Cardiovascular Disease In Smokers Research Articles

Effects of inhaled β‑caryophyllene on vascular stiffness in smokers: A randomized, double‑blind, placebo‑controlled trial.

Approximately 1.14 billion smokers worldwide are at risk of developing tumors, cardiovascular diseases and respiratory diseases. Smoking cessation is the first choice of health care; however, the disease should be attenuated in individuals who never stop smoking, which escalates medical costs. Therefore, alternative options are needed to manage the social burden. The present study proposed an alternative method to prevent such diseases by inhalation of β-caryophyllene (BCP). A placebo-targeted, dose-searching, double-blind, parallel-group comparative study was conducted on 19 subjects. The BCP intervention was performed using a flavor capsule inserted in a cigarette filter. The primary endpoint was the reducibility of brachial-ankle pulse wave velocity (baPWV). The secondary endpoints were confirmation of the bioavailability of BCP inhalation with cigarette smoke, confirmation of the effect of BCP inhalation on respiratory function, and association between respiratory function and blood concentration and baPWV reduction. The BCP concentration in the blood reached 4 ng/ml in the BCP 15% group 10 min after inhalation. The baPWV decreased in BCP-inhaling subjects whose initial baPWV was >1,300 cm/sec. The correlation analyses revealed that the higher the forced expiratory volume in 1 sec, the better the transition of baPWV. Inhaled BCP with cigarette smoke could reduce the baPWV and the risk of cardiovascular diseases in smokers. These findings indicated that with the introduction of BCP capsule-cigarettes in the future, smokers will be able to take care of their health, which may help reduce national medical costs. BCP microcapsules placed in cigarette wrapping paper may possibly reduce the risk of sidestream smoke and contribute to improved public health. This clinical research was retrospectively registered in the University Hospital Medical Information Network (UMIN)-Clinical Trials Registry with the following identifications: UMIN000048510 and UMIN000048512 on August 15, 2022.

Social isolation, social support and loneliness as predictors of cardiovascular disease incidence and mortality

BackgroundPoor social health is associated with increased risk of cardiovascular disease (CVD). Recent research suggests that different social health domains should be considered separately as the implications for health and possible interventions may differ.AimTo assess social isolation, low social support and loneliness as predictors of CVD.MethodsSecondary analysis of 11,486 community-dwelling, Australians, aged 70 years and over, free of CVD, dementia, or significant physical disability, from the ASPirin in Reducing Events in the Elderly (ASPREE) trial. Social isolation, social support (Revised Lubben Social Network Scale), and loneliness were assessed as predictors of CVD using Cox proportional-hazard regression. CVD events included fatal CVD, heart failure hospitalization, myocardial infarction and stroke. Analyses were adjusted for established CVD risk factors.ResultsIndividuals with poor social health were 42 % more likely to develop CVD (p = 0.01) and twice as likely to die from CVD (p = 0.02) over a median 4.5 years follow-up. Interaction effects indicated that poorer social health more strongly predicted CVD in smokers (HR 4.83, p = 0.001, p-interaction = 0.01), major city dwellers (HR 1.94, p < 0.001, p-interaction=0.03), and younger older adults (70-75 years; HR 2.12, p < 0.001, p-interaction = 0.01). Social isolation (HR 1.66, p = 0.04) and low social support (HR 2.05, p = 0.002), but not loneliness (HR 1.4, p = 0.1), predicted incident CVD. All measures of poor social health predicted ischemic stroke (HR 1.73 to 3.16).ConclusionsAmong healthy older adults, social isolation and low social support may be more important than loneliness as cardiovascular risk factors. Social health domains should be considered in future CVD risk prediction models.

