Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxia-inducible factor 1 (HIF-1) is a basic-helix-loop-helix transcription factor that plays essential roles in mammalian development and physiology. HIF-1 is a heterodimer composed of HIF-1alpha and HIF-1beta subunits. The expression and activity of the HIF-1alpha subunit are tightly regulated by cellular O2 concentration. Under hypoxic conditions, HIF-1 activates the transcription of genes encoding erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, and other genes whose protein products increase O2 delivery or facilitate metabolic adaptation to hypoxia. HIF-1 is essential for embryonic vascularization and survival, neovascularization in ischemic myocardium, hypoxia-induced pulmonary vascular remodeling, and tumor vascularization. HIF-1alpha is overexpressed in the majority of common human cancers and their metastases, due to the presence of intratumoral hypoxia and as a result of mutations in genes encoding oncoproteins and tumor suppressors. Pharmacologic manipulation of HIF-1 levels may provide a novel therapeutic approach to diseases that represent the most common causes of mortality in Western society, including cancer, chronic lung disease, and myocardial ischemia.
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PMID:Expression of hypoxia-inducible factor 1: mechanisms and consequences. 1060 34

Hypoxia plays a fundamental role in the pathophysiology of common causes of mortality, including ischemic heart disease, stroke, cancer, chronic lung disease, and congestive heart failure. In these disease states, hypoxia induces changes in gene expression in target organs that either fail to result in adequate adaptation or directly contribute to disease pathogenesis. Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator that is expressed in response to cellular hypoxia and mediates multiple cellular and systemic homeostatic responses to hypoxia. Recent studies have provided evidence that important pathophysiological responses to hypoxia in pulmonary hypertension, myocardial ischemia, and cancer are mediated by HIF-1. Pharmacologic and gene therapy strategies designed to modulate HIF-1 activity may represent a novel and effective therapeutic approach to these common disorders.
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PMID:Hypoxia, HIF-1, and the pathophysiology of common human diseases. 1084 54

The widespread use of antibacterial agents for prophylaxis has altered surgical practice markedly in the past 20 years and now represents one of the most frequent uses of antibiotics in hospitals, accounting for as many as half of all antibiotics prescribed. The present study was undertaken to determine the patterns of and reasons for antibacterial agent usage by today's practicing plastic surgeons in Israel. A survey of 78 Israeli plastic surgeons certified by the Israeli Association of Plastic Surgery was conducted. Questionnaires were mailed to all the certified plastic surgeons; 66 (84.6%) were completed and returned. The results indicate that prophylactic antibiotics are administered in a high percentage of aesthetic and reconstructive surgeries except for those in eyelids and nose. Most of the surgeons prefer to prescribe cephalosporins as their antibiotics of choice and the timing of administration is before or at the beginning of surgery. Placement of drains did not change the decision to use prophylaxis. Diabetes mellitus, steroid treatment, and chronic lung disease have a direct influence on the decision to use antibiotics; however, conditions such as ischemic heart disease, hypertension, and cigarette smoking do not influence their use. Personal experience was the main reason for prescribing antimicrobial agents. We conclude that although the infection rate in aesthetic and reconstructive operations is extremely low, most Israeli plastic surgeons still prefer to administer prophylactic antibiotics though no scientific hard data is available.
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PMID:Prophylactic antibiotics in aesthetic and reconstructive surgery. 1095 95

