Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Reduction of Smoking in Cardiac Patients (ROSCAP) Study is a randomized controlled trial to test the effectiveness of a smoking reduction strategy to decrease tobacco-related harm, promote cessation, and improve biochemical and clinical indicators of toxin exposure among patients with heart disease. We analyzed baseline characteristics of patients enrolled for participation to investigate predictors of spontaneous smoking reduction prior to study enrollment. Past reducers were more likely to be males (p=.009) and had higher past peak smoking level (p<.0001) than nonreducers. Gender and number of heart disease diagnoses predicted the occurrence of spontaneous reduction and its extent. Age and a history of chronic obstructive pulmonary disease also predicted the extent of reduction. Cotinine and nicotine levels per cigarette per day were significantly higher among past spontaneous reducers than nonreducers. Spontaneous reduction is common among medically ill smokers. Past history of heart disease is a strong predictor of prior reduction. There is evidence of compensation among past spontaneous reducers.
Nicotine Tob Res 2005 Apr
PMID:Predictors of smoking reduction without formal intervention. 1603 85

Smoking is the leading preventable cause of illness and premature death in Germany, claiming over 110,000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema and a variety of cancers. The overwhelming majority of smokers begin tobacco use before they reach adulthood. Among those young people who smoke, the average age is now 13-14. In Germany, about 39% of male and 31% of female adults (age 18-60 years) continue to smoke, despite information about the unequivocally negative health consequences of smoking. The exact mechanisms of smoking-related vascular disease are not yet known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction mainly by increased inactivation of nitric oxide by oxygen-derived free radicals. Smoking also increases oxidative modification of LDL and is associated with lower HDL plasma levels. Smoking induces a systemic inflammatory response with increased leukocyte count and elevation of the C-reactive protein level. Importantly, the prothrombotic effects of smoking have been repeatedly demonstrated to cause alterations in platelet function, imbalance of antithrombotic vs prothrombotic factors, and decrease of fibrinolytic activity. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counselling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every smoker should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment. A framework for tobacco control measures is necessary to reduce tobacco consumption and exposure to tobacco smoke. Recommendations on specific tobacco control interventions are: 1. increase in tobacco taxes; 2. comprehensive tobacco advertising bans; 3. legislation prohibiting smoking in work and public places; 4. prohibiting the sales of tobacco products to persons under 18; 5. comprehensive disclosure of the physical, chemical and design characteristics of all tobacco products; 6. training of health professionals to promote smoking prevention and cessation interventions; and 7. development of a national network of smoking cessation treatment services.
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PMID:[Prevention of coronary heart disease: smoking]. 1625 91

The prevalence of smoking is greater and smoking restrictions are less common in rural areas in comparison to urban areas. Consequently, rural smokers and their families are at increased risk for adverse health consequences from smoking. The presence of home smoking restrictions (i.e., limiting or banning cigarette smoking in the home) can be a mediator for smoking cessation and can reduce health risks for those who live with smokers. The purpose of the present study was to identify correlates of home smoking restrictions among rural smokers. We surveyed 472 smokers from 40 rural Kansas primary care practices who were enrolled in a smoking cessation intervention study. We assessed the prevalence of home smoking restrictions and examined the relationship between such restrictions, demographic variables, comorbid diagnoses, and psychosocial measures of smoking abstinence self-efficacy and motivation to quit. Complete home smoking restrictions were found among 25.4% of rural smokers with an additional 28.3% reporting some restrictions. Restrictions were associated with younger age, higher controlled motivation to quit (i.e., motivation from external pressure), the presence of children under age 6 years living in the home, fewer friends who smoke, and a partner who does not smoke. Smokers with a comorbid diagnosis of high cholesterol, chronic lung disease, or heart disease were less likely to have restrictions. Most smokers in rural primary care practices do not have home smoking restrictions, particularly those without children or a nonsmoking partner and those with significant risk factors for smoking-related illnesses. These patients may be critical targets for broaching issues of home smoking restrictions.
Nicotine Tob Res 2006 Jun
PMID:Correlates of home smoking restrictions among rural smokers. 1680 Dec 93

Pharmacotherapy is a critical adjunct to smoking cessation therapy. Little is known about relative preferences for these agents among smokers in primary care settings. In the context of a population-based clinical trial, we identified 750 smokers in primary care practices and independent of their readiness to quit offered them a free treatment course of either bupropion or transdermal nicotine replacement (TNR). Smokers opting for pharmacotherapy completed standardized contraindication screens that were reviewed by the patient's primary care physician. Most participants (67%) requested pharmacotherapy. Use of pharmacotherapy was positively associated with higher nicotine dependence and readiness to quit. Of the smokers requesting pharmacotherapy, 51% requested bupropion and 49% requested TNR. Choice of bupropion was related to no history of heart disease and no previous use of bupropion. Although potential contraindications to treatments were identified for 21.7% of bupropion and 6.6% of TNR recipients, physicians rarely felt that these potential contraindications precluded the use of these agents. When cost is removed as a barrier, a large proportion of rural smokers are eager to use smoking cessation pharmacotherapy, especially agents that they have not tried before. Although some comorbid conditions and concurrent drug therapies were considered contraindications, particularly to bupropion, physicians rarely considered these clinically significant risks enough to deny pharmacotherapy.
Nicotine Tob Res 2008 Feb
PMID:Smoking cessation pharmacotherapy preferences in rural primary care. 1823 94

