Events In Smokers Research Articles

The Risk of Adverse Events in Smokers Undergoing Spinal Fusion: A Systematic Review and Meta-Analysis.

Systematic review and meta-analysis. Determine if tobacco use is associated with increased risk of postoperative adverse events within 90days in patients undergoing spinal fusion surgery. Databases were queried to identify cohort studies that directly compared smokers with non-smokers and provided the absolute number of adverse events and the population at risk. Data quality was evaluated using the Quality in Prognosis Studies tool. Risk ratios (RR) and 95% confidence intervals were calculated and compared between studies. The grading of recommendation, assessment, development and evaluation (GRADE) criteria were used to assess the strength of the evidence. Seventeen studies assessing 37897 participants met the inclusion criteria. Of these, 10031 (26.5%) were smokers and 27866 (73.5%) were nonsmokers. The mean age for the study population was 58years, and 45% were males. Smoking was not associated with increased risk of one or more major adverse events within 90days following spine surgery (seven studies, pooled RR 1.13, 95% CI [.75-1.71], I2 = 41%). However, smoking was significantly associated with one or more major adverse events in ≤2 level fusion (three studies, pooled RR 2.46, 95% CI [1.18-5.12], I2 = 0%), but not in fusions of ≥3 levels (four studies, pooled RR .87, 95% CI [.70-1.08], I2 = 0%). Additionally, there was no statistically significant association between smoking and any adverse event, nor increased reoperation risk due to adverse events. In this meta-analysis, tobacco use was not associated with a statistically significant increased risk of adverse events within 90days in patients undergoing spinal fusion surgery. Our results are limited by the variable reporting methodology for both complication rates as well as smoking incidence between the included individual studies.

Heated tobacco products for smoking cessation and reducing smoking prevalence.

Heated tobacco products for smoking cessation and reducing smoking prevalence.

Low testosterone is associated with increased risk of major adverse cardiovascular events in smokers with erectile dysfunction

Abstract Purpose Tobacco cigarette smoking and decreased concentrations of testosterone are major risk factors of erectile dysfunction (ED) and independent predictors of cardiovascular disease (CVD). We investigated, whether testosterone deficiency has a complementary predictive value for CVD events in smokers with ED. Methods A cohort of 398 men with ED and without known atherosclerotic CVD (mean age: 55±10 years) were followed for the occurrence of major adverse cardiovascular events (MACE), (CVD death, coronary artery disease, stroke). Total testosterone (TT) levels were measured in all patients. Results Among the study population, 205 (52%) were smokers. During a mean follow-up of 6 years (range: 1–11 years), 30 (7.5%) patients demonstrated a MACE. Baseline TT levels were significantly lower and prevalence of smoking was higher in the CV-event group than the event-free survival group (P<0.01 and P<0.05, respectively). Kaplan–Meier analysis showed that patients with low TT (≤4.0 ng/mL) had a worse prognosis than patients with TT >4.0 ng/mL (log rank: 6.52, P=0.011), and that smokers had a greater risk of adverse events than never smokers (log rank: 4.42, P=0.04). We then stratified all patients into four groups, on the basis of smoking status (current/never smokers) and low or high TT (≤ or >4.0 ng/mL) and cardiac event-free survival curves were constructed by Kaplan–Meier analysis (figure). The event-free rate in smokers with low TT is significantly lower than that of smokers with low TT or never smokers with normal TT (log rank: 11.3, P=0.02). Smokers with low TT had an almost 4-fold higher risk of MACEs compared to never smokers with normal TT (adjusted hazard ratio: 3.91; P=0.030). Conclusion Cigarette smoking combined with low TT concentration is associated with a shorter event-free period compared with either smoking or testosterone deficiency alone. The measurement of testosterone concentration may be useful to further stratify the risk of ED smokers without known CVD. Funding Acknowledgement Type of funding sources: None. Smoking testosterone deficiency and MACE

Cardiovascular risk of smoking and benefits of smoking cessation.

