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)

Usage of antisclerotic diet with PUFA n-3 from vegetable or animal source in 326 patients with IHD, HL and HBP resulted in positive dynamic of clinical manifestation, blood lipids and coagulogramms of the patients. The favorable changes of membrane lipids and the decrease of intensity of lipid peroxidation was also revealed. The decrease of primary and secondary metabolites of lipid peroxidation could be a result of hypolipidemic effect of the diets and sufficient level of vitamin E. We suppose that vitamin A and b-carotene content of butter "Laplandia" had additional mild antioxidant influence.
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PMID:[Lipid peroxidation in patients with ischemic heart disease, hyperlipidemia and/or hypertension while polyunsaturated omega-3 fatty acids of plant and animal origin were in their diet]. 941 77

Polyunsaturated fatty acids (PUFA), in the form of marine oils, contain a large proportion of n-3 long chain fatty acids and have been recommended as a dietary supplement for patients with ischaemic heart disease. It has also been suggested that consumption of diets rich in polyunsaturated fatty acids renders tissues more susceptible to free radical-mediated lipid peroxidation, a process which has been implicated in the mechanisms by which tissues may become damaged following hypoxia and subsequent reoxygenation. We have examined the effect of supplementation of diets with oils of different PUFA composition and different vitamin E content on the accumulation of fatty acids by rat hearts in comparison with the effects on tissue lipid peroxidation and the response of the heart to a standardised form of oxidative stress. Groups of Wistar rats were fed a vitamin E supplemented (100 mg alpha-tocopherol acetate/kg) diet containing either 10% corn oil, 10% menhaden oil or 10% lard, or a low vitamin E diet (2.5 mg alpha-tocopherol acetate/kg) containing either 10% corn oil, 10% menhaden oil or 10% lard for 82 +/- 3 days. Diets supplemented with menhaden oil had a dramatic effect on the incorporation of n-3 fatty acids into the cardiac tissue and increased the susceptibility of this tissue to lipid peroxidation in vitro. The effect of these changes on damage to isolated hearts subjected to 60 min hypoxia and reoxygenation was examined using a modified Langendorff system. Nutritional manipulation of the tissue fatty acids and vitamin E content had no influence on the release of creatine kinase activity from rat hearts subjected to hypoxia/reoxygenation. Thus these data do not support the hypothesis that consumption of diets rich in polyunsaturated fatty acids renders tissues more susceptible to free radical damage induced by hypoxia/reoxygenation.
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PMID:Dietary polyunsaturated fatty acids, vitamin E and hypoxia/reoxygenation-induced damage to cardiac tissue. 946 53

The hypothesis that oxidative damage due to free radicals is an important cause of aging is the subject of much research and even more interest among the public and lay media. An increasing number of older people are asking whether they should be taking antioxidant vitamins, despite their considerable cost. Epidemiological and laboratory evidence indicates that oxidative damage caused by oxygen free radicals is important in many of the major diseases of older age. It is also clear that a diet high in antioxidants protects against these diseases, including many cancers and ischaemic heart disease. However, it has not been proven whether antioxidant vitamins, taken as dietary supplements, provide the same level of protection as a diet that is rich in fruit and vegetables. Although there appears to be no reason to discourage older people from taking vitamin E (tocopherols) and ascorbic acid (vitamin C), the best advice to give them is to reduce their intake of xenobiotics, to drink tea instead of coffee, and to eat liberal amounts of fruit, vegetables, nuts, soya beans and lentils. The use of beta-carotene as a dietary supplement should be discouraged.
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PMID:Should antioxidant vitamins be routinely recommended for older people? 953 18

