Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The new drug, sumatriptan, used to treat migraine, causes substernal tightness and severe angina-like pain in 3-21% of patients. Several reports have described sumatriptan-induced death, ventricular fibrillation, myocardial infarction, ischaemia and coronary vasospasm. We describe the case of a woman aged 40 years who suffered from bronchial asthma but was without known coronary heart disease. She experienced chest pain after intake of 100 mg sumatriptan orally. ECG was normal and there was no increase in coronary enzymes. Sumatriptan has a weak coronary constrictor effect. Endothelial dysfunction, with reduced release of vasodilating nitric oxide, may potentiate vasoconstriction induced by sumatriptan in the presence of thromboxane A2.
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PMID:[The migraine remedy sumatriptan (Imigran) and coronary heart disease]. 766 66

This review of controlled outcome research on Autogenic Training complements the literature by pooling narrative and quantitative approaches, by including only studies with experimental controls, by integrating the English and German literature, and by adding research findings published since the last review. Whereas previous reviews have already reported positive effects of Autogenic Training for migraine, insomnia, and test anxiety, additional supportive findings for angina pectoris, asthma, childbirth, eczema, hypertension, infertility, Raynaud's disease, and recovery from myocardial infarction are discussed here. The impact of protocol variations on outcome is described, and the specificity of Autogenic Training relative to other stress management techniques is highlighted. Quantitative findings suggested that Autogenic Training was associated with medium-sized pre- to posttreatment effects ranging from d = .43 for biological indices of change to d = .58 for psychological and behavioral indices thus matching effect sizes for other biobehavioral treatment techniques like biofeedback and muscular relaxation. Length of treatment did not affect clinical outcome. The discussion emphasizes how narrative and quantitative strategies complement one another.
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PMID:Autogenic training: a narrative and quantitative review of clinical outcome. 781 86

beta-Adrenergic blocking agents are used for the treatment of angina pectoris, cardiac arrhythmia, hypertension, anxiety attacks, thyrotoxicosis, migraine and glaucoma. Owing to their sedative effect, they are also used as doping agents in sport. All beta-blockers have an alkanol amine side chain terminating in a secondary amino group in their structure. The pKa values vary from 9.2 to 9.8. Because some beta-blockers are hydrophilic and some lipophilic, simultaneous determination is difficult. In this work, a method based on micellar electrokinetic capillary chromatography (MECC) was developed for the separation and determination of beta-blockers in serum. The phosphate buffer 0.08 M (pH 6.7) solution contained 15 mM N-cetyl-N,N,N-trimethylammonium bromide. Nine parent beta-blockers could be separated in a single run and the concentrations determined by internal standard (ephedrine) method. The simple clean-up procedure consisted of enzyme hydrolysis (Helix pomatia), protein precipitation, and filtration through 0.5-microns PTFE membranes. The MECC method exhibited good repeatability and a linear range of 75-300 micrograms/ml. The method was successfully applied after concentration to the determination of propranolol in real samples.
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PMID:Determination of nine beta-blockers in serum by micellar electrokinetic capillary chromatography. 791 2

beta-Adrenergic blocking agents are of therapeutic value in the treatment of migraine and various cardiovascular disorders (angina pectoris, cardiac arrhythmia, hypertension). Owing to their sedative effect, they are also used as doping agents in sport. A characteristic feature of beta-blockers is the alkanolamine side-chain terminating in a secondary amino group. The pKa values vary from 9.2 to 9.8. Because some beta-blockers are hydrophilic and some lipophilic, simultaneous determination is difficult. In this work, a method based on micellar electrokinetic capillary chromatography (MECC) was developed for the separation and determination of beta-blockers. The 0.08 M phosphate buffer (pH 7.0) solution contained 10 mM N-cetyl-N,N,N-trimethylammonium bromide (CTAB). Ten parent beta-blockers in human urine could be separated in a single run and determined quantitatively by the internal standard (2,6-dimethylphenol) method. Neither endogenous compounds in urine nor caffeine and its metabolites interfered with the analysis. The clean-up procedure for urine consisted of a simple filtration through 0.5-microns PTFE membranes. The MECC method exhibited good repeatability and a linear range of 25-150 micrograms/ml. The method was applied to determination of oxprenolol in real samples.
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PMID:Determination of ten beta-blockers in urine by micellar electrokinetic capillary chromatography. 809 37

The classification of Raynaud's phenomenon has been complicated by various confusing labels, including Raynaud's disease and Raynaud's syndrome. To improve clarity and to allow for uniformity in reporting, most investigators agree that only the terms primary and secondary Raynaud's phenomenon should be used for patient classification. The prevalence of Raynaud's phenomenon seems to vary among different populations and different climates, suggesting genetic and environmental influences on its expression. The concept that Raynaud's phenomenon is the manifestation of a generalized vasospastic disorder has been addressed by studies of migraine headaches, variant angina, and the pulmonary vascular circulation. Current data suggest that the pathophysiology of Raynaud's phenomenon is complex and multifactorial, involving the endothelium, neuroreceptor expression, and locally produced mediators that affect vascular responses. New and old diagnostic tools used to measure digital circulation continue to be tested in an effort to define a better method of evaluating patients. Occupational causes of Raynaud's phenomenon continue to be an important health problem despite efforts to control vibratory tool usage. The role of beta-blockers in the induction of Raynaud's phenomenon has been questioned, but the use of chemotherapeutic agents is a definite risk factor. A new radical surgical approach for severe refractory Raynaud's phenomenon was described. Intravenous prostaglandins continue to appear helpful in the treatment of severe Raynaud's phenomenon, and oral prostaglandins are beginning to be studied.
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PMID:Raynaud's phenomenon. 811 41