Smoking increases mortality from all causes and has a crucial role in atherosclerotic cardiovascular disease (ASCVD). Active smoking and secondhand smoke exposure determine more than 30% of coronary heart disease (CHD) mortality. The exact mechanisms of cardiovascular damages are not well known, but the detrimental effect of smoking on endothelial function has long been recognized. Smoking elicits oxidative processes, negatively affects platelet function, fibrinolysis, inflammation and vasomotor function; all these proatherogenic effects double the 10-year risk of fatal events in smokers compared to non smokers. An intriguing issue about smoking is the vulnerability of female gender. The mortality from cardiovascular diseases (CVDs) is higher in female than male smokers and female smokers show a 25% higher risk of developing CHD than men with the same exposure to tobacco smoke. This female vulnerability seems to be related to genes involved in thrombin signaling. The effects of smoking cessation have also been extensively studied. Cessation at an early age (40 years) has an impressive 90% reduction in the excess risk of death. In this review we report recent data about the causal link between smoking and CVDs and about the benefits of smoking cessation.

Influence of smoking on CYP2C19 genetic variants and clopidogrel efficacy in patients with minor stroke or transient ischaemic attack.

Studies suggest that smoking affects clopidogrel efficacy. However, whether it influences the association between CYP2C19 genetic variants and clopidogrel efficacy is not clear. In total, 2961 patients from the CHANCE trial were involved in this substudy and were successfully genotyped for two single-nucleotide polymorphisms of CYP2C19 (*2 and *3). The Cox proportional risk regression model was used to evaluate the interactions between CYP2C19*2 and CYP2C19*3 carrier status and clopidogrel efficacy stratified by smoking status. There were marginal significant interactions between CYP2C19*2 and CYP2C19*3 allele carrier status and antiplatelet treatment regimen for the risk of recurrent stroke and composite events (P=0.054, P=0.051, respectively) amongst smokers, but not in non-smokers. Amongst smokers, clopidogrel plus aspirin decreased the recurrence rate of stroke compared with aspirin alone in non-carriers (3.8% vs. 11.8%, hazard ratio 0.32, 95% confidence interval 0.15-0.65, P=0.002), but not in carriers. Similar results were also found for the recurrence rate of composite events in smokers. No significant difference was found for hemorrhage events in any group. Amongst patients with minor stroke or transient ischaemic attack, marginal significant interactions between CYP2C19*2 and CYP2C19*3 allele carrier status and clopidogrel efficacy were found in smokers but not in non-smokers. Amongst smokers, clopidogrel plus aspirin might decrease the recurrence rate of stroke in non-carriers of *2 and *3 alleles of CYP2C19 compared with aspirin alone. However, caution should be taken to interpret our findings in view of several limitations in our study.

Abstract WP517: Influence of Smoking on CYP2C19 Genetic Variants and Clopidogrel Efficacy in Patients with Minor Stroke or TIA

Background and Purpose: Whether smoking has an effect on the association between CYP2C19 genetic variants and clopidogrel efficacy is not clear. This study was aimed to estimate the influence of smoking on the association between CYP2C19 genetic variants and clopidogrel efficacy among patients with minor stroke and TIA. Methods: In total of 2961 patients from the CHANCE trial were involved in this substudy and successfully genotyped for both two single-nucleotide polymorphisms of CYP2C19 (*2 and *3). Current smokers were defined as those who smoked at least five cigarettes per day in the last month. The primary clinical efficacy outcome of this study was a new stroke. Cox proportional risk regression model was used to evaluate the interactions between CYP2C19 loss-of-function allele (*2 and *3) carrier status and clopidogrel efficacy stratified by smoking status. Results: There were marginal significant interactions between CYP2C19 loss-of-function carrier status and antiplatelet treatment regimen for the risk of recurrent stroke and composite events (p = 0.054, p = 0.051, respectively) among smokers, but not in non-smokers. Among smokers, clopidogrel plus aspirin decreased the recurrence rate of stroke compared with aspirin alone in noncarriers (3.8% vs 11.8%, hazard ratio [HR], 0.32; 95% confidence interval [CI], 0.15-0.65, p = 0.002), but not in carriers (8.1% vs 10.8%, HR, 0.73; 95% CI, 0.46-1.17, p = 0.19). Similar results were also found for the recurrence rate of composite events in smokers. No significant difference was found for hemorrhage events in all groups. Conclusions: Among patients with minor stroke or TIA, marginal significant interactions were found between CYP2C19 loss-of-function carrier status and clopidogrel efficacy in smokers, but not in non-smokers. It seemed that among smokers, clopidogrel plus aspirin might decrease the recurrence rate of stroke in noncarriers of CYP2C19 loss-of-function allele compared with aspirin alone.

