Summary. Background: Dextromethorphan (DM) is reported to reduce the inflammation-mediated degeneration of dopaminergic neurons. Objective: The goal of this study was to test if DM can improve the endothelial dysfunction and inflammatory markers in heavy smokers. Patients and methods: Forty habitual smoking healthy male volunteers (mean age, 31.5 ± 1.4 years) were randomly given either DM (120 mg day) or a placebo for 6 months. We determined endothelial function using the brachial artery diameter changes in flow-mediated dilatation (FMD) and measured their inflammatory and oxidative markers. A sex-and-age matched non-smoking group (n = 20) was compared as normal parameters. Results: Habitual smokers showed impaired baseline endothelial function in FMD (smoking vs. non-smoking: 6.3 ± 1.8 vs. 10.2 ± 2.3% respectively, P < 0.01). Without change in smoking behavior, lipid and metabolic parameters, a significant increase in FMD was found in the DM-treated group (32%), accompanied by a decrease in high-sensitivity C-reactive protein (hs-CRP), phospholipase A 2 , matrix metalloproteinase-3, interleukin 6 (IL-6) and tumor necrosis factor-a receptor II (TNF-a RII) (all P < 0.05), but unchanged in von Willebrand factor (VWF)and plasminogen activator inhibitor-1 (PAI-1). An increase in plasma glutathione peroxidase and a decrease in spot urinary excretion of 8-epi-prostaglandin F 2a were found in DM-treated smokers. Conclusions: Our study suggests that a 6-month treatment with DM can improve endothelial function and attenuate vascular oxidative stress and inflammation markers in habitual smokers.

No abstract

Stenting is a potential alternative treatment for carotid artery stenosis. Direct stenting may, theoretically, reduce the risk of embolism by minimizing plaque manipulation before tissue scaffolding is achieved. The results of direct carotid stenting are reported and compared with those of stenting with predilatation. One hundred and seventy-four carotid artery stenoses were treated from July 1998 to February 2002, with 84 lesions directly stented (Group 1) and the other 90 lesions stented after predilatation (Group 2). The criteria for direct stenting were minimal luminal diameter (MLD) > 1 mm and no visible thrombus angiographically. Technical success rates of the two groups were both 100%, without any cross-over. Reference vessel diameter and lesion length did not differ between the two groups. In Group 1, diameter stenosis was lower (79 ± 8 vs 92 ± 7%, P < 0.001) and MLD was larger (1.1 ± 0.5 vs 0.4 ± 0.4 mm, P < 0.001) than that in Group 2, but the final MLD (4.7 ± 0.9 vs 4.7 ± 0.9 mm, P = 0.94) of the two groups were not statistically different. The periprocedural ipsilateral stroke or death rates were also similar in the two groups (2/84 vs 4/90, P = 0.68). It was concluded that if the MLD of carotid stenosis is larger than 1 mm and no thrombus is present, direct stenting could be carried out safely with results comparable to that of stenting after predilatation.