The management of XXXX .

@entity1 @entity1289 @entity101 @entity39 @entity75 @entity117 @entity1406 @entity1188 @entity204 @entity583 @entity67 @entity2165 @entity715 @entity1002
Greater understanding of the underlying pathophysiology of @entity583 ( @entity583 ) has led to more aggressive management and lower mortality, both in-hospital and long term. @entity583 results mainly from @entity715 of the @entity1188 -related coronary artery. The ensuing @entity39 evolves over a 6-12 h period providing a time window for interventions designed to reduce eventual @entity1188 size. The most appropriate interventions are those which restore coronary artery patency and hence myocardial blood flow as soon as possible. Occasionally, disruption of the occluding thrombus and compression of the underlying @entity75 is best achieved by direct percutaneous transluminal coronary angioplasty. For the vast majority however, revascularisation by drug therapy is more appropriate. As soon as possible, all @entity1 without contraindications should be offered oral @entity117 and intravenous thrombolysis, usually with streptokinase but occasionally with tissue plasminogen activator. @entity1 in whom these agents are contraindicated should be considered for intravenous beta-blockade using @entity2165 or @entity1406 to reduce myocardial demand and hence @entity1188 size. @entity1 with large @entity1188 , @entity67 , @entity1002 or @entity101 should be considered for early @entity1289 inhibitor therapy. Other agents may be valuable symptomatically, but have no proven role in reducing @entity1188 size or mortality. After the first 24 h, the main aims of management are to assess the likelihood of later ischaemic events or @entity204 (risk stratification) and hence to choose appropriate long term secondary prophylaxis.
