Antiplatelet therapy after percutaneous coronary intervention.
There is intense interest in the relationship between inflammation, thrombosis, platelet aggregation, and hyperlipidemia in patients with coronary artery disease. The specific role of inflammation with its linkage to the coagulation cascade has been well studied. A number of inflammatory markers have been identified which can be used for risk stratification in patients with acute coronary syndromes. Patients with acute coronary syndromes at the time of presentation often have an underlying inflammatory state which needs therapy with antiplatelet regimens including now increasingly frequently clopidogrel in addition to the standard of aspirin. In those patients who are treated medically for their acute coronary syndromes, long-term treatment with dual antiplatelet therapy has been documented to be associated with improved outcome. In patients who undergo an invasive approach with placement of intracoronary stents, the importance of dual antiplatelet therapy is increased. Drug-eluting stents are now used in approximately 90% of all interventional procedures. There is evidence to suggest that while these patients have improved outcome in terms of a decreased need for subsequent procedures to treat restenosis, there is the potential for late subacute stent thrombosis. When late subacute stent thrombosis occurs, it results in mortality or infarction in 40-60% of patients. Dual antiplatelet therapy is therefore recommended for an increasingly longer time in this patient group. At the present time, protocols indicate 3 months for one of the drug-eluting stents and 6 months for the other. However, increasingly longer antiplatelet therapy is being used clinically. Assessment of platelet function during follow-up is as yet early. There are issues about which specific test to use and the definition of platelet hyperreactivity. In the future, more individually targeted therapy may be possible if we can more adequately assess the degree of hyperreactivity and underlying inflammation.
Holmes
David R
DR
Mayo Clinic, Rochester, MN 55905, USA. holmes.david@mayo.edu
D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use; D000077407:Cilostazol; D000077144:Clopidogrel; D003328:Coronary Thrombosis / Q000209:etiology / Q000517:prevention & control*; D004351:Drug Resistance; D004359:Drug Therapy, Combination; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D015607:Stents / Q000009:adverse effects; D013777:Tetrazoles / Q000009:adverse effects / Q000627:therapeutic use; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors
D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D000077144:Clopidogrel; D000077407:Cilostazol; D013988:Ticlopidine; D001241:Aspirin