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

Lipoprotein(a) was discovered by chance by Berg in 1963; after twenty years of research, the chemical, physical and metabolic characteristics of Lp(a) are now known. This lipoprotein forms the missing link between the lipid metabolism and the coagulation-fibrinolysis process. The A. describe its similarity to plasminogen, its capacity to delay coagulum or embolus destruction and highlight its structural and functional similarity to lipid metabolism. To day, a total of 6 Lp(a) isoforms have been identified with different molecular weights: in addition, the inverse proportion between the isoforms' molecular weight and Lp(a) plasma concentration has been demonstrated. Lp(a) is not the product of the metabolism of other lipoproteins nor is it a catabolite of LDL; it is produced ex-novo and does not apparently exchange its proteic fraction with other lipoproteins. The paper also examines the question of whether Lp(a) is a plasma marker which increases during the formation of atherosclerotic plaque or whether it should not be considered an atherogenetic factor. To this end the possible mechanisms by which Lp(a) is deposited in plaque are examined. Lastly, the paper reviews all studies concerning the relationship between Lp(a), ischemic cardiopathy and cerebrovascular disease.
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PMID:[Lipoprotein(a): structure, metabolism and atherosclerotic disease]. 146 28

Although the number of cardiovascular deaths associated with environmental tobacco smoke cannot be predicted with absolute certainty, the available evidence indicates that environmental tobacco smoke increases the risk of heart disease. The effects of environmental tobacco smoke on cardiovascular function, platelet function, neutrophil function, and plaque formation are the probable mechanisms leading to heart disease. The risk of death due to heart disease is increased by about 30% among those exposed to environmental tobacco smoke at home and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present. Even though considerable uncertainty is a part of any analysis on the health affects of environmental tobacco smoke because of the difficulty of conducting long-term studies and selecting sample populations, an estimated 35,000-40,000 cardiovascular disease-related deaths and 3,000-5,000 lung cancer deaths due to environmental tobacco smoke exposure have been predicted to occur each year. The AHA's Council on Cardiopulmonary and Critical Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. The council strongly supports efforts to eliminate all exposure of nonsmokers to environmental tobacco smoke. This requires that environmental tobacco smoke be treated as an environmental toxin, and ways to protect workers and the public from this health hazard should be developed. According to a 1989 Gallup survey commissioned by the American Lung Association, 86% of nonsmokers think that environmental tobacco smoke is harmful and 77% believe that smokers should abstain in the presence of nonsmokers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Environmental tobacco smoke and cardiovascular disease. A position paper from the Council on Cardiopulmonary and Critical Care, American Heart Association. 163 35

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

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

Clinical and necropsy findings are described in 56 patients with mitral valve prolapse: 15 patients, aged 16 to 69 years (mean 39), died suddenly and mitral valve prolapse was the only cardiac condition found at necropsy (hereafter called isolated mitral valve prolapse); the remaining 41 patients had other conditions that were capable of being fatal. Of the latter 41 patients, 7, aged 17 to 59 years (mean 45), had associated congenital heart disease, and 34 patients, aged 17 to 70 years (mean 52), had no associated congenital cardiac abnormalities. Compared with the 34 patients without associated congenital heart disease and with nonmitral valve prolapse conditions capable in themselves of being fatal, the 15 patients who died suddenly with isolated mitral valve prolapse were younger (mean age 39 +/- 17 versus 52 +/- 15 years; p = 0.01), more often women (67% versus 26%; p = 0.008) and had a lower frequency of mitral regurgitation (7% versus 38%; p = 0.02). The 15 patients dying suddenly with isolated mitral valve prolapse also were less likely to have evidence of ruptured chordae tendineae (29% versus 67%; p = 0.04). The frequency of increased heart weight (67% versus 59%), a dilated mitral valve anulus (80% versus 81%), a dilated tricuspid valve anulus (17% versus 17%), an elongated anterior mitral leaflet (86% versus 54%), an elongated posterior mitral leaflet (79% versus 77%) and fibrous endocardial plaque under the posterior mitral leaflet (73% versus 63%) was similar between the two groups. The severity of the prolapse (mild 20% versus 11%; moderate 27% versus 58%; severe 53% versus 32%) also was similar between the two groups. Thus, persons with mitral valve prolapse dying suddenly without another recognized condition tend to be relatively young women without mitral regurgitation.
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PMID:Morphologic comparison of patients with mitral valve prolapse who died suddenly with patients who died from severe valvular dysfunction or other conditions. 199 30

