Anticoagulation after intracoronary stent implantation

The success of percutaneous transluminal coronary angioplasty (PTCA) is limited by vessel dissection with subsequent vessel occlusion in the acute phase and by restenosis chronically. The implantation of intracoronary stents allows to manage acute complications more efficiently and reduce restenosis rate. Anticoagulation and inhibition of platelet function play an important role in reducing the risk of stent thrombosis triggered by the thrombogenic surface of the stents available today. Among the risk factors for stent thrombosis are stent implantations in emergency situations, a low coronary blood flow secondary to more distal stenoses or to small vessel diameter, and several stents implanted in a single vessel region. In 2 large randomized studies (BENESTENT, STRESS), combination therapy using aspirin, dipyridamole, dextrane, and heparin continued by warfarin lead to a high incidence of bleedings and vascular complications at the site of arterial punction. Subsequent studies documented that dipyridamole and dextrane do not improve the outcome after stent implantation. Recently, the combination of aspirin and ticlopidine has been show to reduce the rate of stent thrombosis; with coronary stents implanted optimally anticoagulation may be handled without warfarin. Most stent thromboses occur even if anticoagulation is monitored and controlled accurately. The search for markers to predict stent thrombosis such as the prothrombin fragment F1+2 or the thrombin-antithrombin complex has not been successful so far. The direct antithrombin hirudin, platelet receptor blockers such as the antibody 7E3, and new stents with reduced thrombogenic surface offer new perspectives in anticoagulation with stent implantation.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

The success of percutaneous transluminal coronary angioplasty (PTCA) is limited by vessel dissection with subsequent vessel occlusion in the acute phase and by restenosis chronically.

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