Coronary Artery Calcium Scores and Atherosclerotic Cardiovascular Disease Risk Stratification in Smokers

ObjectivesThis study assessed the utility of the pooled cohort equation (PCE) and/or coronary artery calcium (CAC) for atherosclerotic cardiovascular disease (ASCVD) risk assessment in smokers, especially those who were lung cancer screening eligible (LCSE). BackgroundThe U.S. Preventive Services Task Force recommended and the Centers for Medicare & Medicaid Services currently pays for annual screening for lung cancer with low-dose computed tomography scans in a specified group of cigarette smokers. CAC can be obtained from these low-dose scans. The incremental utility of CAC for ASCVD risk stratification remains unclear in this high-risk group. MethodsOf 6,814 MESA (Multi-Ethnic Study of Atherosclerosis) participants, 3,356 (49.2% of total cohort) were smokers (2,476 former and 880 current), and 14.3% were LCSE. Kaplan-Meier, Cox proportional hazards, area under the curve, and net reclassification improvement (NRI) analyses were used to assess the association between PCE and/or CAC and incident ASCVD. Incident ASCVD was defined as coronary death, nonfatal myocardial infarction, or fatal or nonfatal stroke. ResultsSmokers had a mean age of 62.1 years, 43.5% were female, and all had a mean of 23.0 pack-years of smoking. The LCSE sample had a mean age of 65.3 years, 39.1% were female, and all had a mean of 56.7 pack-years of smoking. After a mean of 11.1 years of follow-up 13.4% of all smokers and 20.8% of LCSE smokers had ASCVD events; 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during the follow-up. One SD increase in the PCE 10-year risk was associated with a 68% increase risk for ASCVD events in all smokers (hazard ratio: 1.68; 95% confidence interval: 1.57 to 1.80) and a 22% increase in risk for ASCVD events in the LCSE smokers (hazard ratio: 1.22; 95% confidence interval: 1.00 to 1.47). CAC was associated with increased ASCVD risk in all smokers and in LCSE smokers in all the Cox models. The C-statistic of the PCE for ASCVD was higher in all smokers compared with LCSE smokers (0.693 vs. 0.545). CAC significantly improved the C-statistics of the PCE in all smokers but not in LCSE smokers. The event and nonevent net reclassification improvements for all smokers and LCSE smokers were 0.018 and −0.126 versus 0.16 and −0.196, respectively. ConclusionsIn this well-characterized, multiethnic U.S. cohort, CAC was predictive of ASCVD in all smokers and in LCSE smokers but modestly improved discrimination over and beyond the PCE. However, 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during follow-up.

Cardiovascular and neuropsychiatric risks of varenicline and bupropion in smokers with chronic obstructive pulmonary disease

BackgroundVarenicline and bupropion are effective smoking cessation treatments, but there are concerns about their safety in smokers with COPD.ObjectiveTo investigate whether varenicline and bupropion are associated with serious adverse cardiovascular...

Cannabinoids and haemostasis.