Histochemical and immunohistochemical investigations were performed on tissue obtained from the right heart side in three patients subjected to valve, replacement operations because of severe carcinoid heart disease. Extensive fibrotic changes were present on the endocardium of the right atrium, the papillary muscles of the tricuspid valve and the leaflets of the tricuspid and pulmonic valves of all patients. The main constituent of the lesions was a stroma with abundant acid mucopolysaccharides and collagen but devoid of stainable elastic components. The lesions were in some areas sharply delineated from the normal endocardium, but often also extended into the endocardium and myocardium. Small to medium sized vessels were demonstrated histochemically in the lesions and confirmed by positive immunoreaction against endothelial and smooth muscle cells. The moderate number of mesenchymal cells within the lesions had immunoreactivity consistent with muscle cells which seemed to have a very low proliferating activity. The histochemical and immunohistochemical techniques used confirmed some earlier observations in carcinoid heart disease but also rendered new information contradicting previous findings. The infiltrative nature of the carcinoid plaque gives a new dimension to the carcinoid heart disease. The etiology still remains obscure and well known growth factors for connective tissue such as platelet derived growth factor (PDGF) do not seem to be directly involved in the process.
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PMID:Histochemical and immunohistochemical morphology of carcinoid heart disease. 202 24

We investigated the association of elevated serum low density lipoprotein (LDL) cholesterol levels, smoking and hypertension with different manifestations of carotid atherosclerosis in a population-based sample of 720 Eastern Finnish men aged 42, 48, 54 or 60 years, examined in the Kuopio Ischaemic Heart Disease Risk Factor Study. Carotid atherosclerosis was assessed with high-resolution B-mode ultrasonography. Men who had neither a history nor symptoms of cardiovascular disease with serum LDL cholesterol concentration in the highest tertile (4.17 mM or more) had 3.40-fold (95% confidence interval (CI) 1.98-5.84) age-, smoking- and hypertension-adjusted probability of intimal-medial thickening as compared to men in the lowest serum LDL cholesterol tertile. The odds ratio for carotid plaque versus intimal-medial thickening was only 1.03 (95% CI 0.47-2.28). The respective odds ratios for smoking (28 pack-years or more) were 1.62 (95% CI 0.79-3.32) and 3.02 (95% CI 1.41-6.47) and those for hypertension were 1.10 (95% CI 0.70-1.73) and 0.99 (95% CI 0.53-1.84). Our findings suggest that elevated serum LDL cholesterol concentration associates with an increased risk of common carotid arterial wall thickening, whereas smoking is associated more strongly with carotid plaques than intimal-medial thickening. Our cross-sectional data do not support association between hypertension and either manifestation of carotid atherosclerosis.
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PMID:Association of serum low density lipoprotein cholesterol, smoking and hypertension with different manifestations of atherosclerosis. 208 21

This review summarizes selected topics discussed at one of the major congress events in cardiovascular medicine in Great Britain in 1989. The congress was attended during its five days duration by 800 participants from nearly 40 countries. The scientific programme, consisting of invited state-of-art lectures, was divided into following basic topics: coronary heart disease including risk and prevention, arhythmias, hypertension, heart failure, structural heart disease, cardiac imaging and costs-effectiveness of cardiology. The aim of the review is to bring nearer the creative atmosphere and the very advanced postgraduate level of this cardiologic meeting. Due to the actual medico-social importance of current strategies in management of ischemic heart disease and malignant arrhythmias in Czechoslovakia, special interest is devoted to these problems. Based on congress lectures an overview of the atherosclerotic plaque pathology and resulting therapeutic and prognostic implications for the management of unstable angina and myocardial infarction is given. Selected aspects of thrombolytic therapy and its impact on coronary vessel wall and myocardium are discussed, too. Some contemporary problems and updated concepts of both drug and intervention treatment of malignant ventricular arrhythmias are highlighted in a more extensive way, confronting congress speakers and recent publications.
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PMID:[Cardiology '89. Present trends in cardiovascular medicine at the Congress of Cardiology '89 in London April 1989]. 233 60

