Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the demographic and clinicolaboratory features of postdialysis fatigue (PDF), we enrolled 85 patients on maintenance hemodialysis in a cross-sectional study using validated questionnaires and chart review. Forty-three patients complained of fatigue after dialysis. On formal testing using the Kidney Disease Questionnaire, the PDF group had statistically greater severity of fatigue and somatic complaints than the group of patients without subjective fatigue (P = 0.03 and 0.04, respectively). On a scale measuring intensity of fatigue (1 = least to 5 = worst), the PDF group average was 3.4 +/- 1.2. PDF subjects reported that 80% +/- 25% of dialysis treatments were followed by fatigue symptoms. In 28 (65%) of patients, the symptoms started with the first dialysis treatment. They reported needing an average of 4.8 hours of rest or sleep to overcome the fatigue symptoms (range, 0 to 24 hours). There were no significant differences between patients with and without PDF in the following parameters: age; sex; type of renal disease; presence of diabetes mellitus, heart disease (congestive, ischemic), or chronic obstructive lung disease; blood pressure response to dialysis; type or adequacy of dialysis regimen; hematocrit; electrolytes; blood urea nitrogen; creatinine; cholesterol; albumin; parathyroid hormone; ejection fraction; and use of antihistamines, benzodiazepines, and narcotics. In the fatigue group, there was significantly greater use of antihypertensive medications known to have fatigue as a side effect (P = 0.007). Depression was more common in the fatigue group by Beck Depression score (11.6 +/- 8.0 v 7.8 +/- 6.3; P = 0.02). We conclude that (1) postdialysis fatigue is a common, often incapacitating symptom in patients on chronic extracorporeal dialysis; (2) no routinely measured parameter of clinical or dialytic function appears to predict postdialysis fatigue; and (3) depression is highly associated with postdialysis fatigue, but the cause-effect relationship is unclear.
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PMID:Postdialysis fatigue. 915 12

A 48-year-old woman with no cardiovascular risk factors was admitted to the hospital because of acute dyspnea. At 27-year-old, she developed Hodgkin's disease, that was successfully treated with splenectomy, combined chemotherapy (nitrogen mustard, vincristine, procarbazine, prednisone-MOPP regimen) and radiotherapy (4500 rads). At 43-year-old the lymphoma relapsed and she had further chemotherapy with doxorubicin, bleomycin, vinblastina and dacarbazine. After this treatment, she had an episode of pulmonary edema, attributed to doxorubicin acute cardiotoxicity. She responded to digitalis and diuretics and was discharged with an electrocardiogram (ECG) showing left bundle branch block and a normal echocardiogram. The patient enjoyed good health for several years and 4 months before the present admission the ECG and echocardiogram were unchanged. On this admission there were signs of left ventricular failure with acute pulmonary edema, and a new soft apical murmur (3-4 Levine). The patient required endotracheal intubation and high doses of diuretics, digitalis and vasodilators. The cardiac enzymes were negative, the serial ECGs confirmed left bundle branch block, while the echocardiogram showed moderate to severe mitral regurgitation, akinesia of the interventricular septum and inferior wall with dilation of the left ventricle. A previous silent myocardial infarction was suspected. After recovery, she underwent cardiac catheterization confirming akinesia of the interventricular septum and inferior wall with moderate mitral regurgitation, while coronary angiography showed a critical ostial stenosis of the right coronary artery. In view of a dipyridamole-thallium scan negative for myocardial viability, reperfusion was not attempted. With changes in radiotherapeutic techniques, the incidence of radiation-induced heart disease (pericarditis, myocarditis, conduction abnormalities and, rarely, occlusive coronary artery disease) is declining. Nevertheless, after irradiation of the chest and mediastinum a longterm cardiological follow-up is useful in selecting patients at higher risk of radiation-induced coronary artery disease, who will eventually require coronary angiography and reperfusion intervention.
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PMID:[Silent myocardial infarction in a patient treated with radiation therapy and polychemotherapy for Hodgkin's lymphoma]. 928 80

