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

The prevention of cardiovascular disease antedates our current preoccupation with risk factors for coronary heart disease and hypertension. Indeed, earlier preventive efforts have in part been so successful that many people have forgotten that they existed. The almost forgotten entity, beriberi heart disease, was first prevented in 1883 by Takaki of Japan. With diphtheria, it was the identification of the causative bacillus by Klebs in 1883, leading finally to the development of diphtheria toxoid by Ramon in 1923, which resulted in the disappearance of diphtheritic heart disease. Success in the attack on syphilitic heart and vascular disease began with Bordet and Gengou in 1901 with the discovery of the phenomenon of complement fixation, and with the formulation of Salvarsan by Ehrlich in 1907. The story of the prevention of rheumatic fever has a large cast of characters, but special recognition must be given to Coburn for his observations confirming the role of the hemolytic streptococcus published in 1931 and showing the prophylactic value of sulfanilamide published in 1939. The important association of maternal rubella with congenital heart malformations was revealed by Gregg in 1941. Alcoholic heart disease was identified particularly by Brigden and Evans in 1957 and 1959, respectively. In relation to coronary and hypertensive heart disease, the names of Anitschkow (1933), Leary (1935), and Keys (1948) in relation to diet, of Freis (1967) in the field of hypertension treatment, of White (1927) in relation to physical exercise, and of English, Willius, and Berkson (1940) and Hammond and Horn (1954) in the role of cigarette smoking, deserve special recognition.
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PMID:Background of the prevention of cardiovascular disease. II. Arteriosclerosis, hypertension, and selected risk factors. 266 Oct 54

In a 12-year follow-up study of 610 persons (239 black and 371 white) in Evans County, Georgia, psychologic distress as measured by total score on the Health Opinion Survey, a 20-item questionnaire, was a predictor of mortality. The hazard ratio, comparing the 95th percentile score with the median, was 1.93 (97.5% confidence interval (CI) 1.42-2.62), controlling for age, race, and sex; there was no interaction with these variables. A purer measure of distress symptomatology, based on 18 of the questionnaire items, was also predictive of mortality. The hazard ratio was 1.94 (97.5% Cl 1.33-2.82), controlling for age, race, sex, and the item, "Do you have any sickness or illness problems at the present time?"; no interactions with the latter variables were found. This pattern was not affected in any major way by several modifications of the analyses: 1) controlling also for smoking, serum cholesterol, Quetelet index (weight (kg)/height (m)2), diastolic blood pressure, a social network index, and a social class index; 2) excluding persons with a diagnosis (in 1968) of chronic heart disease, angina pectoris, myocardial infarction, stroke, transient cerebral ischemic attach, or diabetes mellitus, or whose deaths were due to neoplastic disease; and 3) restricting the analyses to the last half of the follow-up period to explore the role of incipient or early physical illness in producing the association. With the restricted samples, confidence intervals included 1.00, which may be attributed to both the substantially smaller samples and the slightly reduced strength of the effect. The evidence is consistent with a causal role for psychologic distress, as measured by the Health Opinion Survey, in subsequent mortality rates.
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PMID:Psychologic distress as a predictor of mortality. 281 89

The safety and convenience of the transvenous approach to long-term endocardial pacing are well established, but its principal drawback is electrode displacement. The reported incidence of this complication varies between 3.0% to 36.7%, and is highest in the early post-implantation period before endocardial fixation of the electrode tip. Recently Brewster and Evans determined that the electrode displacement rate in 21 published series averaged 14.3%. However, the Inter Society Committee on Heart Diseases (ICHD) report on pacemakers states that a rate of early displacement greater than 5% calls for a critical review of results. The training and expertise of the persons inserting the pacemaker electrodes undoubtedly are major factors which determine the proper transvenous placement of permanent cardiac electrodes. This paper deals with our clinical experience of 353 patients who received permanent transvenous pacemakers during the period September 1, 1974 through March 1, 1979, with emphasis on problems and complications encountered and overall results.
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PMID:Three hundred and fifty-three consecutive patients with permanent transvenous pacemakers. 616 May 38

