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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over one quarter of the risk of death due to the sudden infant death syndrome (cot death) is attributable to maternal smoking. Maternal smoking during pregnancy and infancy is one of the most important avoidable risk factors for infant death. Nicotine is a drug of addiction. Many young smokers are addicted to nicotine and develop withdrawal symptoms on stopping. Smoking is an important marker for other types of drug abuse, e.g. alcohol, cannabis and cocaine. The earlier children start smoking, the greater the risk of lung cancer and heart disease. Smoking affects immunity and has been associated with an increased risk of acquiring human immunodeficiency virus-1 infection.
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PMID:Smoking and the young. 146 39

Cigarette smoking has been causally linked to atherosclerotic heart disease. The mechanism by which cigarette smoking causes heart disease has not, however, been determined. Nicotine has been shown to lead to increases in plasma epinephrine and norepinephrine following smoking. Catecholamines have been shown to lead to increases in blood glucose. This paper demonstrates that cigarette smoking is associated with increases in average blood glucose as measured by glycosylated hemoglobin levels in smokers compared with nonsmokers. Fifteen nondiabetic smokers had an average glycosylated hemoglobin of 6.82% (SD = 1.06%), which is higher than the 5.63% (SD = .49%, t = 3.98, P less than .001) found for 23 nonsmokers. The average glycosylated hemoglobin level of the smokers is in the range found for patients with well-controlled diabetes. These data suggest that elevated blood glucose may contribute to atherogenesis in cigarette smokers.
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PMID:The effects of cigarette smoking on glycosylated hemoglobin in nondiabetic individuals. 276 87

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

Smoking tobacco contributes to and exacerbates many chronic diseases of aging, including hypertension, stroke, COPD, heart disease, and atherosclerosis. It is also associated with an increased risk of peptic ulcers and of cancers of the lungs and oral cavity. Older patients generally continue to smoke because of physiologic and psychological addiction to nicotine. Nicotine administration through gum or patch eases the symptoms of nicotine withdrawal for highly-tolerant patients. Detecting and treating alcohol abuse, depression, or life stress may then make it easier to motivate the patient to quit smoking. Physician advice combined with follow-up visits and phone calls has been shown to be one of most effective methods of getting patients to stop smoking.
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PMID:Smoking cessation: clinical steps to improve compliance. 838 53

Recent findings have demonstrated that terminally differentiated adult ventricular myocytes are capable of repairing DNA that has been damaged by exposure to oxygen free radicals. Despite the potential importance of DNA repair in cells that may survive many decades after injury, little is known about the mechanisms or regulation of repair. Since tobacco use has a well-defined role in the epidemiology and pathophysiology of heart disease, we tested the effects of nicotine on repair of free radical damaged plasmids by whole-cell protein extracts from adult myocytes. Exposure to a concentration of 25 microM nicotine increased incorporation of (32P)dCTP into damaged plasmids by 16%, and 50 or 100 microM nicotine increased incorporation by 32%. Nicotine did not alter the rate or amount of poly (ADP-ribose) on the major protein acceptor of molecular weight 113-116 kDa. Inhibition of DNA polymerase activity with pyridoxal 5'-phosphate revealed greater plasmid degradation in the presence of nicotine. We conclude that nicotine enhances DNA degradation and the increased repair is a consequence of this greater degradation.
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PMID:The effect of nicotine on DNA repair in adult myocytes. 973 35

Tobacco use is a global health care problem. Repetitive exposure to nicotine produces neuroadaptation resulting in nicotine dependence. Cigarette smoking is particularly addictive due to the repeated delivery of bolus doses of nicotine to the bloodstream. Although compulsive tobacco use is sustained by nicotine addiction, it is the toxic combustion products in tobacco smoke such as carbon monoxide and oxidant gases that adversely affect the cardiovascular system. Smoking cessation produces significant health benefits and is a very cost-effective intervention. Evidence that nicotine is the addictive component of tobacco provides the rationale for using nicotine replacement therapy to aid cessation. Nicotine replacement therapy doubles successful smoking cessation rates and evidence-based guidelines for the treatment of tobacco addiction recommend routine use of nicotine replacement therapy, particularly in heavily dependent smokers. Success rates of up to 40% can be achieved in specialist clinics. Despite early concerns regarding the safety of nicotine replacement therapy in smokers with heart disease, it is now clear that the health risks of using nicotine replacement therapy to assist such patients to stop, or significantly reduce, smoking far outweigh any treatment-related risks.
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PMID:Diagnosis and treatment of nicotine dependence with emphasis on nicotine replacement therapy. A status report. 1068 82

This gender-specific research study compares the relative effectiveness of two theory-based interventions targeting women who smoke. Women with coronary artery disease (CAD; n = 53) or CAD risk factors (n = 107) were randomly assigned to either coping-skills Relapse Prevention (RP) treatment or an educational/supportive treatment based on Health Belief Model (HBM) principles. RP was comparable, but not superior to HBM treatment, as indicated by the lack of differential smoking outcomes at 3 and 6 months. RP was more effective than HBM for women with low self-efficacy, as predicted. The presence of a smoking-related disease had a substantial effect on smoking status, in that the odds of being abstinent at 6 months were 2.2 times greater for non-diagnosed women when compared with CAD women. These findings indicate that more potent relapse prevention interventions are needed to increase cessation rates in women who smoke, especially those with established heart disease.
Nicotine Tob Res 1999 Mar
PMID:Smoking cessation in women with cardiac risk: a comparative study of two theoretically based therapies. 1107 92

