Carotid angioplasty and stenting versus carotid endarterectomy: randomized trial in a community hospital.

OBJECTIVES: The goal of this study was to determine whether carotid angioplasty and stenting (CAS) is equivalent to carotid endarterectomy (CEA) in patients with symptomatic carotid stenosis >70% by a randomized, controlled trial in a community hospital. BACKGROUND: Carotid angioplasty and stenting has been suggested to be as effective as CEA for treatment of symptomatic carotid artery stenosis. METHODS: A total of 104 patients presenting with cerebrovascular ischemia ipsilateral to carotid stenosis were selected randomly for CEA or carotid stenting and followed for two years. RESULTS: Stenosis decreased to an average of 5% after CAS. The patency of the reconstructed artery remained satisfactory regardless of the technique as determined by sequential ultrasound. One death occurred in the CEA group (1/51); one transient ischemic attack occurred in the CAS group (1/53); no individual sustained a stroke. The perception of procedurally related pain/discomfort was similar. Hospital stay was similar, although the CAS group tended to be discharged earlier (mean = 1.8 days vs. 2.7 days). Complications associated with CAS prolonged hospitalization when compared with those sustaining a CEA-related complication (mean = 5.6 days vs. 3.8 days). Return to full activity was achieved within one week by 80% of the CAS group and 67% of the patients receiving CEA. Hospital charges were slightly higher for CAS. CONCLUSIONS: Carotid stenting is equivalent to CEA in reducing carotid stenosis without increased risk for major complications of death/stroke. Because of shortened hospitalization and convalescence, CAS challenges CEA as the preferred treatment of symptomatic carotid stenosis if a reduction in costs can be achieved.

Inhibition of neutrophil and monocyte defensive functions by nicotine.

To learn more about the effects of smokeless tobacco on the defensive functions of neutrophils, we studied the influence of nicotine on these cells in vitro, looking at their bactericidal activity against oral pathogens, and at their ability to produce microbicidal reactive oxygen species (oxygen radicals). Exposure of human blood neutrophils to nicotine (0.01% to 0.1%) inhibited their ability to kill Actinomyces naeslundii, Actinobacillus actinomycetemcomitans, and Fusobacterium nucleatum. Although these concentrations of nicotine are high, such concentrations are relevant to phagocytes in the gingival sulcus, because smokeless tobacco contains 0.5% to 3.5% nicotine by dry weight. Nicotine had no such inhibitory effect when the killing assay was performed in an anaerobic environment, implying that nicotine preferentially affected oxygen-dependent killing mechanisms. To further investigate the effects of nicotine on production of oxygen radicals, neutrophils were primed with lipopolysaccharide and triggered with f-met-leu-phe or phorbol ester in the presence of nicotine. Nicotine inhibited production of superoxide anion (measured by reduction of cytochrome c) and hydrogen peroxide (measured by oxidation of phenol red). Nicotine inhibition of superoxide production was reversible by washing away the nicotine. By observing that nicotine inhibited the reduction of cytochrome c by reagent potassium superoxide, we determined that nicotine directly absorbed superoxide. In addition, by examining nicotine inhibition of the uptake of oxygen by neutrophils, we determined that nicotine also interfered with the production of oxygen radicals by these cells. Nicotine also inhibited production of superoxide and interleukin-1 beta by monocytes. Nicotine did not affect the viability of neutrophils and monocytes, as determined by their ability to exclude trypan blue dye. Inhibition of the aerobic antimicrobial functions of neutrophils and monocytes by nicotine may alter the microbial ecology of the oral cavity, and this might be one mechanism by which nicotine compromises the oral health of users of tobacco products.