Influences of smoking on central blood pressure in hypertensive subjects

Abstract Background/Introduction Smoking is known to induce systemic vascular damage, leading to cardiovascular diseases. Recent studies demonstrated that central blood pressure has a greater impact on cardiovascular events than brachial blood pressure. Purpose We investigated influences of habitual smoking on central systolic blood pressure (CSBP) in hypertensive subjects. Methods A total of 5630 subjects (male = 2622, 51.7±12.0 year-old at baseline), who visited our hospital for a physical check-up at least twice during the last 10 years and underwent CSBP measurement at each visit, were enrolled, and they were divided into three groups; normotensive (n=4634), non-treated hypertensive (n=91) and treated hypertensive subjects (n=905). Then, the influences of smoking on the average and yearly changes of CSBP (median follow-up 5 years) were analyzed. Brachial blood pressure (oscillometer) and radial artery pressure waveforms (tonometer) were recorded using an automated device, and the pressure corresponding to the second systolic peak of radial pressure waveforms was taken as CSBP (HEM-9000AI, Omron Healthcare, Kyoto). Hypertension was defined as brachial BP ≥140/90mmHg or the use of antihypertensive medications. A yearly change in CSBP was calculated in each subject by linear regression analysis using longitudinal data. Results The average CSBP was higher in habitual smokers than in non-smokers when analyzed in normotensive (109.1±11.7 vs. 107.6±12.8 mmHg, p&amp;lt;0.001) and non-treated hypertensive subjects (150.7±14.8 vs. 142.8±16.7 mmHg, p&amp;lt;0.05), whereas in hypertensive subjects under medication the average CSBP was lower in smokers than in non-smokers (124.6±12.4 vs. 127.8±13.6 mmHg, p&amp;lt;0.01). Smoking status did not affect yearly changes of CSBP in normotensive (habitual smokers vs. non-smokers; 1.38±6.00 vs. 1.44±6.04 mmHg/year), treated hypertensive (−0.16±7.08 vs. −0.66±8.24 mmHg/year), and non-treated hypertensive subjects (4.09±15.1 vs. −0.53±10.3 mmHg/year). Conclusions Habitual smoking increases CSBP, however, antihypertensive medications counteract the unfavorable effects of smoking on CSBP. These results imply a new pathway underlying the development of cardiovascular diseases in smokers. Unfavorable changes in the cardiovascular system caused by smoking may quite slowly progress that short period of observation in the present study could not have detected enhanced yearly increases of CSBP by smoking. Funding Acknowledgement Type of funding sources: None.

EFFECTS OF SMOKING ON CENTRAL BLOOD PRESSURE

Abstract Objective: Smoking is known to induce systemic vascular damage, leading to cardiovascular diseases. Recent studies demonstrated that central blood pressure has a greater impact on cardiovascular events than brachial blood pressure. We investigated effects of habitual smoking on central systolic blood pressure (CSBP) in the general population. Design and method: A total of 5630 subjects (male = 2622, 51.7 ± 12.0 year-old at baseline), who visited our hospital for a physical check-up at least twice during the last 10 years and underwent CSBP measurement at each visit, were enrolled, and effects of smoking on the average and yearly changes of CSBP (median follow-up 5 years) were analyzed. Brachial blood pressure (oscillometer) and radial artery pressure waveforms (tonometer) were recorded using an automated device, and the pressure corresponding to the second systolic peak of radial pressure waveforms was taken as CSBP (HEM-9000AI, Omron Healthcare, Kyoto). Hypertension was defined as brachial BP &gt; = 140/90mmHg or the use of antihypertensive medications. A yearly change in CSBP was calculated in each subject by linear regression analysis using longitudinal data. Results: The average CSBP during the follow-up was higher in habitual smokers than in non-smokers when analyzed in normotensive (n = 4634, 109.1 ± 11.7 vs. 107.6 ± 12.8 mmHg, p &lt; 0.001) and non-treated hypertensive subjects (n = 91, 150.7 ± 14.8 vs. 142.8 ± 16.7 mmHg, p &lt; 0.05), whereas in hypertensive subjects under medication the average CSBP was lower in smokers than in non-smokers (n = 905, 124.6 ± 12.4 vs. 127.8 ± 13.6 mmHg, p &lt; 0.01). Although smoking status did not affect yearly changes of CSBP in both normotensive (habitual smokers vs. non-smokers; 1.38 ± 6.00 vs. 1.44 ± 6.04 mmHg/year) and treated hypertensive subjects (-0.16 ± 7.08 vs. -0.66 ± 8.24 mmHg/year), the unfavorable effect of smoking on yearly increase of CSBP was found in non-treated hypertensive subjects (4.09 ± 15.1 vs. -0.53 ± 10.3 mmHg/year). Conclusions: Habitual smoking increases CSBP especially in subjects with hypertension, however, antihypertensive medications counteract the unfavorable effects of smoking on CSBP. These results imply a new pathway underlying the development of cardiovascular diseases in smokers. Unfavorable changes in the cardiovascular system caused by smoking may quite slowly progress that short period of observation in the present study could not have detected enhanced yearly increases of CSBP by smoking.