Although inhibitors of angiotensin-converting enzyme (ACE) have improved the treatment of chronic heart failure (CHF), mortality related to this disorder remains unacceptably high. Results from studies started more than 25 years ago in Sweden suggested that long-term therapy with beta-blockers could improve hemodynamics and increase survival in patients with CHF; this hypothesis is confirmed by the results of six double-blind, randomized, placebo-controlled trials (MDC, CIBIS, ANZ, US Carvedilol Study, CIBIS II and MERIT-HF) who enrolled about 9000 patients with CHF. In these trials beta-blockers (metoprolol, bisoprolol or carvedilol) where added to the stable usual treatment of each patient (ACE-inhibitors, diuretics, digoxin). Baseline characteristics of patients enrolled into the beta-blocker or placebo arm were similar in all these studies. Specifically the mean patient's age was < 60 years, with a mean left ventricular ejection fraction of 25-26%, 30% of enrolled patients were in NYHA functional class II and 60% in NYHA functional class III, CHF was due to ischemic heart disease in about 60% of patients. The average follow-up for all the trials was 14.5 +/- 5.6 months. On the whole in patients on beta-blocker treatment there is a 33.3% reduction in total mortality rate, a 34.2% reduction in cardiac death rate, a 37.7% reduction in sudden death rate, and a 41.7% reduction in worsening heart failure mortality rate. Moreover, in beta-blocker patients there is a 31.7% reduction in all-cause readmissions to hospital and a 26% reduction in the combined end point (total mortality and hospital readmission). Beta-blockers improved ventricular function but there was no significant improvement in functional capacity. In conclusion, the results of the six trials considered indicate that there is convincing evidence supporting a favorable effect of beta-blockade on the risk of death and readmission to hospital in patients with dilated cardiomyopathy with systolic dysfunction, aged < 70 years, in NYHA functional class II-III. The effects of these drugs in CHF patients a) with normal left ventricular ejection fraction, b) aged > 65-70 years, c) in NYHA functional class IV, and d) with comorbilities such as obstructive lung disease, diabetes, peripheral arterial diseases, require additional study.
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PMID:[The use of beta blockers in heart failure: clinical studies]. 1099 5

Modern therapy for both cardiovascular disease and obstructive lung disease involves diametrically opposed manipulations of the beta-adrenoceptor. Beta-agonists reduce airflow limitation and improve symptoms among patients with obstructive lung disease while beta-blockers reduce symptoms, recurrent myocardial ischaemia and all-cause mortality among patients with ischaemic heart disease. There is biological plausibility for beta-agonists leading to adverse cardiovascular outcomes, and observational trials have raised concern about the safety of beta-agonists among patients with cardiovascular disease. Although there are many potential causal and noncausal explanations for these observational findings, the implications from these studies are the same. Physicians should be careful when prescribing beta-agonists for patients at risk for ischaemic heart disease. Furthermore, careful consideration should be given to distinguish symptoms caused by cardiovascular versus respiratory aetiologies.
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PMID:Risk of myocardial ischaemia and beta-adrenoceptor agonists. 1149 Nov 85

Successful simultaneous operation for cardiac and lung disease was performed in a 71-year-old man with lung carcinoma and ischemic heart disease. Chest CT scan revealed a mass in the right lower lobe and absence of mediastinal lymphadenopathy. Coronary angiography revealed significant stenosis of the left anterior descending artery, circumflex artery and right coronary artery. We performed concomitant video-assisted right lower lobectomy with mediastinal lymph node dissection as a form of less invasive surgery and triple coronary artery bypass grafting under cardiopulmonary bypass. Curative surgery for lung carcinoma and complete revascularization for ischemic heart disease were completed. The postoperative course was uneventful.
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PMID:[Concomitant lobectomy by video-assisted thoracic surgery and coronary artery bypass grafting: report of a case]. 1199 25

Cigarette smoking has been implicated in the pathogenesis of ischemic heart disease, emphysema, obstructive lung disease and neoplastic disorders. More than 1000 constituents of smoke, including many oxidants, pro-oxidants, free radicals and reducing agents, have been identified. The activities of erythrocyte superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), which are the important components of antioxidant defense system, were measured in 100 healthy volunteers. This study included heavy smokers (consuming cigarettes > or = 20 per day; n=30, group I), light smokers (consuming cigarettes<20 per day; n=30, group II), passive smokers (exposed to cigarette smoke in the indoor environment; n=20, group III), and non-smokers (n=20, the control group). While activities of SOD and CAT in erythro cytes were significantly lower in groups I, II and III than in the control group (p<0.01 for all), mean erythrocyte GSH-Px activity in group III was higher than that in groups l, II and in controls. These results suggest that the increased oxidative stress occurs in smokers, owing to the free radicals present in smoke. It might cause a decrease in antioxidant enzyme activities and oxidant/antioxidant imbalance. We also observed that passive smokers were affected by the environmental smoke to the same extent as active smokers.
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PMID:The changes of superoxide dismutase, catalase and glutathione peroxidase activities in erythrocytes of active and passive smokers. 1221 58

