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

The results of the catamnestic study of case reports and records of postmortem examination of 102 patients with bronchial asthma (BA) aged 47 to 88 years who died at a general hospital during 1976-1988 indicate that in the overwhelming majority of cases, there took place death "with asthma" rather than death "from asthma". At the same time the dominant pathology was coronary heart disease (acute coronary failure, myocardial infarction, progressive heart failure associated with atherosclerotic and postinfarction cardiosclerosis). Emphasis is laid on the fact that according to the autopsy data, the rate of the recognized stenosing atherosclerosis of the coronary arteries considerably exceeded the number of cases of coronary heart disease documented clinically (typical angina pectoris of effort, significant macrofocal myocardial infarction). The characteristic features of the group under observation included an unexpectedly frequent combination of BA and malignant neoplasms (24 cases), including lung cancer in 13 of these cases.
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PMID:[An analysis of the causes of death in bronchial asthma patients (based on the data from a 13-year prospective observation)]. 236 7

Despite increasing scientific evidence for a causal role of tobacco smoking in lung cancer and coronary heart disease, an alternative hypothesis was put forward several decades ago. The constitutional hypothesis has stated that there are genetic or other common factors, which predispose both to smoking and disease. A critical test of this hypothesis was considered the pattern of occurrence of disease in monozygotic (MZ) twin pairs in which one is a smoker and the other never has been a smoker. Initial twin studies found only small differences in the mortality of smoking and nonsmoking twins of discordant pairs. In the Finnish Twin Cohort, a population-based panel of adult like-sexed twin pairs, a questionnaire study carried out in 1975 permitted identification of 2488 twin pairs discordant for cigarette smoking. Analyses of total mortality and mortality due to coronary heart disease and lung cancer indicate that the smoking members of discordant MZ pairs are at higher risk than their nonsmoking cotwins; increased mortality of smoking cotwins was also found on 21-year follow-up of smoking-discordant pairs in Sweden. Incidence data and noninvasive studies of atherosclerosis in the Finnish sample provide confirmatory evidence for the causal role of smoking in the etiology of coronary heart disease and lung cancer.
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PMID:Cigarette smoking as a cause of lung cancer and coronary heart disease. A study of smoking-discordant twin pairs. 239 91

To determine the relative importance of multiple interrelated factors that have been considered to contribute to pulmonary infarction, the authors performed a discriminant analysis on consecutively autopsied patients with pulmonary embolism. From the clinic records of 45 individuals, the authors tabulated the underlying illness, history of valvular or ischemic heart disease, right and left ventricular failure, sepsis, shock, malignancy, premortem functional status, and the clinician's suspicion of pulmonary embolism. At postmortem examination, the authors measured and recorded the extent of emphysema, pneumonia, neoplasia, pulmonary vascular atherosclerosis; thickness and dilatation of both cardiac ventricles; the presence of valvular heart disease; the number, diameter, and amount of occlusion of the pulmonary arteries that contained thromboemboli; the extension of the clot, the size of the infarct; the Reid-Index; and the thickness of pulmonary and bronchial arterial wall. The major determinants of infarction were as follows: poor premortem functional status, the number of lobes having emboli, left ventricular failure, and the presence of lung cancer. The authors then tested the equation generated from these patients on 21 additional patients. The discriminant function correctly classified 81% of first group and predicted the occurrence of infarction in new patients with 70% accuracy. The size of the infarct was most correlated with the use of vasodilators and the embolic burden.
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PMID:Factors associated with pulmonary infarction. A discriminant analysis study. 401 73

Mortality among workers of the rubber industry was assessed following the observation of the cohort comprised of 6,978 male workers who had started their employment in the plant producing rubber footwear during the years 1945-1973, and worked for, at least, three months. The condition of the cohort was assessed for December 31, 1990. Standardised mortality rate (SMR) was used as a measurement tool and it was calculated by means of the man-year method. The general population of Poland was taken as the reference population. General mortality in the cohort was significantly higher than in the reference population (2020 death, SMR = 110). Significant excess mortality due to atherosclerosis (205 deaths, SMR = 135) and cirrhosis of the liver (48 deaths, SMR = 170) was also noted. Total number of deaths due to malignant neoplasms-421-was slightly higher than expected. Significant excess of the bladder cancer (13 deaths, SMR = 357), the larynx cancer (23 deaths, SMR = 180) and the lung cancer (148 deaths, SMR = 122) was revealed. Significantly increased risk of the large intestine cancer (15 deaths, SMR = 242) was observed in the subcohort of workers employed in direct production departments.
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PMID:[Mortality among workers of the rubber industry. III. Results of further observation of the male cohort]. 747 45