Combined aortic valve and coronary artery calcifications in lung cancer screening as predictors of death from cardiovascular disease.

Smoking is a major risk factor for both cardiovascular disease (CVD) and lung cancer. Aortic valve calcification (AVC) and coronary artery calcification (CAC) are both due to atherosclerotic disease. We aim to investigate whether AVC on low-dose CT (LDCT) predicts death from CVD in smokers beyond that provided by CAC. We reviewed a prospective cohort of 8618 smokers enrolled in LDCT screening for lung cancer in New York State between June 2000 and December 2005. As of December 2009, 169 of the 643 deaths were due to CVD; median follow-up time was 96.4months. Visual AVC was assessed as being absent (AVC = 0) or present (AVC > 0). CAC ordinal scores of 0-12 were categorized into three validated prognostic categories (0, 1-3, and 4-12). Cox proportional hazards regression analysis was used to assess whether AVC > 0 increased the risk of CVD death, after adjustment for CAC categories and other risk factors. The prevalence of AVC significantly increased (p < 0.0001) with the increasing severity of the CAC categories; Pearson, Spearman, and Kendall's correlation coefficients showed a significant correlation between AVC and CAC with r = 0.29, ρ = 0.32, and τB = 0.28 (all p values < 0.0001), respectively. CAC and AVC were significant predictors of CVD death when considered alone using multivariable Cox regression analysis (adjusted HR of CAC = 1.57, p = 0.04; adjusted HR of AVC = 1.39, p = 0.045). When AVC > 0 and CAC ≥ 4, the hazard ratio was 2.35 (95%CI 1.57-3.50) compared with the reference group of AVC = 0 and CAC < 4, when adjusted for other risk factors. The presence of AVC identified on LDCT is a significant predictor of future CVD death, particularly for those with ordinal CAC score ≥ 4. • Aortic valve calcification (AVC) and coronary artery calcification (CAC) are both due to atherosclerotic disease. The prevalence of AVC in lung cancer screening cohort significantly increased with the increasing severity of CAC. • CAC and AVC were significant predictors of cardiovascular disease (CVD) death when considered alone. Participants who underwent lung cancer screening with AVC > 0 and CAC ≥ 4 had more than a 2-fold increased risk of CVD death than the group with AVC = 0 and CAC < 4, when adjusted for other risk factors.

Total and differential leukocyte count and oxygen saturation of hemoglobin changes in healthy smokers and non-smokers

