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)

Intravenous unfractionated heparin (UFH) is associated with several limitations, including short duration of action, poor bioavailability, unpredictable anticoagulant response, a risk of heparin-induced thrombocytopenia (HIT), and disease reactivation following early discontinuation. Because of these limitations, there is interest in the development of newer antithrombotic strategies. Low-molecular-weight heparins (LMWHs) offer potential benefits over standard heparin and allow the opportunity for subcutaneous self-administration for longer periods. In the acute phase of unstable angina, LMWHs have been shown to be superior to placebo and at least as effective as UFH in reducing death, myocardial infarction and recurrent angina. Trials of longer-term therapy with LMWHs are in progress. Although animal studies have suggested that LMWHs, by reducing neo-intimal proliferation, may prevent restenosis following coronary angioplasty, clinical trials have been disappointing. However, an initial study with the LMWH enoxaparin (Lovenox/Clexane) and ticlopidine after elective stenting (ENTICES) showed a reduction in stent thrombosis and ischaemic events. This has led to a further trial of antiplatelet therapy versus Lovenox plus antiplatelet therapy for patients with an increased risk of stent thrombosis (ATLAST). Further studies are assessing the role of diffusion and pressure-driven and mechanical devices to deliver high and sustained local intravascular concentrations of heparin.
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PMID:Current roles and future possibilities for low-molecular-weight heparins in unstable angina. 979 Feb 85

Acute coronary syndromes are responsible for the deaths of tens of thousands of patients every year. Rupture of coronary atheromatous plaques with resultant luminal thrombosis is the cause in most cases. Although great steps forward have been taken in the management of acute myocardial infarction (MI) and unstable angina (UA), new therapeutic strategies are required to reduce further the incidence and risk of these events. At present, aspirin, nitrates and heparin are the conventional treatments for unstable angina. Aspirin, in combination with a thrombolytic agent or with percutaneous transluminal coronary angioplasty (PTCA), has been shown to be effective in reducing mortality in acute MI. Heparin is conventionally used in all PTCA procedures, whereas its efficacy in enhancing the therapeutic role of thrombolytic agents remains uncertain and may depend on the thrombolytic agent used. PTCA, which is also an effective therapy for stable angina, can be complicated by intimal dissection and thrombosis in a minority of cases, with vessel restenosis leading to recurrent symptoms in approximately 30% of cases. A number of new agents are being evaluated in both acute coronary syndromes and PTCA. These can be classified as adenosine diphosphate (ADP) receptor antagonists, Factor Xa inhibitors (low-molecular weight heparin [LMWH], direct thrombin inhibitors, new thrombolytic agents and glycoprotein IIb/IIIa receptor blockers. Of the latter, the most studied is abciximab, the Fab fragment of the chimeric monoclonal antibody, 7E3. This is a potent inhibitor of platelet aggregation. Four major clinical studies of PTCA in high-risk patients have demonstrated clear efficacy of abciximab in reducing acute ischaemic complications, mainly by reducing the frequency of MI and the need for repeat revascularisation. Unlike other glycoprotein IIb/IIIa receptor blockers, both short- and long-term efficacy have been demonstrated. Its impact on the rate of restenosis after PTCA is unclear. Abciximab's role in an era of intracoronary stent implantation is undergoing further study (with encouraging early results). Its role in other situations, such as the early (non-angioplasty) management of unstable angina and its ability to enhance the efficacy of thrombolytic agents, is under active investigation.
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PMID:Abciximab (Reopro): a clinically effective glycoprotein IIb/IIIa receptor blocker. 1599 12