The attenuation of intracellular production of cyclic guanosine monophosphate (cGMP) has been known as a mechanism of nitrate tolerance. A recent in vitro study have shown an increase in superoxide levels and a reduced activation of guanylate cyclase in tolerant vessels. We investigated the preventive effect of an antioxidant, vitamin E, on the development of nitrate tolerance. In this double-blind, placebo-controlled study, 24 normal volunteers and 24 patients with ischemic heart disease (IHD patients) were randomized to receive either vitamin E (200 mg t. i. d.; vitamin E group) or placebo (placebo group). Vasodilator response to nitroglycerin was assessed with forearm plethysmography by measuring the change in the forearm blood flow before and 5 min after sublingual administration of 0.3 mg nitroglycerin, and at the same time, blood samples were taken from veins to measure the platelet cGMP level. Measurements of the forearm blood flow and blood sampling were obtained serially at baseline (day 0), 3 days after taking vitamin E or placebo alone (day 3), and 3 days after application of a 10 mg/24 hr nitroglycerin tape concomitantly with oral vitamin E or placebo (day 6). The response of forearm blood flow (%FBF) and cGMP (%cGMP) after sublingual nitroglycerin on day 0(%FBF: normal volunteers 32 +/- 12% vs 31 +/- 11%, IHD patients 35 +/- 15% vs 34 +/- 15%; %cGMP: normal volunteers 38 +/- 10% vs 35 +/- 11%, IHD patients 37 +/- 11% vs 38 +/- 12%; vitamin E group as placebo group) and day 3(%FBF: normal volunteers 33 +/- 9% vs 32 +/- 12%, IHD patients 35 +/- 12% vs 33 +/- 13%, %cGMP: normal volunteers 38 +/- 10% vs 37 +/- 11%, IHD patients 36 +/- 14% vs 37 +/- 10%, vitamin E group vs placebo group) were not different between the two groups. On day 6 %FBF and %cGMP in the placebo group were significantly lower compared with day 0, and there were significant differences in them between the two groups (%FBF: normal volunteers 30 +/- 12% vs 17 +/- 9%, p < 0.01; IHD patients 28 +/- 14% vs 17 +/- 8%, p < 0.01; %cGMP: normal volunteers 35 +/- 11% vs 8 +/- 5%, p < 0.01; IHD patients 38 +/- 10% vs 12 +/- 4%, p < 0.01, vitamin E group vs placebo group). In conclusion, the combination therapy with vitamin E is potentially a useful method to prevent the development of nitrate tolerance.
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PMID:[Randomized, double-blind, placebo-controlled study of supplemental vitamin E on attenuation of the development of nitrate tolerance]. 955 81

Lipid peroxidation contributes to myocardial reperfusion injury. The indenoindole H290/51, a lipid peroxidation inhibitor with balanced lipophilicity and a considerably higher antioxidative capacity than that of vitamin E, was tested for its myocardioprotective effect against reperfusion injury. Coronary-ligated pigs were subjected to 45 min of myocardial ischemia followed by 240 min of reperfusion. Starting five minutes prior to reperfusion, H290/51 (n = 6) or vehicle (n = 6) was retrogradely infused via a coronary vein for 30 min. The total dose of H290/51 was 1 microM in 300 ml fluid (10 ml/min). In addition to the hemodynamics, left ventricular (LV) wall segment shortening (%SS) was measured by sonomicrometry. The LV area at risk and infarct size were measured by means of Evans blue and triphenyl tetrazolium chloride staining. The hemodynamics did not change significantly during the study, and no differences were found between the two groups. In the H 290/51-treated pigs, %SS of the ischemic area recovered from 1.9% at the end of ischemia to 9.1% after 120 min (p < .05) and to 16.2% at 240 min (p < .01). There was no significant recovery in the vehicle group. The LV area at risk was approximately 20% of LV. Infarct size as a percentage of LV and of the area at risk was significantly smaller in the H290/51 group (9+/-3% and 46+/-11%) than in the control group (18+/-6%; p < .05 and 83+/-5%; p < .01). H290/51 effectively protected the myocardium at risk in the setting of myocardial ischemia followed by reperfusion. This effect was reflected by diminished infarct size and improved functional recovery.
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PMID:The lipid peroxidation inhibitor indenoindole H290/51 protects myocardium at risk of injury induced by ischemia-reperfusion. 958 2

