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

The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
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PMID:Passive smoking and heart disease. Epidemiology, physiology, and biochemistry. 191 25

1,3-Butadiene (BD), a gas widely used in the rubber industry, is also present in automotive exhaust and in the vapor phase of environmental tobacco smoke (ETS; approximately 400 micrograms/cigarette). The threshold limit value (TLV) for BD which was 10 ppm, has now been reduced to 2 ppm. Extensive investigations of workers have identified very few statistically significant increases in BD-associated cancer mortality. However, two studies have reported increased BD-associated mortality from arteriosclerotic heart disease in black workers in the BD rubber industry. The cockerel is a sensitive animal model for studying effects of environmental agents on arteriosclerosis development. Previous studies showed that inhaled environmental levels of ETS significantly accelerate arteriosclerosis. Surprisingly, the carcinogen-rich tar fraction of ETS was ineffective. The elevated risk of death from arteriosclerotic heart disease in black BD workers and the high BD level in the vapor phase of ETS, raised the question of whether BD would accelerate arteriosclerosis in cockerels. Here, cockerels breathed either 20 ppm BD or filtered air (6 h/day, 80 days). Blinded measurements showed no differences between groups in plaque frequency or location. However, plaque sizes were significantly larger in BD-treated cockerels than in controls--results nearly identical to those reported earlier for ETS-exposed vs. air-exposed cockerels. This indicates that BD may contribute to the atherogenicity of ETS and provides experimental support for the recent reduction in the TLV for BD.
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PMID:Butadiene inhalation accelerates arteriosclerotic plaque development in cockerels. 890 24

ETS contains numerous toxins. Robust epidemiologic evidence implicates ETS as a cause of lung cancer and as a primary cause and source of exacerbation of excess respiratory disease. There is also increasing evidence that ETS may be associated with other outcomes, including heart disease. There is currently little doubt that ETS is an important and avoidable health hazard. Unfortunately, ETS is frequently encountered in the workplace--where it is no safer than in other environments and where it presents hazards to exposed workers and to others. A unique aspect of workplace ETS is that exposure is rarely an outcome of essential manufacturing, extraction, or service delivery processes. Moreover, ETS exposure, with its growing list of known hazards, is preventable by engineering or policy means. Implementation of policies to prevent workplace ETS can be highly effective while entailing low costs and yielding primary and secondary benefits to employers and employees. ACOEM strongly supports an increase in the scope and effectiveness of policies and efforts that protect against exposure to ETS in the workplace and elsewhere. To that end, ACOEM supports voluntary, regulatory, and legislative initiatives to eliminate ETS from the workplace, including public spaces such as bars, casinos, restaurants, schools, day-care centers, and public transportation. ACOEM also encourages employers to provide employee training concerning the health hazards of ETS and voluntary personal smoking-cessation programs.
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PMID:Epidemiologic basis for an occupational and environmental policy on environmental tobacco smoke. 1112 75

Congenital heart defects comprise the most common form of major birth defects, affecting 0.7% of all newborn infants. Jacobsen syndrome (11q-) is a rare chromosomal disorder caused by deletions in distal 11q. We have previously determined that a wide spectrum of the most common congenital heart defects occur in 11q-, including an unprecedented high frequency of hypoplastic left heart syndrome (HLHS). We identified an approximately 7 Mb 'cardiac critical region' in distal 11q that contains a putative causative gene(s) for congenital heart disease. In this study, we utilized chromosomal microarray mapping to characterize three patients with 11q- and congenital heart defects that carry interstitial deletions overlapping the 7 Mb cardiac critical region. We propose that this 1.2 Mb region of overlap harbors a gene(s) that causes at least a subset of the congenital heart defects that occur in 11q-. We demonstrate that one gene in this region, ETS-1 (a member of the ETS family of transcription factors), is expressed in the endocardium and neural crest during early mouse heart development. Gene-targeted deletion of ETS-1 in mice in a C57/B6 background causes, with high penetrance, large membranous ventricular septal defects and a bifid cardiac apex, and less frequently a non-apex-forming left ventricle (one of the hallmarks of HLHS). Our results implicate an important role for the ETS-1 transcription factor in mammalian heart development and should provide important insights into some of the most common forms of congenital heart disease.
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PMID:Deletion of ETS-1, a gene in the Jacobsen syndrome critical region, causes ventricular septal defects and abnormal ventricular morphology in mice. 1994 20

Using a novel noninvasive, visible-light optical diffusion oximeter (T-Stat VLS Tissue Oximeter; Spectros Corporation, Portola Valley, CA) to measure the tissue oxygen saturation (StO2) of the buccal mucosa, the correlation between StOz and central venous oxygen saturation (ScvO2) was examined in children with congenital cyanotic heart disease undergoing a cardiac surgical procedure. Paired StO2 and serum ScvO2 measurements were obtained postoperatively and statistically analyzed for agreement and association. Thirteen children (nine male) participated in the study (age range, 4 days to 18 months). Surgeries included Glenn shunt procedures, Norwood procedures, unifocalization procedures with Blalock-Taussig shunt placement, a Kawashima/ Glenn shunt procedure, a Blalock-Taussig shunt placement, and a modified Norwood procedure. A total of 45 paired StO2-ScvO2 measurements was obtained. Linear regression demonstrated a Pearson's correlation of .58 (95% confidence interval [CI], .35-.75; p < .0001). The regression slope coefficient estimate was .95 (95% CI, .54-1.36) with an interclass correlation coefficient of .48 (95% CI, .22-.68). Below a clinically relevant average ScvO2 value, a receiver operator characteristic analysis yielded an area under the curve of .78. Statistical methods to control for repeatedly measuring the same subjects produced similar results. This study shows a moderate relationship and agreement between StO2 and ScvO2 measurements in pediatric patients with a history of congenital cyanotic heart disease undergoing a cardiac surgical procedure. This real-time monitoring device can act as a valuable adjunct to standard noninvasive monitoring in which serum SyvO2 sampling currently assists in the diagnosis of low cardiac output after pediatric cardiac surgery.
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PMID:Correlation of a novel noninvasive tissue oxygen saturation monitor to serum central venous oxygen saturation in pediatric patients with postoperative congenital cyanotic heart disease. 2369 83