vascular effects suggests that drugs without a significant activity on blood vessels may be effective in the treatment of migraine.

Afferent Pathways↗
PubMed1996

Oral sumatriptan in the acute treatment of migraine and migraine recurrence in general practice.

We investigated the efficacy, safety and tolerability compared with placebo of a second dose of oral sumatriptan 100 mg in 1349 general practice patients who had already treated a moderate or severe migraine headache with 100 mg sumatriptan 4 h earlier. Headache was relieved by the first sumatriptan dose in about 70% of patients, but the second dose did not produce significantly more relief than placebo, either in non-responders or in the group as a whole, nor did it reduce other symptoms (photophobia, nausea, vomiting, etc.) at 8 h, or influence the incidence of headache recurrence. The drug was well-tolerated, and a further single dose was effective in treating recurrence after initial relief. A single 100 mg dose of sumatriptan is an effective acute treatment for migraine. A second dose should be reserved for treating headache recurrence.

Acute Disease↗
PubMed1996

Sumatriptan inhibits the release of CGRP and substance P from the rat spinal cord.

The possible presynaptic action of the anti-migraine drug sumatriptan on primary afferent fibres containing substance P and/or calcitonin gene-related peptide was investigated on superfused rat horizontal spinal cord slices with attached dorsal roots. Electrical stimulation of dorsal roots triggered a significant overflow of both peptides; this could be reduced by sumatriptan in a concentration-dependent manner. As expected from the involvement of 5-HT1B/1.D beta receptors, methiothepin, (-)tertatolol and GR 127,935, but not WAY 100,635, prevented the inhibitors effect of sumatriptan. These data support the idea that the anti-migraine action of sumatriptan may involve, at least in part, a presynaptic inhibitory control of nociceptive (trigeminovascular) substance P- and/or calcitonin gene-related peptide-containing sensory fibres.

Animals↗
PubMed2005

The effect of early intervention with sumatriptan tablets on migraine-associated productivity loss.

OBJECTIVE: Impaired performance, which can considerably impact employee output, occurs when employees attempt to continue work with inadequate treatment while experiencing a migraine episode. This analysis examined productivity loss as a result of migraine after treatment with sumatriptan tablets and patients' usual non-triptan therapy when pain was mild (early intervention) versus when pain was moderate/severe. METHODS: The authors conducted a retrospective analysis of data on 6803 migraine days reported by 251 subjects who participated in a clinical trial. RESULTS: Although early intervention significantly reduced productivity loss compared with treatment when pain was moderate/severe for both sumatriptan and non-triptan therapy, productivity loss was consistently lower for sumatriptan than non-triptan therapy for all predose pain intensity levels. CONCLUSIONS: These findings suggest that the pharmaco-economic benefits of early intervention with sumatriptan tablets, like the clinical benefits, exceed those of delayed intervention.

Adult↗
PubMed2001

Efficacy of sumatriptan in the treatment of migraine: a review of the literature.

Advanced practice nurses treat many patients, including children and adolescents, with migraine headaches. Management of headache episodes requires a delicate balance of prophylactic and abortive therapies. Sumatriptan has been used effectively to treat adult patients with migraine headaches, but its efficacy in children has not been established. Results of a literature review provide strong evidence supporting the use of sumatriptan in treating adults with migraine headaches. Some evidence also exists for using sumatriptan to treat migraines in pediatric patients. Open prospective studies used small convenience samples, thus limiting the external validity of the research findings. Two randomized, double-blind, placebo-controlled, crossover trials found conflicting results for the efficacy of sumatriptan in the treatment of pediatric migraine. Further research is needed to determine its efficacy in children.

Adult↗
PubMed1992

Effect of sumatriptan, a new selective 5HT1-like agonist, on liquid gastric emptying in man.

Paired studies were carried out on 12 healthy male subjects to compare the effect of intravenous doses of the 5-HT1-like agonist sumatriptan (GR43175; 3 mg), 10 mg metoclopramide and saline control on the rate of gastric emptying of a radiolabelled liquid test-meal. Intravenous administration of metoclopramide accelerated gastric emptying by decreasing the lag period, while intravenous administration of sumatriptan delayed gastric emptying by increasing the lag period. The observation that sumatriptan causes a delay in gastric emptying in normal healthy volunteers, but relieves nausea and vomiting during migraine attacks, suggests that sumatriptan may be acting via a central mechanism to relieve symptoms of nausea and vomiting associated with migraine.

Adult↗
PubMed1992

Lack of effect of flunarizine on the pharmacokinetics and pharmacodynamics of sumatriptan in healthy volunteers.

Twenty-four healthy subjects completed a double-blind, placebo controlled, parallel group study to evaluate the effect of treatment with flunarizine on the pharmacokinetics and pharmacodynamics of sumatriptan, a 5HT1-like agonist. Subjects received a single oral 200 mg dose of sumatriptan on the eighth day of a once daily treatment with either flunarizine 10 mg or matching placebo. There were no significant differences between treatments in relation to Cmax (82.3 ng ml-1 in the absence and 81.4 ng ml-1 in the presence of flunarizine), AUC (368 ng ml-1 h in the absence and 360 ng ml-1 in the presence) and elimination half-life (2.2 h in the absence and 2.4 h in the presence of flunarizine) of sumatriptan. Similarly pretreatment with flunarizine was not found to have any clinically significant effect on the pharmacodynamics of sumatriptan as measured by pulse rate, blood pressure and ECG.

Administration, Oral↗
PubMed1995

A comparison of the contractile effects of 5-hydroxytryptamine, sumatriptan and MK-462 on human coronary artery in vitro.

