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INTRODUCTION: High blood pressure in hypertensive smokers is affected by nicotine consumption. This study aimed to evaluate the effect of smoking cessation treatments on blood pressure in hypertensive smokers. METHODS: A total of 113 hypertensive smokers on antihypertensives during smoking cessation treatment in the randomized controlled trial GENTSMOKING were considered for analysis. At Baseline (T0) and Week 12 (T12), systolic and diastolic blood pressure (SBP and DBP), and heart rate (HR) were measured using a semi-automated digital oscillometric device. Mean arterial pressure (MAP) and delta differences for SBP, DBP, HR, and MAP were calculated. Smoking cessation was confirmed by measuring carbon monoxide (CO) in exhaled air. RESULTS: After 12 weeks of treatment, 72 participants ceased smoking (cessation group) and 41 did not (no cessation group). At T0, there was no statistically meaningful difference between groups with respect to age, body mass index, CO, and daily cigarette consumption. At T12, daily cigarette consumption and CO had decreased in both groups (p<0.001). The cessation group showed decreased SBP (131 ± 2 vs 125 ± 2 mmHg, p=0.004), DBP (79 ± 1 vs 77 ± 1 mmHg, p=0.031), MAP (96 ± 1 vs 93 ± 1 mmHg, p=0.005), and HR (79 ± 1 vs 74 ± 1 beats/min, p=0.001), and increased body weight (77.4 ± 2.1 vs 79.2 ± 2.2 kg, p<0.001). No significant differences were seen for these variables in the no cessation group. Decrease in blood pressure was significantly higher among hypertensive participants with SBP ≥130 mmHg: SBP (145 ± 2 vs 132 ± 2 mmHg, p<0.001), DBP (85 ± 2 vs 80 ± 1 mmHg, p=0.002), MAP (105 ± 1 vs 97 ± 1 mmHg, p<0.001), and HR (81 ± 2 vs 74 ± 2 beats/min, p=0.002). A positive correlation was found between HR and CO (r=0.34; p=0.001). CONCLUSIONS: Smoking cessation treatment reduced blood pressure in hypertensive smokers, allowing them to reach therapeutic targets for hypertension management. Smoking cessation has a positive impact on hypertension treatment; therefore, it should be encouraged in clinical practice. CLINICALTRIALSGOV IDENTIFIER: NCT03362099.

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INTRODUCTION: Smoking cessation is the best strategy for reducing tobacco-related morbimortality. The goal of this randomized controlled trial was to test whether using the genetically favorable markers to choose a smoking cessation drug treatment (precision medicine) was superior to using the most effective drug (varenicline) in terms of abstinence rates. Additionally, combination therapy was tested when monotherapy failed. METHODS: This partially blind, single-center study randomized (1:1) 361 participants into two major groups. In the genetic group (n=184), CYP2B6 rs2279343 (genotype AA) participants started treatment with bupropion, and CHRNA4 rs1044396 (genotype CT or TT) participants started treatment with varenicline; when genetic favorable to both, participants started treatment with bupropion, and when favorable to neither, on both drugs. In the control group (n=177), participants started treatment with varenicline, regardless of genetic markers. Drug treatment lasted 12 weeks. Efficacy endpoints were abstinence rates at Weeks 4, and Weeks 8-12, biochemically validated by carbon monoxide in exhaled air. Participants who did not achieve complete abstinence at Week 4, regardless of group, were given the choice to receive combination therapy. RESULTS: Abstinence rates were 42.9% (95% CI: 36-64) in the control group versus 30.4% (95% CI: 23-37) in the genetic group at Week 4 (p=0.01); and 74% (95% CI: 67-80) versus 52% (95% CI: 49-64) at Week 12 (p<0.001), respectively. The strategy of combining drugs after Week 4 increased abstinence rates in both groups and the significant difference between genetic and control groups was maintained. CONCLUSIONS: Results show that using these selected genetic markers was inferior to starting treatment with varenicline (control group), which is currently the most effective smoking cessation drug; moreover, the addition of bupropion in cases of varenicline monotherapy failure improves the efficacy rate until the end of treatment. CLINICAL TRIAL IDENTIFIER: NCT03362099.