Elements of the endocannabinoid system (cannabinoid receptors CB1, CB2, CBPT and CBED, endocannabinoids, enzymes involved in the synthesis and metabolism of endocannabinoids) are located on the structures involved in the process of hemostasis. An increasing level of endocannabinoids was also observed in some pathological conditions, which may occur in disorders of hemostasis. At the same time, disconcertingly, there is an increased number of reports about incidents of cardiovascular events in smokers of marijuana. Experimental and clinical studies demonstrated multidirectional, often contradictory, effects of cannabinoids on hemostasis, including effects of the compounds on platelets, vascular endothelium, fibrinolysis and plasma coagulation systems. The mechanisms of action of cannabinoids on homeostasis depend on the cannabinoid receptors CB1, CB2, CBPT and CBED, receptors of other systems stimulated by endocannabinoids, as well as metabolites of endocannabinoids and nitrogen oxide. The range of biological functions of endo- and plant cannabinoids, expanded to include the process of hemostasis, may constitute a condition for their recognition as a new factor responsible for thromboembolism in smokers of marijuana, in pathological disorders with increased levels of endocannabinoids and in individuals with polymorphisms of FAAH C385A and A385A. On the other hand, there are compelling reasons for anti‑hemostatic action of cannabinoids.

Associations Between Cardiovascular Risk Factors, Inflammation, and Progression of Carotid Atherosclerosis Among Smokers.

The high risk of cardiovascular events in smokers requires adequate control of other cardiovascular risk factors (CVRFs) to curtail atherosclerosis progression. However, it is unclear which CVRFs have the most influence on atherosclerosis progression in smokers. In 260 smokers aged 40-70 included in a smoking cessation trial, we analyzed the association between traditional CVRFs, high-sensitivity C-reactive protein (hs-CRP), smoking cessation and 3-year progression of carotid intima-media thickness (CIMT, assessed by repeated ultrasound measurements) in a longitudinal multivariate model. Participants (mean age 52 years, 47% women) had a mean smoking duration of 32 years with a median daily consumption of 20 cigarettes. Baseline CIMT was 1185 μm (95% confidence interval [CI]: 1082-1287) and increased by 93 μm (95% CI: 25-161) and 108 μm (95% CI: 33-183) after 1 and 3 years, respectively. Age, male sex, daily cigarette consumption, systolic blood pressure (SBP), but neither low-density lipoprotein cholesterol nor hs-CRP, were independently associated with baseline CIMT (all P ≤ .05). Baseline SBP, but neither low-density lipoprotein cholesterol nor hs-CRP, was associated with 3-year atherosclerosis progression (P = .01 at 3 years). The higher the SBP at baseline, the steeper was the CIMT increase over 3-year follow-up. We found an increase of 26 μm per each 10-mmHg raise in SBP at 1 year and an increase of 39 μm per each 10 mmHg raise in SBP at 3 years. Due to insufficient statistical power, we could not exclude an effect of smoking abstinence on CIMT progression. Control of blood pressure may be an important factor to limit atherosclerosis progression in smokers, besides support for smoking cessation. Among 260 smokers aged 40-70 years with a mean smoking duration of 32 years, baseline SBP was associated with atherosclerosis progression over 3 years, as measured by CIMT (P = .01 at 3 years), independently of smoking variables and other CVRFs. The higher the SBP at baseline, the steeper was the CIMT increase over 3-year follow-up. Our findings emphasize the importance of focusing not only on smoking cessation among smokers, but to simultaneously control other CVRFs, particularly blood pressure, in order to prevent future cardiovascular disease.

Treatment of hypertension in patients with coronary artery disease: a scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension.

1. Relationship Between Hypertension and CAD e437 2. Prevention of Cardiovascular Events in Patients With Hypertension and CAD e443 3. BP Goals e445 4. Management of Hypertension in Patients With CAD and Stable Angina e449 5. Management of Hypertension in Patients With ACS e451

Functional Interactions of Varenicline and Nicotine With nAChR Subtypes Implicated in Cardiovascular Control