Background: Inflammatory markers are altered in smokers and smoking has been proved as one of the main causative factors for cardiovascular diseases (CVDs), inflammatory diseases, and oxidative stress stimulation. An alteration in hematological parameters and oxygen saturation of hemoglobin is expected with smoking tobacco. Aim and Objective: This study has been planned with the aim to evaluate the changes associated with the extent of adverse effects of tobacco smoking in total and differential leukocyte count (DLC) and oxygen saturation of hemoglobin in healthy smokers and non-smokers. Materials and Methods: A total of 150 healthy adults were participated in this cross-sectional study. Anthropometric measurements such as height, weight, and body mass index were taken, and information of smoking habits were obtained by a questionnaire. Blood samples were taken for the estimation of total and DLC using MS-9 automated hematology cell counter. Oxygen saturation of hemoglobin was done using fingertip pulse oximeter Nidek Medical 5300. Results: Our results showed a statistically significant rise in the total leukocyte count (TLC) (P < 0.001), lymphocyte count (P < 0.001), granulocyte count (P < 0.01), and monocyte count (P < 0.02) and showed a statistically significant decrease in SpO2 (P < 0.04) in smokers as compared to non-smokers. Conclusion: The study has shown that altered values of TLC and DLC and oxygen saturation of hemoglobin in smokers should be considered during diagnosis, interpretation of result, and treatment of patients. A high TLC and DLCs exhibited in this research may be responsible for chronic inflammation and subsequent high risk of CVD in smokers. Therefore, quitting smoking should be encouraged for better health.

Smoking-induced risk of future cardiovascular disease is partly mediated by cadmium in tobacco

TPS 771: Diet and lifestyle, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background: Smoking is a strong risk factor for cardiovascular disease (CVD) and causes exposure to cadmium, which is a pro-atherosclerotic metal. Cadmium exposure has also been shown to increase the risk of CVD, even after adjustment for smoking. Our hypothesis was that part of the risk of CVD in smokers may be mediated by cadmium exposure from tobacco smoke. We examined this hypothesis in a mediation analysis, trying to assess how much of the smoking-induced CVD risk could be explained via cadmium. Methods: We used prospective data on CVD (incidence and mortality) in a Swedish population-based cohort of 4304 middle-aged men and women (the Malmö Diet and Cancer Study). Blood cadmium was analyzed in base-line samples from 1991 - 1994, and clinical events were followed up for 16–19 years based on registry data. Mediation analysis was conducted to evaluate the indirect effect (via cadmium) of smoking on CVD. Survival was analyzed by the accelerated failure time (AFT) model and the Aalen additive hazard model. Results: The mean blood cadmium level in the study population was 0.43 μg/L (median 0.24 μg/L) and increased with recent and current smoking. As expected, shorter survival time (AFT model) and higher incidence rate (Aalen model) were found in current smokers for all CVD outcomes and this effect seemed to be partly mediated by cadmium. For the sum of acute myocardial infarction, bypass grafts and percutaneous coronary intervention, and death in ischemic heart disease, about half of the increased risk of such events in current smokers was mediated via cadmium, with similar results for the AFT and Aalen models. Conclusion Cadmium plays an important role in smoking-induced CVDs.

Smoking-induced risk of future cardiovascular disease is partly mediated by cadmium in tobacco: Malm\xf6 Diet and Cancer Cohort Study

BackgroundSmoking is a strong risk factor for cardiovascular disease (CVD) and causes exposure to cadmium, which is a pro-atherosclerotic metal. Cadmium exposure has also been shown to increase the risk of CVD, even after adjustment for smoking. Our hypothesis was that part of the risk of CVD in smokers may be mediated by cadmium exposure from tobacco smoke. We examined this hypothesis in a mediation analysis, trying to assess how much of the smoking-induced CVD risk could be explained via cadmium.MethodsWe used prospective data on CVD (incidence and mortality) in a Swedish population-based cohort of 4304 middle-aged men and women (the Malmö Diet and Cancer Study). Blood cadmium was analyzed in base-line samples from 1991, and clinical events were followed up for 16–19 years based on registry data. Mediation analysis was conducted to evaluate the indirect effect (via cadmium) of smoking on CVD. Survival was analyzed by the accelerated failure time (AFT) model and the Aalen additive hazard model.ResultsThe mean blood cadmium level in the study population was 0.43 μg/L (median 0.24 μg/L) and increased with recent and current smoking. As expected, shorter survival time (AFT model) and higher incidence rate (Aalen model) were found in current smokers for all CVD outcomes and this effect seemed to be partly mediated by cadmium. For the sum of acute myocardial infarction, bypass grafts and percutaneous coronary intervention, and death in ischemic heart disease, about half of the increased risk of such events in current smokers was mediated via cadmium, with similar results for the AFT and Aalen models.ConclusionsCadmium plays an important role in smoking-induced CVDs. This provides evidence for mechanisms and is of importance for both individuals and policy makers.

