Drug Eluting Stents and Stent Thrombosis
Blockages in coronary arteries (coronary stenoses) reduce blood flow to the heart and may result in symptoms of anginal chest pain, heart attack (myocardial infarction), heart failure and even sudden death. Many patients with these conditions require treatment to relieve the blockages. Traditionally this has been done by coronary bypass surgery. From 1980's, interventional cardiology techniques like angioplasty and stenting has overtaken bypass surgery as the treatment of choice as they offer good results without the morbidity of major surgery. However, patients treated with these techniques have greater chances of recurrence of blockages. This is due to the development of restenosis at the site of stenting or angioplasty.
The introduction of drug eluting stents (DES) in the late 1990's was a major landmark in coronary interventions. They could reduce restenosis due to the effects of the drug, the Achilles heel of coronary stents, thus reducing the need for repeat intervention. However, a new problem has surfaced with their use - an increased rate of late stent thrombosis. Stent thrombosis refers to the development of clots within the stent blocking blood flow suddenly and this almost invariably results in a heart attack.
All stents are to some degree thrombogenic, ie, they promote clotting. This tendency is overcome by antiplatelet therapy to reduce clotting at least till the stented part heals by endothelialization. Drug eluting stents appear to be more thrombogenic than bare stents. Stent thrombosis is often a catastrophic event leading to acute myocardial infarction or even death. Delayed reendothelialization of the stented segment due to the effects of the drug has been thought as the mechanism for stent thrombosis. Particularly disturbing are the reports of late stent thrombosis more than a year after stent implantation. Such events are generally associated with stoppage of antiplatelet therapy.
A recently reported study by Kuchulakanti et al in Circulation is one of the first to evaluate the correlates of stent thrombosis. They found that stent thrombosis was significantly higher in patients with diabetes, acute postprocedural renal failure, and chronic renal failure. There were more bifurcation lesions, type C lesions, and a trend for smaller-diameter stents. Discontinuation of clopidogrel was higher in these patients (36.8% versus 10.7%). Multivariate analysis detected cessation of clopidogrel therapy, renal failure, bifurcation lesions, and in-stent restenosis as significant correlates of stent thrombosis. The follow up period in this study was 12 months.
The current best practice to reduce the incidence of stent thrombosis in patients treated with DES (sirolimus and paclitaxel) is to give dual antiplatelet therapy with aspirin and clopidogrel for at least 12 months. Thereafter, patient should be on aspirin lifelong. Aspirin should never be stopped even if the patient is undergoing surgery. As one cardiologist put it: "In the current era, there is no surgery which cannot be done without stopping aspirin". One should still recognize that there may still be instances where aspirin need to be withheld as in intracranial surgery or bleeding. In such situations, time off antiplatelets should be minimized.
Newer drug eluting stents which have a biopolymer coating are claimed not to interfere with endothelial healing. One might hope that they will reduce the risks of late stent thrombosis, while still maintaining low restenosis rates.
The introduction of drug eluting stents (DES) in the late 1990's was a major landmark in coronary interventions. They could reduce restenosis due to the effects of the drug, the Achilles heel of coronary stents, thus reducing the need for repeat intervention. However, a new problem has surfaced with their use - an increased rate of late stent thrombosis. Stent thrombosis refers to the development of clots within the stent blocking blood flow suddenly and this almost invariably results in a heart attack.
All stents are to some degree thrombogenic, ie, they promote clotting. This tendency is overcome by antiplatelet therapy to reduce clotting at least till the stented part heals by endothelialization. Drug eluting stents appear to be more thrombogenic than bare stents. Stent thrombosis is often a catastrophic event leading to acute myocardial infarction or even death. Delayed reendothelialization of the stented segment due to the effects of the drug has been thought as the mechanism for stent thrombosis. Particularly disturbing are the reports of late stent thrombosis more than a year after stent implantation. Such events are generally associated with stoppage of antiplatelet therapy.
A recently reported study by Kuchulakanti et al in Circulation is one of the first to evaluate the correlates of stent thrombosis. They found that stent thrombosis was significantly higher in patients with diabetes, acute postprocedural renal failure, and chronic renal failure. There were more bifurcation lesions, type C lesions, and a trend for smaller-diameter stents. Discontinuation of clopidogrel was higher in these patients (36.8% versus 10.7%). Multivariate analysis detected cessation of clopidogrel therapy, renal failure, bifurcation lesions, and in-stent restenosis as significant correlates of stent thrombosis. The follow up period in this study was 12 months.
The current best practice to reduce the incidence of stent thrombosis in patients treated with DES (sirolimus and paclitaxel) is to give dual antiplatelet therapy with aspirin and clopidogrel for at least 12 months. Thereafter, patient should be on aspirin lifelong. Aspirin should never be stopped even if the patient is undergoing surgery. As one cardiologist put it: "In the current era, there is no surgery which cannot be done without stopping aspirin". One should still recognize that there may still be instances where aspirin need to be withheld as in intracranial surgery or bleeding. In such situations, time off antiplatelets should be minimized.
Newer drug eluting stents which have a biopolymer coating are claimed not to interfere with endothelial healing. One might hope that they will reduce the risks of late stent thrombosis, while still maintaining low restenosis rates.
posted by drheart at
9:06 AM
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