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INTRODUCTION: Varenicline effectively helps smokers quit by reducing withdrawal symptoms and blocking the reward of smoking. However, most quitters return to smoking within one year. 'Cue Restricted Smoking' is a behavioral technique designed to increase quit rates by asking smokers attempting to quit to restrict smoking to the standing position, while alone, in an isolated area facing a wall, with the cigarette as the only stimulus. METHODS: Using retrospective clinic records we compared quit rates in 281 smokers (50% males) instructed in the cue restricted smoking cessation method during 2016-2018 to quit rates in 324 smokers (46% males) advised to completely stop smoking on the target quit date which we previously used during 2011-2014. All were prescribed varenicline for 12 weeks alone, with the addition of bupropion if needed after 4 weeks. Follow-up consisted of behavioral support at 4-6 visits during active drug treatment and telephone counselling at 24 and 52 weeks. The smoking cessation rate was confirmed with exhaled carbon monoxide at the clinic visit at 12 weeks and only by telephone at 52 weeks. RESULTS: The mean age of smokers was 49 years in both groups and the number of cigarettes smoked daily was similar (18/day in the cue restricted vs 19/day in the target quit day group). The smoking cessation rate at 12 weeks was 75% in the cue restricted versus 45% in the target quit day group (relative risk, RR=1.8; 95% CI: 1.4-2.2, p<0.001). At 52 weeks the quit rate was 65% vs 34%, respectively (RR=1.9; 95% CI: 1.5-2.4, p<0.001). CONCLUSIONS: Cue restricted smoking was associated with a substantially increased chance of quitting compared with standard advice during treatment with varenicline. These results should be further studied in a randomized controlled trial.

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OBJECTIVE: The aim of this study was to investigate cytogenetic and cytotoxic damage through the evaluation of micronuclei (MN) and metanuclear anomalies in the oral mucosa of electronic cigarette (e-cig) users. STUDY DESIGN: The patients were recruited into 4 groups: e-cig users, smokers, former smokers, and nonsmokers (control). The samples were collected by means of exfoliative cytology of the lateral region of the tongue and the floor of the mouth. The smears obtained were fixed and stained by the Feulgen method for investigation of MN and metanuclear anomalies. RESULTS: A significant difference was observed for MN frequency only between the smoker and control groups. As for metanuclear anomalies, significant differences were observed: karyolysis between: smokers and control, e-cig and control, as well as former smokers; karyorrhexis: between smoker and control; binucleation: between e-cig and former smoker, as well as control; broken eggs: between e-cig and all other groups; nuclear bud: between e-cig and former smokers, as well as control. CONCLUSIONS: E-cig and alcohol users presented genotoxicity and cytotoxicity in the oral mucosa cells. The use of e-cigs and alcohol by former smokers can cause more damage to the cells of the oral mucosa compared to those who have not used e-cigs.

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INTRODUCTION: Smoking is considered the leading cause of preventable morbidity and mortality worldwide. Studies have sought to identify predictors of response to smoking cessation treatments. The aim of this study was to analyze a possible association of target gene expression for smoking cessation with varenicline. METHODS: We included 74 smokers starting treatment with varenicline. Gene expression analysis was performed through the custom RT² Profiler qPCR array assay, including 17 genes. Times for sample collection were before the start of therapy (T0) and two weeks (T2) and four weeks (T4) after the start of treatment. RESULTS: For gene expression analysis, we selected 14 patients who had success and 13 patients resistant to varenicline treatment. Success was considered to be when a patient achieved tobacco abstinence until the fourth week of treatment and resistant was when a patient had not stopped smoking as of the fourth week of treatment. We observed a significant difference for CHRNA7 gene expression: in the resistant group, samples from T2 and T4 had lower expression compared with T0 (fold change: 0.38, P = 0.007; fold change: 0.67, P = 0.004; respectively). CONCLUSION: This exploratory clinical study, searching for a possible predictor of effectiveness for varenicline, reaffirmed the association of the α7 nAChR subunit for nicotine dependence and smoking therapy effectiveness with varenicline.

