Stefan Agewall

Atorvastatin normalizes endothelial function in healthy smokers

Endothelial function is known to predict cardiovascular disease. The aim of the present study was to examine whether endothelial function in smokers with normal cholesterol levels could be normalized by treatment with 80 mg of atorvastatin in comparison with a control group. Healthy smokers (n=20) and non-smokers (n=20) were randomized to receive 80 mg of atorvastatin or placebo in an open randomized cross-over study, followed by measurement of endothelial functional [FMD (flow-mediated dilation)]. At baseline, smokers had a lower FMD compared with the non-smoking group (2.2+/-0.5 and 4.5+/-0.8% respectively; P<0.05). In the smoking group, FMD increased significantly (P<0.05) to 4.0+/-0.8% during treatment with atorvastatin and returned to basal levels during placebo (2.3+/-0.6%). In the non-smoking group, FMD was unaffected by both atorvastatin and placebo. The net change of total cholesterol or LDL (low-density lipoprotein)-cholesterol was not associated with the net change in FMD when the study group was considered as a whole or the smoking group was considered separately. In conclusion, improved endothelial function was observed in a group of smokers when they were received 80 mg of atorvastatin, whereas atorvastatin had no effect on endothelial function in the non-smoking group. The improved FMD among smokers was independent of the decrease in LDL-cholesterol during atorvastatin treatment. The results show that poor endothelial function in smokers with normal lipid levels can be improved by a statin treatment.

Glucose intolerance is associated with C-reactive protein and intima-media anatomy of the common carotid artery in patients with coronary heart disease

Aimsu2003 The purpose of this study was to examine the relationship between glucose intolerance and levels of hsCRP, calculated intima‐media area (cIMa) of the carotid artery and flow‐mediated dilation of the brachial artery in 122 patients with a myocardial infarction 1–12 months before inclusion and without known diabetes mellitus.

Snus is not harmless

Recently, Rodu and Cole [1] suggested that the low smoking-related mortality among Swedish men probably is due to their use of snus [Swedish smokeless tobacco]. The authors claim that snus produces a very low risk for cardiovascular disease. However, they do not mention the study of Bolinder et al. [2], which showed a 40% increased risk for cardiovascular death among snus users. This study is the largest study in this area. It was a prospective cohort study of 135,036 industry employees, who were followed for cause-specific mortality during a 12-year period. In this study, the risk was even more pronounced among men aged 35 to 54 years old. The risk for cardiovascular death increased by 110% for snus users compared to nontobacco users. A more than doubled risk is certainly not a very low risk. There are a few small case-control studies that have failed to show a significant cardiovascular risk among snus users [3]. Snus dipping is addictive. The nicotine levels increase soon after placing snus in the mouth and this causes a blood pressure elevation and an increased heart rate. There are reports suggesting that snus causes leukoplakia and irreversible gingival recessions [4]. Recently, it was reported that snus has an acute negative effect on endothelial function [5]. I agree that most data indicate that cigarette smoking is associated with a higher cardiovascular risk than snus is. However, snus dipping is not a harmless substitute for cigarette smoking. Snus dipping is addictive, has acute effects on blood pressure, heart rate and endothelial function. The largest study showed a 110% increased risk for cardiovascular death in male snus users, aged 35 to 54 years old. It is important to see both sides of the coin, especially if the United States Smokeless Tobacco Company sponsors a study and the authors serve as consultants to the sponsor.