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular disease and work place exposures. 638 Apr 27

This study determined if reported decreases in the delta subunit of ATP synthase and nuclear-encoded cytochrome c oxidase subunits in hearts of copper-deficient rats were secondary to the heart disease pathology or due to lack of the trace element. Male weanling Long-Evans rats were randomly divided into six groups: rats fed a copper-adequate or copper-deficient diet (with free access) with or without 5% dimethyl sulfoxide (DMSO) in the drinking water and rats pair-fed the copper-adequate or copper-deficient diet without DMSO treatment. After 4 wk, rats in the groups fed the copper-deficient diet had lower liver superoxide dismutase and heart cytochrome c oxidase activities compared with groups fed the copper-adequate diet. Administration of DMSO, an antioxidant, and energy restriction (pair-feeding) partially blocked cardiac hypertrophy in rats fed the copper-deficient diet. Greater mitochondrial volume density and mitochondrial:myofibrillar ratio and disrupted myofibrils and basal laminae were observed in the hearts from rats fed the copper-deficient diet and not treated with DMSO compared with hearts from groups fed the copper-adequate diet. The DMSO-treated rats fed the copper-deficient diet had hearts with intact structure but enlarged mitochondria compared with other groups fed the copper-deficient diet. The delta subunit of ATP synthase and the nuclear-encoded cytochrome c oxidase subunits IV and V were depressed in rats fed a copper-deficient diet regardless of antioxidant treatment and pair-feeding. These data suggest that the effects of copper deficiency upon ATP synthase and cytochrome c oxidase proteins are not due to the cardiac pathology.
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PMID:Low levels of ATP synthase and cytochrome c oxidase subunit peptide from hearts of copper-deficient rats are not altered by the administration of dimethyl sulfoxide. 820 36

Optison is a new echocardiographic contrast agent, designed for IV injection, that is very useful in delineating cardiac structures during ultrasound examination. Because Optison could be a valuable adjunct in the diagnosis and evaluation of congenital heart disease, this study was undertaken to assess its effects on the blood-brain barrier when introduced directly in the cerebral circulation, as might occur with some congenital lesions. In this study, Sprague-Dawley rats were anesthetized, and Optison, at various dosages, was injected into the carotid artery. After this, Evans blue dye, a marker for blood-brain barrier disruption, was injected at different time intervals. Gross and histologic examination of the animals' brains revealed disruption of the blood-brain barrier that appeared to be Optison-dosage-dependent. Although the mechanism for this disruption is unclear, it may be related to the use of octofluoropropane gas used in the Optison as a contrast medium. Further studies are necessary to determine the pathologic consequences of Optison's effects on the blood-brain barrier.
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PMID:Optison (FS069) disrupts the blood-brain barrier in rats. 1100 29

Diseases of the heart are the No. 1 killer in industrialized countries. Brain injury can develop as a result of cerebral ischemia-reperfusion due to stroke (brain attack) and other cardiovascular diseases. Learning about the disease is the best way to reduce disability and death. We present here whether gene repair activities are associated with neuronal death in an ischemia-reperfusion model that simulates stroke in male Long-Evans rats. This experimental stroke model is known to induce necrosis in the ischemic cortex. Cerebral ischemia causes overactivation of membrane receptors and accumulation of extracellur glutamate and intracellular calcium, which activates neuronal nitric oxide synthase, causing damage to lipids, proteins, and nucleic acids, and reduces energy sources with consequent functional deterioration, leading to cell death. Restoration processes normally repair genes with few errors. However, ischemia elevates oxidative DNA lesions despite these repair mechanisms. These episodes concurrently occur with the induction of immediate-early genes that critically activate other late genes in the signal transduction pathway. Damage, repair, and transcription of the c-FOS gene are presented here as examples, because Fos peptide, one of the components of activator protein 1, activates nerve growth factor and repair mechanisms. The results of our studies show that treatments with 7-nitroindazole, a specific inhibitor of nitric oxide synthase known to attenuate nitric oxide, oxidative DNA lesions, and necrosis, increase intact c-fos mRNA levels after stroke. This suggests that the accuracy of gene expression could be accounted for the recovery of cellular function after cerebral injury.
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PMID:Ischemia-reperfusion-related repair deficit after oxidative stress: implications of faulty transcripts in neuronal sensitivity after brain injury. 1256 81