Increased eryptosis in smokers is associated with the antioxidant status and C-reactive protein levels

Cigarette smoking has been linked with oxidative stress and inflammation. In turn, eryptosis, the suicidal erythrocyte death similar to apoptosis that can be triggered by oxidative stress, has been associated with chronic inflammatory diseases including atherosclerosis. However, the link between smoking and eryptosis has not been explored so far. The aim of the present study was to determine the level of eryptotic erythrocytes in healthy male smokers (n = 21) compared to non-smokers (n = 21) and assess its relationship with systemic inflammation (CRP) as well as with antioxidant defense (GSH) and their resistance to ex-vivo induced hemolysis. Smoking caused an increase in phosphatidylserine translocation outside the erythrocyte membrane (hallmark of eryptosis), significantly correlated to the plasma level of CRP (r = 0.546) and GSH concentration in erythrocytes (r=−0.475). With respect to non-smokers, smokers show a marginal increase of total leucocytes and erythrocyte volume, no modifications of the RBC resistance to oxidative stress-induced hemolysis and hematological and lipid parameters unvaried. We conclude that the inflammatory status (high CRP levels) and RBC oxidative stress (low GSH levels) caused by cigarette smoking are associated with an increase of eryptotic erythrocytes, a yet unknown relationship potentially involved with atherosclerosis and cardiovascular disease in smokers.

A Japanese cross-sectional multicentre study of biomarkers associated with cardiovascular disease in smokers and non-smokers

We performed a cross-sectional, multicentre study in Japan to detect the differences in biomarkers of exposure and cardiovascular biomarkers between smokers and non-smokers. Several clinically relevant cardiovascular biomarkers differed significantly between smokers and non-smokers, including lipid metabolism (high-density lipoprotein cholesterol concentrations – lower in smokers), inflammation (fibrinogen and white blood cell count – both higher in smokers), oxidative stress (8-epi-prostaglandin F2α – higher in smokers) and platelet activation (11-dehydro-thromboxane B2 – higher in smokers) (p ≤ 0.0001). These results provide further evidence showing that cardiovascular biomarkers can discriminate smokers from non-smokers, and could be used to evaluate the risks associated with tobacco products.

Effect of cigarette smoking on insulin resistance risk

ObjectivesSmoking is one of the main risk factors for cardiovascular disease (CVD). The mechanism(s) of the effects of smoking on CVD are not clearly understood; however, a number of atherogenic characteristics, such as insulin resistance have been reported. We aim to investigate the effects of cigarette smoking on insulin resistance and to determine the correlation between this parameter with smoking status characteristics. Study designThis study was conducted on 138 non-smokers and 162 smokers aged respectively 35.6±16.0 and 38.5±21.9 years. All subjects are not diabetic. MethodsFasting glucose was determined by enzymatic methods and insulin by chemiluminescence method. Insulin resistance (IR) was estimated using the Homeostasis Model of Assessment equation: HOMA-IR=[fasting insulin (mU/L)×fasting glucose (mmol/L)]/22.5. IR was defined as the upper quartile of HOMA-IR. Values above 2.5 were taken as abnormal and reflect insulin resistance. ResultsCompared to non-smokers, smokers had significantly higher levels of fasting glucose, fasting insulin and HOMA-IR index. These associations remained significant after adjustment for confounding factors (age, gender, BMI and alcohol consumption). A statistically significant association was noted between the smoking status parameters, including both the number of cigarettes smoked/day and the duration of smoking, and fasting insulin levels as well for HOMA-IR index. Among smokers, we noted a positive correlation between HOMA-IR index and both plasma thiocyanates and urinary cotinine. ConclusionOur results show that smokers have a high risk to developing an insulin resistance and hyperinsulinemia, compared with a matched group of non-smokers, and may help to explain the high risk of cardiovascular diseases in smokers.

