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)

Thromboembolic disease is a common medical condition which, if untreated, carries a significant risk of morbidity and mortality. Treatment with anticoagulant therapy, while clearly beneficial, may expose patients to potentially serious side effects. A thoughtful risk-benefit assessment is therefore crucial before initiating therapy. Thromboembolic disease involves syndromes of both the venous and arterial circulation, and its pathogenesis is best understood by considering the elements of Virchow's Triad. This model defines the risk factors for venous thromboembolism and allows us to classify surgical and medical patients into low, moderate and high risk groups. Similar analysis allows risk assessment for patients prone to cardiogenic embolism resulting from nonvalvular atrial fibrillation, ischaemic heart disease, rheumatic heart disease and valvular prostheses. All anticoagulant therapy is prophylactic. Primary prophylaxis involves instituting anticoagulant therapy in patients at risk, before thromboembolism occurs, while secondary prophylaxis involves treating patients with established disease. The 2 major anticoagulants, heparin and warfarin, differ in their mechanism of action, mode of administration and methods of monitoring. Either may be used as primary or secondary prophylaxis. Heparin, because it acts immediately, is the drug of choice for the short term treatment of thromboembolic disease. Warfarin is the drug of choice for long term oral maintenance therapy. The principal complication of heparin therapy is haemorrhage, although thrombocytopenia and osteoporosis may also occur; the complications of warfarin include haemorrhage and skin necrosis. The risks of complications vary with the underlying thromboembolic disease. After the benefits of treatment are weighed against the risks of complications, recommendations for therapy can be established. The use of anticoagulants in pregnancy is especially complex. Here heparin is probably the preferred agent since, unlike warfarin, it does not cross the placenta and is nonteratogenic.
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PMID:Risk-benefit assessment of anticoagulant therapy. 202 54

Cafergot is a combination of ergotamine tartrate and caffeine and may cause symptoms of peripheral vascular insufficiency. Iatrogenic ergotism should be suspected in any patient exhibiting ischemic symptoms while receiving this medication. Progression to fulminant necrosis and gangrene can occur. Two cases are presented and the management reviewed. This effect of ergotamine tartrate and caffeine may be an idiosyncratic hypersensitivity reaction with therapeutic doses or may result from excessive medication. Iatrogenic ergotism occurs most often in women in their mid-thirties with migraine syndrome. By alpha-adrenergic agonism, as well as by possible interactions with prostaglandins, calcium, and serotonin, ergotamine causes vasoconstriction of both arteries and veins. The angiographic pattern of spasm, collateral formation, and intravascular thrombi is typical. Treatment of ergotism depends on the severity of the symptoms and the possibility of gangrene. Discontinuation of ergotamine, cigarette smoking, and caffeine may be all that is necessary in most patients. Nitroprusside is the drug of choice in the treatment of acute vascular insufficiency from ergotism, but in a less urgent situation, prazosin has also been effective. Intra-arterial balloon dilatation has also been helpful. Other forms of therapy have been supportive and the results inconsistent. Cafergot should be used with extreme caution in patients with renal or hepatic failure, peripheral vascular disease, or pregnancy. Relative contraindications include hypertension, ischemic heart disease, and Raynaud's phenomenon.
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PMID:Recognition and treatment of arterial insufficiency from cafergot. 372 91

Sumatriptan, a 5HT1-like receptor agonist, is a completely new treatment principle for migraine. In an extensive international programme of controlled clinical trials, sumatriptan, 6 mg subcutaneously and 100 mg orally, was superior to placebo in reducing headache and associated symptoms. The response rate for subcutaneous sumatriptan (70-84% after 1 h and 81-87% after 2 h) was higher than for oral sumatriptan (50-67% after 2 h). Additional doses did not increase efficacy. Oral sumatriptan was superior to Cafergot (2 mg ergotamine plus 200 mg caffeine) and somewhat better than aspirin (900 mg) plus metoclopramide (10 mg). Recurrence of migraine occurred in approximately 40% of attacks. Side effects were generally mild and short-lived in the controlled clinical trials. However, in clinical practice sumatriptan has subsequently caused rare cases of heart ischemia and sumatriptan is contraindicated in patients with a history of ischemic heart disease.
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PMID:Sumatriptan for the treatment of migraine attacks--a review of controlled clinical trials. 839 70