[ XXXX therapy in @entity1187 ].

@entity1 @entity1187 @entity556 @entity583 @entity548 @entity63 @entity20806 @entity1459 @entity715 @entity5582
Intracoronary @entity715 is fundamental in the pathogenesis of @entity1187 , although the causes of @entity715 are still unclear. As @entity556 generation is crucial for @entity715 formation, the inhibition of @entity556 is a primary aim to prevent the evolution of an initial repair process into a pathological @entity715 . @entity556 inhibition can be achieved by several drugs. Heparin is the principal @entity5582 drug currently used in acute syndromes; it acts mainly by binding to @entity5582 III and increasing its inhibitory effect on @entity556 and other coagulation factors. The heparin- @entity5582 III complex, however, does not inhibit @entity715 -bound @entity556 ; moreover, iv heparin requires frequent laboratory monitoring and dose adjustments. Despite these limitations, continuous infusion of i.v. heparin has been found to be effective in @entity1459 and in @entity583 , especially when treated with accelerated rt-PA. New @entity5582 drugs that selectively and directly inhibit @entity556 are hirudin, its synthetic derivate hirulog, and @entity20806 . These drugs have several theoretical advantages over heparin: greater stability of the aPTT--with the need for less laboratory monitoring--and greater efficacy--associated mainly with its capacity to inhibit clot-bound @entity556 . Clinical pilot studies seem to indicate a greater antithrombotic efficacy compared with heparin, but a greater number of @entity548 events in @entity1 with @entity583 receiving thrombolysis. In conclusion, the use of heparin is certainly indicated in @entity1 with @entity1459 and persistent @entity63 and in @entity583 treated with accelerated rt-PA. The use of new @entity5582 drugs, although promising, requires further clinical evaluation.