During the 1991 Gulf War, the Iraqi army set Kuwait oil wells on fire. Wells and some oil refineries were burned, resulting in Kuwait and the surrounding Gulf region being exposed to toxic gases. The oil fires reached their peak in February 1991. On March 7, the fires in some fields were still burning at peak strength. Sulfur dioxide, particulates, carbon monoxide, and nitrogen oxides were emitted into the atmosphere. All of these substances can cause adverse health effects, which vary according to concentration and duration of exposure. A survey conducted in Kuwait clinics and emergency rooms showed an increase in upper respiratory irritation consistent with environmental air sampling results, indicating occasional high levels of particulates. Patient visits related to gastrointestinal illness, heart disease, psychiatric illness, chronic bronchitis and emphysema, and bronchiectasis increased during the period following the burning of the oil wells. There was no documented evidence of an increase in visits for acute upper and lower respiratory infections or asthma. Public health workers must recognize the high priority of collecting long-term health data and developing public health systems to assess those data.
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PMID:Environmental surveys conducted in the Gulf region following the Gulf War to identify possible neurobehavioral consequences. 931 49

The serum concentrations of nitrogen oxides, the stable metabolites of nitric oxide, were measured in 61 children during and after cardiopulmonary bypass (CPB) for surgery of congenital heart disease. Overall, there was a small reduction in serum nitrogen oxide concentrations during CPB, from a median of 27.5 (interquartile range 16.6-55.7) to 26.4 (15.3-40.6) mumol/l, followed by an increase in the following 24 h to 33.1 (21.3-46.7) mumol/l. The largest postoperative increases in nitrogen oxides occurred in children who developed renal impairment, or were treated with nitrovasodilators. There was no relationship between changes in serum nitrogen oxides intraoperatively and early changes in pulmonary vascular resistance, and a weak positive relationship between changes in serum nitrogen oxides and early postoperative changes in cardiac index (r2 = 0.09, p = 0.04). We found no evidence for increased activation of the L-arginine nitric oxide pathway during CPB; and the reduction in nitric oxide metabolites that occurred during CPB were of doubtful significance to pulmonary or systemic haemodynamic changes in the postoperative period.
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PMID:Altered activation of the L-arginine nitric oxide pathway during and after cardiopulmonary bypass. 941 53

Radiocontrast nephrotoxicity, which has increased in incidence with widespread use of radiological methods in medicine, is a serious complication of radiocontrast materials. In this study, we have prospectively investigated whether children with cyanotic congenital heart disease are at risk for radiocontrast nephrotoxicity with the use of a nonionic low osmolar contrast agent. Thirty-five children (17 cyanotic and 18 acyanotic patients) who underwent diagnostic cardiac catheterization were subjects of the study. The age range was from five days to 13 years. The volume of contrast material was 3.11 +/- 1.37 ml/kg in cyanotic patients and 2.67 +/- 0.86 ml/kg in acyanotic patients. Blood samples and timed urine samples were taken from all patients 24 hours before and 48 hours after cardiac catheterization. Blood urea nitrogen, creatinine, sodium, and phosphorus in serum, and creatinine and N-acetyl-beta-D-glucosamine in urine were analyzed. There was not a statistically significant difference between the values before and after angiography. As a result, we could find no evidence of radiocontrast nephrotoxicity with the use of a nonionic contrast agent in cyanotic and acyanotic patients who underwent cardiac angiography.
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PMID:Evaluation of renal functions in children with congenital heart disease before and after cardiac angiography. 967 35

