Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Safety information was pooled from 4,859 patients, mainly treated in controlled clinical trials with a dispersible tablet of sumatriptan or by a subcutaneous injection, and from 1,164 patients who received placebo by these routes. Safety monitoring involved collection of all adverse events, regardless of their relationship to treatment, and included routine laboratory screening tests and some special investigations. Individuals experienced several groups of symptoms that might be considered to be features of migraine itself or of the post-migraine period or due to treatment. The commonest complaints were an unpleasant taste or pain on injection. After oral sumatriptan (100-300 mg), some events (nausea, malaise) were characteristic of migraine and others (fatigue, sedation, weakness) were characteristic of the recovery period. With subcutaneous sumatriptan (4-8 mg) similar events were observed, but certain distinctive symptoms variously described as heaviness, pressure sensation, tingling, feelings of heat or warmth, were more common and affected various parts of the body. Their early onset and transient nature suggests some pharmacological mechanism, as yet not identified. Despite the mixed picture of symptoms recorded after treatment, they were not serious, they were transient and they were accepted by patients. Close patient monitoring allowed detailed evaluation of any possible cardiovascular side-effects as seen with other anti-migraine agents, particularly ergotamine. The evidence is reassuring but, since experience in patients with symptomatic ischaemic heart disease is limited, it is recommended that they should initially be treated with sumatriptan under medical supervision for their first two or three attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety and tolerability of sumatriptan: an overview. 165 42

Sumatriptan is a potent and selective agonist at a vascular serotonin1 (5-hydroxytryptamine1; 5-HT1) receptor subtype (similar to 5-HT1D) and is used in acute treatment of migraine and cluster headache. Following administration of sumatriptan 100mg orally, relief of migraine headache (at 2 hours) was achieved in 50 to 67% of patients compared with 10 to 31% with placebo in controlled clinical trials. In a comparative study, oral administration of sumatriptan 100mg consistently achieved significantly greater response rates than a fixed combination of ergotamine 2mg plus caffeine 200mg during 3 consecutive migraine attacks (66 vs 48% for first attack). Oral sumatriptan 100mg was also more effective than aspirin 900mg plus metoclopramide 10mg orally in a similar study. In the majority of controlled clinical trials, headache relief (at 1 hour after administration) was achieved in 70 to 80% of patients with migraine receiving sumatriptan 6mg subcutaneously compared with 18 to 26% of placebo recipients. Approximately 40% of patients who initially responded to oral or subcutaneous sumatriptan experienced recurrence of their headache, usually within 24 hours, but the majority of these patients responded well to a further dose of sumatriptan. Patients with cluster headache were treated for acute attacks with sumatriptan 6mg subcutaneously or placebo in 2 crossover trials. Headache relief was achieved within 15 minutes in 74 and 75% of patients receiving sumatriptan in these studies compared with 26 and 35%, respectively, with placebo. Patients receiving sumatriptan 12mg had a similar response rate as those receiving 6mg, but the higher dose was associated with an increased incidence of adverse events. Based on extensive safety data pooled from controlled clinical trials, sumatriptan is generally well tolerated and most adverse events are transient. The most frequently reported adverse events following oral administration include nausea, vomiting, malaise, fatigue and dizziness. Injection site reactions (minor pain and redness of brief duration) occur in approximately 40% of patients receiving subcutaneous sumatriptan, although the incidence appears to be markedly reduced when patients self-administer the drug with an auto-injector. Chest symptoms (mainly tightness and pressure) occur in 3 to 5% of sumatriptan recipients, but have not been associated with myocardial ischaemia except in a few isolated cases. Sumatriptan is contraindicated in patients with ischaemic heart disease, angina pectoris including Prinzmetal (variant) angina, previous myocardial infarction and uncontrolled hypertension, but is not contraindicated in patients with migraine and asthma. Data from long term studies in acute treatment of migraine and cluster headache suggest that sumatriptan remains effective and well tolerated over several months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sumatriptan. A reappraisal of its pharmacology and therapeutic efficacy in the acute treatment of migraine and cluster headache. 751 61