Malondialdehyde (MDA)-modified and oxidized low density lipoproteins (LDL) have been demonstrated in atherosclerotic lesions. Elevated titers of autoimmune antibodies specific for MDA-modified LDL predicted the progression of carotid atherosclerosis and of myocardial infarction. Recently, elevated levels of MDA-modified LDL were detected in the plasma of patients with ischemic heart disease, whereas, elevated levels of oxidized LDL were detected in the plasma of patients with ischemic heart disease and of heart transplant patients with post-transplant cardiovascular disease. Although increased levels of autoimmune antibodies against oxidatively modified LDL and increased levels of oxidized LDL antigen appear to be associated with atherosclerotic cardiovascular disease, there is to date no direct proof of the causal role of oxidized LDL in atherothrombosis. However, the decreased risk of cardiovascular disease associated with the administration of antioxidants (e.g. vitamin E), estrogen supplementation and increased levels of high density lipoproteins (HDL) may, at least partially, be due to the inhibition of oxidation of LDL or to the reversal of the atherothrombotic effects of oxidized LDL.
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PMID:Oxidation of low density lipoproteins in the pathogenesis of atherosclerosis. 969 39

Several studies report that among the antioxidant agents used to reduce injury after myocardial ischemia/reperfusion, analogues of vitamin E (VE) seem to have a significant efficacy. Raxofelast is a potent antioxidant agent under investigation, structurally related to VE, having an excellent bioavailability and favourable physicochemical properties. We assessed raxofelast in a rat model of myocardial damage induced by 1 h of left coronary artery occlusion followed by 6 h of reperfusion. Myocardial ischemia/reperfusion produced: wide tissue necrosis (50.3+/-10.3%); membrane peroxidation, evaluated by assessing cardiac malondialdehyde (MAL) (87.8+/-15.8 nmol/g tissuev 9.53+/-2.4 nmol/g tissue) and plasma conjugated dienes (CD) (8.73+/-1.86 DeltaABS/mlv 1.61+/-0.45 DeltaABS/ml); endogenous antioxidant wasting [cardiac VE=23.5+/-10.2 nmol/g tissuev 61.4+/-13.4 nmol/g tissue, cardiac reduced glutatione (GSH)=2.15+/-1.23 micromol/g proteinv 7.34+/-0.92 micromol/g protein and cardiac superoxide dismutase (SOD)=8.9+/-4.1 U/mg proteinv 17. 5+/-4.2 U/mg protein]; depressed mean arterial blood pressure (MAP) (61.4+/-5.8 mmHgv 85.3+/-6.2 mmHg); heart rate (HR) (275+/-35 beats/minv 368+/-34 beats/min) and left-ventricular derivative developed force (LV dP/dtmax) (1050+/-187 mmHg/sv 2520+/-194 mmHg/s); and cardiac neutrophil accumulation, evaluated by assessing cardiac myeloperoxidase (MPO) (9.23+/-2.1 U/g tissuev 0.92+/-0.12 U/g tissue). Administration of raxofelast (25, 50 and 100 mg/kg i.p. 5 min after occlusion) limited myocardial necrosis (22.3+/-14.8%P<0. 005, following the highest dose), reduced lipid peroxidation (MAL=43. 5+/-14.7 nmol/g tissueP<0.001 and CD=4.01+/-2.21 DeltaABS/mlP<0.001, following the highest dose), restored the endogenous antioxidants VE (52.8+/-14.2 nmol/g tissueP<0.001, following the highest dose), SOD (14.2+/-2.7 U/mg proteinP<0.001, following the highest dose) and GSH (4.92+/-1.33 micromol/g proteinP<0.005, following the highest dose), improved hemodynamic parameters (MAP=68.1+/-5.3 mmHgP<0.05, HR=317+/-27 beats/minP<0.05, LV dP/dtmax=1427+/-143 mmHg/sP<0.05, following the highest dose) and reduced myocardial neutrophil infiltration (MPO=5.1+/-1.5 U/g tissueP<0.001, following the highest dose). These data suggest that raxofelast could be considered a useful drug to reduce myocardial infarction.
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PMID:Beneficial effect of raxofelast, an hydrophilic vitamin E analogue, in the rat heart after ischemia and reperfusion injury. 973 36