Cigarette reduction has been proposed as a treatment goal for smokers who are not interested in stopping completely. This randomized controlled trial was designed to determine the effect of a smoking reduction intervention on smoking behavior, symptoms of heart disease, and biomarkers of tobacco exposure. It included 152 patients with heart disease who did not intend to stop smoking in the next 30 days. Participants were randomly assigned to smoking reduction (SR) or usual care (UC). SR subjects received counseling and nicotine replacement therapy to encourage > or =50% reduction in cigarettes per day (CPD). They were followed at 1, 3, 6, 12 and 18 months to assess smoking, heart disease symptoms, quality of life and nicotine, cotinine, carbon monoxide (CO), white blood cell (WBC) count, fibrinogen, hs-C-reactive protein (hs-CRP), F2-isoprostane, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and 1-hydroxypyrene (1-HOP). At 6 months SR participants reduced by 10.9 CPD, compared with 7.4 CPD in UC (difference NS). At 18 months, 9/78 SR vs. 9/74 UC participants quit smoking. There were no significant differences between treatment groups in angina, quality of life or adverse events, nicotine, cotinine, CO, WBC count, fibrinogen, hs-CRP, F2-isoprostane, total NNAL or 1-HOP levels at any time point. To determine if smoking reduction, regardless of treatment condition, was associated with improved outcomes, we compared all subjects at 6 months to baseline (mean reduction in CPD from 27.4 to 18.1, p<.01). There were no significant changes in outcome variables except CO, which decreased by 5.5 ppm (p<.01). There were also no significant improvements considering only subjects who reduced by > or =50%, or those who had no history of reduction prior to enrollment in the study. The SR intervention did not significantly reduce CPD or toxin exposure, or improve smoking cessation or clinical outcomes compared to UC. These results emphasize the importance of abstinence for smokers with heart disease to minimize health risks from tobacco.
Nicotine Tob Res 2008 Mar
PMID:Smoking reduction fails to improve clinical and biological markers of cardiac disease: a randomized controlled trial. 1832 66

Since 2000, the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study has been collecting information on cardiovascular disease (CVD) and its risk factors from 1,214 Alaska Natives of the Norton Sound region, a population with increasing rates of heart disease and stroke. Because smoking was reported in a large proportion of the participants, this analysis was undertaken to evaluate smoking patterns and their relation to other risk factors and to CVD. The relationships among smoking habits and demographic factors, body mass index, plasma fibrinogen, prevalent hypertension, and carotid plaque were evaluated. Eighty percent of participants had smoked 100+ cigarettes in their lifetime. Fifty-seven percent of women and 63% of men (p = .12) were current smokers: one in four smokers had quit. Current smokers (OR = 2.1; 95% CI = 1.1-3.8) and those who had quit <5 years ago (OR = 1.6; 95% CI = 1.1-2.2) were more likely than non-smokers to have carotid plaque. Pack-years smoked also were correlated with carotid plaque. The high prevalence of smoking and low rates of cessation in this population demonstrate an urgent need for smoking prevention and cessation programs among Alaskan Eskimos of the Norton Sound region and other Alaska Native groups.
Nicotine Tob Res 2008 Mar
PMID:Prevalence of smoking and its relationship with carotid atherosclerosis in Alaskan Eskimos of the Norton Sound region: the GOCADAN study. 1832 67

Smoking cessation can reduce both morbidity and mortality among patients who have heart disease. China has the largest number of smokers in the world, and most smokers have low motivation to quit. Regular smoking cessation services are almost nonexistent in China, and little is known about the psychometric properties of instruments in assessing smoking self-efficacy in Chinese, whose cultures differ greatly from those of Westerners. The present study tested the psychometric properties of the Chinese version of the Smoking Self-Efficacy Questionnaire (SEQ-12) among 1,841 Chinese smokers who had heart disease, including (a) factorial structure using confirmatory factor analysis, (b) reliability with Cronbach's alpha, (c) concurrent validity, and (d) predictive validity of successful quitting. Confirmatory factor analysis of the SEQ-12 revealed a modified two-factor model that provided a good fit to the data; item 6 ("urge to smoke") was an indicator for the external stimuli subscale rather than for the internal stimuli subscale. Internal consistency coefficients (.77 for external stimuli and .88 for internal stimuli) were acceptable. Baseline self-efficacy scores were significantly associated positively with stage of readiness to quit, and negatively with cigarettes smoked per day and Fagerstrom Test for Nicotine Dependence (FTND) score. Multivariate logistic regression analysis showed that successful quitting at 1 month and at 3 months were predicted by higher external stimuli score, fewer cigarettes smoked per day, lower FTND scores, and being in the intervention group. We concluded that the Chinese version of the SEQ-12 is a valid and reliable instrument for Chinese cardiac patients who smoke. The SEQ-12 can be used to assess smokers' self-efficacy so that appropriate smoking cessation interventions can be provided.
Nicotine Tob Res 2008 Aug
PMID:An evaluation of the psychometric properties of the Smoking Self-Efficacy Questionnaire (SEQ-12) among Chinese cardiac patients who smoke. 1868 78