It has been suggested that varenicline-induced activation of nicotinic acetylcholine receptors (nAChRs) could play a role in the cardiovascular (CV) safety of varenicline. However, since preclinical studies showed that therapeutic varenicline concentrations have no effect in models of CV function, this study examined in vitro profiles of varenicline and nicotine at nAChR subtypes possibly involved in CV control. Concentration-dependent functional effects of varenicline and nicotine at human α3β4, α3α5β4, α7, and α4β2 nAChRs expressed in oocytes were determined by electrophysiology. The proportion of nAChRs predicted to be activated and inhibited by concentrations of varenicline (1mg b.i.d.) and of nicotine in smokers was derived from activation-inhibition curves for each nAChR subtype. Human varenicline and nicotine concentrations can desensitize and inhibit nAChRs but cause only low-level activation of α3β4, α4β2 (<2%), α7 (<0.05%), and α3α5β4 (<0.01%) nAChRs, which is consistent with literature data. Nicotine concentrations in smokers are predicted to inhibit larger fractions of α3β4 (48%) and α3α5β4 (10%) nAChRs than therapeutic varenicline concentrations (11% and 0.6%, respectively) and to inhibit comparable fractions of α4β2 nAChRs (42%-56%) and α7 nAChRs (16%) as varenicline. Nicotine and varenicline concentrations in patients and smokers are predicted to cause minimal activation of ganglionic α3β4* nAChRs, while their functional profiles at α3β4, α3α5β4, α7, and α4β2 nAChRs cannot explain that substituting nicotine from tobacco with varenicline would cause CV adverse events in smokers who try to quit. Other pharmacological properties that could mediate varenicline-induced CV effects have not been identified.

Dysfunction of Endothelial Progenitor Cells from Smokers and Chronic Obstructive Pulmonary Disease Patients Due to Increased DNA Damage and Senescence

Cardiovascular disease (CVD) is a major cause of death in smokers, particularly in those with chronic obstructive pulmonary disease (COPD). Circulating endothelial progenitor cells (EPC) are required for endothelial homeostasis, and their dysfunction contributes to CVD. To investigate EPC dysfunction in smokers, we isolated and expanded blood outgrowth endothelial cells (BOEC) from peripheral blood samples from healthy nonsmokers, healthy smokers, and COPD patients. BOEC from smokers and COPD patients showed increased DNA double-strand breaks and senescence compared to nonsmokers. Senescence negatively correlated with the expression and activity of sirtuin-1 (SIRT1), a protein deacetylase that protects against DNA damage and cellular senescence. Inhibition of DNA damage response by silencing of ataxia telangiectasia mutated (ATM) kinase resulted in upregulation of SIRT1 expression and decreased senescence. Treatment of BOEC from COPD patients with the SIRT1 activator resveratrol or an ATM inhibitor (KU-55933) also rescued the senescent phenotype. Using an in vivo mouse model of angiogenesis, we demonstrated that senescent BOEC from COPD patients are dysfunctional, displaying impaired angiogenic ability and increased apoptosis compared to cells from healthy nonsmokers. Therefore, this study identifies epigenetic regulation of DNA damage and senescence as pathogenetic mechanisms linked to endothelial progenitors' dysfunction in smokers and COPD patients. These defects may contribute to vascular disease and cardiovascular events in smokers and could therefore constitute therapeutic targets for intervention.

T5 Circulating endothelial progenitor cells in smokers and patients with COPD are dysfunctional due to increased DNA damage and senescence

IntroductionCardiovascular disease (CVD) is a major cause of death in smokers, particularly in patients with chronic obstructive pulmonary disease (COPD). Circulating endothelial progenitor cells (EPC) are required for endothelial homeostasis,...