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BACKGROUND: The identification of variants in genes involved in nicotine metabolism may have implications for the pharmacological therapy of smoking. In the scenario of precision medicine, the aim of this study was to evaluate a possible association of cytochrome P450 2A6 and 2B6 polymorphisms with varenicline pharmacotherapy. METHODS: The present study included 167 patients treated with varenicline in monotherapy who were from a cohort study of 1049 patients (treated with smoking cessation drugs: nicotine replacement therapy, bupropion, varenicline, or combinations of same). Smoking cessation success was considered for patients who completed 6 months of continuous abstinence. The CYP2A6 rs1801272 and rs28399433 and CYP2B6 rs8109525 polymorphisms were genotyped by real-time PCR using the TaqMan® platform. RESULTS: Patients with AG or GG genotypes for CYP2B6 rs8109525 had a higher success rate of smoking cessation with varenicline (51.2%) compared with carriers of the AA genotypes (33.3%, P = 0.03, n = 167). The AG or GG genotypes were also associated with a higher odds ratio of success, even in a multivariate analysis adjusting for potential confounders (OR = 2.01; 95%CI = 1.01 to 4.00; P = 0.047). CONCLUSION: CYP2B6 rs8109525 was associated with a higher success rate of smoking cessation with varenicline treatment. This finding may be useful in pharmacogenomic strategies for smoking cessation therapy.

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O tabagismo é a principal causa evitável de morte, e é associado ao desenvolvimento de doenças cardiovasculares, respiratórias e câncer. Existem fortes evidências de que o controle do tabagismo tem boa relação de custo-efetividade quando comparado com outras intervenções de redução de riscos e prevenção de doenças. As bases da Convenção-Quadro para Controle do Tabaco da Organização Mundial da Saúde (CQCT/OMS) oferecem, por meio de artigos, guias e protocolos, rotina de atuação, além da oportunidade de colaboração e cooperação técnica entre os diversos países para abordar conjuntamente problemas que transcendem suas fronteiras. A OMS, objetivando facilitar a aplicação do tratado, lançou um pacote de intervenções para redução de demanda por produtos do tabaco de impacto comprovado, com experiência de implementação reconhecida e com políticas que podem ser aplicadas em qualquer país do mundo, o MPOWER. M >Monitor:monitorar da epidemia. P >Protect: proteger a população contra a fumaça do tabaco. O Offer:oferecer ajuda para deixar de fumar. W >Warn: advertir sobre os perigos do tabaco. E >Enforce: fazer cumprir a proibição da publicidade, promoção e patrocínio. R >Raise: aumentar impostos dos produtos do tabaco

Smoking is the leading avoidable cause of death, and is associated with the develo-pment of cancer, cardiovascular and respiratory diseases. There is strong evidence that tobacco control is cost-effective compared to other risk-reduction and disease prevention interventions. The bases of the World Health Organization Framework Convention on Tobacco Control (WHO FCTC) offer, through articles, guides and protocols, both a road map and the opportunity for collaboration and technical cooperation among the different countries to jointly address issues that transcend their borders. With a view to facilitating the implementation of the treaty, WHO has launched a package of interventions with proven impact, geared towards reducing the demand for tobacco products, with recognized implementation experience and policies that can be applied in any country in the world, MPOWER. M- Monitor tobacco use and prevention policies. P- Protect people from tobacco smoke. O- Offer help to quit tobacco use. W- Warn about the dangers of tobacco. E- Enforce bans on tobacco advertising, promotion and sponsorship. R- Raise taxes on tobacco

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BACKGROUND: The identification of variants in the nicotinic acetylcholine receptor (nAChR) subunit genes associated with smoking phenotypes are increasingly important for prevention and treatment of nicotine dependence. In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (CHRNA3), cholinergic receptor nicotinic alpha 5 (CHRNA5) and cholinergic receptor nicotinic beta 3 (CHRNB3) polymorphisms were associated with nicotine dependence severity, and to investigate possible pharmacogenetics markers of smoking cessation treatment. METHODS: This study cohort enrolled 1049 smoking patients who received pharmacological treatment (varenicline, varenicline plus bupropion, bupropion plus/or nicotine replacement therapy). Smoking cessation success was considered for patients who completed 6 months of continuous abstinence. Fagerström test for nicotine dependence (FTND) and Issa situational smoking scores (Issa score) were analyzed for nicotine dependence. CHRNA2 (rs2472553), CHRNA3 (rs1051730), CHRNA5 (rs16969968 and rs2036527) and CHRNB3 (rs6474413) polymorphisms were genotyped by high resolution melting analysis. RESULTS: Females with GA and AA genotypes for CHRNA5 rs16969968 and rs2036527 polymorphisms had higher success rate in smoking cessation treatment: 44.0% and 56.3% (rs16969968), 41.5% and 56.5% (rs2036527), respectively, compared with carriers of the GG genotypes: 35.7% (rs16969968), 34.8% (rs2036527), (P = 0.03, n = 389; P = 0.01, n = 391). The GA or AA genotypes for the rs16969968 and rs2036527 were associated with higher odds ratio for success in women (OR = 1.63; 95% CI = 1.04 to 2.54; P = 0.03 and OR = 1.59, 95% CI = 1.02 to 2.48; P = 0.04; respectively). We did not find association of these polymorphisms with nicotine dependence related scores. Polymorphisms in the CHRNA2, CHRNA3 and CHRNB3 genes were not associated with the phenotypes studied. CONCLUSION: CHRNA5 rs16969968 and rs2036527 were associated with higher success rate in the smoking cessation treatment in women. These findings might contribute to advances in personalized medicine.