Nicotine, the addictive component of tobacco, is thought to be at least partially responsible for the deleterious effects of smoking such as heart disease and cancer. Evidence shows that nicotine is an immunomodulator and that one of its possible mechanisms is regulation of apoptosis, or programmed cell death, in immune cells. This study examined the effects and the mechanisms of action of nicotine on dexamethasone (DEX)-induced apoptosis in murine immune cells by examining the expression of levels of the 17-kDa active caspase-3, a marker of apoptosis. Thymocytes and splenocytes from adult BALB/c female mice were incubated with concentrations of nicotine correlating to those found in the blood and tissue of smokers (0.01 microg/ml [0.022 microM] and 1 microg/ml [2.2 microM]), concurrently with 100 nM DEX, to induce apoptosis. Cytosolic protein fractions were analyzed by Western blotting with polyclonal antibodies that recognize the active form of caspase-3. The data showed that nicotine significantly blocked the formation of the DEX-induced 17-kDa caspase-3 subunit expression. This downregulation ranged from 65% to 100% of the active caspase-3 expressed in cultures treated with DEX alone. Addition of d-tubocurarine chloride (dTC), a general nicotinic receptor antagonist, inhibited nicotine downregulation of the DEX-induced active caspase-3 expression, providing evidence that this action of nicotine was receptor-mediated. These data support that nicotine is an important immunomodulator at the level of immune cell apoptosis, a process thought to be a contributory mechanism of autoimmunity, cardiovascular disease, and carcinogenesis.
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PMID:Nicotine inhibition of apoptosis in murine immune cells. 1168 2

The adverse effects of tobacco smoking on the cardiovascular system are well established. Effects of nicotine on the heart, in contrast, are not well characterized. Understanding specific effects of nicotine on the heart and on blood volume is relevant to (a) elucidating the mechanisms by which nicotine may contribute to heart disease and (b) determining potential risks associated with nicotine products used in smoking cessation or to treat various medical conditions. The present experiment investigated effects of continuous nicotine administration for 14 days (0, 6, or 12 mg/kg/day) on heart histopathology and blood volume (a measure of hemoconcentration) in 59 male and 59 female rats of two strains (Sprague-Dawley and Long-Evans). Following nicotine administration, animals were sacrificed and blood volume was measured. Heart length; heart weight; left ventricle, right ventricle, lateral wall, anterior wall, and posterior wall thicknesses; and intraventricular width (i.e., septum) were measured. Nicotine reduced heart weight, heart length, and overall blood volume. Females were more sensitive than males to the effects of nicotine on heart weight. In contrast, males were more sensitive than females to the effects of nicotine on heart length. Together, these findings suggest that males and females differ in their sensitivity to nicotine's cardiac effects.
Nicotine Tob Res 2003 Jun
PMID:Effects of nicotine on heart dimensions and blood volume in male and female rats. 1279 29

Tobacco smoking is the main risk factor associated with chronic destructive periodontal disease. No other known factor can match the strength of smoking in causing harm to the periodontium. The harmful effects manifest themselves by interfering with vascular and immunologic reactions, as well as by undermining the supportive functions of the periodontal tissues. The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the ensuing clinical symptoms of bone loss, attachment loss, pocket formation, and eventually tooth loss. A review of the international literature that has accumulated over the past 20 years offers convincing evidence that smokers exhibit greater bone loss and attachment loss, as well as more pronounced frequencies of periodontal pockets, than non-smokers do. In addition, tooth loss is more extensive in smokers. Smoking, thus, considerably increases the risk for destructive periodontal disease. Depending on the definition of disease and the exposure to smoking, the risk is 5- to 20-fold elevated for a smoker compared to a never-smoker. For a smoker exposed to heavy long-life smoking, the risk of attracting destructive periodontal disease is equivalent to that of attracting lung cancer. The outcome of periodontal treatment is less favorable or even unfavorable in smokers. Although long-term studies are rare, available studies unanimously agree that treatment failures and relapse of disease are predominantly seen in smokers. This contention is valid irrespective of treatment modality, suggesting that smoking will interfere with an expected normal outcome following commonplace periodontal therapies. The majority of available studies agree that the subgingival microflora of smokers and non-smokers are no different given other conditions. As a consequence, the elevated morbidity in smokers does not depend on particular microflora. The mechanisms behind the destructive effects of smoking on the periodontal tissues, however, are not well understood. It has been speculated that interference with vascular and inflammatory phenomena may be one potential mechanism. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing. Smoking research over the past two decades has brought new knowledge into the domains of periodontology. Even more so, it has called into question the prevailing paradigm that the disease is primarily related to intraoral factors such as supra- and subgingival infection. Smoking research has revealed that environmental and lifestyle factors are involved in the onset and progression of the disease. Being the result of smoking, destructive periodontal disease shares a common feature with some 40 other diseases or disorders. As a consequence, periodontal disease should be regarded as a systemic disease in the same way as heart disease or lung disease. Thus, chronic destructive periodontal disease in smokers is initiated and driven by smoking. Its progression may or may not be amplified by unavoidable microbial colonization.
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PMID:Tobacco smoking and chronic destructive periodontal disease. 1549 Feb 98


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