Despite major improvements in antiplatelet therapy, thrombotic events remain the primary cause of death after percutaneous coronary interventions.^1,2 Sirolimus-eluting stents and polymer-based paclitaxel-eluting stents have been shown to reduce neointimal hyperplasia and risk of restenosis without increasing the risk of stent thrombosis.^3-7 Operators are now using drug-eluting stents for a wide variety of clinical and anatomic situations, many of which have not been evaluated in randomized studies.^8-10 We analyzed the incidence, predictors, and clinical outcome of stent thrombosis at 9-month follow-up in an observational cohort study.

Background —Despite the increasing use of stents, few reports have described human coronary artery morphology early and late after stenting. Methods and Results —Histology was performed on 55 stents in 35 coronary vessels (32 native arteries and 3 vein grafts) from 32 patients. The mean duration of stent placement was 39±82 days. Fibrin, platelets, and neutrophils were associated with stent struts ≤11 days after deployment. In stents implanted for ≤3 days, only 3% of struts in contact with fibrous plaque had >20 associated inflammatory cells compared with 44% of struts embedded in a lipid core and 36% of struts in contact with damaged media ( P <0.001). Neointimal growth determined late histological success, and increased neointimal growth correlated with increased stent size relative to the proximal reference lumen area. Neointimal thickness was greater for struts associated with medial damage than struts in contact with plaque ( P <0.0001) or intact media ( P <0.0001). When matched for time since treatment, neointimal cell density in stented arteries was similar to that in unstented arteries that had undergone balloon angioplasty and showed similar proteoglycan deposition. Conclusions —Morphology after coronary stenting demonstrates early thrombus formation and acute inflammation followed by neointimal growth. Medial injury and lipid core penetration by struts result in increased inflammation. Neointima increases as the ratio of stent area to reference lumen area increases. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis.

Aims The role of aspirin in patients with coronary artery disease (CAD) is well established, yet patients happen to discontinue aspirin according to physician’s advice or unsupervised. We thus undertook a systematic review to appraise the hazards inherent to aspirin withdrawal or non-compliance in subjects at risk for or with CAD.

Patients with substantial carotid artery narrowing are at increased risk for major stroke,^1-6 but the pathogenic mechanisms linking carotid atherosclerosis and ischemic brain injury still need to be fully clarified.Clinical trials designed to evaluate the beneficial effects of endarterectomy in symptomatic and asymptomatic patients have focused on carotid stenosis severity and plaque ulceration as risk factors for cerebrovascular events. The results of the European Carotid Surgery Trial^2,3 and the North American Symptomatic Carotid Endarterectomy Trial(NASCET)^4,5 suggest that surgery is indicated for stroke prevention when stenosis is more than 70%. TheNASCET study showed that among symptomatic patients with high-grade carotid stenosis (>70%) not treated by surgery, the 2-year rate of any ipsilateral stroke was 26.0% for major stroke and 13.1% for fatal stroke.⁵ The Asymptomatic Carotid Atherosclerosis Study⁷ suggested that indications for carotid endarterectomy could be broadened to include asymptomatic patients with carotid stenosis of more than 60% and that the aggregate risk over 5 years for ipsilateral stroke and any perioperative stroke was estimated at 11.0% for asymptomatic patients treated medically.