Endothelial dysfunction, caused in part by reduced NO bioavailability, is a feature of hypercholesterolemia, hypertension, smoking, and atherosclerosis. We examined whether cholesterol, blood pressure, smoking status, and polymorphisms in the endothelial NO synthase gene (NOS 3) influence NO production (as assessed by the plasma levels of nitrogen oxides, NO(x)) in middle-aged men. We also determined whether plasma NO(x) or NOS 3 genotype predicted the risk of is chemic heart disease (IHD). We studied 3052 men who were initially free of IHD and recruited from 9 UK primary care practices. Blood pressure, age, body mass index, serum cholesterol, and smoking status were assessed at baseline and annually over 8.1 years of follow-up, and all IHD events were recorded. DNA samples were screened for 4 NOS 3 gene polymorphisms: -786 T/C, -922 A/G, 894 G/T (which predicts a Glu(298)-->Asp amino acid substitution in the mature protein), and a 27-bp tandem repeat in intron 4 (eNOS4a/4b). NO(x) was measured in plasma samples obtained on entry in 1121 participants from North Mymms and Chesterfield general practices, together with an additional 571 recruits selected at random. Genotype frequencies were in Hardy-Weinberg equilibrium, and linkage disequilibrium was detected between all the NOS 3 polymorphismsstudied, with the strongest allelic association being detected between -922 A/G and -786 T/C polymorphisms in the gene promoter (Delta=0.90, P<0.001). Plasma NO(x) was lower in smokers than in nonsmokers in the North Mymms (10.8+/-4.5 versus 11.8+/-4.6 micromol/L, P=0.13), Chesterfield (8.4+/-3.6 versus 9.9+/-4.0 micromol/L, P=0.01), and random samples (10.7+/-5.1 versus 11.7+/-4.7 micromol/L, P=0.03). A weak but significant inverse relationship was detected between plasma NO(x) and serum cholesterol only in the North Mymms data set (r=-0.14, P=0.02). No relationship was detected between plasma NO(x) and any of the NOS 3 polymorphisms, nor was there any association between any NOS 3 polymorphism and risk of an IHD event in either smokers or nonsmokers. These data support the hypothesis that the endothelial dysfunction observed in the blood vessels of smokers is related to reduced NO bioactivity but indicate that NOS 3 genotype does not influence significantly the level of plasma NO(x) or the risk of IHD in this population sample of middle-aged British men.
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PMID:Genetic and environmental determinants of plasma nitrogen oxides and risk of ischemic heart disease. 1171 97

Melatonin was found to be a potent free radical scavenger in 1993. Since then over 800 publications have directly or indirectly confirmed this observation. Melatonin scavenges a variety of reactive oxygen and nitrogen species including hydroxyl radical, hydrogen peroxide, singlet oxygen, nitric oxide and peroxynitrite anion. Based on the analyses of structure-activity relationships, the indole moiety of the melatonin molecule is the reactive center of interaction with oxidants due to its high resonance stability and very low activation energy barrier towards the free radical reactions. However, the methoxy and amide side chains also contribute significantly to melatonin's antioxidant capacity. The N-C=O structure in the C3 amide side chain is the functional group. The carbonyl group in the structure of N-C=O is key for melatonin to scavenge the second reactive species and the nitrogen in the N-C=O structure is necessary for melatonin to form the new five membered ring after melatonin's interaction with a reactive species. The methoxy group in C5 appears to keep melatonin from exhibiting prooxidative activity. If the methoxy group is replaced by a hydroxyl group, under some in vitro conditions, the antioxidant capacity of this molecule may be enhanced. However, the cost of this change are decreased lipophility and increased prooxidative potential. Therefore, in in vivo studies the antioxidant efficacy of melatonin appears to be superior to its hydroxylated counterpart. The mechanisms of melatonin's interaction with reactive species probably involves donation of an electron to form the melatoninyl cation radical or through an radical addition at the site C3. Other possibilities include hydrogen donation from the nitrogen atom or substitution at position C2, C4 and C7 and nitrosation. Melatonin also has the ability to repair damaged biomolecules as shown by the fact that it converts the guanosine radical to guanosine by electron transfer. Unlike the classical antioxidants, melatonin is devoid of prooxidative activity and all known intermediates generated by the interaction of melatonin with reactive species are also free radical scavengers. This phenomenon is defined as the free radical scavenging cascade reaction of the melatonin family. Due to this cascade, one melatonin molecule has the potential to scavenge up to 4 or more reactive species. This makes melatonin very effective as an antioxidant. Under in vivo conditions, melatonin is often several times more potent than vitamin C and E in protecting tissues from oxidative injury when compared at an equivalent dosage (micromol/kg). Future research in the field of melatonin as a free radical scavenger might be focused on: 1), signal transduction and antioxidant enzyme gene expression induced by melatonin and its metabolites, 2), melatonin levels in tissues and in cells, 3), melatonin structure modifications, 4), melatonin and its metabolites in plants and, 5), clinical trials using melatonin to treat free radical related diseases such as Alzheimer's, Parkinson's, stroke and heart disease.
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PMID:Chemical and physical properties and potential mechanisms: melatonin as a broad spectrum antioxidant and free radical scavenger. 1189

