[Stents in interventional cardiology].
Since the first percutaneous transluminal coronary angioplasty performed by A. Gruentzig in 1977, percutaneous coronary interventions have become the most important treatment modality for coronary heart disease. Coronary angioplasty carried a significant risk of coronary flow-limiting dissections and restenosis during the first six months following the procedure. Two main studies comparing percutaneous transluminal coronary angioplasty and coronary stenting (STRESS and BENESTENT) performed in 1994 showed a significant reduction in restenosis rate using stents. Thus, until now stents are the most widely used devices for coronary intervention despite two problems: subacute stent thrombosis (1-2%) and still high restenosis rate (5-40%). Subacute stent thrombosis occurs within the first month after stent placement and can be prevented using the double antiplatelet regimen with aspirin and clopidogrel. Some risk of subacute thrombosis remains beyond the first month when drug-eluting stents are used. This requires prolonged antiplatelet therapy. Drug-eluting stents are the most significant innovation in interventional cardiology. They can reduce the incidence of restenosis in native stable coronary arteries to 3-5%. However, the long-term studies comparing bare-metal stents and drug-eluting stents did not show any significant differences in the rate of major adverse cardiac events (death, myocardial infarction), especially in patients with diabetes after the treatment of bifurcational lesions. According to proposed recommendations, drug-eluting stents should be used in small vessels, restenotic lesions, and in saphenous vein grafts. Despite some disadvantages, the results of coronary stenting using drug-eluting stents continue to improve.
Grinius
Virgilijus
V
Institute of Cardiology, Clinic of Cardiology, Kaunas University of Medicine, Sukileliu 17, Kaunas, Lithuania. virgilijusg@yahoo.com
Navickas
Ramūnas
R
Unikas
Ramūnas
R
D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D000077144:Clopidogrel; D023903:Coronary Restenosis / Q000517:prevention & control*; D003328:Coronary Thrombosis / Q000209:etiology / Q000517:prevention & control*; D048909:Diabetes Complications; D016503:Drug Delivery Systems; D004359:Drug Therapy, Combination; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D005500:Follow-Up Studies; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000627:therapeutic use; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D011239:Prednisolone / Q000008:administration & dosage / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D020123:Sirolimus / Q000008:administration & dosage / Q000627:therapeutic use; D015607:Stents / Q000009:adverse effects / Q000592:standards; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D000893:Anti-Inflammatory Agents; D005343:Fibrinolytic Agents; D007166:Immunosuppressive Agents; D010975:Platelet Aggregation Inhibitors; D011239:Prednisolone; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin; D020123:Sirolimus