Effects of cigarette smoking on HDL quantity and function: Implications for atherosclerosis

Cigarette smoking has been identified as an independent and preventable risk factor for atherosclerosis and cardiovascular disease. Population studies have shown that plasma high density lipoprotein (HDL) cholesterol levels are inversely related to the risk of developing cardiovascular disease. Cigarette smoking is associated with reduced HDL cholesterol levels. Cigarette smoking can alter the critical enzymes of lipid transport, lowering lecithin: cholesterol acyltransferase (LCAT) activity and altering cholesterol ester transfer protein (CETP) and hepatic lipase activity, which attributes to its impact on HDL metabolism and HDL subfractions distribution. In addition, HDL is susceptible to oxidative modifications by cigarette smoking, which makes HDL become dysfunctional and lose its atheroprotective properties in smokers. Therefore, cigarette smoking has a negative impact on both HDL quantity and function, which can explain, in part, the increased risk of cardiovascular disease in smokers.

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.

1980 – Effect of cigarette smoking on insulin resistance risk

Smoking is one of the main risk factors for cardiovascular disease (CVD). The mechanism(s) for the effects of smoking on CVD are not clearly understood; however, a number of atherogenic characteristics such as insulin resistance have been reported. We aim to investigate the effects of cigarette smoking on insulin resistance and to determine the correlation between this parameter with smoking status characteristics. This study was conducted on 138 nonsmokers and 162 smokers aged respectively 35.55±16.03 and 38.47±21.91 years. All subjects are not diabetics. Fasting glucose was determined by enzymatic methods and insulin by chemiluminescence method. Insulin resistance (IR) was estimated using the Homeostasis Model of Assessment equation: HOMA-IR = [fasting insulin (mU/L) × fasting glucose (mmol/L)] /22.5. IR was defined as the upper quartile of HOMA-IR. Values above 2.5 were taken as abnormal and reflect insulin resistance. Compared to non-smokers, smokers had significantly higher levels of fasting glucose, fasting insulin and HOMA-IR index. A statistically significant association was noted between the smoking status parameters, including both the number of cigarettes smoked/day and the duration of smoking, and fasting insulin levels as well for HOMA-IR index. Among smokers, we noted a positive correlation between HOMA-IR index and both plasma thiocyanates and urinary cotinine. The findings show that smokers have a high risk to developing an insulin resistant, hyperinsulinaemic, compared with a matched group of non-smokers, and may help to explain the high risk of cardiovascular diseases in smokers.

Fruit and vegetable intake and smoking cessation

In cohort studies, fruit and vegetable (F&V) intake is associated with lower cardiovascular diseases (CVDs). Former smokers often have a higher F&V intake than current smokers. If a high intake of F&V precedes smoking cessation, the latter may explain the favorable association between F&V intake and CVD among smokers. The objective was to assess whether higher F&V intake precedes smoking cessation. The study population comprised 1056 male smokers from Lille (France) and Belfast (Northern Ireland) aged 50-59 years on inclusion in 1991. At baseline, participants completed self-administered questionnaires related to smoking habits, demographic, socioeconomic factors and diet. At the 10-year follow-up, smoking habits were assessed by mailed questionnaire. After 10 years, 590 out of 1056 smokers had quit smoking (70.7% of smoker in Lille and 37.8% in Belfast). After adjusting for center, consumption of F&V was associated with quitting (odds ratio (OR) for high versus low F&V intake: 1.73; 95% confidence interval (CI): (1.22-2.45); P-trend=0.002). After further adjustment for sociodemographic factors, body mass index and medical diet, the association was still statistically significant (OR: 1.59; 95% CI (1.12-2.27); P-trend = 0.01). In a model fully adjusted for age, smoking intensity, alcohol consumption and physical activity, the association was no longer significant (P = 0.14). Higher F&V intake precedes smoking cessation. Hence, smoking cessation could affect the causal interpretation of the association between F&V and CVD in smokers.