One hundred sixty-eight opiate addicts, whose hearts were submitted for necropsy study, were examined with prime focus on modes of death and types of cardiac abnormalities. Twenty various modes of death were identified: active infective endocarditis or its consequences in 67 (40%), drug overdose in 39 (24%), coronary artery disease in 14 (8%), pulmonary granulomatosis in 7 (4%) and 15 various diseases (7 cardiac and 8 noncardiac) in the remaining 41 (24%) patients. Of the 168 hearts examined, only 7 (4%) were normal. Although infective endocarditis (active, healed or both) was most common (80 [48%] patients), there was a broad range of other cardiac abnormalities present: cardiomegaly in 114 (68%) (including 22 patients without another cardiac abnormality), coronary artery disease in 35 (21%), acquired valvular heart disease in 16 (10%), myocardial heart disease in 14 (8%) and a congenital cardiac anomaly in 19 (11%). Of the 35 hearts with various coronary artery diseases, 28 had significant (greater than 75%) narrowing of the cross-sectional area of 1 or more of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaque. Of 112 coronary arteries in these 28 hearts, 52 (46%) were significantly narrowed (a mean of 1.9 of the 4 major coronary arteries/patient). In 27 of these 28 cases, each 5-mm segment of the 4 major coronary arteries was examined histologically. Of the 1,435 five-mm segments examined, 189 (13%) were narrowed 76 to 100% in cross-sectional area by plaque; 347 (24%), 51 to 75%; 336 (23%), 26 to 50%; and 563 segments (39%) were narrowed 0 to 25% in cross-sectional area by plaque. The percents of 5-mm segments narrowed 76 to 100% in cross-sectional area were greater in those patients with (128 of 793 [16%]) than without (61 of 642 [9%]) clinical evidence of myocardial ischemia (p = 0.001). In this study a very high frequency of cardiac abnormalities (161 [96%]) was found at necropsy and most deaths (97 [58%]) were related to cardiac disease. Although death was most often due to diseases whose association to opiate addiction is well recognized (such as infective endocarditis, drug overdose and pulmonary granulomatosis from the venous injection of talc), several other modes of death were present. Most prominent among these was coronary artery disease (14 patients [8%]).
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PMID:Modes of death and types of cardiac diseases in opiate addicts: analysis of 168 necropsy cases. 280 61

This investigation was undertaken to study the prevalence of amoxycillin-resistant oral streptococci in normal healthy patients and patients with a cardiac condition, susceptible to infective endocarditis. Samples of supragingival dental plaque were collected from two test groups, children with congenital heart disease and adults with a history of rheumatic fever, and two control groups comprising normal healthy children and normal healthy adults. Bacteria from these samples were grown on a medium selective for oral streptococci, as well as on the same medium containing known concentrations of amoxycillin. The results indicate that a high percentage of rheumatic heart patients and children with congenital heart disease harboured amoxycillin-resistant oral streptococci. The level of amoxycillin resistance in the plaque of adults with rheumatic heart disease was significantly greater than in that of normal adults. In view of the high percentage of patients at risk harbouring amoxycillin-resistant streptococci, it is important that the individual clinical situation be monitored. Perhaps antibiotic sensitivity tests should be performed to select an appropriate antibiotic for prophylaxis of infective endocarditis.
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PMID:Amoxycillin-resistant streptococci in dental plaque. 363 61


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