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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.
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PMID:Smoking and cardiovascular disease. 149 5

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major components of cigarette smoke which is believed to be partly responsible for the deleterious effect of cigarette smoke. There was significant alteration in the concentration of glycosaminoglycans (GAG) in rats exposed to cigarette smoke. Administration of nicotine to rats has been found to decrease many of GAG fractions in the aorta, liver and heart and increase in the lungs. The increase in GAG now observed in lung tissue in rats administered nicotine and those exposed to cigarette smoke may be involved in the increased incidence of lung cancer in smokers. Increased activity of many of GAG hydrolysing enzymes indicates increased degradation of GAG. Sulphate metabolism in the liver is also significantly altered by nicotine. Thus administration of nicotine to rats caused alteration in the metabolism of GAG which are similar to those observed on exposure of rats to cigarette smoke, indicating that nicotine content of the tobacco smoke may partly be responsible for the effect on GAG observed on exposure to cigarette smoke.
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PMID:Effect of nicotine on glycosaminoglycan metabolism in rats. 151 30

Cigarette smoking is associated with an increased risk and extent of advanced atherosclerotic vascular disease in peripheral as well as coronary arteries. The likelihood of claudication, amputation, stroke, abdominal aortic aneurysm, and failure of vascular reconstruction is higher in smokers than nonsmokers. Smoking exerts its deleterious effects through many interactive mechanisms. Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypertension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are elevated plasma, free fatty acids, elevated vasopressin, and a thrombogenic balance of prostacyclin and thromboxane A2. Chronic smoking is associated with a tendency for increased serum cholesterol, reduced high density lipoprotein, and other lipid effects that contribute to atherosclerosis. In addition to rheologic and hematologic changes from increased erythrocytes, leukocytes, and fibrinogen, smokers have alterations in platelet aggregation and survival that produce thrombosis. Considering the ubiquitous repercussions of this menace, vascular surgeons should play an active role in motivating their patients to quit smoking.
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PMID:The peripheral vascular consequences of smoking. 206 25

Chronic exposure to cigarette smoke causes an imbalance in both PGI2 and TXA2 production which is believed to favor the development of atherosclerosis. Nicotine, a major constituent of smoke, has been shown to adversely alter arachidonic acid metabolism. To determine whether varying doses of nicotine in cigarettes would influence the extent of PGI2/TXA2 alterations, male Sprague-Dawley rats were chronically exposed (7 days/wk/6 mo.) to smoke from University of Kentucky Reference cigarettes containing "low" nicotine (3A1), "high" nicotine (2R1) and "low" nicotine cigarettes spiked with enough nicotine to deliver amounts equivalent to the 2R1. COHb levels were monitored to confirm smoke inhalation. No differences in body weights were observed between treatment groups, but all were significantly lower than sham. Aortic PGI2 formation was not significantly depressed by any of the treatment groups compared to shams. Platelet TXA2 production was elevated in all treatment groups compared to shams, irrespective of nicotine content. In the rat smoking model, low nicotine cigarettes do not appear to be an advantage over higher nicotine cigarettes.
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PMID:Alterations in prostacyclin and thromboxane formation following chronic exposure to high and low nicotine cigarettes in rats. 330 20

Nicotine was fed to rats for 6 weeks, as a weight adjusted dose equivalent to that of a human being smoking 50 to 100 cigarettes per day. Those rats fed nicotine developed hypercholesterolaemia. Scanning electron microscopy showed the porosity of the hepatic sinusoidal endothelium of nicotine fed animals was about 40% that of control animals. The decline in porosity was found to be due to a reduction in diameter rather than number of fenestrae. We believe that this decreased hepatic sinusoidal porosity may alter cholesterol homeostasis by increasing the circulation time of chylomicron remnants too large to pass through the fenestrae. This phenomenon may be an aetiological factor in the known correlation between cigarette smoking, atherosclerosis, and coronary heart disease in humans.
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PMID:Nicotine decreases the porosity of the rat liver sieve: a possible mechanism for hypercholesterolaemia. 339 Mar 86

Smoking has been linked to the development and progression of atherosclerosis but the mechanism by which smoking exerts its deleterious effects remains unknown. This study was designed to examine in a systematic way the effects of nicotine and carbon monoxide on platelets, arterial walls, and the heart. Results of experiments designed to assess the effect of nicotine and carbon monoxide on the production of prostacyclin (PGI2) by the rabbit heart are reported. Animals exposed to carbon monoxide had the carboxyhemoglobin raised to at least 12% by breathing an atmosphere enriched with carbon monoxide. Nicotine was infused at 50 micrograms/kg/hr for 1 week. Nicotine was measured by gas/liquid chromatography. PGI2 was measured by radioimmunoassay of 6-keto-PGF1 alpha, and its biologic activity was assessed by inhibition of platelet aggregation. Nicotine is concentrated in the heart and blood vessel wall and causes a statistically significant reduction in PGI2 production. Carbon monoxide raised PGI2 production significantly in all chambers, and the combination of nicotine and carbon monoxide further raised PGI2 production. The difference between the effects of nitrogen and carbon monoxide alone and nitrogen and a combination of nitrogen and carbon monoxide was significant in all chambers. It is hypothesized that nicotine exerts a direct metabolic effect in lowering PGI2 production. Carbon monoxide may make the endothelial cell relatively hypoxic, a powerful stimulus of PGI2 production, or less likely exert a direct toxic effect on the endothelial cell.
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PMID:Prostacyclin production by the heart: effect of nicotine and carbon monoxide. 354 37

