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

118 patients with lung cancer who underwent treadmill exercise electrography (ECG) as part of their preoperative evaluation, were investigated for postoperative events. On the treadmill exercise ECG 27 patients were positive and 91 were negative. The more elderly patients tended to reveal ischemic findings in treadmill exercise ECG. Of the 71 patients with normal of result by ECG at rest, 15 patients (21.1%) had postoperative ischemic change on ECG. As a result, it was considered that this examination was insufficient to detect latent ischemic heart disease. The patients who had a discontinued at stage 2 or less of the Bruce protocol and had a negative result by treadmill exercise ECG, were classified as insufficient group and separated from the others. (27/118 patients). This group consisted of advanced age (p < 0.05) who tended to experience postoperative events. In the sufficient group, patients showed ischemic events predominantly on ECG at postoperative period (p < 0.01). We concluded that as preoperative screening of heart disease prior to lung cancer surgery ECG at rest was not adequate while treadmill exercise ECG was useful.
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PMID:[Preoperative evaluation of cardiac disease for patients with lung cancer: usefulness of treadmill exercise electrocardiogram]. 1003 70

One study after another is finding strong associations between a variety of human illness and exposure to environmental tobacco smoke (ETS). A 1986 report by the U.S. Surgeon General concluded that ETS is a cause of disease, including lung cancer, in healthy nonsmokers. Other reports have documented causal associations between ETS and lower respiratory tract infections, middle ear disease and exacerbation of asthma in children, heart disease, retardation of fetal growth, sudden infant death syndrome, and nasal sinus cancer. However, the findings from many of these studies remain controversial. A number of scientists remain skeptical about the association between ETS and serious illness in nonsmokers, charging that scientific journals either fail to publish pro-tobacco findings and meta-analyses or disregard those that are published. They also claim that many epidemiological studies declare causal associations based on marginal odds ratios.
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PMID:Double exposure. Environmental tobacco smoke. 1044 19

Health objectives, developed by the United States Department of Health and Human Services, were published recently in the document entitled Healthy People 2000: National Health Promotion and Disease Prevention Objectives. They were developed to guide national and local health policy toward actions to increase the health of the nation. To effectively apply these objectives locally, epidemiologists and health planners must work together. Through collaboration, the Healthy People 2000 objectives can be prioritized to guide health policy and planning on a regional basis. The purpose of this study was to assess certain health status indicators in southwestern Pennsylvania to determine whether it was likely that the year 2000 targets would be met if trends from the past 20 years were to continue. The following mortality rates were analyzed: heart disease, homicide, breast cancer, colon cancer, lung cancer, suicide, motor vehicle accidents, work-related injury, and infant mortality. In addition, incidence of the following diseases was evaluated against the year 2000 targets: gonorrhea, primary and secondary syphilis, measles, tuberculosis, and AIDS. By employing epidemiological principles and considering strategic planning needs, it is possible to prioritize some of the health care needs in local areas for the next decade.
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PMID:Epidemiologic indicators of health status to guide health care management decision making. 1013 Feb 41

The concentrations of environmental tobacco smoke (ETS) to which workers are exposed have been measured, using nicotine or other tracers, in diverse workplaces. Policies restricting workplace smoking to a few designated areas have been shown to reduce concentrations of ETS, although the effectiveness of such policies varies among work sites. Policies that ban smoking in the workplace are the most effective and generally lower all nicotine concentrations to less than 1 microg/m3; by contrast, mean concentrations measured in workplaces that allow smoking generally range from 2 to 6 microg/m3 in offices, from 3 to 8 microg/m3 in restaurants, and from 1 to 6 microg/m3 in the workplaces of blue-collar workers. Mean nicotine concentrations from 1 to 3 microg/m3 have been measured in the homes of smokers. Furthermore, workplace concentrations are highly variable, and some concentrations are more than 10 times higher than the average home levels, which have been established to cause lung cancer, heart disease, and other adverse health effects. For the approximately 30% of workers exposed to ETS in the workplace but not in the home, workplace exposure is the principal source of ETS. Among those with home exposures, exposures at work may exceed those resulting from home. We conclude that a significant number of U.S. workers are exposed to hazardous levels of ETS.
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PMID:Exposure of U.S. workers to environmental tobacco smoke. 1035 May 18