The objective of our study was to investigate the safety and efficacy of high-dose methyl prednisolone (MP) in modifying the systemic inflammatory response (SIR) to cardiopulmonary bypass (CPB) and to compare its efficacy with low-dose MP in children undergoing cardiac surgery for congenital heart disease. Thirty children with congenital heart disease undergoing CPB were randomly assigned to two groups: group 1 (n = 15) received 30 mg/kg MP by an intravenous infusion for 30 minutes and group 2 (n = 15) received 2 mg/kg intravenously, before the onset of CPB. Postoperative clinical parameters were recorded, and serum interleukin (IL)-6 and 8 levels, acute phase reactants, and blood biochemistry were determined serially for both groups. In both groups plasma IL-6 and 8 levels were elevated above the preoperative levels at 2 and 24 hours after declamping. The peak levels were obtained at 2-hour samples. The difference between the two groups in terms of postoperative IL-6 and 8 levels was not statistically significant. C-reactive protein (CRP) levels and polymorphonuclear leukocyte counts, postoperative core temperature, duration of mechanical ventilation, period of stay in intensive care unit, oxygenation indices, and biochemical parameters of patients did not significantly differ in the two groups. Only 1 patient in group 1 had elevated liver enzymes, blood urea nitrogen, and creatinine in the postoperative period. No significant complications were observed due to treatment with high-dose MP. Although postoperative IL and CRP levels indicated a SIR in our patients, the clinical picture was apparently affected in only 1 patient and she was in the high-dose MP group. CPB initiates a SIR that is associated with an increase in neutrophil count, CRP, and IL-6 and 8 levels. High-dose (30 mg/kg) MP was not superior to low-dose (2 mg/kg) in blunting the SIR to CPB in pediatric patients undergoing open-heart surgery.
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PMID:Systemic inflammatory response related to cardiopulmonary bypass and its modification by methyl prednisolone: high dose versus low dose. 1217 Mar 62

Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. However, hyperglycemia, as an independent risk factor, directly causes cardiac damage and leads to diabetic cardiomyopathy. Diabetic cardiomyopathy can occur independent of vascular disease, although the mechanisms are largely unknown. Previous studies have paid little attention to the direct effects of hyperglycemia on cardiac myocytes, and most studies, especially in vitro, have mainly focused on the molecular mechanisms underlying pathogenic alterations in vascular smooth-muscle cells and endothelial cells. Thus, a comprehensive understanding of the mechanisms of diabetic cardiomyopathy is urgently needed to develop approaches for the prevention and treatment of diabetic cardiac complications. This review provides a survey of current understanding of diabetic cardiomyopathy. Current consensus is that hyperglycemia results in the production of reactive oxygen and nitrogen species, which leads to oxidative myocardial injury. Alterations in myocardial structure and function occur in the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. Oxidative stress, induced by reactive oxygen and nitrogen species derived from hyperglycemia, causes abnormal gene expression, altered signal transduction, and the activation of pathways leading to programmed myocardial cell deaths. The resulting myocardial cell loss thus plays a critical role in the development of diabetic cardiomyopathy. Advances in the application of various strategies for targeting the prevention of hyperglycemia-induced oxidative myocardial injury may be fruitful.
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PMID:Oxidative stress and diabetic cardiomyopathy: a brief review. 1221 71

Acute and chronic ischaemic diseases are among the main death reasons and civilized world menace. Branched chain amino acids (BCAAs): valine (Val), leucine (Leu), and isoleucine (Ile) are the main source of nitrogen to glutamine (Gln) and alanine (Ala) synthesis in muscles. In numerous cachexy-producing illnesses such as cancer, sepsis, diverse injuries and heart diseases increased consumption of BCAAs occurs. In myocardial ischemia BCAAs derived from the mobilization of muscle protein may be an important alternative energy substrate for the heart. BCAAs are oxidative energy substrates for the heart and may exert anabolic effects on myocardial protein (8). The aim of our study was to determine branched chain amino acids (BCAAs) concentrations in blood plasma of patients with chronic and acute ischeamic heart disease and to find out changes that those amino acids undergo during the first five days of patients' hospitalization.
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PMID:Branched chain amino acids (BCAAs) in heart diseases (ischaemic heart disease and myocardial infarction). 1614 56


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