The effect of chronic oral nicotine intake on plasma low density lipoprotein (LDL) clearance, lipid transfer protein, and lecithin:cholesterol acyltransferase (LCAT) was examined in male atherosclerosis susceptible squirrel monkeys. Eighteen yearling primates were divided into two groups: 1) Controls fed isocaloric liquid diet; and 2) Nicotine monkeys given liquid diet supplemented with nicotine at 6 mg/kg body wt/day for a two-year period. Averaged over 24 months of treatment, animals in the Nicotine group had significantly higher levels of plasma and LDL cholesterol compared to Controls while plasma LCAT activity was similar for both groups. Following simultaneous injection of 3H LDL and 14C high density lipoprotein (HDL) cholesteryl ester (CE), removal of the latter was not altered by oral nicotine while plasma clearance of 3H LDL was dramatically delayed in Nicotine monkeys. Transfer of 14C HDL CE to very low density lipoprotein (VLDL)-LDL particles was greatly accelerated in the Nicotine group vs Controls while the reciprocal movement of 3H LDL CE to HDL was only higher in experimental animals at two time points following injection of the isotopes. Results from this study provide evidence that one major detrimental effect of long-term oral nicotine use is an increase in the circulating pool of atherogenic LDL which is due to: 1) accelerated transfer of lipid from HDL; and 2) impaired clearance of LDL from the plasma compartment. Diminished removal of LDL is of particular importance because an extended residence time of these particles in circulation would increase the likelihood of their deposition in the arterial wall.
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PMID:Oral nicotine impairs clearance of plasma low density lipoproteins. 371 25

Nicotine consumption is one of the most important avoidable risk factors for atherosclerosis and cardiovascular, pulmonary as well as many other diseases. In daily practice one cannot always clearly detect whether a patient remains really abstinent. 68 patients following consultations for risk factors were included in this study. Smoking habits were evaluated by means of a questionnaire and by measurement of carbon monoxide concentration in the breath; also the cotinine concentrations in saliva and urine were investigated during consultation. Cotinine is one of the most important metabolic product of nicotine. Smokers showed significantly increased carbon monoxide concentrations in the breath as well as increased cotinine concentrations in urine and saliva. Anamnestic information from patients about their nicotine consumption correlated well with the cotinine concentration in urine and saliva (r = 0.54). The best correlation was found between creatine-corrected cotinine concentration and cigarette consumption on the day preceding in measurement (p < 0.001, r = 0.66). It is not clear if and to what extent cotinine determination may qualify for the evaluation of passive smoking; however, measurement of cotinine concentrations in saliva (or urine) represents a good biochemical parameter for the control of nicotine abstinence.
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PMID:[Cotinine--a useful biomarker for tobacco use?]. 763 Oct 97

Patient care and research in clinical vascular surgery have traditionally and appropriately focused on the complications of atherosclerosis. Without question, however, the clinical field of vascular surgery encompasses a number of areas other than clinical vasospasm as exemplified by Raynaud's syndrome. At the Clinical Research Center at the Oregon Health Sciences University, during the past 20 years the vascular surgery unit has maintained an active research program in Raynaud's syndrome and to date has enrolled and longitudinally followed more than 1000 patients with this affliction. There has been an opportunity to participate in the long-term management of this large population with emphasis both on natural history and vascular laboratory diagnosis and treatment. Raynaud's syndrome is a condition characterized by episodic digital ischemia in response to cold or emotional stimuli. The incidence is greater in women, and it is more frequent in areas with a cool, damp climate. Raynaud's usually affects the hands and fingers, but it may affect the feet and toes as well. The classical Raynaud's attack is tricolor and consists of blanching of the digits resulting from cessation of arterial flow, then cyanosis upon rewarming. This is followed by reactive hyperemia, which causes the digits to turn red. Raynaud's syndrome is classified into two groups: vasospastic or obstructive. Vasospastic Raynaud's is generally cold-induced. Nicotine, stress, and caffeine are associated with vasospasm. Obstructive Raynaud's is observed in association with other diseases such as connective tissue disorders, atherosclerosis, traumatic occlusion, Buerger's disease, and occupational related disorders. The diagnosis of Raynaud's is based on differentiating between vasospasm and obstruction and detecting the presence of associated disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Raynaud's syndrome: diagnosis and treatment. 774 70

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


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