Out of a number of 2113 of COLD ambulatory cases followed-up over 20 years, 170 cases of death were registered. The causes were: heart in 54%, cancer in 42% among which 37% lung cancer, exceeding 8 times the mean figures on the whole country. These diseases: COLD, atherosclerosis inducing heart disease and lung cancer have common risk factors which unbalance respiratory homeostasis. By obstructing the airways they lead to cellular O2 deficit. In this way the cell is compelled to shift to anaerobic glycolysis in order to supply the bioenergy necessary for life, resulting in malignancy mutagenesis. On a control group of 166 cases of lung cancer a ventilatory impairment was noted in the history: obstructive syndrome in 63.8%, restrictive syndrome in 28.3%, which means chronic respiratory insufficiency.
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PMID:[Chronic obstructive bronchopneumonia (COBP), a precancerous state through destabilization of body homeostasis and bioenergetics]. 776 2

The mechanisms by which exposure to cigarette smoke dramatically increase the incidence and severity of atherosclerosis and the incidence of lung cancer, chronic obstructive airways disease, and emphysema are incompletely understood. Epidemiologic evidence has suggested a modifying role for antioxidant micronutrients, including tocopherols and carotenoids, in these disease processes. It has been suggested that oxidants in cigarette smoke could be involved. We exposed freshly obtained human plasma to the gas phase of cigarette smoke to assess its effects on tocopherols, carotenoids, and retinol. Exposure to cigarette smoke led to the depletion of most of the lipophilic antioxidants in 20 mL human plasma. The order of disappearance was lycopene > alpha-tocopherol > trans-beta-carotene++ > (lutein + zeaxanthin) = cryptoxanthin > gamma-tocopherol = retinol. However, despite a substantial loss of alpha-tocopherol, there was very little peroxidative damage to lipids, and no detectable change in the content of polyunsaturated fatty acid-rich cholesterol esters. We conclude that a wide spectrum of lipophilic micronutrients undergo degradation when exposed to gas-phase cigarette smoke. The relevance of these in vitro findings to possible cigarette smoke-induced depletions of respiratory tract lipophilic antioxidants remains to be clarified.
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PMID:Destruction of tocopherols, carotenoids, and retinol in human plasma by cigarette smoke. 859 20

Nicotine, a major component of cigarette smoke, plays an important role in the development of cardiovascular disease and lung cancer in smokers. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis and the level of lipid peroxides is increased in smokers. In rats fed a high-fat diet, the tissue concentration of lipid peroxides was found to be increased. On nicotine administration along with a high-fat diet an additive effect was observed in lipid peroxidation and free radical scavengers. The activities of scavenging enzymes superoxide dismutase, catalase and glutathione reductase were found to be decreased, while the glutathione concentration and activity of glutathione peroxidase were enhanced.
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PMID:Effect of nicotine on antioxidant defence mechanisms in rats fed a high-fat diet. 884 84

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major toxic components of cigarette smoke that is believed to be partly responsible for the deleterious effect of cigarette smoke. Alcohol intake is another major risk factor for the development of cardiovascular disease. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis. The concentration of lipid peroxides is found to be increased in alcohol-treated rats. On nicotine administration along with alcohol, an additive effect was observed in lipid peroxidation and the antioxidant defence mechanism. The activity of scavenging enzymes superoxide dismutase, catalase and glutathione reductase was found to be decreased, while the activity of glutathione peroxidase and the concentration of glutathione were increased.
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PMID:Additive effect of alcohol and nicotine on lipid peroxidation and antioxidant defence mechanism in rats. 885 16