Smoking is one of the leading preventable causes of disease, disability, and death in the USA and leads to more than 400,000 preventable deaths per year. Nicotine is the major alkaloid present in tobacco smoke, and many of the negative effects of smoking are attributed to nicotine. Nicotine is not only the addictive component of tobacco smoke, but also highly associated with carcinogenesis and induces oxidative stress. Furthermore, the administration of nicotine via subcutaneous mini-osmotic pumps or by injection is an established method in preclinical studies for this area of research. Thus, preclinical research on the negative effects of tobacco smoke and tobacco addiction has focused primarily on the effects of nicotine. However, there are over 4,500 components found in tobacco smoke, many of which are highly toxic. Other components may also contribute to the addictive properties of tobacco smoke. Furthermore, the negative effects of tobacco smoke are not isolated to the smoker but can have negative effects to those exposed to the secondhand smoke (SHS) stream. SHS exposure is the third leading cause of preventable death. Approximately 38,000 deaths per year are attributed to SHS exposure in the USA. SHS exposure increases the risk of heart disease by approximately 30% and is associated with increased risk of stroke, cancer, type II diabetes, as well as pulmonary disease. Thus, methods of administering tobacco smoke in a controlled environment will further our understanding of tobacco addiction and the role tobacco smoke in other disease states. Moreover, combining smoke exposure with proteomics can lead to the discovery of biomarkers that can be potentially useful tools in screening, early diagnosis, prevention, and treatment of diseases caused by SHS.
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PMID:Methods in tobacco abuse: proteomic changes following second-hand smoke exposure. 2223 25

Inhalation of drugs for therapeutic effects is not a recent innovation as illicit drugs have been 'smoked' for millennia. Nicotine delivery 'devices' in convenient packaged cartons of cigarettes are simple to use, inexpensive per dose and accessible to people of most ages and lung function, but of course their use leads to increased cancer, emphysema, heart disease and other medical and societal problems. In contrast, many inhalation pharmaceutical medical devices are expensive, nonportable, inconvenient, and/or are used improperly thus leading to poor therapeutic benefit. We review the current state of the art with respect to aerosol delivery, inhalation devices and the ability to personalize the treatment and management of lung disease. The confluence of many drivers will lead to more programmable and flexible devices in the future: the transition from the blockbuster model to customized therapy, technological advancements (e.g., smartphones) and cultural changes including social networking.
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PMID:Personalizing aerosol medicine: development of delivery systems tailored to the individual. 2283 56

Clinical studies have demonstrated that cigarette smoking is strongly associated with insulin resistance and heart disease. Nicotine is considered the primary toxin constituent associated with smoking. However, the distinct molecular mechanism of nicotine-induced cardiac dysfunction remains unclear. Cardiomyocytes with nicotine-induced insulin resistance are characterized by decreased glucose uptake, as measured by 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose (2-NBDG), a fluorescent derivative of glucose, and reactive oxygen species (ROS) generation. Immunoblotting was used to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), extracellular signal-related kinase (ERK) and phosphoinositide 3-kinase (PI3K, p85, Y607). We determined the impact of nicotine on insulin resistance and Nrf2, phospho-ERK and phospho-PI3K expression in the myocardial tissue of a mouse model. Nicotine increased ROS production and depressed insulin-induced glucose uptake in cardiomyocytes. Pretreatment with N-acetyl-L-cysteine (NAC), an antioxidant, reversed nicotine-inhibited glucose uptake induced by insulin. Nicotine exposure directly inhibited Nrf2 and increased ERK phosphorylation in cardiomyocytes, which were obstructed by NAC. Further exploration of signaling cascades revealed nicotine-induced ROS involved in inhibiting PI3K/Nrf2 and activating ERK in cardiomyocytes. Moreover, the mouse model treated with nicotine showed glucose intolerance and impaired insulin tolerance accompanied by inhibited PI3K/Nrf2 and increased ERK in myocardial tissues. Thus, nicotine induces insulin resistance via the downregulation of Nrf2 activity in cardiomyocytes, which is a potential mechanism of the pharmacological effects of nicotine. This study identified potential therapeutic targets against nicotine-related cardiovascular diseases.
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PMID:Nicotine induces insulin resistance via downregulation of Nrf2 in cardiomyocyte. 3131 24


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