168 CIRCULATING ENDOTHELIAL PROGENITOR CELLS IN SMOKERS ARE DYSFUNCTIONAL DUE TO INCREASED DNA DAMAGE AND SENESCENCE

Introduction Cardiovascular disease (CVD) is a major cause of death in smokers, particularly in patients with chronic obstructive pulmonary disease (COPD). Circulating endothelial progenitor cells (EPC) are required for endothelial homeostasis, and their dysfunction contributes to CVD. DNA damage has also been recognized as an important contributor to CVD. Our aim was to investigate whether EPC from smokers and COPD patients are dysfunctional, and to investigate the role of DNA damage pathways in mediating endothelial dysfunction in these patients. Methods To investigate EPC dysfunction in smokers, we isolated and expanded blood outgrowth endothelial cells (BOEC) from peripheral blood samples of healthy non-smokers, healthy smokers and COPD patients. The mononuclear fraction was placed in culture in the presence of endothelial growth factors and BOEC colonies appeared between days 7 and 24. BOEC colonies were expanded and used at passages 4 to 6 for all experiments. Endothelial senescence was measured by senescence-associated β-galactosidase (SA-β-Gal) activity. Expression of sirtuin (SIRT)-1 and of markers of senescence and DNA damage were measured by Western blotting and/or immunofluorescence confocal microscopy. SIRT1 activity was measured using a SIRT1 fluorescent activity assay kit. To investigate in vivo function, BOEC were labelled with Vybrant DiI Cell-Labelling Solution, mixed with Matrigel and injected subcutaneously into the back of NOD.CB17-Prkdcscid/NcrCrl mice. Seven days later, the mice were sacrificed and the plugs were harvested and cryosectioned. Results In vitro, BOEC from smokers and COPD patients showed increased DNA double-strand breaks (measured by γ-H2AX, 53BP1) and senescence (senescence associated-β-galactosidase activity, p16 and p21 levels) compared to non-smokers. Senescence negatively correlated with sirtuin-1 (SIRT1) expression and activity, a protein deacetylase that inhibits DNA damage and cellular senescence. Inhibition of DNA damage response by silencing of ataxia telangiectasia-mutated (ATM) kinase resulted in up-regulation of SIRT1 expression and decreased senescence. Interestingly, treatment of BOEC from COPD patients with the SIRT1 activator resveratrol or a selective ATM inhibitor rescued the senescent phenotype. Using the in vivo Matrigel plug angiogenesis assay, BOEC from COPD patients displayed reduced ability to form capillary-like structures and increased DNA damage, senescence and apoptosis (measured by 53BP1, p16, TUNEL and cleaved-caspase 3 staining) compared to non-smokers. Conclusions BOEC from smokers and COPD patients show reduced angiogenesis in vivo and display increased DNA damage and senescence, associated with reduced SIRT1 expression. These defects may contribute to endothelial dysfunction and cardiovascular events in smokers and COPD patients and could potentially constitute therapeutic targets for intervention.

Short‐acting anticholinergic bronchodilation does not increase cardiovascular events in smokers with mild to moderate pulmonary obstruction

We hypothesized that bronchodilation in patients with chronic obstructive pulmonary disease (COPD) increases the smoke-related risk to develop cardiovascular disease, and aimed to study the effect of short-acting anticholinergic bronchodilation and smoking on cardiovascular events. We performed a secondary analysis on data from the Lung Health Study, a large randomized clinical trial of smokers with mild to moderate pulmonary obstruction, 35-60 years old, without cardiovascular comorbidity. We used Cox proportional survival analysis, controlling for several confounders, to study the effect on 5-year risk of fatal and/or non-fatal cardiovascular events. Secondary outcome encompassed fatal and non-fatal coronary events. Of 2745 participants, 23 (0.8%) died of cardiovascular disease. One hundred and sixty-two participants were hospitalized for a cardiovascular event, and 94 participants due to a coronary event. Survival analysis revealed no effect between smoking and short-acting anticholinergic bronchodilation on fatal and/or non-fatal cardiovascular events, hazard ratio = 1.12 (0.58-2.19), nor on coronary events, hazard ratio = 1.46 (0.60-3.56). Our study results show that short-acting anticholinergic bronchodilation had no detrimental effect on cardiovascular disease in smokers with mild to moderate pulmonary obstruction.