The adverse effects of tobacco smoking on the cardiovascular system are well established. Effects of nicotine on the heart, in contrast, are not well characterized. Understanding specific effects of nicotine on the heart and on blood volume is relevant to (a) elucidating the mechanisms by which nicotine may contribute to heart disease and (b) determining potential risks associated with nicotine products used in smoking cessation or to treat various medical conditions. The present experiment investigated effects of continuous nicotine administration for 14 days (0, 6, or 12 mg/kg/day) on heart histopathology and blood volume (a measure of hemoconcentration) in 59 male and 59 female rats of two strains (Sprague-Dawley and Long-Evans). Following nicotine administration, animals were sacrificed and blood volume was measured. Heart length; heart weight; left ventricle, right ventricle, lateral wall, anterior wall, and posterior wall thicknesses; and intraventricular width (i.e., septum) were measured. Nicotine reduced heart weight, heart length, and overall blood volume. Females were more sensitive than males to the effects of nicotine on heart weight. In contrast, males were more sensitive than females to the effects of nicotine on heart length. Together, these findings suggest that males and females differ in their sensitivity to nicotine's cardiac effects.
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PMID:Effects of nicotine on heart dimensions and blood volume in male and female rats. 1279 29

Endocardial lesions are caused not only by inflammatory processes but also by myocardial ischemia, resulting in endocardial thrombosis and cerebral embolism. We deviced a method for direct visualization of endocardial damages by a novel dye image cardioscopy with Evans blue and examined its feasibility in patients with heart disease. The dye was injected into the left ventricle before and after endomyocardial biopsy. Endocardial surface was stained in dark blue in 63% of patients with angina pectoris before biopsy. After biopsy, the biopsied portions were stained in blue in all. The results indicate that endocardium is damaged even in apparently intact LV in patients with ischemic heart disease and that endomyocardial biopsy causes severe endocardial damages.
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PMID:Percutaneous dye image cardioscopy for detection of endocardial lesions. 1849 44

Stress-induced cardiomyopathy (SIC) is a form of acute heart disease triggered by extreme psychological stress. In patients who develop SIC, the outward symptoms are almost indistinguishable from acute myocardial infarction (AMI). However, some important criteria differentiate patients with SIC from those with AMI. Patients with SIC: (1) experience some form of extreme psychological stress from minutes to hours before developing heart disease, (2) do not suffer from atherosclerosis or coronary artery obstruction, and 3) exhibit abnormal ballooning of the left ventricle. In the present study, the resident-intruder (RI) social defeat test was investigated as a potential rat model for stressed-induced cardiomyopathy. Adult Long-Evans rats were implanted with a biotelemetry transmitter for ECG recordings and habituated for two weeks. An intruder rat was placed in the cage of a resident rat behind a wire-mesh partition for 5 min. The partition was then removed for 5 min to allow direct contact between the intruder and resident rats. After this interval, the wire-mesh partition was replaced and the intruder rat remained behind the partition for an additional 50 min. Behavioral responses were noted and ECG recordings were collected during the entire 60-min testing period. Upon completion of the test, the intruder rat was removed from the cage of the resident rat and sacrificed. The heart was examined and blood was collected. Heart weight/body weight ratio, left ventricle/body weight ratio, heart length, plasma corticosterone levels, and plasma troponin I levels of intruder rats were significantly higher as compared to control rats. Intruder rats significantly increased their heart rate during the first 5 min of the RI test. It is concluded that the RI test to induce social defeat is a novel rodent paradigm for modeling stress-induced cardiomyopathy in the human.
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PMID:An animal model of stress-induced cardiomyopathy utilizing the social defeat paradigm. 2396 81


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