A retrospective cohort study of 55,407 U.S. railroad workers has been called the most definitive study linking exposure to diesel exhaust (DE) with lung cancer in humans. However, reanalysis of data from this study suggests caution in interpreting this study as demonstrating such a link. Although workers who rode trains had a significantly elevated lung cancer mortality relative to clerks and signalmen (who were assumed to be unexposed), shop workers did not, despite convincing evidence that these workers had the highest exposures to DE. Mortality from heart disease and cirrhosis of the liver were also significantly elevated among train riders, which suggests that these workers had a substantially different lifestyle from other workers, and raises the possibility that their elevated lung cancer mortality may be related to lifestyle rather than to DE exposure. Smoking information was not available for this cohort. A positive, monotone dose-response trend in lung cancer mortality with increasing duration of exposure found by the original investigators was not present when age was controlled more carefully and years of exposure quantified more accurately. Instead, a negative dose-response trend for lung cancer was seen among exposed workers based on either duration of exposure or quantitative measures of cumulative exposure. Similar negative trends were seen with several broad categories of mortality, including all causes. These negative trends are possibly a result of incomplete follow-up that was most severe among workers with the longest tenures. A sizable fraction of deaths occurring during the last 4 years of follow-up evidently were not identified, and there is evidence that follow-up in earlier years was also incomplete. At the very least, problems with the follow-up should be rectified before any conclusions are drawn about the carcinogenicity of DE in this cohort.
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PMID:Lung cancer mortality and diesel exhaust: reanalysis of a retrospective cohort study of U.S. railroad workers. 1038 Jan 56

Dyspnea is a frequent and devastating symptom among advanced cancer patients and is often difficult to control. However, there has been considerably less emphasis in the literature on the appropriate characterization and management of this symptom than of other cancer-related symptoms. The purpose of this paper is to review issues relating to the prevalence, causes, prognosis and treatment of dyspnea in patients with advanced cancer. A Medline search of the literature published from 1966 to February 1999 was conducted. Dyspnea occurs in 21-78.6% of advanced cancer patients and is reported to be from moderate to severe in 10-63% of the patients. The frequency and severity of dyspnea increase with the progression of the disease and/ or when death is approaching. Lung cancer patients with dyspnea have shorter survival than patients with other types of cancer. Dyspnea can be a direct effect of the cancer, an effect of therapy or not related to the cancer or therapy. In addition to cancer, patients may suffer from chronic obstructive pulmonary disease, congestive heart failure, nonmalignant pleural effusion, pneumonitis, air flow obstruction, or bronchospasm associated with asthma. In the absence of lung or heart disease, dyspnea may be a clinical expression of the syndrome of overwhelming cachexia and asthenia or of severe asthenia. Many different causes may co-exist in a patient. Whenever possible, an attempt should be made to treat underlying cancer. Radiotherapy and chemotherapy may relieve dyspnea also in patients who fail to achieve a major objective response. Symptomatic measures in addition to specific treatments for the underlying cancer and/or other pulmonary and cardiovascular diseases are indicated. Oxygen therapy has proved effective in hypoxemic and nonhypoxemic patients. The role of transfusion therapy to relieve anemia-related dyspnea in advanced and terminal cancer patients is still controversial. Oral, subcutaneous and intravenous opioids are effective but underused in these patients, whereas currently available evidence does not support the clinical use of nebulized opioids. While benzodiazepines are frequently used in patients with dyspnea, these drugs were ineffective in four out of five randomized controlled trials. Other components of the symptom expression are better managed by supportive counseling, occupational therapy or physiotherapy. While the mechanism of breathing and the consequences of different pathologic conditions for both respiratory function and gas exchange are well known, the genesis and pathophysiology of dyspnea as a symptom are much less well understood. Palliative care assessment should be focused on dyspnea as a symptom rather than on the functional and gas exchange abnormalities. Increased research on the appropriate management of dyspnea is needed.
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PMID:Management of dyspnea in advanced cancer patients. 1042 43

