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- Lunell, Erik, et al.
(författare)
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Steady-state nicotine plasma levels following use of four different types of Swedish snus compared with 2-mg Nicorette chewing gum: A crossover study
- 2005
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Ingår i: Nicotine & Tobacco Research. - : Oxford University Press (OUP). - 1469-994X .- 1462-2203. ; 7:3, s. 397-403
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Tidskriftsartikel (refereegranskat)abstract
- The present study evaluated nicotine plasma levels achieved following 1 day's regular use of four commonly used brands of Swedish portion snus and 2-mg Nicorette chewing gum. The study also estimated the amount of sodium chloride extracted from each snus sachet to identify potential risks for exacerbation of heart failure and hypertension with the use of Swedish snus. Extracted dose of nicotine, area under the venous plasma concentration-time curve (AUC), maximum plasma nicotine concentration (C-max) of the last (12th) dosing interval, and the Cm,, and AUC ratios versus Nicorette were calculated. Relative brioavailable dose was calculated using AUC of 2-mg Nicorette gum as the reference. The mean extracted nicotine doses were 2.74 +/- 0.80, 1.55 +/- 0.68, 2.00 +/- 0.56, and 1.08 +/- 0.94 mg/sachet for General, Catch Licorice, Catch Mini, and Catch Dry Mini snus, respectively. The approximate bioavailable dose of nicotine from snus was 40%-60% of the extracted dose. The steady-state nicotine plasma concentration-time curve for the weakest brand, Catch Dry Mini portion snus, did not differ significantly from that of the 2-mg Nicorette gum. The AUC and C-max for Catch Licorice I g and Catch Mini 0.5 g portion snus were twice those for the 2-mg Nicorette gum; for the strongest brand, General, these values were 21/2 times those for Nicorette gum. The differences in AUC and C-max versus the 2-mg Nicorette gum were statistically significant (p=.020). Nicotine plasma levels with General portion snus were sustained at higher levels than current nicotine replacement therapy products, peaking at 29.0 +/- 8.5 ng/ml, and more closely mimicking cigarette smokers' nicotine plasma levels. The risks of aggravation of heart failure and hypertension with respect to increased salt load from the use of snus appeared to be negligible.
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- Mariscalco, Giovanni, et al.
(författare)
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Are current smokers paradoxically protected against atrial fibrillation after cardiac surgery?
- 2009
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Ingår i: Nicotine & tobacco research. - : Oxford University Press (OUP). - 1462-2203 .- 1469-994X. ; 11:1, s. 58-63
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The hyperadrenergic condition following surgical stress and inotropic drugs have been identified as leading causes for postoperative atrial fibrillation (AF). Smokers are characterized by higher catecholamine levels and tolerance. We tested the hypothesis that smoking patients are less prone to develop postoperative AF. METHODS: A total of 3,245 coronary artery bypass and valvular procedures were reviewed. Predictors of AF and interaction between variables were explored by multivariable logistic regression. AF-predictive scores were created and validated for goodness of fit, and receiver operating characteristic curves were created. RESULTS: Postoperative AF occurred in 26% of patients. Smokers accounted for 15% of the study population and demonstrated a reduced incidence of postoperative AF compared with nonsmoking individuals (20% vs. 27%, p < .001). Multivariate analysis revealed a significant interaction between smoking status and inotropic support requirement. The AF-protective effect of smoking was confounded by inotropic drugs. However, when we excluded from analysis the patients with inotropic support, smoking conferred a 46% risk reduction of AF (odds ratio [OR] = 0.54, 95% CI = 0.34-0.87, p = .011). In addition, age, valvular surgery, and hypertension were independently associated with AF. Postoperative AF increased the length of hospitalization, without affecting hospital mortality. AF was associated with an increased 1-year mortality (p = .002). DISCUSSION: Current smokers are less prone to develop AF after cardiac surgery. Our data support the hypothesis that hyperadrenergic state and catecholamines are key mechanisms in the pathophysiology of postoperative AF.
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