The relationship between migraine and cardiopathy has not been sufficiently established and controversy exists concerning its favoring role in coronary disease. Likewise, specific cephalea ("bregmatic") has been proposed as a manifestation of myocardial ischemia. With the aim of investigating this topic a protocol which collected the history and morphology of previous migraine, cephalea during the angina episode and cephalic response to vasodilators to 40 consecutive patients with acute myocardial infarction (AMI) admitted to the Coronary Unit of the Hospital 12 de Octubre in Madrid was applied. The results were compared with a control group. Migraine was more frequent in patients with AMI (25%) than in the control group (18.5%). Likewise, the beginning was later and the rhythm of the episodes greater. No specific cephalea was identified. The pain response to the nitrites did not depend on migraine history. The data suggests that determined forms of migraine may represent a risk factor of coronary disease. Epidemiologic studies are required to better know the natural history of the migraine.
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PMID:[Migraine and acute myocardial infarction]. 780 57

Sumatriptan is a potent and selective agonist at the vascular 5HT1 receptor which mediates constriction of certain large cranial blood vessels and/or inhibits the release of vasoactive neuropeptides from perivascular trigeminal axons in the dura mater following activation of the trigeminovascular system. The mode of action of this drug in migraine and cluster headache is discussed. On the basis of a detailed review of all published trials and available data from post-marketing studies, the efficacy, safety, tolerability and the place of oral and subcutaneous sumatriptan in the treatment of both conditions are assessed. A number of double-blind clinical trials have demonstrated that sumatriptan 100 mg administered orally is clearly superior to placebo in the acute treatment of migraine headache and achieves significantly greater response rates than ergotamine or aspirin. In other studies, 70 to 80% of patients receiving sumatriptan 6 mg sc experienced relief of migraine headaches by 1 or 2 h after administration, and patients consistently required less rescue medication for unresolved symptoms. Sumatriptan was also effective in relieving associated migraine symptoms like nausea and vomiting. Sumatriptan was equally effective regardless of migraine type or duration of migraine symptoms. Overall, approximately 40% of patients who initially responded to oral or subcutaneous sumatriptan experienced recurrence of their headache usually within 24 h, effectively treated by a further dose of this drug. In 75% of patients with cluster headache treated with sumatriptan 6 mg sc, relief was achieved within 15 min. Based on pooled study data, sumatriptan is generally well tolerated and most adverse events are transient. Adverse events following oral administration include nausea, vomiting, malaise, fatigue and dizziness. With the subcutaneous injection, injection site reactions occur in approximately 30%. Chest syumptoms are reported in 3 to 5% but have been associated with myocardial ischaemia only in rare isolated cases. The recommended dosage of sumatriptan at the onset of migraine symptoms is 100 mg orally or 6 mg subcutaneously. The recommended dosage for cluster headache is 6 mg sumatriptan sc. Sumatriptan must not be given together with vasoconstrictive substances, e.g., ergotamines, or with migraine prophylactics with similar properties, e.g., methysergide. Sumatriptan should not be given during the migraine aura. It is contraindicated in patients with ischaemic heart disease, previous myocardial infarction, Prinzmetal (variant) angina and uncontrolled hypertension.
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PMID:Migraine and cluster headache--their management with sumatriptan: a critical review of the current clinical experience. 853 93

The view that the era of modern medicine began with the introduction of the sulfonamides is supported by a standard textbook of pharmacology that refers to the years 1908-35 as being characterized by "therapeutic nihilism". However, a survey of several sources listing some of the treatments then available yields 15 infectious, 7 deficiency and 3 endocrine disorders amenable to cure. In addition, palliation that even today would be considered rational could be given for congestive heart failure, angina pectoris, asthma, epilepsy, migraine, and Parkinson's disease, to mention only a few. A total of 38 surgical, pharmacological, nutritional and physical remedies were identified, many of them still in use. These findings represent a minimum estimate as the review was not exhaustive, being aimed chiefly at recapturing the therapeutic atmosphere prevailing 75 years ago. Nothing in the textbooks of medicine, pharmacology and treatment suggests that physicians of the 1920's lacked either the means or the enthusiasm for treating their patients.
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PMID:Therapeutic nihilism? 860 44

There have been hints over the years about the involvement of purines in pain, and we now have direct evidence with the cloning and characterisation of extracellular receptors for ATP (P2X-purinoceptors) on nociceptive sensory neurons. In this article, a hypothesis is put forward about the sources of ATP released to activate these receptors in three different pain conditions--as a cotransmitter from sympathetic nerves in causalgia and reflex sympathetic dystrophy; from endothelial cells in vascular pain, including migraine and angina; and from tumour cells in cancer. These findings are leading to an active search for selective P2-purinoceptor antagonists to alleviate pain.
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PMID:A unifying purinergic hypothesis for the initiation of pain. 866 73

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.
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PMID:Vasospasm-induced myocardial infarction with sumatriptan. 868 77


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