Information on obstructive lung disease (OLD) deaths is generally derived from the underlying cause of death on the death certificate. This neglects information on other conditions mentioned and may underestimate the burden of disease. Descriptive analyses of all conditions mentioned on the death certificate for all decedents where OLD (chronic obstructive pulmonary disease or asthma) was mentioned as a contributing cause of death were conducted for England and Wales for 1993-1999. OLD was mentioned in 312,664 or 8.0% of all deaths. OLD comprised the underlying cause of death in 59.8% of deaths with any mention of OLD. Where OLD was not the underlying cause of death, the leading causes by the International Classification of Disease version 9 chapter were diseases of the circulatory system, neoplasms, and non-OLD diseases of the respiratory system. The top single causes were acute myocardial infarction, other ischaemic heart disease, and lung cancer. The current analysis confirms that using the underlying cause of death underestimates the contribution of obstructive lung disease to mortality in England and Wales, in contrast to myocardial infarction where underlying cause of death captures most (94%) mentions on the death certificate.
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PMID:What do chronic obstructive pulmonary disease patients die from? A multiple cause coding analysis. 1462 Oct 89

The aim of this study is to contribute to the emerging field of quantification of Health Impact Assessment (HIA), by analysing how different relative risks affect the burden of disease for various socio-economic groups (SES). Risk analysis, utilising attributable and impact fraction, raises several methodological considerations. The present study illustrates this by measuring the impact of changed distribution levels of smoking on lung cancer, ischemic heart disease (IHD), chronic obstructive lung disorder (COLD) and stroke for the highest and lowest socio-economic groups measured in disability adjusted life years (DALY). The material is based on relative risks obtained from various international studies, smoking prevalence (SP) data and the number of DALY based on data available for Sweden. The results show that if smoking would have been eliminated (attributable fraction, AF), the inequality between the highest and lowest socio-economic groups may decrease by 75% or increase by 21% depending on the size of the relative risk. Assuming the same smoking prevalence for the lowest socio-economic group as for the highest (impact fraction), then the inequality may decrease by 7-26%. Consequently, the size of the relative risk used may have a significant impact, leading to substantial biases and therefore should be taken into serious consideration in HIA.
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PMID:Using risk analysis in Health Impact Assessment: the impact of different relative risks for men and women in different socio-economic groups. 1472 Jun 39

Fetal growth retardation is a result of a complex pathology caused by multiple factors of fetal, placental, and maternal origin. Hormones and growth factors released as a result of maternal-fetal physiological interactions play an importance role in fetal well being and fetal outcome. Intrauterine Growth Retardation (IUGR) is associated with significant perinatal and childhood morbidity. It is estimated that 13.7 million infants are born annually with IUGR, comprising 11% of all births in developing countries. Both maternal malnutrition and anemia are associated with various degrees of fetal growth retardation. The relationship between decreasing birth weight percentiles and increasing fetal morbidity and mortality has been demonstrated by several investigators and epidemiological studies suggest that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischemic heart disease, diabetes, and obstructive lung disease in adult life (Barker's Hypothesis). Maternal anemia and/or malnutrition are recognized to be the most frequent cause of IUGR and SGA birth in developing countries like India. In order to investigate adaptive mechanisms by the fetus to overcome the growth disadvantage caused due to maternal nutritional limitations, we examined the quantitative variations in hormonal and growth factor profiles in paired cord blood and maternal samples obtained from neonates born to malnourished and/or anemic mothers. The results of our study show that: 1) The percentage of small for gestational age (SGA) neonates born to malnourished and anemic mothers was significantly higher than those born to mothers who were either malnourished or anemic; 2) Significantly higher levels of GH, PRL, HPL and IGF-1 were observed in the cord blood of neonates born to malnourished and anemic mothers indicative of an adaptive response on part of the fetus to over come an in-utero growth disadvantage; 3) The anoxemia-related fetal perturbations may have unique features that make them distinct from nutrient deficiency-related IUGR. Thus, these novel observations are relevant to the context of the ongoing scientific debate on Barker's hypothesis.
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PMID:Effect of maternal malnutrition and anemia on the endocrine regulation of fetal growth. 1547 29


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