stent thrombosis


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stent thrombosis

A blood clot that forms inside a device inserted into a blood vessel to keep that vessel open.

Patient Care

Stents are deployed in completely obstructed or partially blocked arteries to keep blood flowing through them to the organs they supply. When this blood flow stops due to clotting within the stent, the organ may become ischemic and die. To reduce the risk of clotting within a stent, patients use antiplatelet drugs, like aspirin, dipyridamole, or clopidogrel, and medications to lower serum lipid levels. Tobacco cessation, and healthy lifestyle changes (eating lighter, exercising regularly) may also be helpful.

See also: thrombosis
References in periodicals archive ?
Pathological correlates of late drug-eluting stent thrombosis: strut coverage as a marker of endothelialization.
The objective of the current study was to determine short term outcomes of LMCA stenting by using drug eluting stents in terms of major in hospital complicatins like death, fatal or non fatal myocardial infaction, acute or sub acute stent thrombosis, urgent CABG angiographic evidence of restosis and target vessel revascularization in carefully selected patients with normal left ventricular (LV) systolic function as an alternative treatment to CABG.
Taking two antiplatelet drugs after stenting is standard procedure to prevent stent thrombosis. It is effective in 98.5 percent of patients, which is why these drugs are universally prescribed.
The patient was transferred to the cardiac catheterization laboratory, where coronary angiography revealed stent thrombosis in the proximal LAD, causing 100% occlusion (Figure 2a).
This led to inadequate platelet inhibition resulting in two-vessel stent thrombosis. In patients with heterozygous [CYP2C19.sup.*]2 alleles, higher doses of clopidogrel have been shown to overcome the genetic resistance and improve the platelet inhibition [10].
All four studies reported stent thrombosis, myocardial infarction/acute coronary syndrome, all-cause mortality, and major bleeding event.
At 6 months of follow-up, the study endpoint (death from cardiovascular causes, nonfatal myocardial infarction, or stent thrombosis) was 2.3% in both groups.
At one year, researchers found that high platelet reactivity was significantly associated with stent thrombosis (1.3 percent vs.
Secondary clinical endpoints include stent thrombosis and major adverse cardiac events (MACE) at 30, 60, 180, 360 and 540 days.
EC dysfunction denotes the beginning of atherosclerotic processes, and extensive damage of EC lining is supposed to trigger stent thrombosis (3).