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

Carvedilol competitively blocks beta 1, beta 2 and alpha 1 receptors. The drug lacks sympathomimetic activity and has vasodilating properties that are exerted primarily through alpha 1-blockade. Animal models indicate that carvedilol confers protection against myocardial necrosis, arrhythmia and cell damage caused by oxidising free radicals, and the drug has no adverse effects on plasma lipid profiles. Recent data have confirmed the antihypertensive efficacy of carvedilol in patients with mild to moderate essential hypertension. Carvedilol has similar efficacy to other beta-blocking agents, calcium antagonists, ACE inhibitors and hydrochlorothiazide. Carvedilol also improves exercise tolerance and ischaemic symptoms in patients with stable angina pectoris. Significant reductions in serious cardiac events after acute myocardial infarction and in frequency and severity of ischaemic events in patients with unstable angina have also been demonstrated. Interest in the use of carvedilol in patients with congestive heart failure (CHF) has culminated in the publication of a cumulative analysis of data from 1094 patients with mild to severe CHF who participated in the US Carvedilol Heart Failure Study Program (4 trials). After a median follow-up of 6.5 months, a significant overall reduction in mortality relative to placebo (3.2 vs 7.8%) was revealed in patients who had received carvedilol 6.25 to 50 mg twice daily (plus diuretics and ACE inhibitors). All-cause mortality, risk of hospitalisation for cardiovascular reasons and hospitalisation costs were also reduced significantly (by 65, 28% and 62%, respectively) in these trials. In addition, the Australia and New Zealand Heart Failure Research Collaborative Group showed a 26% reduction in the combined risk of death or hospitalisation with carvedilol 12.5 to 50 mg/day relative to placebo after a mean 19-month follow-up period in 415 patients with CHF (relative risk 0.74). Adverse events with carvedilol appear to be less frequent than with other beta-blocking agents, are dosage-related and are usually seen early in therapy. Events most commonly reported are related to the vasodilating (postural hypotension, dizziness and headaches) and the beta-blocking (dyspnoea, bronchospasm, bradycardia, malaise and asthenia) properties of the drug. Carvedilol appears to date to have little effect on the incidence of worsening heart failure. Concomitant administration of carvedilol with some medications requires monitoring. Carvedilol is therefore likely to have a beneficial role in the management of controlled CHF, but further clinical studies are required to show the place of beta-adrenoceptor blocking therapy in general in this indication, and the position of carvedilol relative to other similar agents. Carvedilol is also confirmed as effective in the management of mild to moderate hypertension and ischaemic heart disease.
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PMID:Carvedilol. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disorders. 921 Oct 87

Shift work and night work in particular have been associated with sleep difficulties, general malaise, fatigue, peptic ulceration, ischaemic heart disease, cigarette smoking and adverse pregnancy outcome. The medical conditions previously regarded as making individuals unsuitable for shift work show wide ranging patho-physiological activity and there is no published evidence for any such condition to be regarded an absolute reason to exclude an individual from shift work. The fulfilment of the legal obligations of the Working Time Regulations 1998 is neither prescribed nor constrained in any way. It is advisable therefore to build on existing health procedures where they are in effect. Periodic health questionnaires can offer health professionals an opportunity to detect any disorder likely to be aggravated by shift work or by a combination of shift work, job demands and workplace conditions. A further purpose of the questionnaire is the assessment of ability to undertake shift work duties. However, health questionnaires are neither sensitive nor specific enough to be used to select applicants or employees for shift work, since they do not consistently predict tolerance of shift work or subsequent health problems. Whether employers should offer anything more than a simple questionnaire will depend on the culture of the company and accessibility of health services. Screening programmes affect many people relative to the few who benefit and with existing knowledge, periodic general health examinations performed in asymptomatic subjects have limited predictive or preventive value.
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PMID:Shift work, health, the working time regulations and health assessments. 1045 93