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BACKGROUND: In the oral cavity, genomic instability is caused by long-term exposure to carcinogens. The aim of this study was to evaluate the relationship between smoking and DNA ploidy. METHODS: Cytological material was obtained from patients participating in the Outpatient Smoking Treatment Program of the Heart Institute (INCOR-HCFMUSP), and of the Discipline of Oral Medicine (ICT-UNESP). The inclusion criteria for all groups were the absence of a history of malignant tumors, absence of clinical signs of changes in the selected area, and alcohol consumption of less than 3 units per week. Group 1:30 smokers before smoking cessation treatment; Group 2:30 non-smokers; Group 3:30 ex-smokers abstinent for at least 1 year. Cytological smears were collected from the floor of the mouth and border of the tongue and stained by Feulgen. Aneuploidy was evaluated using the ACIS® III system. RESULTS: The Kruskal-Wallis test showed no statistically significant difference (P = .4383) between the groups studied. No association between tobacco consumption and aneuploidy was observed in group 1 (P = 1) or group 2 (P = .68; Fisher's exact test). CONCLUSION: Smoking was not associated with changes in DNA content or the incidence of aneuploidy in normal oral mucosa.

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BACKGROUND: Smoking restriction laws have spread worldwide during the last decade. Previous studies have shown a decline in the community rates of myocardial infarction after enactment of these laws. However, data are scarce about the Latin American population. In the first phase of this study, we reported the successful implementation of the law in São Paulo city, with a decrease in carbon monoxide rates in hospitality venues. OBJECTIVE: To evaluate whether the 2009 implementation of a comprehensive smoking ban law in São Paulo city was associated with a reduction in rates of mortality and hospital admissions for myocardial infarction. METHODS: We performed a time-series study of monthly rates of mortality and hospital admissions for acute myocardial infarction from January 2005 to December 2010. The data were derived from DATASUS, the primary public health information system available in Brazil and from Mortality Information System (SIM). Adjustments and analyses were performed using the Autoregressive Integrated Moving Average with exogenous variables (ARIMAX) method modelled by environmental variables and atmospheric pollutants to evaluate the effect of smoking ban law in mortality and hospital admission rate. We also used Interrupted Time Series Analysis (ITSA) to make a comparison between the period pre and post smoking ban law. RESULTS: We observed a reduction in mortality rate (-11.9% in the first 17 months after the law) and in hospital admission rate (-5.4% in the first 3 months after the law) for myocardial infarction after the implementation of the smoking ban law. CONCLUSIONS: Hospital admissions and mortality rate for myocardial infarction were reduced in the first months after the comprehensive smoking ban law was implemented.

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BACKGROUND: Considering the pharmacokinetic and pharmacodynamic aspects of different medications, it is plausible that the age of a smoker could affect the half-life of these drugs. The aim of this study was to compare the effectiveness of smoking cessation drugs (nicotine replacement therapy, bupropion, and varenicline) used either in isolation or in combination in adults under and over 60 years of age. METHODS: Data were collected from 940 Brazilian patients participating in a smoking cessation program. Participants were prescribed smoking cessation medication to be used for at least 12 weeks and were followed for 52 weeks. RESULTS: Cessation rates were significantly different among younger and older participants who were using nicotine replacement therapy (NRT) alone. Being over 60 years of age was significantly associated with increased cessation success among those who used NRT alone (OR 2.34, 95% CI: 1.36 to 4.04, p = 0.002). The effectiveness of varenicline and bupropion were not significantly different according to age groups. CONCLUSION: Using age as a predictor for tailoring smoking cessation drugs might potentially lead to a more individualized prescription of smoking cessation therapy. These results should be tested in randomized controlled trials.

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