Influence of Smoking Combined with Another Risk Factor on the Risk of Mortality from Coronary Heart Disease and Stroke: Pooled Analysis of 10 Japanese Cohort Studies

Background: In spite of the importance of a multifactorial approach to preventing cardiovascular disease in smokers, most information on the combined adverse effects of smoking and hypertension or high serum cholesterol on cardiovascular disease has been derived from Western populations, and coronary heart disease was often used as the only endpoint. Therefore, the present large-scale pooled analysis attempted to provide reliable information on the adverse effects of the coexistence of smoking and hypertension or high serum cholesterol on the risk of mortality from coronary heart disease and stroke in both, individuals and the entire population in Japan. Methods: A total of 27,385 male and 39,207 female participants aged 40–89 years were enrolled from 10 well-qualified Japanese cohort studies with a mean follow-up of 10.1 years. Hazard ratios and their corresponding 95% confidence intervals in smokers who had hypertension or high serum cholesterol were estimated for men and women separately using a Cox proportional hazards regression model that included age, body mass index, cohort and either serum total cholesterol or systolic blood pressure as covariates. Fractions of deaths attributable to the coexistence of these risk factors were also calculated. Results: The multivariate-adjusted hazard ratios in male and female current smokers with hypertension, compared with those with neither factor were 2.57 (95% confidence intervals, 1.51–4.38) and 6.14 (3.49–10.79) for coronary heart disease, and 3.28 (1.89–5.71) and 1.61 (0.81–3.18) for cerebral infarction, respectively. The fractions of deaths attributable to the coexistence of current smoking and hypertension in men and women were 24.6 and 9.6% for coronary heart disease and 28.1 and 2.0% for cerebral infarction, respectively. Smokers with high serum cholesterol were broadly comparable to hypertensive smokers only with respect to coronary mortality risk; the hazard ratios, compared with those with neither factor were 4.19 (2.33–7.53) for men and 3.90 (1.57–9.67) for women. The fraction of coronary deaths attributable to the coexistence of current smoking and high serum cholesterol was 6.3% in men and 2.2% in women. There was no interaction between smoking habit and blood pressure or serum total cholesterol for these two subtypes in both men and women. Conclusions: Particular attention should be given to smokers who have concomitant hypertension or high serum cholesterol for preventing deaths due to cardiovascular disease. From a public health perspective in Japan, priority should be given to hypertensive smokers, since this group makes a large contribution to the burden of both coronary and cerebral infarction deaths.

Etude de l'activité de la paraoxonase 1 (PON1) et du profil lipidique dans une population de fumeurs tunisiens

This study aims at examine the effect of cigarettes smoking on paraoxonase 1 (PON1) activity and lipid profile. Our study included 102 smokers aged 35.5 +/- 16.0 years and 98 non-smokers aged 38.5 +/- 21.9 years. Total cholesterol (TC), triacylglycerols (TG), HDL cholesterol (CHDL) and LDL-cholesterol (cLDL) were determined by enzymatic colorimetric methods. ApoA1 and ApoB and Lp(a) were analyzed by immunoturbidimetry on Konélab 30, PON1 activity was measured by a kinetic method. Plasma CT, TG, cLDL, Lp(a) and ApoB/ApoA1 ratio appeared significantly higher in the smokers when compared to nonsmokers, since cHDL levels were lower. In addition, TG values were significantly higher in subjects smoking more than 30 cigarettes/day as compared to those smoking 5-10 cigarettes/day. We noted a significant decrease of PON1 activity in smokers compared to non smokers (94 +/- 104 vs 158 +/- 133 IU/L), with regression of PON1 activity according number of cigarettes/day. In conclusion, hypertriglyceridemia, low levels of cHDL, high levels of ApoB/ApoA1 and significant decrease of PON1 activity confirm the high risk of cardiovascular diseases in smokers.