Smoking in Dialysis Patients: A Systematic Review and Meta-analysis of Mortality and Cardiovascular Morbidity

Cigarette smoking is associated with increased cardiovascular morbidity and mortality in the general population, but the effect of smoking on these outcomes in the dialysis population is less well studied. Systematic review and meta-analysis of cohort studies. Adults treated with long-term hemodialysis or peritoneal dialysis. SELECTION CRITERIA FOR INCLUDED STUDIES: Cohort studies of unselected dialysis patients reporting the association between smoking status and cardiovascular morbidity and/or mortality. Smoking status (determined using patient report). (1) All-cause or cardiovascular mortality; (2) incident cardiovascular events. We identified 34 studies that fulfilled all inclusion criteria. Of these, 26 studies provided data for smoking and mortality and 10 (n = 6,538) were included in a meta-analysis. The pooled HR for all-cause mortality in smokers compared with nonsmokers was 1.65 (95% CI, 1.26-2.14; P < 0.001). 11 studies provided data for smoking and incident cardiovascular events; 5 (pooled n = 845) were included in a meta-analysis. The pooled HR for composite cardiovascular events in smokers compared with nonsmokers was 1.01 (95% CI, 0.98-1.05; P = 0.4). Data for these meta-analyses were heterogeneous. Few individual studies assessed smoking as the primary variable of interest. Active smoking is associated with a significant increase in all-cause mortality in dialysis patients, although there was no corresponding increased risk of cardiovascular events.

Varenicline and the Evaluation of Neuropsychiatric Adverse Events in Smokers

Varenicline, a selective partial agonist of α4β2 subunits of nicotinic acetylcholine receptors, has been shown to be efficacious relative to placebo as summarized in a meta-analysis of clinical trials of smokers without significant psychiatric comorbidities (1). In these studies, neuropsychiatric adverse events (NPAEs) on varenicline were infrequent and comparable to placebo. In the postmarketing period, however, various NPAEs have been reported to occur in individuals taking varenicline.

High Blood Viscosity Is Closely Associated With Cigarette Smoking and Markedly Reduced by Smoking Cessation

Cigarette smoking is an independent risk factor for cardiovascular events such as myocardial infarction and stroke. To date, a useful and convenient method of predicting such events in smokers has not been established. The rheological properties of blood assessed by the microchannel method reflect the blood's viscosity and the state of microthrombus formation, which may predict cardiovascular thrombotic events. Blood fluidity was assessed in 74 smoking patients (54 men, 20 women, mean age 57.9 years) by measuring the blood passage time (BPT) in an aliquot (100 µl) of blood using the Micro Channel Array Flow Analyzer. BPT was significantly related with smoking variables such as daily consumption of tobacco (r = 0.236, P = 0.044), Brinkman's index (r = 0.252, P = 0.033), the Fagerstrom Test for Nicotine Dependence (r = 0.257, P = 0.029), and the score of a self-rating depression scale (r = 0.236, P < 0.05). Multivariate regression analysis revealed that an independent BPT determinant was daily consumption of tobacco (r = 0.326, P = 0.045). Furthermore, smoking cessation markedly decreased BPT from 63.0 s to 49.7 s (P = 0.002) at 3 months after the start of therapy. Unfavorable blood rheology is closely associated with cigarette smoking and may reflect increased cardiovascular risk in smokers. The study results also suggest that such risk can be reduced after only 3 months of smoking cessation.

The effects of cigarette smoking on script-driven imagery in smokers with and without posttraumatic stress disorder

The study investigated the effects of smoking a nicotinized or denicotinized cigarette on craving, affect and posttraumatic stress disorder (PTSD) symptoms while recalling neutral, stressful and traumatic events in smokers with and without PTSD. Smokers completed laboratory sessions during which they were presented with audiotapes of personalized scripts followed by smoking a cigarette. The effect of the script and cigarette conditions on dependent variables was evaluated. There was a main effect of script type across groups for smoking craving, negative affect and PTSD symptoms, with increased symptoms in trauma and stressful conditions. Responses were significantly higher in PTSD smokers. Smoking either cigarette type resulted in decreased craving, negative affect and PTSD symptoms in both groups. A second script presentation following smoking elicited similar responses, suggesting the ameliorative effect of having smoked a cigarette was short-lived. These results support that context and non-pharmacologic effects of smoking are important variables in smoking craving and mood, particularly in smokers with PTSD.