Alpha-tocopherol (vitamin E) may play a role in the treatment of arterial thromboembolic disease, possibly by inhibiting platelet aggregation. Thus far, no clinical evidence exists for this effect. The objective of this study was to assess the effect of alpha-tocopherol supplementation on gingival bleeding either in combination with acetylsalicylic acid (ASA) or without it. This study was an end-point examination of a random sample of male smokers who had participated in a controlled clinical trial, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) for 5-7 years. The study included 409 men aged 55-74 years of whom 191 received alpha-tocopherol supplementation (50 mg/day); 56 used ASA, 30 received both and 132 received neither. Gingival bleeding was examined by probing with a WHO probe and reported as a percentage of bleeding sites adjusted by the logistic regression model. Gingival bleeding was more common in those who received alpha-tocopherol compared with nonreceivers among subjects with a high prevalence of dental plaque (P < 0.05). ASA alone increased bleeding only slightly. The highest risk of gingival bleeding was among those who took both alpha-tocopherol and ASA (33.4% of probed sites bleeding vs 25.8% among subjects taking neither alpha-tocopherol nor ASA, P < 0.001). In the ATBC Study, more deaths from haemorrhagic stroke and fewer from ischaemic heart disease were observed among those participants who received alpha-tocopherol compared with those who did not. Based on the results of the present study and the ATBC Study, we conclude that alpha-tocopherol supplementation may increase the risk of clinically important bleedings, particularly when combined with ASA.
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PMID:Increased tendency towards gingival bleeding caused by joint effect of alpha-tocopherol supplementation and acetylsalicylic acid. 992 Mar 56

Autoantibodies against oxidized low density lipoprotein (oxLDL) have been proposed to be independent predictors of atherosclerotic vascular disease. Because the levels of autoantibodies against oxLDL and cardiolipin might be modified by the presentation and severity of coronary heart disease (CHD), we measured their levels in patients with different manifestations of CHD (n=415, mean age 61 years, range 33 to 74 years) in a subset of the European Action on Secondary Prevention through Intervention to Reduce Events (EUROASPIRE) study. There were 109 patients with coronary artery bypass surgery, 106 patients with balloon angioplasty, 101 patients with acute myocardial infarction, and 99 patients with acute myocardial ischemia. Autoantibodies were measured by ELISA. Food records and fatty acid profiles of serum cholesteryl esters were used to evaluate dietary intake. Anti-oxLDL antibodies were significantly higher in the group with acute myocardial infarction than in other groups in men (coronary artery bypass surgery 1.91+/-1. 41, balloon angioplasty 2.11+/-2.19, acute myocardial infarction 2. 52+/-2.05, and acute myocardial ischemia 1.96+/-1.78; P=0.022, mean+/-SD) but not in women. The titers of anti-cardiolipin antibodies did not differ among the patient groups. Neither of the autoantibodies was associated with recurrent coronary events. Anti-oxLDL and anti-cardiolipin autoantibodies were not correlated with serum total cholesterol, high density lipoprotein cholesterol, or triglycerides, except that in women anti-oxLDL antibodies and triglycerides were positively correlated (r=0.225, P=0.011). In men, anti-cardiolipin antibodies were higher in the lowest quartiles of dietary intakes of vitamin E and polyunsaturated fat. Dietary intakes of vitamin E and polyunsaturated fat were correlated (r=0. 588, P<0.001). In conclusion, autoantibodies against oxLDL were associated with myocardial infarction in men. Anti-cardiolipin autoantibodies were inversely correlated with dietary intakes of vitamin E and polyunsaturated fat in men with CHD.
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PMID:Autoantibodies against oxidized low-density lipoprotein and cardiolipin in patients with coronary heart disease. 1063 19

In the 80's, three retrospective studies showed an inverse relation between fish consumption and ischemic heart disease (IHD) mortality. In parallel, fish fats containing the polyunsaturated fatty acid eicosapentaenoic (EPA) were shown to impair platelet aggregation and thromboxane formation. The results of the large prospective Diet and Reinfarction (DART) Study in the secondary prevention of myocardial infarction have further supported the possibility of potential interrelationships between diet and thrombogenic factors with respect to IHD. More recently these concepts have been confirmed and extended in the prospective Lyon Heart Study. However, in the latter in addition to changes in the content of EPA, changes in other well known variables (i.e. leukocytes and vitamin E) often abnormal in subjects prone to arterial thrombosis have been found. From studies on polygenic disorders, we have learned that by lowering the threshold and becoming a susceptibility gene, a polymorphism can lead to an effect assuming that it is present in the appropriate milieu. Nutrients have been shown to affect major determinants of myocardial ischemia such as fibrinogen or factor VII. However, the extent to what these and other hemostatic variables have been affected in studies devoted to dietary prevention of ischemia remains presently elusive.
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PMID:Nutrition and thrombogenic factors. 1071 34


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