Influence of C-159T SNP of the CD14 gene promoter on lung function in smokers

CD14, a co-receptor for endotoxin, plays a significant role in regulating the inflammatory response to this agent. The C-159T single nucleotide polymorphism (SNP) in the CD14 gene promoter is an important regulator of CD14 expression, with TT homozygotes having increased expression of CD14. This SNP has been linked to pathogenesis of asthma and with cardiovascular diseases in smokers. We hypothesize that CD14 also plays a role in the pathophysiology of COPD in smokers who are exposed to endotoxin contained in cigarette smoke as well as endotoxin derived from Gram-negative microbes colonizing their airways. To assess the effect of the C-159T SNP of the CD14 gene promoter on lung function, we recruited 246 smokers 40 years of age or older with a range of 10-156 pack-year smoking exposures. The TT genotype was associated with lower lung function in smokers with a moderate smoking history. However, the CC genotype was associated with decreased lung function in heavy smokers (>56 pack years). The effect of CC genotype on severity of COPD is analogous with the effect of this genotype in risk for asthma. CD14 may be a factor in the pathophysiology of COPD, as it is in asthma and smoking-related cardiovascular diseases.

Association of Smoking With Aortic Wave Reflection and Central Systolic Pressure and Metabolic Syndrome in Normotensive Japanese Men

The influences of smoking habits on blood pressure (BP) may have been underestimated substantially on the basis of conventional measurements. We compared the radial augmentation index (AI), brachial and central pressures, and prevalence of the metabolic syndrome (MetS) among never smokers, former smokers, and current smokers in a population of Japanese healthy men. A total of 443 normotensive men who entered the health checkup program was divided into four groups according to smoking status; i.e., never smokers (n = 117), former smokers (n = 165), current mild to-moderate smokers (n = 105), and current heavy smokers (n = 56). Radial pulse waveforms were obtained using radial tonometry (HEM-9000AI), and the AI and late systolic pressure in the radial artery, an estimate of central systolic pressure, were measured. The AI was significantly higher in current smokers than both never and former smokers. Central systolic pressure was significantly higher in both current and former smokers than never smokers, although brachial systolic pressure was not significantly different among these groups. The MetS was more prevalent in current smokers than never smokers. Smoking habits have substantially different effects on the AI and central systolic pressure despite a similar level of brachial systolic pressure. Along with higher prevalence of the MetS, elevated AI and central systolic pressure may be potential mechanisms responsible for an increased risk of cardiovascular disease in smokers.

An Evaluation of the Clinical Evidence on the Role of Inflammation and Oxidative Stress in Smoking-Mediated Cardiovascular Disease

The number of fatalities due to cardiovascular disease (CVD) continues to be far ahead of loss of human life caused by any other type of disease worldwide. According to the WHO, the annual global tobacco death toll is already 8.4 million and will reach 10 million by the year 2025. However, in contrast to other modifiable primary risk factors for CVD such as obesity, primary prevention strategies for smokers unable to quit are not available to date. This Review, by adopting the principles of evidence-based medicine, summarizes the most recent clinical studies on CVD in smokers, and concludes by suggesting a novel primary prevention strategy for CVD in smokers unable to quit. Evidence gathered from mechanistic studies involving basic research as well as large population-based approaches point to oxidative stress as the major insult imposed by cigarette smoke (CS), and a state of systemic inflammation, as signified by increased hs (high sensitivity) CRP levels in smokers, as the decisive pro-atherogenic response of the body to the initial insult. Since we identified oxidative stress induced by heavy metals as a significant pro-atherogenic activity of CS, strategies aimed at detoxifying heavy metals and combating inflammation appear as plausible approaches to counteract the accelerated onset of CVD in smokers. For this purpose, we discuss metal chelating agents and statins as promising novel primary prevention strategies in smokers unable to quit.