There are two major dietary sources of vitamin A: easily absorbed retinyl palmitate in foods of animal origin, and poorly bioavailable carotenoids from plant foods. Plasma retinol is tightly controlled, probably by regulation of retinol-binding protein (RBP) formation in the liver, and only hormonal factors (e.g. oral contraceptives) and infection will alter the homeostasis. Delivery of retinol to the tissues is facilitated by the RBP-retinol complex; however, there is evidence that this mechanism can be bypassed when very high doses of vitamin A are given. Some retinyl ester may be released to tissues from chylomicrons when the latter bind to tissue lipoprotein receptors during their passage from the gut to the liver following a meal. High-dose vitamin A therapy is a means of rapidly improving vitamin A status in persons with sub-optimal vitamin A nutrition but there are dangers of toxic symptoms (e.g. teratogenicity) from excess vitamin A usage. Evidence is presented to suggest that the plasma retinol: RBP may be a guide to optimal vitamin A status, since values less than one frequently occur in less-developed countries and during infection. In contrast to plasma retinol, plasma carotenoids reflect the dietary intake of plant foods. However, absorption is limited by poor bioavailability and a saturable uptake mechanism in competition with other phytochemicals. Recent work on bioavailability suggests that the calculation of plant food vitamin A activity should be re-examined. Illness has little influence on plasma levels except by suppressing appetite. Carotenoids are generally regarded as non-toxic yet intervention studies with beta-carotene in smokers have been associated with increased lung cancer and heart disease. Some carotenoids are important as vitamin A precursors, but the physiological importance of their antioxidant properties is not known and consequently the amount needed for optimal nutrition is uncertain.
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PMID:Optimal nutrition: vitamin A and the carotenoids. 1046 90

Smoking--once a socially accepted behavior--is the leading preventable cause of death and disability in the United States. During the first decades of the 20th century, lung cancer was rare; however, as cigarette smoking became increasingly popular, first among men and later among women, the incidence of lung cancer became epidemic (Figure 1). In 1930, the lung cancer death rate for men was 4.9 per 100,000; in 1990, the rate had increased to 75.6 per 100,000 (1). Other diseases and conditions now known to be caused by tobacco use include heart disease, atherosclerotic peripheral vascular disease, laryngeal cancer, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, intrauterine growth retardation, and low birthweight. During the latter part of the 20th century, the adverse health effects from exposure to environmental tobacco smoke also were documented. These include lung cancer, asthma, respiratory infections, and decreased pulmonary function (2).
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PMID:Tobacco use--United States, 1900-1999. 1057 92

In 1994 the U.S. Occupational Health and Safety Administration (OSHA) published a study of risk assessment for heart disease and lung cancer resulting from workplace exposure to environmental tobacco smoke (ETS) among nonsmokers. This assessment is currently being revised. The present article considers different possible approaches to a risk assessment for heart disease among nonsmokers resulting from workplace ETS exposure, reviews the approach taken by OSHA in 1994, and suggests some modifications to that approach. Since 1994 the literature supporting an association between ETS exposure and heart disease among never smokers (sometimes including long-term former smokers) has been strengthened by new studies, including some studies that have specifically considered workplace exposure. A number of these studies are appropriate for inclusion in a meta-analysis, whereas a few may not be due to methodological problems or problems in exposure definition. A meta-analysis of eight relative risks (either rate ratios or odds ratios) for heart disease resulting from workplace ETS exposure, based on one reasonable selection of appropriate studies, yields a combined relative risk of 1.21 (95% confidence interval [CI], 1.04-1.41). This relative risk, which is similar to that used by OSHA in 1994, yields an excess risk of death from heart disease by age 70 of 7 per 1000 (95% CI 0.001-0.013) resulting from ETS exposure in the workplace. This excess risk exceeds OSHA's usual threshold for regulation of 1 per 1000. Approximately 1,710 excess ischemic heart disease deaths per year would be expected among nonsmoking U.S. workers 35-69 years of age exposed to workplace ETS.
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PMID:Risk assessment for heart disease and workplace ETS exposure among nonsmokers. 1059 43

Gene-environment interactions are thought to be critical for several diseases such as cancer, diabetes, heart disease and asthma. Cancer is a result of multiple gene-environment interactions occurring over several decades. During tumor development the cell accumulates multiple genetic changes, which generate the transformed phenotype, i.e. a cell with increased genetic instability. Lung cancer is a useful model for the study of the interplay between genetic factors and environmental exposure since the primary etiology is well established. Several polymorphic enzymes that may be important determinants of susceptibility have been demonstrated. Data also provide evidence for sex differences in lung cancer susceptibility. Furthermore, certain chemical carcinogens may contribute to the carcinogenic process in the lung epithelial cells by inducing genomic instability either directly or indirectly through inflammatory processes.
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PMID:Gene-environment interactions in human lung cancer. 1072 Jul 36


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