1. MK-462 (N,N-dimethyl-2-[5-(1,2,4-triazol-1-ylmethyl)-1H- indol-3-yl]ethylamine) is a novel selective 5-HT1D-receptor agonist which in clinical trials has been shown to be an effective antimigraine agent. As angiographic studies have shown that sumatriptan (an established 5-HT1D-receptor agonist) can cause coronary artery vasoconstriction in patients, we compared the effects of MK-462 with those of 5-HT and those of sumatriptan, on isolated segments of human coronary artery in vitro. 2. Coronary arteries were obtained from explanted hearts from patients (n = 22, 2 females, 20 males, aged 21-60 years) undergoing cardiac transplantation. Endothelium-denuded ring segments of coronary artery, 2mm long were mounted in organbaths for isometric tension recording. For each arterial ring segment, a cumulative concentration-effect curve to either 5-HT, sumatriptan or MK-462 was determined. After maximal response to each agonist had been obtained, ketanserin (a 5-HT2 receptor antagonist) 0.6 microM was added to the tissue bath, followed by methiotepin (0.6 microM) and the reduction in tension produced by the addition of each antagonist was determined. 3. Out of 22 coronary arteries studied, only 10 showed any response (contraction) to 5-HT. Not all arteries which responded to 5-HT contracted in response to both sumatriptan and MK-462 (one ring from each artery being exposed to a single agonist in each case).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vessels↗
PubMed2004

Effects of chronic sumatriptan and zolmitriptan treatment on 5-HT receptor expression and function in rats.

Triptans are commonly used anti-migraine drugs and show agonist action mainly at serotonin 5-HT(1B/1D/1F) receptors. It is not known whether frequent or long-term treatment with these drugs would alter 5-HT receptor function. We investigated the effects of protracted (14-18 days) sumatriptan and zolmitriptan treatment in rats on 5-HT(1) receptor mRNA expression and function in tissues related to migraine pathophysiology. RT-PCR analysis revealed that 5-HT(1B/1D/1F) receptor mRNA was reduced in the trigeminal ganglion after treatment with either triptan (reduction by: sumatriptan 39% and zolmitriptan 61% for 5-HT(1B); 60%vs 41% for 5-HT(1D); 32%vs 68% for 5-HT(1F)). Sumatriptan attenuated 5-HT(1D) receptor mRNA by 49% in the basilar artery, whereas zolmitriptan reduced 5-HT(1B) mRNA in this tissue by 70%. No change in 5-HT(1) receptor mRNA expression was observed in coronary artery and dura mater. Chronic triptan treatment had no effect in two functional assays [sumatriptan mediated inhibition (50 mg/kg, i.p.) of electrically induced plasma protein extravasation in dura mater and 5-nonyloxytryptamine-stimulated [(35)S]guanosine-5'-O-(3-thio)triphosphate binding in substantia nigra]. Furthermore, vasoconstriction to 5-HT in isolated basilar artery was not affected by chronic triptan treatment, while it was slightly reduced in coronary artery. We conclude that, although our treatment protocol altered mRNA receptor expression in several tissues relevant to migraine pathophysiology, it did not attenuate 5-HT(1) receptor-dependent functions in rats.

Animals↗
PubMed2004

Effects of sumatriptan on capsaicin-induced carotid haemodynamic changes and CGRP release in anaesthetized pigs.

It is suggested that during a migraine attack capsaicin-sensitive trigeminal sensory nerves release calcitonin gene related peptide (CGRP), resulting in cranial vasodilatation and central nociception. Hence, inhibition of trigeminal CGRP release may prevent the above vasodilatation and, accordingly, abort migraine headache. Therefore, this study investigated the effects of sumatriptan (100 and 300 microg/kg, i.v.) on capsaicin-induced carotid haemodynamic changes and on CGRP release. Intracarotid (i.c.) infusions of capsaicin (10 microg/kg/min, i.c.) increased total carotid, arteriovenous anastomotic and capillary conductances as well as carotid pulsations, but decreased the difference between arterial and jugular venous oxygen saturations. Except for some attenuation of arteriovenous anastomotic changes, the capsaicin-induced responses were not affected by sumatriptan. Moreover, i.c. infusions of capsaicin (0.3, 1, 3 and 10 microg/kg/min, i.c.) dose-dependently increased the jugular venous plasma concentrations of CGRP, which also remained unaffected by sumatriptan. The above results support the contention that the therapeutic action of sumatriptan is mainly due to cranial vasoconstriction rather than trigeminal (CGRP release) inhibition.

Animals↗
PubMed1990

Sumatriptan (GR43175) inhibits cyclic-AMP accumulation in dog isolated saphenous vein.

Sumatriptan (GR43175) contracts rings of dog isolated saphenous vein by an action at 5-HT1-like receptors. We have now examined the effects of sumatriptan on prostaglandin E2(PGE2)-stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in this tissue. Sumatriptan and 5-hydroxytryptamine (5-HT) produced a concentration-dependent inhibition of PGE2-stimulated cyclic AMP accumulation (EC50 values of 250 nM and 80 nM respectively), responses that were mimicked by 5-carboxamidotryptamine but not by U-46619 or methoxamine. The response to sumatriptan (1 microM) was antagonised by methiothepin (1 microM), but not by metergoline (0.1 microM), spiperone (1 microM) or ondansetron (GR38032, 1 microM). These results suggest that 5-HT1-like receptors which mediate contraction of the dog isolated saphenous vein are negatively coupled to adenylate cyclase in this preparation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