The clinical significance of rapid monomorphic ventricular tachycardia (VT) (> 270 beats/min), also called ventricular flutter, remains controversial in patients without documented spontaneous sustained VT. The aim of this study was to evaluate the outcome of 115 patients with ischaemic heart disease, aged 58 +/- 10 years, without spontaneous ventricular arrhythmias, but who had inducible ventricular flutter during programmed ventricular stimulation. The patients underwent stimulation to evaluate the prognosis after myocardial infarction or to investigate a malaise with or without loss of consciousness. Sustained ventricular flutter was the only inducible arrhythmia in all patients. The mean left ventricular ejection fraction (LVEF) was 42 +/- 14%. During an average follow-up period of 66 +/- 43 months, 31 deaths, including 27 of cardiac causes, were observed. The 1, 5, and 11 year survival of the whole population was 94, 79 and 64% respectively. In univariate analysis, anterior wall myocardial infarction, a low LVEF, the presence of non-sustained ventricular tachycardia (NSVT) on 24 hour Holter monitoring and Class III antiarrhythmic treatment, were poor prognostic factors (p 0.05). In multivariate analysis, the only independent predictive factors of mortality were low LVEF (p = 0.006), the presence of NSVT on Holter monitoring (p = 0.003) and the absence of betablocker therapy (p = 0.015). Medical therapy with betablockers or the implantation of an automatic defibrillator may be indicated in these patients at higher risk.
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PMID:[Long-term follow up of 115 patients with ischemic heart disease and ventricular flutter induced by programmed ventricular stimulation in the absence of ventricular arrhythmia]. 1056 1

A 74 year-old Japanese woman, who had suffered from Lambert-Eaton myasthenic syndrome (LEMS), Sjoegren's syndrome, and discoid lupus erythematosus for 10 years and had been successfully controlled by 3,4-diaminopyridine and prednisolone, began to suffer from chest discomfort at night. Stress-induced myocardial ischemia in the left ventricular anterior septum was detected by thallium-201 scintigraphy. After diltiazem was prescribed, she began to feel systemic malaise and weakness in both thighs. She stopped taking diltiazem and the symptoms improved. Coronary angiography revealed 75% stenosis with calcification in the middle of the left anterior descending artery. After atherectomy with a lotablator and coronary stenting, diltiazem was prescribed. She felt malaise again, but continued taking diltiazem. After three months a follow-up coronary angiography showed no restenosis in the lesion and diltiazem was stopped. The weakness and malaise disappeared and her muscle strength recovered. LEMS is an autoimmune disorder of peripheral cholinergic transmission in which autoantibodies to the presynaptic P/Q-type voltage-gated calcium channels (VGCC) decrease the release of acetylcholine at the neuromuscular junction resulting in muscle weakness. P/Q-type VGCC regulates most of the neurotransmitter release and L-type VGCC regulates the remainder. L-type VGCC blockers are thought to have little effect on the neuromuscular junction. but they should be used very carefully. even in the remission stage of LEMS, because of preexisting neuromuscular blocking in transmission.
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PMID:Exacerbation of Lambert-Eaton myasthenic syndrome caused by an L-type Ca2+ channel antagonist. 1262 45

Ondansetron is a serotonin receptor antagonist used widely in the prophylaxis and treatment of postoperative nausea and vomiting (PONV) and vomiting associated with cancer chemotherapy. The common side effects of ondansetron are fever, malaise, diarrhoea, constipation, and allergic reactions. Extra-pyramidal reactions are rare and cardiovascular side effects are even rarer. Even though its clinical safety has been established in a large number of studies, its adverse effects have been reported and these include cardiovascular events like acute myocardial ischemia and arrhythmias in adults.([1]) Studies of its adverse effects in children are few. We report a rare adverse effect of ondansetron in a 14-year-old girl, presenting as ventricular tachycardia.
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PMID:Ondansetron induced fatal ventricular tachycardia. 2004 Sep 55

Despite established exposure limits and safety standards, and the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO, or from longer exposures to lower levels. Common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often go on to develop neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus and Parkinsonian-like syndrome. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.
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PMID:Hyperbaric oxygen therapy for carbon monoxide poisoning. 2510 87

Despite established exposure limits and safety standards as well as the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. Common symptoms can include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury manifested by neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.
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PMID:Carbon monoxide poisoning. 3217 57


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