A mortality cohort study was carried out on 11,224 men with pneumoconiosis diagnosed during the period 1970-1985. The cohort was selected from among subjects entered into the National Register of Occupational Diseases and included 7,065 coal miners, 924 employees of underground work enterprises, 1,796 workers of the metallurgical industry and iron and nonferrous foundries, as well as 1,439 refractory materials, china, ceramics, and quarry workers. The cohort was traced up to the end of 1991. The mortality of all groups enrolled in the study, as compared with that of general male population of Poland, showed a statistically significant excess of overall mortality (SMRs ranging from 105; 95% confidence interval [CI]: 100-110 to 136; CI: 121-153) as well as a great excess of deaths from diseases of the respiratory system (SMRs from 383; 95% CI: 345-424 to 588; 95% CI: 457-744). In workers of the metallurgical industry, foundries, and those from refractory materials, china, and ceramics manufacturing plants as well as quarries, a statistically significant excess of deaths from infectious diseases (mostly tuberculosis) was found (SMRs: 503; 95% CI: 364-677 and 286; 95% CI: 177-437, respectively). Mortality from lung cancer was significantly elevated only in the group of metallurgical industry and iron and nonferrous foundry workers (SMR: 159; 95% CI: 124-201). In the remaining subcohorts, no significant excess of deaths from lung cancer was noted. The study does not support the hypothesis on the role of exposure to crystalline silica in the induction of lung cancer. Significantly lower mortality was seen for diseases of the circulatory system (SMR: 89; 95% CI: 82-96), hypertensive disease (SMR: 63; 95% CI: 38-98), cerebrovascular disease (SMR: 79; 95% CI: 62-99), atherosclerosis (SMR: 79; 95% CI: 66-93), and injuries and poisonings (SMR: 50; 95% CI: 38-64) in coal miners. In addition, lower mortality was noted for cerebrovascular disease (SMR: 56; 95% CI: 32-91) and injuries and poisonings (SMR: 34; 95% CI: 17-61) in metallurgical industry and iron and nonferrous foundry workers.
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PMID:Mortality among different occupational groups of workers with pneumoconiosis: results from a register-based cohort study. 891 18

DNA adducts are biomarkers evaluating the biologically effective dose of carcinogens, which reflects, more realistically than the external exposure dose, an enhanced risk of developing cancer. Likewise, inhibition of DNA adduct formation can be assumed as an indicator of decreased risk. Molecular dosimetry techniques can be exploited in anticarcinogenicity studies in animal models as well as in Phase II clinical chemoprevention trials. We have extensively used these end points in animal studies using individual carcinogens and complex mixtures. As assessed by 32P-postlabelling, DNA adducts were formed in the liver of rats fed a diet supplemented with 2-acetylaminofluorene. DNA adducts were detected by synchronous fluorescence spectrophotometry (SFS) in rat liver, lung, heart and testis following intratracheal (l.t) instillations of benzo[a]pyrene. The whole-body exposure of rats to mainstream cigarette smoke resulted in the appearance of DNA adducts in lung, heart, aorta and kidney, whereas adducts were not detected by SFS in liver, brain, oesophagus and testis. Moreover, typical diagonal radioactive zones and multiple DNA adducts were revealed by 32P-postlabelling in the tracheal epithelium, nasal mucosa, aorta and testis of smoke-exposed rats. Formation of adducts to lung DNA, as assessed by both 32P-postlabelling and SFS, also occurred in rats receiving i.t. instillations of air particulate extracts from polluted urban and rural areas. The oral administration of the thiol N-acetylcysteine (NAC) significantly inhibited the formation of DNA adducts in all organs of the rats exposed to the aforementioned carcinogens, which correlated with the parallel inhibition of biochemical, cytogenetic and histopathological alterations as well as with inhibition of preneoplastic and neoplastic lesions in rodents. Our working hypothesis is that DNA adducts in trachea/lung, heart and aorta may be associated with lung cancer, cardiomyopathies and atherosclerosis, respectively. DNA adducts were consistently detectable in the DNA of smooth muscle cells from abdominal aorta specimens taken at surgery from atherosclerotic patients. Even broader are the consequences of mitochondrial (mt) DNA impairment, which has been associated with aging, cancer, and other degenerative diseases. Our data show that adduct levels are consistently higher in mtDNA than in the nuclear DNA in different organs of rats exposed either to benzo[a]pyrene, 2-acetylaminofluorene or cigarette smoke. NAC significantly decreased the formation of adducts to mtDNA when administered with drinking-water. Inhibition of adducts to nuclear DNA is one of the end points evaluated in ongoing Phase II chemoprevention trials in high-risk individuals.
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PMID:Adducts to nuclear DNA and mitochondrial DNA as biomarkers in chemoprevention. 892 39


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